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Rickettsiae
The document discusses rickettsial diseases caused by various genera such as Rickettsia, Orientia, and Ehrlichia, focusing on their morphology, transmission, symptoms, and diagnostic methods. It details specific infections like epidemic typhus, rocky mountain spotted fever, and scrub typhus, along with their vectors, clinical manifestations, and laboratory confirmation techniques. Treatment approaches, including antibiotics and the importance of early intervention, are also emphasized alongside preventive measures.
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Introduction by Dr. Anil Kumar, an Associate Professor in Microbiology.
Rickettsiae are gram-negative pleomorphic rods with muramic acid in cell walls, containing both DNA and RNA, visible under a microscope.
Discussion of Rickettsiae family, including Rickettsia, Orientia, Ehrlichia, and Coxiella, named after Howard Taylor Ricketts.
Rickettsiae are obligate intracellular parasites of arthropods like fleas and ticks, not transmitted human-to-human.
Rickettsial species associated with diseases: R. prowazekii (Epidemic typhus), R. typhi (Endemic typhus), R. rickettsii (Rocky Mountain spotted fever), etc.
Transmission mechanism to humans through arthropod bites, multiplication at the site, and localization in vascular endothelium.
Classification into groups: Typhus (Epidemic & Endemic) and Spotted fever.
Epidemic typhus, caused by R. prowazekii with a vector of human body louse, has a 20-30% mortality rate if untreated.
Reactivation of latent R. prowazekii in previously infected individuals resulting in mild illness.
Endemic typhus caused by R. typhi; vector is rat flea with rats as a reservoir.
Most serious spotted fever form caused by R. rickettsii; characterized by rash appearing earlier than in typhus.
Benign febrile illness caused by Liponyssoides sanguineus with self-limiting vesicular rash.
Potential complications include pneumonia, heart failure, multi-organ failure, and various inflammation issues.
Diagnosis methods include isolation and serological tests, clinical specimen handling is critical.
Serological tests using Weil-Felix test for antibody detection and other techniques for confirmation.
Early treatment with doxycycline preferred; vector control significant for prevention.
Causative agent Orientia tsutsugamushi; transmission through chiggers; diagnostic black eschar from bites.
Symptoms include fever and rash; diagnosis based on clinical signs and serological tests.
Treatment should be early and may include doxycycline; alternative antibiotics discussed.
Emphasizing the preventable and treatable nature of scrub typhus with quick clinical action.
Coxiella burnetii as causative agent in Q fever; global spread, transmission via inhalation of infected particles.
Suggested laboratory culture methods and potential treatment options against Q fever.
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Rickettsiae
- 1. Dr. Anil Kumar AssociateProfessor Microbiology.
- 2. Morphology They aregram negative pleomorphic rods Cell wall contains muramic acid Have both DNA and RNA Can be seen under light microscope Susceptible to antibiotics Held back by bacterial filters
- 3. Rickettsiae Family- Rickettsiaceae-four genera ◦ Rickettsia ◦ Orientia ◦ Ehrlichia ◦ Coxiella
- 4. Rickettsiae • Rickettsia namedafter HOWARD TAYLOR RICKETTS died of Typhus fever contracted during his studies • Discovered spotted fever rickettsia (1906)
- 5. • Obligate intracellular parasite •Gram negative pleomorphic rods • Parasite of arthropods – fleas, lice, ticks and mites. • No Human to human transmission. Rickettsia inside the host cell TICK FLEA LICE MITE
- 6. Rickettsial species andits disease • R. prowazekii – Epidemic typhus, Brill- Zinsser disease – Human body louse • R. typhi – Endemic typhus – Rat flea • R. rickettsii – Rocky-Mountain spotted fever-Ticks • R. conori – Boutonneuse fever - Ticks • R. australis – Australian tick typhus - Ticks • R. siberica – Siberian tick typhus - Ticks • R. akari – Rickettsial pox - Mites
- 7. GENERAL PATHOGENESIS • Rickettsiaare transmitted to humans by the bite of infected arthropod vector. • Multiply at the site of entry and enter the blood stream. • Localise in the vascular endothelial cells and multiply to cause thrombosis lead to rupture & necrosis. RICKETTSIA INSIDE THE ENDOTHELIAL CELLS
- 8. Rickettsial infections- classification •Typhus fever group - Epidemic typhus/Brill-Zinsser typhus - Endemic typhus • Spotted fever group - Rocky mountain spotted fever - Siberian tick typhus - Boutonneuse fever - Australian tick typhus - Rickettsial pox
- 9. EPIDEMIC TYPHUS (CLASSICALTYPHUS) Cause: Rickettsia prowazekii Vector: Human body louse ( Pediculus humanus corporis) Human head louse ( Pediculus humanus capitis) Incubation period – 5-21 days Mortality rate is 20-30% in untreated cases. LICE
- 10. SYMPTOMS • Severe headache •Chills • Generalised myalgia • High fever ( 39-410C) • Vomiting • Macular rash after 4-7 days – first on trunk and spreads to limb. • Lacks conciousness.
- 11. Brill –Zinsser/ Recrudescenttyphus • This occur after the person recovered from epidemic typhus and reactivation of the rickettsia prowazekii which remained latent for years. • Mild illness and low mortality rate.
- 12. ENDEMIC TYPHUS (MURINETYPHUS) • R. typhi • Vector: Rat flea (Xenopsylla cheopis) • Reservoir: Rat • Infection occurs after rat flea bite
- 13. Spotted fever group Rockymountain spotted fever •Most serious form •Cause – R. rickettsii •Infection occurs after tick bite •Incubation period – 1 week •More similar to typhus fever but the rash appears earlier and is more prominent.
- 15. • The clinicalsymptoms of other spotted fevers are very similar to Rocky mountain spotted fever Early (macular) rash on sole of foot. Late petechial rashes on palm and forearm.
- 16. Rickettsial pox • Benignfebrile illness with vesicular rash resembling chickenpox. • Vector: Liponyssoides sanguineus • Reservoir: Domestic mouse ( Mus musculus) • Self-limiting, non-fatal.
- 17. Complications of rickettsial diseases •Bronchopneumonia • Congestive heart failure • Multi-organ failure • Deafness • Disseminated intravascular coagulopathy (DIC) • Myocarditis (inflammation of heart muscle) • Endocarditis (inflammation of heart lining) • Glomerulonephritis (inflammation of kidney)
- 18. LABORATORY DIAGNOSIS • Isolationfrom experimental animals • Serology Specimens: Blood – collected in febrile illness Note: Rickettsia is highly infectious so specimens should be handled very carefully.
- 19. ISOLATION • Blood isinoculated in guinea pigs/mice. • Observed on 3rd – 4th week. • Animal responds to different rickettsial species can vary Symptoms: • Rise in temperature – all species. • Scrotal inflammation,swelling,necrosis – R.typhi, R.conori, R.akari ( except R.prowazekii)
- 20. Serology • Reliable testto confirm rickettsial diseases • Antibody detection by Weil-felix test • Antigen detection by IFA
- 21. • Heterophile agglutinationtest using non motile proteus strains (OX 19, OX 2, OX K) to find rickettsial antibodies in patient’s serum. Procedure: • Serum is diluted in three separate series of tubes followed by the addition of equal amount of OX19,OX2,OXK in 3 separate series of tubes. • Incubation at 370C for overnight. • Observe for agglutination. WEIL-FELIX TEST
- 22. INTERPRETATION OF WEIL-FELIX TEST •Strong Agglutination with OX 19 – means epidemic & endemic typhus. • Strong agglutination with OX 19 & OX 2 – means Spotted fever • Strong agglutination with OX K – Scrub typhus (Scrub typhus by Orientia tsutsugamushi (one of the rickettsial disease)
- 23. IMMUNOFLUORESCENT ANTIBODY TECHNIQUE– UTILISES FLUORESCENT ANTIBODY TO DETECT RICKETTSIAL ANTIGEN IN INFECTED TISSUES
- 24. Other Serological tests •Complement fixation test • Latex agglutination test • Enzyme immunoassay All tests uses rickettsial antigens only to detect rickettsial antibodies.
- 25. Treatment • Treatment shouldbe started early in the first week of illness. • Doxycycline (first choice) • Tetracycline (alternate)
- 26. PROPHYLAXIS • Vector control •Live vaccine & killed vaccine are available but not much effective
- 27. Scrub typhus • Orientiatsutsugamushi – causative agent • Formerly-R.tsutsugamushi -R.orientalis • Tsutsugam=dangerous • Mushi = insect /mite • It is a place disease • Found only in area with suitable climate plenty of moisture ,Japan, China, Australia,
- 28. Disease transmission Transmitted tohumans and rodents by the bite of infected larvae of the trombiculid mite Leptotrombidium deliense (“chiggers” also known as Chigger – borne typhus). The bite of the mite leaves a characteristic black eschar that is useful to the doctor for making the diagnosis.
- 29. Scrub typhus Symptoms : •fever , • headache , • conjunctival congestion • Regional lymphadenopathy • Maculo papular rash • Pneumonia • Encephalitis
- 30. DIFFERENTIAL DIAGNOSIS Shouldbe differentiated from 1. Malaria 2. Arbovirus infections 3. Leptospirosis 4. Meningococcal disease 5. Typhoid 6. Infectious mononucleosis 7. Brucellosis 8. Toxoplasmosis
- 31. Investigation Decreased lymphocytecount Thrombocytopenia Raised liver enzymes Hypoalbuminemia and albuminuria Features of organ failure
- 32. Diagnosis Isolation ordetection in clinical specimens. Serological tests: tool in the diagnosis. immunoflourescence is the test of choice. Latex agglutination, indirect haemagglutination, immunoperoxidase assay, ELISA and polymerase chain reaction (PCR) are other tests.
- 33. Nested PCRmore sensitive than the serological test - prolonged persistence of O. tsutsugamushi DNA in blood - despite clinical recovery . No current diagnostic test is sufficiently practical for use in rural areas.
- 34. Dipstick testusing a dot blot immunoassay format ◦ Accurate, rapid, easy to use, and relatively inexpensive. ◦ Best currently available test for diagnosis in rural areas. ◦ Not available commercially
- 35. Weil-Felix test Weil-Felixtest (W-F) using Proteus OXK strain is commercially available. Only 50% positivity during second week. Minimum positive titer is 1:80 or a four fold rise Awareness of the antigenic diversity of R. tsutsugamushi strains in a given area.
- 36. Diagnosis Diagnosis ofscrub typhus is based upon the geographical history, physical signs and is confirmed by the rapid response to specific chemotherapy
- 37. Treatment Early treatmentshows better outcomes and faster resolution than delayed treatment. Should be started mainly on clinical grounds. Tetracycline, 500 mgs, QID or doxycyclin 200 mgs, OD X 7 days is treatment of choice.
- 38. Supportive measures Goodgeneral care Fluid balance Antibiotics for secondary infections Management of Acute renal failure
- 39. Chloramphenicol, 500mgs,QID is an alternative. Poor response to conventional therapy: Rifampicin, 900 mgs per day for a week Favorable outcome with flouroquinolones . Azithromycin - proved more effective than doxycyclin in doxycyclin-susceptible and doxycyclin-resistant strains.
- 40. Oral antibioticsin mild cases Injectables for seriously ill. Emerging resistance to tetracycline
- 41. Case fatality rateis 10-60 % Lab diagnosis is similar to ricketssial diseases but mice is preferred weil felix is also important
- 42. Conclusion 1. Scrub typhusis preventable and treatable disease 2. Should be suspected in any PUO esp with exposure to vegetation 3. Early treatment is effective 4. Should not wait for lab results
- 43. Q (Query )Fever ◦ Widespread in India (first record from Gurkha troops in Dehradun 1940; 400 cases; Kalra and Taneja 1953) ◦ Coxiella burnetii ◦ Worldwide distribution ◦ Inhalation of dust from env of infected animals ◦ Fever, fatigue, pneumonitis, endocarditis, abortions& fetal death at term; similar disease in animals usually livestock ◦ Ticks, mammals ◦ No rash
- 44.
- 45. Lab 1.Culture - yolk sac of chicken embryo cell cultures 2. Serology – CFT,IFA 3. Isolation of Coxiella from blood, sputum and other clinical specimens possible. But not recommended due to laboratory infection
- 46. Vaccines ◦ Formalinkilled whole cells trichloro acetic acid extracts ◦ live attenuated vaccine Treatment : Doxycycline Endocardits : combination therapy ◦ Tetracycline +Co- trimoxazole ◦ Tetracycline+ Rifampicin
- 47. sis 1. Lymphnode biopsy-smear – staining with silver stains 2. Culture –chocolate agar and columbia agar with 5%sheep blood and tryptic soy agar – prolonged incubation
- 48.