Rickettsia are obligate intracellular bacteria that are transmitted to humans through arthropod bites such as ticks, lice, fleas, and mites. They infect endothelial cells and cause vasculitis. There are three main groups - epidemic typhus group, scrub typhus group, and spotted fever group. Rocky Mountain spotted fever is caused by Rickettsia rickettsii and transmitted by ticks. It presents with acute fever, rash, and potentially life-threatening complications if not treated promptly with doxycycline or chloramphenicol. Laboratory diagnosis involves serologic tests to detect antibodies. Prevention involves avoiding tick and insect bites.

1. Rickettsia
Dr Kamran Afzal
Asst 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 Rickettsia
Bacteria infect Blockade of small
vascular blood vessels
endothelium & skin rashes
Enter 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 Rickettsiae
Epidemic typhus group
R. prowazekii Epidemic typhus South America
and Africa
Recrudescent typhus Worldwide
Sporadic typhus United States
R. typhi Endemic Murine typhus Worldwide
Scrub typhus group
O. tsutsugamushi Scrub typhus Asia, northern
Australia
Spotted 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 bites
Removed multiple arthropods after jungle trips

33. The owner of the rats had been in hospital
with hepato-renal failure