Rickettsiae

lecture for MBBS students
Rickettsia named after HOWARD
TAYLOR RICKETTS died of Typhus fever contracted during his studies
Discovered spotted fever rickettsia (1906)
Obligate intracellular parasite
Gram negative pleomorphic rods
Parasite of arthropods – fleas, lice, ticks and mites.
No Human to human transmission.
Rickettsia are 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

1. Dr. Anil Kumar
Associate Professor
Microbiology.

2. Morphology
They are gram 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 named after 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 and itsdisease
•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. GENERALPATHOGENESIS
•Rickettsia are
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.
RICKETTSIAINSIDE
THEENDOTHELIAL
CELLS

8. Rickettsialinfections-classification
•Typhus fevergroup
-Epidemic typhus/Brill-Zinssertyphus
-Endemictyphus
•Spotted fevergroup
-Rocky mountain spottedfever
-Siberian ticktyphus
-Boutonneusefever
-Australian ticktyphus
-Rickettsialpox

9. EPIDEMIC TYPHUS (CLASSICAL TYPHUS)
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 ( 39-41
0C)
•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 (Xenopsyllacheopis)
•Reservoir:Rat
•Infection occurs after rat fleabite

13. Spotted fevergroup
Rocky mountain 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 clinical symptoms 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. Rickettsialpox
•Benign febrile 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 heartfailure
•Multi-organfailure
•Deafness
•Disseminated intravascular coagulopathy(DIC)
•Myocarditis (inflammation of heartmuscle)
•Endocarditis (inflammation of heartlining)
•Glomerulonephritis (inflammation ofkidney)

18. LABORATORY DIAGNOSIS
•Isolation from experimental animals
•Serology
Specimens:
Blood –collected in febrile illness
Note: Rickettsia is highly infectious so
specimens should be handled very carefully.

19. ISOLATION
•Blood is inoculated in guinea pigs/mice.
•Observed on 3
rd –4
th 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 test to confirm rickettsialdiseases
•Antibody detection by Weil-felixtest
•Antigen detection by IFA

21. •Heterophile agglutination test 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 37
0
C for overnight.
•Observe for agglutination.
WEIL-FELIXTEST

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 should be 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. Diseasetransmission
Transmitted to humans and
rodents bythe 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 ,
•conjunctivalcongestion
•Regional lymphadenopathy
•Maculopapularrash
•Pneumonia
•Encephalitis

30. DIFFERENTIAL DIAGNOSIS
Should be differentiated from
1.Malaria
2.Arbovirus infections
3.Leptospirosis
4.Meningococcal disease
5.Typhoid
6.Infectious mononucleosis
7.Brucellosis
8.Toxoplasmosis

31. Investigation
Decreased lymphocyte count
Thrombocytopenia
Raised liver enzymes
Hypoalbuminemia and albuminuria
Features of organ failure

32. Diagnosis
Isolation or detection 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 PCR more 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 test using 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-Felix test (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 of scrub typhus is based upon
the geographical history, physical signs and
is confirmed by the rapid response to
specific chemotherapy

37. Treatment
Early treatment shows 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
Good general 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 antibiotics in mild cases
Injectables for seriously ill.
Emerging resistance to tetracycline

41. Case fatality rate is 10-60 %
Lab diagnosis is similar to ricketssial
diseases but mice is preferred
weilfelixis also important

42. Conclusion
1.Scrub typhus is 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. Q fever-cycle-Coxiella burnetii

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
◦Formalin killed 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. Thank you