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Rickettsiaceae
Dr.M.Malathi
Postgraduate
Department of Microbiology
Chengalpattu Medical College
Synopsis
• Genus Rickettsia
• Genus Orientia
• Genus Ehrlichia
----------------------------------------------------------------
• Genus Coxiella
• Genus Bartonella
Introduction
• Intracellular growth
• Transmitted by blood sucking arthropod
vectors
• Howard Taylor ricketts (1906) – Discovered
spotted fever rickettsia – died of typhus fever
contracted during his studies
Characteristics
• Small GNB
• Virus like , cannot be seen under ordinary light
microscope
• Obligate intracellular parasite
TYPHUS FEVER GROUP
• Epidemic typhus
• Recrudescent typhus (Brill Zinsser disease)
• Endemic typhus
Epidemic typhus
• Causative agent: R.prowazekii
• Vertebrate host : Humans
• Human body louse : Pediculus humanus
corporis
Lice
• Pathogenesis:
Lice become infected by feeding on
ricketssiaemic patients  multiply in the gut
of lice  appear in feces in 3 to 5 days 
infection transmitted from person to person
• When the contaminated louse feces is rubbed
through the minute abrasions caused by
scratching
• Occasionally by aersols of dried louse feces
through inhalation or through the conjuctiva
• Incubation period is 5 to 15 days
• Fever with chills
• Characteristic rash – 4th or 5th day
• Stuporous and delirious
• Case fatality – 40%
Eschar
Recrudescent typhus
• Latent infection in whom recovered from
epidemic typhus
• Reactivation
• Hence no extrahuman reservoir
Endemic typhus
• Causative agent: R. typhi
• Host: Rats, Humans
• Vector: Flea – Xenopsylla cheopsis
• Pathogenesis:
Rickettsia multiplies in the gut of the flea  shed in
faeces  humans
Flea
• Humans acquire the disease:
1. The bite of infected fleas, when their saliva or
feces is rubbed in
2. Through aerosols of dried feces
3. By ingesting food recently contaminated with
infected rat urine or flea feces
Human infection is a dead end
PERSON TO PERSON TRANSMISSION DOES NOT
OCCUR
SPOTTED FEVER GROUP
• Common soluble antigen
• Multiply in the nucleus as well as in the
cytoplasm of host cells
• All transmitted by ticks except R.akari (Mite
borne)
• Tick typhus
• Rickettsial pox
Tick typhus
• Transovarian transmission – in ticks – both
vector and reservoir
• Larval stage or adult ticks – infective form to
vertebrate hosts
• Transmitted to human by tick bite
Tick
• Rocky mountain spotted fever – most serious
type
• Causative agent : R.rickettsii
• Indian tick typhus – R.conori
• Tick: Rhipicephalus sanguineus
Rickettsial pox
• Self limited, non fatal, vesicular exanthem
• Similar to chicken pox
• Vesicular or varicelliform rickettsiosis
• Causative agent: R.akari
• Reservoir : Domestic mouse
• Vector : mite (Transovarial transmission)
Pathogenesis in humans
• Transmitted to humans by arthropod vectors
through bite or feces
• Ricketssaie multiply locally and enter the
blood
• Localised chiefly in the vascular endothelial
cells  thrombus formation  occlusion of
vascular lumen
• Clinical features : acute febrile illness,
septicemia with maculopapular rash and fever
• The long survival of rickettsiae in various
organs and lymphatic tissues in infected
humans and animals is a distinctive feature in
its pathogenesis.
Specimen
• Smears from infected tissues
• Blood
Morphology
• Pleomorphic coccobacilli
• Non motile , non capsulated
• 0.3 – 0.6 * 0.8 – 2 um
• Gram negative, but do not stain well
• Under electron microscope  three layered
cell wall
cultivation
• Unable to grow in cell free media
• Growth occurs in the cytoplasm of infected
cells
• Optimum temperature – 32 to 35deg C
• Cultivated in yolk sac of developing chick
embryos, also grow on HeLa, Hep-2, Detroit 6
continuous cell lines
Resistance
• Rapidly destroyed at 56degC
• Destroyed at room temp also
• Hence when seperated from host  preserve
in skimmed milk or a suspending medium
containing sucrose, potassium phosphate and
glutamate (SPG medium)
Antigenic structure
• Spotted fever rickettsiae  A, B proteins
• Third surface antigen  alkali stable
polysaccharide  found in some rickettsiae
and in some strains of the Proteus bacilli
Who am i?
Neil Mooser Reaction
• R.typhi and R.prowazekii – similar
• When male guinea pigs are inoculated
intraperitoneally with blood from a case of
endemic typhus or with a culture of R.typhi 
develop fever and characteristic scrotal
inflammation.
• Scrotum enlarged and testes cannot be pushed
back into the abdomen because of inflammatory
adhesions between the layers of the tunica
vaginalis
• Neil – Mooser or tunica reaction
GENUS ORIENTIA
SCRUB TYPHUS (CHIGGER BORNE TYPHUS):
• Causative agent: Orientia tsutsugamushi
• First observed in Japan
• Vector: trombiculid mites
• Mite islands
• Humans bitten by mite larvae (Chiggers)
• Transovarian transmission in mites
Trombiculid mite
• Zoonotic tetrad  O.tsutsugamushi, chiggers,
rats and secondary and transitional forms of
vegetation
• Incubation period – 1 to 3 weeks
• Characteristic Eschar, regional
lymphadenopathy and maculopapular rash
• Three antigenic types : Karp, Gilliam and Kato
GENUS EHRLICHIA
• Small, Gram negative, obligate intracellular
bacteria
• Tick borne
• Cytoplasm of infected phagocytic cells 
grow within phagosomes as mulberry like
clusters  Morula
• Pathogenicity: Three infections
1. Resembles glandular fever. Causative agent is
Ehrlichia sennetsu. Endemic in Japan. Causes
lymphoid hyperplasia and atypical
lymphocytosis. No arthropod vector. Human
infection is suspected to be caused by
ingestion of fish with flukes
• 2. Human monocytic ehrlichiosis – caused by
Ehrlichia chaffeensis. Transmitted by
Amblyomma ticks. Deer and rodents are
reservoir hosts. Human disease with
leukopenia, thrombocytopenia and elevated
liver enzymes
• 3. Human granulocytic ehrlichiosis – either
identical with or closely related to equine
pathogen Ehrlichia equi. Transmitted by ticks.
Deer, cattle and sheep are the suspected
reservoir. Leucopenia and thrombocytopenia
are seen in patients
• Treatment: Doxycline for ehrlichiosis
LABORATORY DIAGNOSIS OF
RICKETTSIAL DISEASES
Specimens
• Blood for culture
• Tissue for culture
• Serum for serological tests
Direct Microscopy
• Light microscope  cant see individual
organism, only aggregations of rickettsial
particles
• Giemsa stain  purple coloured basophilic
inclusions
• Machiavello stain  red coloured inclusions
• Immunofluorescence microscope  skin
biopsies from the centre of the petechial
lesions
Culture
• Yolk sac of embryonated hen`s eggs
• Male guinea pigs or mice
• Tissue culture
Serological test
Weil felix reaction:
• Agglutination test in which sera are tested for
agglutinins to the O antigens of certain non
motile Proteus strains OX 19, OX2, OX K
• Due to sharing of antigen by ricketssiae and
certain strain of proteus
• Tube agglutination test
Other serological tests
• Complement fixation test
• ELISA
• RIA
Molecular methods
• Polymerase chain reaction
TREATMENT
• Tetracycline
• Chloramphenicol
• Ciprofloxacin
GENUS COXIELLA
• Coxiella burnetii
• Causative agent of Q fever ( Query)
• Pleomorphic bacilli
• Obligate intracellular pathogen
• Differs from rickettsia by being
1. More resistant to heat
2. No vector
? ? ?
• Weil felix test cannot be used to diagnose
• Infection is from cattle , sheep and goats
• Zoonotic disease
• Bandicoot are the reservoir
• Transmitted to cattle by ixodid ticks
• Shed in milk of infected animals and
transmitted to humans
Pathogenicity
• Human disease characterised by interstitial
pneumonia
• Coxiella may remain latent in the tissues of
patients of 2 to 3 years
Laboratory diagnosis
• Blood for microscopy
• Culture and serum for serological test
• PCR
Treatment
• Tetracycline
• Macrolide antibiotics
GENUS BARTONELLA
• Tiny GNB
• Transmitted by arthropods
• Pathogenic strains
1. B.bacilliformis
2. B.quintana
3. B.henselae
Bartonella bacilliformis
• Oroya fever
• High mortality
• Late sequel  verruga peruana
• 1885 – Medical student  Daniel Carrion 
inoculated himself with material from verruga
and developed oroya fever and died
• Carrion`s disease
Bartonella quintana
• First world war  trench fever or five day
fever (Million of cases)
• No animal reservoir
• Transmitted by body louse
• Ability to grow in blood agar
Bartonella henselae
• Febrile illness with lymphadenopathy
following a cat scratch  Cat scratch disease
• Isolated from the blood of patients in blood
media after prolonged incubation
• Demonstrated in lymph node biospy smears
and sections by Warthin-Starry staining
• Associated with HIV infected and
immunodeficient personns
• Bacillary angiomatosis
THANK YOU………

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Ricketssiaceae

  • 2. Synopsis • Genus Rickettsia • Genus Orientia • Genus Ehrlichia ---------------------------------------------------------------- • Genus Coxiella • Genus Bartonella
  • 3. Introduction • Intracellular growth • Transmitted by blood sucking arthropod vectors • Howard Taylor ricketts (1906) – Discovered spotted fever rickettsia – died of typhus fever contracted during his studies
  • 4.
  • 5. Characteristics • Small GNB • Virus like , cannot be seen under ordinary light microscope • Obligate intracellular parasite
  • 6.
  • 7. TYPHUS FEVER GROUP • Epidemic typhus • Recrudescent typhus (Brill Zinsser disease) • Endemic typhus
  • 8. Epidemic typhus • Causative agent: R.prowazekii • Vertebrate host : Humans • Human body louse : Pediculus humanus corporis
  • 10. • Pathogenesis: Lice become infected by feeding on ricketssiaemic patients  multiply in the gut of lice  appear in feces in 3 to 5 days  infection transmitted from person to person • When the contaminated louse feces is rubbed through the minute abrasions caused by scratching • Occasionally by aersols of dried louse feces through inhalation or through the conjuctiva
  • 11. • Incubation period is 5 to 15 days • Fever with chills • Characteristic rash – 4th or 5th day • Stuporous and delirious • Case fatality – 40%
  • 13. Recrudescent typhus • Latent infection in whom recovered from epidemic typhus • Reactivation • Hence no extrahuman reservoir
  • 14. Endemic typhus • Causative agent: R. typhi • Host: Rats, Humans • Vector: Flea – Xenopsylla cheopsis • Pathogenesis: Rickettsia multiplies in the gut of the flea  shed in faeces  humans
  • 15. Flea
  • 16. • Humans acquire the disease: 1. The bite of infected fleas, when their saliva or feces is rubbed in 2. Through aerosols of dried feces 3. By ingesting food recently contaminated with infected rat urine or flea feces Human infection is a dead end PERSON TO PERSON TRANSMISSION DOES NOT OCCUR
  • 17. SPOTTED FEVER GROUP • Common soluble antigen • Multiply in the nucleus as well as in the cytoplasm of host cells • All transmitted by ticks except R.akari (Mite borne) • Tick typhus • Rickettsial pox
  • 18. Tick typhus • Transovarian transmission – in ticks – both vector and reservoir • Larval stage or adult ticks – infective form to vertebrate hosts • Transmitted to human by tick bite
  • 19. Tick
  • 20. • Rocky mountain spotted fever – most serious type • Causative agent : R.rickettsii • Indian tick typhus – R.conori • Tick: Rhipicephalus sanguineus
  • 21. Rickettsial pox • Self limited, non fatal, vesicular exanthem • Similar to chicken pox • Vesicular or varicelliform rickettsiosis • Causative agent: R.akari • Reservoir : Domestic mouse • Vector : mite (Transovarial transmission)
  • 22. Pathogenesis in humans • Transmitted to humans by arthropod vectors through bite or feces • Ricketssaie multiply locally and enter the blood • Localised chiefly in the vascular endothelial cells  thrombus formation  occlusion of vascular lumen
  • 23. • Clinical features : acute febrile illness, septicemia with maculopapular rash and fever • The long survival of rickettsiae in various organs and lymphatic tissues in infected humans and animals is a distinctive feature in its pathogenesis.
  • 24.
  • 25. Specimen • Smears from infected tissues • Blood
  • 26. Morphology • Pleomorphic coccobacilli • Non motile , non capsulated • 0.3 – 0.6 * 0.8 – 2 um • Gram negative, but do not stain well • Under electron microscope  three layered cell wall
  • 27. cultivation • Unable to grow in cell free media • Growth occurs in the cytoplasm of infected cells • Optimum temperature – 32 to 35deg C • Cultivated in yolk sac of developing chick embryos, also grow on HeLa, Hep-2, Detroit 6 continuous cell lines
  • 28. Resistance • Rapidly destroyed at 56degC • Destroyed at room temp also • Hence when seperated from host  preserve in skimmed milk or a suspending medium containing sucrose, potassium phosphate and glutamate (SPG medium)
  • 29. Antigenic structure • Spotted fever rickettsiae  A, B proteins • Third surface antigen  alkali stable polysaccharide  found in some rickettsiae and in some strains of the Proteus bacilli
  • 31. Neil Mooser Reaction • R.typhi and R.prowazekii – similar • When male guinea pigs are inoculated intraperitoneally with blood from a case of endemic typhus or with a culture of R.typhi  develop fever and characteristic scrotal inflammation. • Scrotum enlarged and testes cannot be pushed back into the abdomen because of inflammatory adhesions between the layers of the tunica vaginalis • Neil – Mooser or tunica reaction
  • 32.
  • 33. GENUS ORIENTIA SCRUB TYPHUS (CHIGGER BORNE TYPHUS): • Causative agent: Orientia tsutsugamushi • First observed in Japan • Vector: trombiculid mites • Mite islands • Humans bitten by mite larvae (Chiggers) • Transovarian transmission in mites
  • 35. • Zoonotic tetrad  O.tsutsugamushi, chiggers, rats and secondary and transitional forms of vegetation • Incubation period – 1 to 3 weeks • Characteristic Eschar, regional lymphadenopathy and maculopapular rash • Three antigenic types : Karp, Gilliam and Kato
  • 36.
  • 37. GENUS EHRLICHIA • Small, Gram negative, obligate intracellular bacteria • Tick borne • Cytoplasm of infected phagocytic cells  grow within phagosomes as mulberry like clusters  Morula
  • 38. • Pathogenicity: Three infections 1. Resembles glandular fever. Causative agent is Ehrlichia sennetsu. Endemic in Japan. Causes lymphoid hyperplasia and atypical lymphocytosis. No arthropod vector. Human infection is suspected to be caused by ingestion of fish with flukes
  • 39. • 2. Human monocytic ehrlichiosis – caused by Ehrlichia chaffeensis. Transmitted by Amblyomma ticks. Deer and rodents are reservoir hosts. Human disease with leukopenia, thrombocytopenia and elevated liver enzymes
  • 40. • 3. Human granulocytic ehrlichiosis – either identical with or closely related to equine pathogen Ehrlichia equi. Transmitted by ticks. Deer, cattle and sheep are the suspected reservoir. Leucopenia and thrombocytopenia are seen in patients • Treatment: Doxycline for ehrlichiosis
  • 42. Specimens • Blood for culture • Tissue for culture • Serum for serological tests
  • 43. Direct Microscopy • Light microscope  cant see individual organism, only aggregations of rickettsial particles • Giemsa stain  purple coloured basophilic inclusions • Machiavello stain  red coloured inclusions • Immunofluorescence microscope  skin biopsies from the centre of the petechial lesions
  • 44.
  • 45. Culture • Yolk sac of embryonated hen`s eggs • Male guinea pigs or mice • Tissue culture
  • 46. Serological test Weil felix reaction: • Agglutination test in which sera are tested for agglutinins to the O antigens of certain non motile Proteus strains OX 19, OX2, OX K • Due to sharing of antigen by ricketssiae and certain strain of proteus • Tube agglutination test
  • 47.
  • 48. Other serological tests • Complement fixation test • ELISA • RIA
  • 51.
  • 52. GENUS COXIELLA • Coxiella burnetii • Causative agent of Q fever ( Query) • Pleomorphic bacilli • Obligate intracellular pathogen • Differs from rickettsia by being 1. More resistant to heat 2. No vector
  • 53. ? ? ?
  • 54. • Weil felix test cannot be used to diagnose • Infection is from cattle , sheep and goats • Zoonotic disease • Bandicoot are the reservoir • Transmitted to cattle by ixodid ticks • Shed in milk of infected animals and transmitted to humans
  • 55. Pathogenicity • Human disease characterised by interstitial pneumonia • Coxiella may remain latent in the tissues of patients of 2 to 3 years
  • 56. Laboratory diagnosis • Blood for microscopy • Culture and serum for serological test • PCR
  • 58.
  • 59. GENUS BARTONELLA • Tiny GNB • Transmitted by arthropods • Pathogenic strains 1. B.bacilliformis 2. B.quintana 3. B.henselae
  • 60. Bartonella bacilliformis • Oroya fever • High mortality • Late sequel  verruga peruana • 1885 – Medical student  Daniel Carrion  inoculated himself with material from verruga and developed oroya fever and died • Carrion`s disease
  • 61. Bartonella quintana • First world war  trench fever or five day fever (Million of cases) • No animal reservoir • Transmitted by body louse • Ability to grow in blood agar
  • 62. Bartonella henselae • Febrile illness with lymphadenopathy following a cat scratch  Cat scratch disease • Isolated from the blood of patients in blood media after prolonged incubation • Demonstrated in lymph node biospy smears and sections by Warthin-Starry staining
  • 63. • Associated with HIV infected and immunodeficient personns • Bacillary angiomatosis
  • 64.