RICKETTSIACEAE

1. RICKETTSIACEAE DR VIDYA PAI 23-02-15

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4. RICKETTSIACEAE

5. General features • Gram negative bacilli • Obligate intracellular parasitism • Primarily infect arthropods • Transmitted to humans by vectors • In humans infect vascular endothelium • Howard Taylor Ricketts 1906 • Genera- Rickettsia, Orientia, Ehrlichia • (Coxiella, Rochalimaea)

6. General features contd….. • Pleomorphiccoccobacilli • 0.3-0.6by 0.8-2 micron in size • Gram stain not very useful, stain light(G –ve) • Giemsa, Casteneda- bluish purple • Machiavello, Giminez- deep red • Do not grow in culture media. • Yolk sac of chick embryo, HeLa and Hep-2 cell lines- primary isolation • Animal inoculation- Guinea pigs, Mice

7. Replication

8. Classification • Genus Rickettsia- 2 groups of diseases : TUPHUS FEVER, SPOTTED FEVER • Genus Orientia– Scrub typhus • Genus Ehrlichia- Ehrlichiosis

10. Others

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13. Epidemic typhus • Worldwide but common in Russia and East Europe. • 1917-1922- Napolean retreat • 25 million cases & 3 mil.deaths • Socialism Vs Louse • Von Prowazek • Humans- the only natural vertebrate host • Vector- Pediculushumanuscorporis • Incubation period: 5-15 days • Clinical features: fever with chills, skin rash 4th- 5th day(trunk-limbs sparing face, palm, soles); 2nd wk-stupor, delirium.

14. Pathogenesis of typhus fever • Source of infection: Infected patient • Mode of infection: Body louse feces rubbed onto abrasions on skin. • Louse feeds on infected patient Rickettsiae multiply in GIT of the insect & appear in feces in 3-5 days. Louse may be transferred to another person Lice defecate while feeding and when louse feces is rubbed through minute abrasions caused by scratching.( aerosol inhalation/ conjunctiva- dried louse feces) Rickettsemia. • TYPHUS= dhupa (Sanskrit)/ typhos(cloud). • CFR= 40% • Recovery-? Latency in lymphoid tissue ----Recrudescent typhus

15. Brill-Zinsser disease • Reactivation of latent/dormant R. prowazekii • Rickettsiae can remain without louse as reservoir.

16. Endemic typhus ----R.typhi/R. mooseri • Fleaborne typhus • Vector-Xenopsyllacheopis • Humans acquire through - Bite of infected flea • Mild disease • No man to man transmission • Worldwide- KASHMIR in India. • Neill Mooser reaction- Tunica reaction to differentiate epidemic from endemic typhus. Male guinea pigs – intraperitoneal inoculation with blood from rickettsemic patient- inflammatory adhesions between the layers of tunica vaginalis- testes cannot be pushed into the abdomen.

18. Tick Typhus • Rocky mountain spotted fever • Siberian tick typhus • Indian tick typhus • R. rickettsii- the first insect transmitted bacterial pathogen to be recognised • Transovarially transmitted in ticks(reservoirs) • RMSF- Dermacentorandersoni, Most serious spotted fever • North and South America • Boutonneuse fever in the mediterranean - Conor • India - Himalayas – Megaw 1917 Ripicephalussanguineus

21. SCRUB TYPHUS • Orientiatsutsugamushi • East Asia, Korea to Indonesia, Australia • Mite larvae (chiggers) • Zoonotic tetrad (Agent. Chiggers, rats, vegetation ) • Tsutsuga= dangerous • Mushi= mite

22. Ehrlichia • Affinity to blood cells • Mulberry like clusters ( morula ) inside the infected cell • Anaplasma/ Cowdria • Tick borne infections of cattle and sheep

23. Types of Ehrlichiosis • E. sennetsu – Sennetsu fever ( lymphoid hyperplasia • E. chaffeensis – Human monocyticehrlichiosis • E. equi - Human granulocytic ehrlichiosis

24. Diagnosis Microscopy Serological Tests (Weil-Felix reaction, ELISA, IF, – Paired sera to be tested. Molecular methods – PCR. Isolation of Rickettsiae – HeLa, Vero cell lines, Chick embryo

25. WEIL FELIX TEST

26. Coxiellaburnetii • Coxiella burnetti is the causative agent of ‘Q-fever’ • Obligate intracellular, gram negative bacterium • Distributed globally • Found in many species of animals

27. Morphology • obligate intracellular pathogen . • gram negative . • Pleomorphic . • size : rods:- 0.2 – 0.4 x 0.4 – 1.0 mc spheres :- 0.3 – 0.4 mc • filterable . • better stained with GIMINEZ and other rickettsiael stains .

28. Culture • Grows well in yolk sac of chick embryos and in various cell cultures .

29. Resistance • Resistant to physical and chemical agents • In pasteurization flash method is effective • Can survive in dust and aerosols • Inactivated by 2% formaldehyde 5% H2O2 1% Lysol .

30. Contd…. • Resistant to heat, drying and disinfectants • Air samples test positive for 2+ weeks • Soil samples test positive for 150+ days

31. History A ZOONOTIC DISEASE • Q stands for Query or Queensland • Origin of disease unknown • First reported cases were in Queensland, Australia

32. Differentiating features from Rickettsiae: 1. Having smaller size 2. Resistance to heat and drying 3. Major route of transmission is- inhalation/ingestion

33. Primary Reservoir -? Bandicoots Goats Cattle Sheep * All eukaryotes can be infected TICKS

34. Bacteria is excreted in: Feces Urine Milk of infected animals

35. Do not touch! Release Into Environment:- • During birthing the organisms are shed in high numbersin amniotic fluids and the placenta • 109 bacteria per gram of placenta

36. Transmission • Most common route is inhalation of aerosols • Consumption of raw • Contaminated dust, manure, birthing products • Tick bites (rare) • Human to human also very rare gsbs.utmb.edu

37. Transmission • Person-to-person (rare) • Transplacental (congenital) • Blood transfusions • Bone marrow transplants • Intradermal inoculation • Possibly sexually transmitted Center for Food Security and Public Health Iowa State University - 2004

38. Who’s at risk? • Farmers, veterinarians, researchers, abattoir (slaughterhouse) workers etc. • People who breed animals • Immunocompromised

39. Acute or Chronic Q fever gsbs.utmb.edu *Bacteria spread through blood

40. Acute Q fever Symptoms : • Asymptomatic • Self-limiting, flu-like disease • Fever, nausea, headaches, vomiting, chest/abdominal pain • Pneumonia & granulomatous hepatitis

41. Chronic Q fever (> 6 months) • Endocarditis & meningoencephalitis • Hepatitis • Spontaneous recovery

42. complications Bacteria may remain latent in tissues for 2-3 years • Hepatitis • Endocarditis • Cirrhosis

43. Host interaction Entry via inhalation Alveolar macrophages encounter bacteria C. burnetii phagocytosed Macrophage C. burnetii R Heinzen, NIAID

44. Host interaction • Replication within phagolysosme • Low pH needed for metabolism • No cellular damage unless lysis occurs • Can invade deeper tissue and cause complications

45. Phagocytosis • Binding/entry into macrophages via: • Integrin Associated Protein (IAP) • Leukocyte Response Integrin (LRI) bacteria macrophage

46. Phagocytosis Phagocytic vesicle Phago-lysosome fusion: bacteria survive and multiplies Lysis of phago-lysosome and macrophage Binding & Entry

47. LAB DIAGNOSISHard to diagnose because: Asymptomatic in most cases Looks like other disease (Flu or cold) Serology continues to be best method PCR, ELISA and other methods WEIL – FELIX test is negative .

48. Contd….. • Bio safety level 3 (BSL-3) facility • Very infectious (one organism causes infection) • Listed by the CDC as a potential bioterrorism agent. • Isolated in cell cultures or embryonated eggs

49. Treatment • Once infected, humans can have life-long immunity • Acute Q fever treated with: doxycycline, chloramphenicol, erythromycin or fluoroquinolones • Chronic Q fever treated with: More than one antibiotic tetracycline and cotrimoxazole for 2 years

50. Vaccines :- • prepared from formalin killed whole cells attenuated strains trichloroacetic acid extracts NOT FOR GENERAL USE.