Rickettsia chlamydia presentation


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Rickettsia chlamydia presentation

  2. 2. Introduction. • Rickettsiae and Chlamydiae- obligate intracellular organisms.(classif. as bacteria) • Rickettsia General features: -parasites of gut cells of athropods. -transmittion- athropod to animal.
  3. 3. Genera of the Family Rickettsiaceae: 1.Rickettsia -11 spp (do not multiply within vacuoles & do not parasitize wbcs. 2. Ehrlichia: - 2 spp obligate intracellular parasites – do not multiply within vacuoles but do parasitize wbcs.
  4. 4. Rickettsia. • 3. Coxiella: – (1 spp) obligate parasite –grows preferentially in vacuoles of host cells. • 4. Baartonella – 3 spp - intracellular parasite which attacks the rbc.
  5. 5. Fundamental differences btn Chlamydiae and rickettsiae. Rickettsiae Chlamydiae Cytochromes +ve No cytochromes Aerobic metabolism Anaerobic metabolism. Multiply by binary fision. Single development cycle.
  6. 6. Similarities Small, pleomorphic coccobacillary forms Obligate intracellular parasites. All contain DNA and RNA. Susceptible to various antibiotics. Cell walls resemble those of Gram –ve bacteria. Require exogenous cofactors from animal cells. Most grow readily in the yolk sac of embryonated eggs and in cell cultures.
  7. 7. Structure of Rickettsia. • Typical rickettsia – Very similar to that of gram-negative bacteria. • Typical envelope: – Innermost cytoplasmic membrane, a thin electron dense rigid cell wall & outer layer • Cell wall – Chemically similar to Gram-ve bacteria i.e contains diamino pimelic acid and no techoic acid. • No discrete nuclear structure.
  8. 8. Metabolism In dil.buffered salt soln: – Unstable, losing both metabolic activity and infectivity for animal cell. In enriched medium: – Can survive for may hrs. Basis for obligate parasitism: – Require rich cytoplasm to stabilize unusually permeable cell membrane. Require exogenous supply of cofactors.
  9. 9. Growth and Multiplication. Transverse binary fission. Under poor nutrition: long filamentous forms. Immediately after division: – Extensive movements through the cytoplasm of the cell. NB: C.burnetii: – Enclosed in a persistent vacuole during growth and division. 6-10 daughter cells form within the host cell before ruptures and releases them.
  10. 10. Host defenses • Both Cellular and Humoral immunity may be important.
  11. 11. Epidemiology • Endemic (murine) typhus: – primarily maintained in rodent populations. – transmitted via the flea. – Humans ( accidental host). • Spotted fever: – Found predominantly in animals. – Transmitted by the tick. – Humans (accidental hosts). • Q fever: – Mostly in animals. – Humans acquire disease primarily by inhalation of contaminated aerosols. • Epidemic typhus and trench fever: – transmitted from human to human via the louse.
  12. 12. Pathogenicity – Transmittion: via arthropod vectors; • Q fever : – via inhalation or ingestion of contaminated milk or food. • The bacteria enter host endothelial cells via an induced phagocytosis. – Phospholipase A may help in penetration. • Replication of the bacteria causes lysis of the host cell and consequent spread to other cells. • Initial replication: – At the site of entry producing a local lesion. – Followed by dissemination via the vascular system producing vasculitis and a skin rash.
  13. 13. Pathogenesis... – The lesions may become necrotic • Virulence : – Probably due to many factors including: • release of endotoxin, • production of immune complexes • hypersensitivity reactions. • A characteristic triad of symptoms include: – fever, – headache and – rash (no rash with Q fever).
  14. 14. Diagnosis. • Clinical: • These diseases present as: – febrile illnesses after exposure to arthropods or animal hosts or aerosols ( endemic areas). – High mortality from Spotted fever (delayed diagnosis). • The spread of the rash ( characteristic): – spread from the trunk to the extremities (centrifugal)- typical for typhus; – spread from the extremities to the trunk (centripetal) -typical for spotted fever.
  15. 15. Diagnosis… Laboratory: 1. Macchiavello stain: - organisms bright red V blue background. 1. Castaneda stain: - blue organisms V red background. 1. Giemsa stain: - bluish purple organisms. 4. Use of immunofluorescent antibodies: NB: The organism can be inoculated into tissue culture and grown over 4-7 days (very hazardous to personnel).
  16. 16. Diagnosis… Confirmative diagnosis: • Serological reaction:(Weil-Felix test): – The production of serum antibody reactive against Proteus OX19, OX2 or OXK antigens is determined • Embryonated eggs. – (Q- Fever) • Cell cultures.
  17. 17. Important Rickettsial diseases of animals Heartwater: Tropical canine Pancytopenia. Equine and Canine Ehrlichiosis. Q- Fever Potomac horse Fever. Salmon poisoning.
  18. 18. Rickettsia of Public health significance Tick-borne:- • Rocky mountain spotted fever (R.rickettsii) – Reservoir (Dog, rodents) • Q-Fever (C. burnetii) – Reservoir (cattle, shoat) • Spotted Fever (R.rhipicephali) – Reservoir (dogs) • Ehrlichiosis (E.canis) – Reservoir (dogs)
  19. 19. Public health… Louse-borne: 1. European epidemic typhus (R.prowazekii) -No animal reservoir 1. Trench Fever (Bartonella) - No animal reservoir. Flea-borne: 1. Endemic murine typhus (R.typhi) -Reservoir- Wild rodents
  20. 20. Public health…. 2.Cat scratch fever/bacillary angiomatosis (Bartonella henselae) Reservoir (domestic cat) Mite-borne: • Scrub typhus(R. tsutsugamushi)reservoir- wild rodents. • Rickettsialpox (r.akari) reservoir House mice. Fly-borne: • Oroyo fever/ Verruga peruana (B. bacilliformis) Reservoir ??
  21. 21. Treatment & Control • Chemotherapeutic: – Tetracycline or – Chloramphenicol • Sanitary: – Arthropod and rodent control are possible but difficult. • Immunological: – No vaccines - currently available.
  22. 22. Chlamydia General characteristics • Species: trachomatis, psittaci • The Chlamydia – Obligate intracellular parasites. • C. trachomatis – Trachoma, – Inclusion conjunctivitis, – Lymphogranuloma venereum (LGV) – nongonococcal urethritis (NGU). I.e, oculourogenital infections. • C. psittaci produces systemic diseases: – psittacosis, – ornithosis and – pneumonitis.
  23. 23. Distinctive properties. • Have two distinct forms:- – Infectious elementary bodies and – Intracellular reticulate bodies. • Elementary bodies attach and are internalized by susceptible host cells. • Once inside, they reorganize into a replicative form (the reticulate body) • Over a 24 hour period: – Reticulate bodies divide and begin to reorganize back into elementary bodies.
  24. 24. Distinctive properties… • 48-72 hours after infection: – The cell is lysed and – numerous infectious elementary bodies released. • The genome of Chlamydia is only 25% the size of E. coli (i.e one of the smallest prokaryotes). • The pathogenic mechanisms employed by Chlamydia - not well understood.
  25. 25. Growth and multiplication.
  26. 26. Metabolism. • No detectable flavoproteins or cytochrome. • Basis of obligate intracelluar parasitism – lack of ATP-generating ability – Obtain ATP from the host cell. • The cells can synthesize : – DNA – RNA and – Protein.
  27. 27. Pathogenesis. • C. psittaci is acquired from infected birds, usually via the respiratory route. • C. trachomatis is spread via the fingers to the urogenital area and vis versa. • Trachoma: – Infection of the epithelial cells of the conjunctiva, producing inclusion bodies. – Vascularization and clouding of cornea along with trichiasis (inward growth of eyelashes) ---- produce scarring leading to blindness.
  28. 28. Pathogenesis…. • Inclusion conjunctivitis – Milder form, – Occurs in both children and adults. • Sexually transmitted nongonococcal urethritis (NGU): – Similar to gonorrhea – Occurs with greater frequency. • Lymphogranuloma venereum (LGV) involving inguinal lymphadenopathy ("buboes") can occur in men
  29. 29. Host defenses. • Chlamydia induce interferon and are sensitive to it. • During infection, antibodies are synthesized but recovery is not generally protective.
  30. 30. Epidemiology. • Trachoma: – prevalent in Africa and Asia, – generally in hot and dry areas. • The organisms are very persistent. – Their habitat : similar to that of Neisseria and Haemophilus. • Infection can occur via: – swimming in unchlorinated pools, – sharing towels or – by passage through the birth canal.
  31. 31. Diagnosis • Clinical: – Diagnosis of trachoma is usually good. – Genital vesicles associated with LGV are characteristic. – NGU can only be suspected in the absence of laboratory findings. • Laboratory: – Iodine stained specimens usually show inclusion bodies. • Tissue culture: – Chlamydia can be cultured in tissue culture and appropriate serological tests performed
  32. 32. Diagnosis Serological diagnosis: • Micro-immunofluorescent tests in tears of patients with eye infections for presence of anti-chlamydia Ab. • Delayed –type skin rexn (hypersensitivity Type IV) (Frei-test) • Rising titer of Ab V chlamydial family Ag in lung infections.
  33. 33. Treatment and Control. • Chlamydia exhibit low pathogenicity in a compromised host. • Chemotherapeutic: – Tetracycline or erythromycin are drugs of choice. • Sanitary: – Good hygiene, – Treatment of sexual partners and – Quarantine of birds all reduce the incidence.
  34. 34. Treatment and control. • Immunological: – No vaccine – available since specific antibodies fail to neutralize elementary bodies in vivo. NB: • Chlamydial d’ses –relatively easy to treat, but: 1.Latency of infection 2.Susceptibility to reinfection.
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