1. RICKETTSIAL DISEASES
Dr. BHUWAN SHARMA
Asst. Professor (Grant Govt. Medical
College)
2. RICKETTSIAE
Rickettsiae
are obligate intracellular
gram negative parasites.
Most are zoonoses spread to humans
by arthropods (except Q fever).
3. Rickettsiae replicate within the
cytoplasm of endothelial cells and
smooth muscle cells of
capillaries, arterioles and small
arteries causing necrotizing
vasculitis.
Most are febrile infections with a
characteristic rash.
An ESCHAR, a black ulcerated
lesion may develop at the site of
inoculation
4. MORPHOLOGY
In smears from infected tissues, rickettsiae
appear as pleomorphic gram negative
coccobacilli
Non motile, Non capsulated
They stain bluish purple with Giemsa and
Castaneda stains
Unable to grow in cell free media
Growth generally occurs in the cytoplasm of
infected cells
5. DISEASES RICKETTSI INSECT MAMMALIAN
AL AGENT VECTOR RESERVOIR
TYPHUS GROUP
a) Epidemic R. prowazekii Louse Human
typhus
b) Murine R. typhi Flea Rodents
typhus
(Endemic typhus)
c) Scrub R. Mite Rodents
typhus tsutsugamushi
6. DISEASES RICKETTSI INSECT MAMMALIAN
AL AGENT VECTOR RESERVOIR
SPOTTED FEVER GROUP
a) Indian tick R. conorii Tick Rodent, Dog
typhus
b) Rocky R. rickettsii Tick Rodents, Dogs
mountain
spotted fever
c) Rickettsial R. akari Mite Mice
pox
7. DISEASES RICKETTSI INSECT MAMMALIA
AL AGENT VECTOR N
RESERVOIR
OTHERS
a) Q fever C. burnetti Nil Cattle,
sheep,goats
b) Trench Rochalimaea Louse Human
fever quintana
8. Rickettsial diseases
Epidemic Indian Tick
Endemic Scrub Q-fever
Typhus Typhus
Typhus Typhus
•Fever
•Fever •Headache
•Fever/chills •Fever •Fever •Headache •Fatigue
•Myalgia •Myalgia •Headache •Rash with •Pneumonia
•Headache •Headache •Rash with eschar, first • No Rash
•Rash (No •Rash (No eschar appear on
eschar) – all eschar) •Lymphadeno- wrist and
over body Trunk> pathy ankle.
except palm extremities
sole & face. •Milder form
of illness.
9. Rickettsial diseases
Rocky
Mountain Rickettsial
Spotted Pox
Fever
•Mild Illness
•Fever •Fever
•Headache •Headache
•Rash (No •Vesicular Rash
eschar) – first with eschar
appear on wrist & •Lymphadenopath
ankle y
•Palms & soles •Resemblance to
involved chicken pox
•Systemic
Complications –
R/S, CVS, CNS,
Renal, Hepatic
10. Among the major group of rickettsioses,
the commonly reported diseases in
India are
Scrub typhus
Murine (Endemic) typhus
Indian tick typhus
Q fever
11. SCRUB TYPHUS IS CONSIDERED IN SOME
DETAIL … WHY?
To be aware of this condition during the
outbreaks of many fevers like DF,CKG Fever,
Leptospirosis & other viral fevers with
secondary infections.
Suspicion of the condition & initiation of
specific therapy cures the condition rapidly
otherwise may lead to serious complications.
12. SCRUB TYPHUS
Causative agent is Rickettsiae
tsutsugamushi.
Found in areas where they harbour the
infected chiggers particularly areas of heavy
scrub vegetations.
I.P. – 10-12 days
13. RESERVOIR: Trombiculid mite which feeds on small
mammals.
MODE OF TRANSMISSION: By bite of infected larval
mites.
Infection occurs during rainy season when the mites
lay their eggs. It is the larva (chigger) that feeds on
vertebrate hosts.
TRANSMISSION CYCLE
MITE------ RATS AND MICE----- MITE---- RATS
AND MICE
MAN
14. CLINICAL FEATURES:
Fever
Chills
Gen. Lymphadenopathy
ESCHAR – A punched out ulcer
covered with a blackened scab
which indicates the location of the
mite bite.
15. Eschar is found only in around
50% of patients.
Eschar is painless and patient
wont complain of it.
Often the patient wont notice it
because of its presence in
concealed sites.
16.
17. ENDEMIC TYPHUS
MURINE OR FLEABORNE TYPHUS
Natural infection in rats
R.typhi (R.mooseri)-causative agent
Vector –Xenopsylla cheopis (rat flea)
Rickettsia multiplies in the gut of the flea
shed in faeces.
Flea is unaffected but remain infectious for
the rest of life
18. Mode of transmission
1. Through the bite of infected fleas, when their
saliva /faeces inoculated in skin through bite
wound.
2. Through aerosols of dried faeces .
3. Ingestion of food contaminated with rat urine
/flea faeces
Human infection is a dead end
Man to man transmission does not occur .
19. CLINICAL FEATURES
• Low grade Fever
• Myalgia
• Headache
• Rash (No eschar) Trunk> extremities
• Milder form of illness than epidemic
typhus.
20. ‘Q’ FEVER
Causative agent- Coxiella burnetti
Zoonosis
Vector –Ixodid ticks
Coxiella abundant in tick faeces , survive in
dried faeces for long periods
Shed in the milk of infected animals
Particularly abundant in products of
conception contaminate environment at
parturition
No arthopod vector involved in transmisson
to humans.
21. Human infection
occupational hazard
Veterinary surgeons
Person handling wool or hides
Meat animal products contaminated with Coxiella
burnetti
Drinking infected milk
Routes of entry
Through skin mucosa
Inhalation
Ingestion
Person to person transmission is rare
Ticks are not important in human infection
22. Human disease
1. Acute systemic infection –interstitial pneumonia
2. Chronic infection – hepatitis ,meningitis ,
endocarditis
3. Spontaneous recovery is usual
Coxiella burnetti is an obligate intracellular
pathogen primarily affect monocytes –
macrophage cells
Remain dormant after recovery in the tissue of
the patient for 2-3 years latent infection
23. In dried faeces or wool it survives for a
year
It cannot be destroyed with pasteurisation
by the holder method but flash method is
effective
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
25. INDIAN TICK TYPHUS
An infectious disease that is caused by Rickettsia
conorii which is transmitted by the brown dog tick
(Rhipicephalus sanguineus).
The disease occurs predominantly in
Mediterranean areas such as India and Africa.
The onset of symptoms is usually sudden and the
incubation period is usually between 6 and 10 days
• Symptoms include fever, headache, rash with
eschar which first appear on wrist and ankle.
Treatment – Doxycyclin/ Tetracyclin.
26. RICKETTSIAL POX
Mildest Rickettsial disease of humans
Self limited , non fatal , vasicular exanthem first
observed in New york 1946
Resembles chicken pox
Also called vesicular /varicelliform Ricketsiosis
R. akari- Causative agent
Reservoir of infection –Domestic mice
Vector – mite
R. akari has also been isolated from wild rodent
in Korea
The disease has also been reported from
Eastern Europe and Korea .
27. ROCKY MOUNTAIN SPOTTED FEVER
Causative agent –R. rickettsii
Vector – Tick
Reservoir – Rodents and dog
Symptoms – Initial signs and symptoms of the
disease include sudden onset of fever, headache,
and muscle pain, followed by development of rash on
wrist and ankle (Palms and soles involved). The
disease can be difficult to diagnose in the early
stages, and without prompt and appropriate treatment
it can be fatal.
• Systemic Complications – R/S, CVS, CNS, Renal,
Hepatic.
28. Rocky Mountain spotted fever remains a
serious and potentially life-threatening
infectious disease. Despite the availability of
effective treatment and advances in medical
care, approximately three to five percent of
patients die from the infection.
Abnormal laboratory findings seen in patients
with Rocky Mountain Spotted Fever may
include thrombocytopenia, hyponatremia, or
elevated liver enzyme levels.
29. INVESTIGATIONS IN RICKETTSIAL DISEASE
PCR
SEROLOGICAL TESTS
• Indirect Flourescent antibody test (IFA) test
( Titer ≥ 1: 200 ),
• the Complement Fixation Test.
• The Weil Felix Test
• IgM ELISA Test: Highly specific test
30. WEIL-FELIX TEST
Agglutination test in which sera are
tested for agglutinins to the O antigens
of certain non motile Proteus strains
OX19, OX2 and OXK. The basis of the
test is the sharing of an Alkali stable
carbohydrate antigen by rickettsiae and
by certain strains of Proteus.
31. WEIL-FELIX TEST (CONTD)
Sera from Epidemic and Endemic typhus
agglutinate OX19 and sometimes OX2.
In tick borne spotted fever, both OX19 and
Ox2 are agglutinated.
OXK agglutinins are found only in scrub
typhus. The test is negative in Rickettsial pox
and Q fever.
32. WEIL-FELIX TEST (CONTD)
False positive reaction may occur in some cases of
urinary or other infections by Proteus and at times
in liver diseases and Typhoid fever.
Hence it is desirable to demonstrate a rise in titer of
antibodies for the diagnosis of rickettsial infections.
A 4 fold rise in agglutinin titres in paired titres is
diagnostic.
33. WEIL-FELIX TEST (CONTD)
However, with a single serum sample
available, the test is suggestive of
infection only at a high cut off titer (≥
1: 320) at which the positive predictive
value and the specificity is reliable.
35. The other serological tests for
Rickettsial diseases including the
specific IgM antibody tests become
positive only in the second week and
a second sample is often required.
Serological tests cannot provide
early diagnosis and a specific
diagnosis may not be available until
after the patient has died or
recovered.
36. TREATMENT
Tetracycline is the DOC.
Doxycycline 100mg Bid PO 7-15 days.
Chloramphenicol 500mg qid PO 7-15 days.
IV Chloramphenicol 150 mg/ kg per day for 5
days.
37. CONTROL
Vector control.
Clearing the vegetation where
rats and mice live.
Rodent control
38. Q1. VECTOR FOR SCRUB TYPHUS ?
• R. Prowazekii
• R. Typhi
• R. tsutsugamushi
• R. conorii
42. Q5. ESCHAR IS THE CHARACTERISTIC FEATURE
OF WHICH OF THE GIVEN DISEASE ?
Rocky Mountain Spotted Fever
Epidemic Typhus
Q- Fever
Scrub Typhus
43. Q6. SPECIFIC ANTIGEN FOR DIAGNOSIS OF
SCRUB TYPHUS IN WEIL-FELIX TEST ?
OX 19
OX 2
Ox K
None
