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RICKETTSIA
Dr. Punit Jhandai
Veterinary Public Health
Department
LUVAS(125004), Hisar RICKETTSIA INSIDE
THE ENDOTHELIAL
CELLS
Introduction
• Obligate intracellular parasite.
• Gram negative
• Parasite of arthropods – fleas, lice, ticks and mites.
• No Human to human transmission.
• Despite the similar name, Rickettsia bacteria do not cause
rickets, which is a result of vitamin D deficiency.
• In the past, positioned somewhere between viruses and
true bacteria.
Introduction
• Pleomorphic coccobacilli
• Non Motile, Non Capsulated.
• Stain bluish purple with Giemsa and deep red with
Machiavello.
• Optimum temp for growth 32-35°C
• Generally occur in cytoplasm of infective cell but in
some case also occur in nucleus of cell.
• Readily inactivated by physical and chemical agents,
rapidly destroyed at 56°C
• Glutamate is key nutrient for rickettsia.
Pathogenesis
• 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 with partial or
complete occlusion of vascular lumen, lead to
rupture & necrosis.
• Overall pathological features of the rickettsial
diseases are similar as the cause acute febrile
illness, characterised by septicemia with
maculopaspular rash and fever.
Rickettsial species and its 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. akari – Rickettsial pox - Mites
EPIDEMIC TYPHUS (CLASSICAL TYPHUS)
Cause: Rickettsia prowazekii
Vector: Human body louse ( Pediculus humanus
corporis) Human head louse ( Pediculus humanus capitis)
Incubation period – 5-15 days
Mortality rate is 30-40% in untreated cases.
Symptoms- Severe headache, Chills , Generalised
myalgia, High fever ( 39-410C), Vomiting, Macular rash
after 4-7 days – first on trunk and spreads to limb.
Brill –Zinsser/ Recrudescent typhus
This occur after the person recovered from
epidemic typhus and reactivation of the rickettsia
prowazekii which remained latent for years.
ENDEMIC TYPHUS (MURINE TYPHUS)
Cause- R. typhi
Vector: Rat flea (Xenopsylla cheopis)
Reservoir: Rat
Infection occurs after rat flea bite
Rickettsia multiply in gut of flea and is shed in
feaces.
Spotted fever group
Rickettsiae of this group multiply in nucleus as well as
in the cytoplasm of the host.
Tick typhus- Transmit Transovarially in ticks, and
transmission to human being is primarily by bite.
Indian tick typhus- caused by R. conori
Vector- Rhipicephalus sanguineus
Rocky mountain spotted fever- Most serious form
Cause – R. rickettsii
Infection occurs after tick(Dermacentor andersoni) bite
Incubation period – 1 week
More similar to typhus fever but the rash appears earlier
and is more prominent.
Rickettsial pox- Mildest rickettsial
Diseases of human, self limiting,
Non fatal, resemble to chicken pox so
Known as vesicular rickettsiosis
Caused by R. akari and transmit by mite
(Mus musculus)
LABORATORY DIAGNOSIS
Direct Microscopy
Culture- Yolk sac of emryonated hens egg, male guinea
pig, cell tissue culture
Serological test- Weil Felix rxn, CFT, IFA, ELISA
LABORATORY DIAGNOSIS
• Isolation from experimental animals
Blood is inoculated 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)
This is known as Neil Mooser Rxn
Specimens: Blood – collected in febrile illness
Note: Rickettsia is highly infectious so specimens should be
handled very carefully.
Serology- Reliable test to confirm rickettsial diseases
Antibody detection by Weil-felix test
Antigen detection by IFA
Weil-felix test- Heterophile agglutination test using
non motile proteus strains (OX 19, OX 2, OX K)
to find rickettsial antibodies in patient’s serum.
Procedure:
1. 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.
2. Incubation at 370C for overnight.
3. Observe for agglutination
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)
IMMUNOFLUORESCENT ANTIBODY TECHNIQUE – UTILISES
FLUORESCENT ANTIBODY TO DETECT RICKETTSIAL
ANTIGEN IN INFECTED TISSUES
Treatment
Treatment should be started early in the first week
of illness.
Doxycycline (first choice)
Tetracycline (alternate)
PROPHYLAXIS
Vector control

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rickettsiabypunit-copy-170914153220.pdf

  • 1. RICKETTSIA Dr. Punit Jhandai Veterinary Public Health Department LUVAS(125004), Hisar RICKETTSIA INSIDE THE ENDOTHELIAL CELLS
  • 2. Introduction • Obligate intracellular parasite. • Gram negative • Parasite of arthropods – fleas, lice, ticks and mites. • No Human to human transmission. • Despite the similar name, Rickettsia bacteria do not cause rickets, which is a result of vitamin D deficiency. • In the past, positioned somewhere between viruses and true bacteria.
  • 3. Introduction • Pleomorphic coccobacilli • Non Motile, Non Capsulated. • Stain bluish purple with Giemsa and deep red with Machiavello. • Optimum temp for growth 32-35°C • Generally occur in cytoplasm of infective cell but in some case also occur in nucleus of cell. • Readily inactivated by physical and chemical agents, rapidly destroyed at 56°C • Glutamate is key nutrient for rickettsia.
  • 4.
  • 5. Pathogenesis • 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 with partial or complete occlusion of vascular lumen, lead to rupture & necrosis. • Overall pathological features of the rickettsial diseases are similar as the cause acute febrile illness, characterised by septicemia with maculopaspular rash and fever.
  • 6.
  • 7. Rickettsial species and its 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. akari – Rickettsial pox - Mites
  • 8. EPIDEMIC TYPHUS (CLASSICAL TYPHUS) Cause: Rickettsia prowazekii Vector: Human body louse ( Pediculus humanus corporis) Human head louse ( Pediculus humanus capitis) Incubation period – 5-15 days Mortality rate is 30-40% in untreated cases. Symptoms- Severe headache, Chills , Generalised myalgia, High fever ( 39-410C), Vomiting, Macular rash after 4-7 days – first on trunk and spreads to limb.
  • 9. Brill –Zinsser/ Recrudescent typhus This occur after the person recovered from epidemic typhus and reactivation of the rickettsia prowazekii which remained latent for years. ENDEMIC TYPHUS (MURINE TYPHUS) Cause- R. typhi Vector: Rat flea (Xenopsylla cheopis) Reservoir: Rat Infection occurs after rat flea bite Rickettsia multiply in gut of flea and is shed in feaces.
  • 10. Spotted fever group Rickettsiae of this group multiply in nucleus as well as in the cytoplasm of the host. Tick typhus- Transmit Transovarially in ticks, and transmission to human being is primarily by bite. Indian tick typhus- caused by R. conori Vector- Rhipicephalus sanguineus
  • 11. Rocky mountain spotted fever- Most serious form Cause – R. rickettsii Infection occurs after tick(Dermacentor andersoni) bite Incubation period – 1 week More similar to typhus fever but the rash appears earlier and is more prominent. Rickettsial pox- Mildest rickettsial Diseases of human, self limiting, Non fatal, resemble to chicken pox so Known as vesicular rickettsiosis Caused by R. akari and transmit by mite (Mus musculus)
  • 12.
  • 13. LABORATORY DIAGNOSIS Direct Microscopy Culture- Yolk sac of emryonated hens egg, male guinea pig, cell tissue culture Serological test- Weil Felix rxn, CFT, IFA, ELISA
  • 14. LABORATORY DIAGNOSIS • Isolation from experimental animals Blood is inoculated 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) This is known as Neil Mooser Rxn Specimens: Blood – collected in febrile illness Note: Rickettsia is highly infectious so specimens should be handled very carefully.
  • 15. Serology- Reliable test to confirm rickettsial diseases Antibody detection by Weil-felix test Antigen detection by IFA Weil-felix test- Heterophile agglutination test using non motile proteus strains (OX 19, OX 2, OX K) to find rickettsial antibodies in patient’s serum. Procedure: 1. 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. 2. Incubation at 370C for overnight. 3. Observe for agglutination
  • 16. 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)
  • 17. IMMUNOFLUORESCENT ANTIBODY TECHNIQUE – UTILISES FLUORESCENT ANTIBODY TO DETECT RICKETTSIAL ANTIGEN IN INFECTED TISSUES
  • 18. Treatment Treatment should be started early in the first week of illness. Doxycycline (first choice) Tetracycline (alternate) PROPHYLAXIS Vector control