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Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
Ricketssia
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Ricketssia

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  • 1. Rickettsia Dr Kamran AfzalAsst Prof Microbiology
  • 2. Rickettsia• General characteristics – Obligate intracellular organisms • Intracellular location varies – Rickettsiae replicate in cytoplasm • R. rickettsiae exception (replicate in nucleus) – Growth slow compared to bacteria – Small, cocco-bacillary bacteria
  • 3. Epidemiology• Transmission – Maintained in arthropods like ticks, lice, fleas and mites – Usually transmitted to human by bite of vector• Organism passed vertically in insect vectors – Trans-ovarially • Louse-borne typhus exception • Louse dies of its infection and does not transmit the organism to its offspring – Human to human transmission via louse• Man is an incidental host
  • 4. Pathogenesis• Rickettsiae infect endothelial cells in small blood vessels – Induced phagocytosis• Lysis of phagosome and entry into cytoplasm – Phospholipase• Replication• Release – Primary lesion is vasculitis
  • 5. Pathogenicity of RickettsiaBacteria infect Blockade of small vascular blood vessels endothelium & skin rashesEnter cells by Vasculitis & endocytosis Thrombosis Multiply Infection of within cell other cells Release of Host cell lysis rickettsia
  • 6. Immunity• Humoral and cell mediated immunity important for recovery – Antibody-opsonized bacteria are killed – CMI develops
  • 7. Clinical features• Early signs and symptoms – History of arthropod vector bite – Sudden fever, nausea, vomiting, severe headache, muscle pain, lack of appetite – The rash first appears 2-5 days – Most often it begins as small, flat, pink, non-itchy spots (macules) on the wrists, forearms, and ankles – These spots turn pale when pressure is applied and eventually become raised on the skin – Skin rashes due to vasculitis
  • 8. • Later Signs and Symptoms – Late (petechial) rash on palms, forearms and trunk – Abdominal pain, joint pains, diarrhea
  • 9. Lab Diagnosis• Indirect immunoflourescence assay (IFA)• ELISA and latex agglutination – Increased IgM titers by the end of the first week of illness – IgG do not appear until 7-10 days after the onset – IgG antibodies are more specific and reliable • other bacterial infections can also cause elevations in riskettsial IgM antibody titers• PCR can detect DNA of 5-10 rickettsiae present in a sample, more specific than antibody-based methods
  • 10. IFA reaction of a positive human Gimenez stain of tick serum hemolymph cells infected with on Rickettsia rickettsii grown in R. rickettsii chicken yolk sacs, 400X
  • 11. Groups of RickettsiaeEpidemic typhus group R. prowazekii Epidemic typhus South America and Africa Recrudescent typhus Worldwide Sporadic typhus United States R. typhi Endemic Murine typhus WorldwideScrub typhus group O. tsutsugamushi Scrub typhus Asia, northern AustraliaSpotted fever group R. rickettsii Rocky Mountain spotted fever Western hemisphere R. akari Rickettsialpox USA, former USSR
  • 12. Epidemic Typhus Group
  • 13. Epidemic Typhus Group• Epidemic typhus or louse-borne typhus – Rickettsia prowazekii – Lice• Endemic or Murine typhus – Rickettsia typhi – Rat Fleas
  • 14. Epidemic Typhus (louse-borne typhus)• Rickettsia prowazekii• Carried by the human body louse• It grows in the GI of the louse then enters as the feces of the louse enters the wound as you scratch the bite• Incubation period approximately 1 week• High fever lasting 2 weeks at least, followed by stupor and rash• Recovery may take months• High mortality if not treated• Complications – Myocarditis, stupor, delirium (Greek “typhos” = smoke)• Anne Frank died of Typhus
  • 15. • Laboratory Diagnosis (Rickettsia prowazekii) – Weil-Felix antibodies - not recommended – Isolation possible but dangerous – Serology • Indirect fluorescent Ab • Latex agglutination tests
  • 16. • Treatment, Prevention and Control – Tetracycline and chloramphenicol – Vaccine available for high risk populations – Louse control measures
  • 17. Endemic or Murine Typhus• Rickettsia typhi• Rodent is the host and is spread by fleas – No transovarian transmission – Normal cycle - rat to flea to rat• Less severe than epidemic typhus – Similar symptoms and treatment• Mortality less than 5 percent
  • 18. • Clinical Syndrome (Endemic or Murine typhus) – Incubation period 1 - 2 weeks – Sudden onset of fever, chills, headache and myalgia – Rash in most cases • Begins on trunk and spreads to extremities (centrifugal spread) – Mild disease - resolves even if untreated
  • 19. • Laboratory Diagnosis – Serology (R. typhi) • Indirect fluorescent antibody test
  • 20. • Treatment, Prevention and Control – Tetracycline and chloramphenicol – Control rodent reservoir
  • 21. Scrub Typhus Group
  • 22. Scrub Typhus• Orientia tsutsugamushi• Japanese “tsutsuga” = small and dangerous• “mushi” = creature• “Scrub” - associated with terrain with scrub vegetation• Vector - chiggers (mite larva)• Reservoir - chiggers and rats – Transovarian transmission – Normal cycle - rat to mite to rat• Humans are accidentally infected
  • 23. • Clinical Syndrome (Scrub Typhus) – Incubation period - 1 to 3 weeks – Sudden onset of fever, chills, headache and myalgia – Maculo-papular rash • Begins on trunk and spreads to extremities (centrifugal spread) – Mortality rates variable
  • 24. • Treatment, Prevention and Control• Tetracycline and chloramphenicol• Measures to avoid exposure to chiggers
  • 25. Spotted Fever Group
  • 26. Rocky Mountain Spotted Fever
  • 27. • Rocky Mountain Spotted Fever• Rickettsia rickettsii Fluorescent Ab staining Vector - Tick
  • 28. • Clinical diagnosis most important – Most common in spring and summer – More common in children <15 yrs – 2-6 days between tick bite and disease – Acute fever, headache, toxicity, myalgia, mental confusion – Rash especially on palms and soles which spreads to trunk (centripetal spread) – Different from scarlet fever • trunk to extremities (centrifugal spread)
  • 29. • Pathogenesis and Immunity – No known toxins or immunopathology – Destruction of cells • Leakage of blood into tissues (rash) • Organ and tissue damage – Humoral and cell mediated immunity important for recovery
  • 30. • Laboratory Diagnosis (R. rickettsii) – Initial diagnosis - clinical grounds – Fluorescent Ab test for Ag in punch biopsy – PCR based tests – Weil-Felix test - no longer recommended – Serology • Indirect fluorescent test for Ab • Latex agglutination test for Ab
  • 31. • Treatment, Prevention and Control – Tetracycline and chloramphenicol • Prompt treatment reduces morbidity and mortality – No vaccine – Prevention of tick bites • protective clothing, insect repellents – Prompt removal of ticks
  • 32. 35-years-old man 3-days H/O fever + chills + headache + vomiting 5 days ceftriaxone and anti- malarials - No response Recovered with doxycycline Multiple bitesRemoved multiple arthropods after jungle trips
  • 33. The owner of the rats had been in hospital with hepato-renal failure

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