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Rickettsiae
1. DR . SHAAN AHMED
JR ,Community Medicine,
NMCH
RICKETTSIAL DISEASES
2. Introduction:-
๏ Rickettsial diseases are considered some of the most covert
emerging or reemerging diseases.
๏ Rickettsial infections are difficult to diagnose clinically
hence occurrence often goes unrecognized.
๏ Failure of timely diagnosis โ Significant morbidity &
mortality.
3. History:-
๏ Hippocrates in 460 BC used the
term Typhus, meaning โsmokeโ
to describe the confused state of
intellect i.e. stupor.
๏ Rickettsia named after HOWARD TAYLOR RICKETTS died
of Typhus fever contracted during his studies discovered
Spotted fever Rickettsia (1906).
๏ It has been documented in India since 1930s with reports of
Scrub typhus from Kumaon region, Assam in soldiers during
2nd world war & Murine typhus from Jabalpur, M.P and
Kashmir.
4. Distribution:-
๏ Epidemic typhus was most formidable disease in past. No
case of this disease reported from South East Asia since
1978.
๏ Endemic typhus prevalent in South-East Asian region and
Western Pacific countries.
๏ Scrub typhus is endemic in Northern Japan, Russia SEA,
Western Pacific Island, China, India and Sri lanka.
๏ Q fever outbreaks are most common in, slaughterhouses
and research facilities.
๏ Trench fever is limited to Central Europe.
๏ Commonly reported diseases in India are Scrub typhus,
Murine typhus, Indian tick typhus, Q fever.
5. Rickettsia inside the
host cell
TICK FLEA LICE MITE
๏ Obligate intracellular parasite.
๏ Gram negative pleomorphic bacteria.
๏ Most are zoonoses spread to humans by
arthropods (except Q fever).
๏ Cannot grow in culture media, but
cultivable only in living tissue.
๏ No human to human transmission.
Rickettsial characteristics:
8. ๏ 1812-1813: Napoleon suffers the greatest loss of troops to
Epidemic typhus.
๏ Typhus was particularly associated with siege warfare
which had a high population density and poor hygiene.
๏ Still endemic in Africa (Burundi, Rawanda, Ethiopia)
and South America (Peru, Bolivia, Ecuador)
9. Epidemic typhus/ Classical typhus
Rickettsial agent: - Rickettsia prowazekii
Insect vector :- Louse
Mammalian Reservoir :- Human, flying squirrels
Transmission :-
Human to human via louse vector, directly in blood, or
as the contaminated louse feces is scratched into the bite
wound, or inhalation of infected louse feces or dust.
Incubation period: 5-21 days
11. Brill โZinsser disease/Recrudescent typhus
(or these days โjail feverโ)
๏ This occurs 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. Control measures
A. Diagnosis:- based on clinical suspicion with Serology
B. Treatment:- Doxycycline (DOC)
C. Preventive measures:-
Delousing - insecticides
Improvement of personal hygiene and living conditions
Louse borne typhus is under WHO surveillance
13. Murine typhus/Endemic typhus
๏ Rickettsial agent: -Rickettsia typhi
๏ Insect Vector: Flea
๏ Mammalian Reservoir: Rodents
๏ Transmission :-
inhalation of infected louse feces or dust.
inoculation into skin with feces of infected fleas.
๏ Incubation period: 1-2 weeks
๏ Symptoms:
Gradual onset- fever,
Headache, myalgia, cough
๏ Rash: > 55% maculopapular rash on trunk
14. Control measures
A. Diagnosis:- liver enzyme elevated
B. Treatment :- Doxycycline (DOC)
C. Preventive measures :-
Residual insecticides โ BHC, Malathion
Rodent control measures in infested areas
15.
16. Scrub typhus
๏ Rickettsial agent : Orientia tsutugamushi
๏ Insect Vector: Mite infective larvae CHIGGERS
๏ Transmission :- larval forms - chiggers found in areas of
scrub vegetations.
Common in military and Jungle warfare, farmers
๏ Mammalian Reservoir: -Rodents
๏ Incubation period: -10-12 days
17. .
๏ Symptoms :-
Acute onset with chills and Fever, headache, myalgia,
Dry cough with Escher- the punched out ulcer covered with
black scab โindicates a site of the bite
Macular rash appears around the 5th day of the bite
Lymphadenopathy
Lymphocytosis
Cardiac and cerebral involvement
19. Control measures
Treatment:- tetracycline (DOC)
Vector control:-
Clearing the vegetation where rats and mice lives
Application of insecticides:- Lindane, Chlordane to the
ground and vegetation
Personal prophylaxis :-
Impregnating clothes and blankets with miticial
chemicals, i.e. benzyl benzoate.
Mite repellant:- Diethyl toluamide application on exposed
skin surfaces.
22. Rocky mountain spotted fever
Rickettsial agent:- R. rickettsii
Insect Vector: - Tick
Mammalian Reservoir: -Rodents, dogs
Incubation period:- 3-7 days
Symptoms:- Abrupt onset fever, chills, headache, myalgia
Rash : first appears in extremities, moves centripetally and
involve palm.
Mortality: 70% if left untreated in elderly
Complications:- HSM, jaundice, myocarditis, uremia, ARDS
23. The clinical symptoms of other spotted fevers are very
similar to Rocky mountain spotted fever
Late petechial rashes on palm
and forearm.
Early (macular) rash on sole
of foot.
24. Control measures
Treatment :- tetracycline (DOC)
Personal prophylaxis :-
Tick infected area should avoided
Disinfection of dogs
Health education about mode of transmission
Clearing the vegetation where rats and mice lives
27. Q fever
Etiology: Coxiella burnetti
Vector : None
Reservoir: Cattle, sheep, goat
MOT: ingestion of dust containing organisms or aerosols
excreted in urine, feces, milk etc.
I.P:- 2-3 wks
C/F:- resembles influenza or non bacterial pneumonia
Individuals at risk : food handlers, veterinarians
Infective endocarditis occasionally in chronic Q fever
28. Control measures
Treatment:- tetracycline (DOC) ,prolong for 18 months.
Preventive measures:-
Pasteurization/boiling of milk
Providing sanitary cattle sheds
Adequate disinfection and disposal of products.
Personal prophylaxis :-
Coxiella vaccination to occupationally exposed workers.
29. Trench fever
Rickettsial agent: - Rochalimaea quintana
Insect vector :- Louse
Mammalian Reservoir :- Human
MOT:- louse feces.
disease limited to central Europe.
30. Diagnosis of Rickettsial Diseases
๏ No rapid laboratory tests are available to diagnose
rickettsial diseases early in the course of illness.
๏ Rise in serum antibody/often do not develop in early
stages.
33. When you Suspect sooner โฆ..
Treatment is easier โฆโฆ.
1.Clinically
2.Tick exposure
3.Epidemiological data
4.Lab features
5.Rapid defervescence with proper antibiotics
Q fever is excluded from the rickettsiaceae family as it doesnโt have an arthropod vector
Rickettsia is classically classified into 2 groups the SFG and typhus group on the basis of antigenic differences in their cell wall.
R. prowazekiiย requires an arthropod vector to infect the human host. In this case, the vector is the body louse,ย Pediculus humanus humanusย (more commonly known asย Pediculus humanus corporis):
Non specific symptom
gangrene of extremities , Untreated cases,
I.P. :- 5-21 days ,8
Case fatality :- 15 to 70%
Who surveillance
1 louse born typhus
2 Malaria
3 Polio
4 Rabies
5 Human influenza RMPTIR
6 Salmonella typhoidโ
7 Relapsing fever
Synonyms: flea-borne typhus, endemic typhus
Xenopsylla chaeopsis
Disease outcome: usually favorable โ low rate of
complications and mortality
The bite caused by a
"strikingly big" engorged tick was almost
uniformly located on the occipital scalp
region. The infection occurred most
commonly in young children: the larger
half of the patients were less than 10 years
of age.
A patient with fever, headache, and myalgia with an eschar in an endemic area is likely to have scrub typhus.
The incubation period is approximately 6โ14 days. Ten to fifty percent of patients may have an eschar โ this variability probably reflects, atleast in part, the extent to which patients are examined. Eschars, which are usually single and in secluded areas such as the axilla and groin, are painless, erythematous papules that develop a central black
scab, resembling a cigarette burn (Fig. 63.3). They are not pathognomonic for scrub typhus, as similar lesions may be produced by spotted
fever group rickettsioses. Chiggers are minute and, unlike ticks, are not normally noticed. Patients may scratch off the characteristic black scab. Lymphadenopathy is more frequent than in sympatric murine typhus [2]. Headache, myalgia, and dry cough frequently occur; a maculopapular erythematous rash occurs in a minority of patients
[1,2]. Deafness, tinnitus, and conjunctival suffusion occur. Severe disease can manifest as pneumonitis, acute respiratory distress
syndrome, jaundice with mildly raised transaminases, meningoencephalitis,coagulopathy, multi-organ failure, acute renal failure, acute
transverse myelitis, myocarditis, and Guillain-Barrรฉ syndrome. Why some, and not others, develop severe disease is not understood.
Mortality is positively correlated with blood bacterial load [5].
Orientia
tsutsugamushi DNA has been demonstrated in cerebrospinal fluid
(CSF), with normal glucose, a mild increase in white cell density
(ranging from 11โ88% lymphocytes) and raised protein [7]. Scrub
typhus appears to be less severe in children, but there have been no prospective comparisons between children and adults from the same
population. Scrub typhus can cause serious adverse effects for mother
and baby in pregnancy [8]. The majority of scrub typhus patients are not diagnosed or treated. The differential diagnosis
would include spotted fever group rickettsiosis, which would also be
expected to respond to tetracyclines. Scrub typhus eschars could be
confused with the lesions of anthrax, tularemia, chancroid, lymphogranuloma
venereum, and injury. In the absence of an eschar, few
clinical features are helpful. Murine typhus, leptospirosis, Q fever,
dengue, hemorrhagic fever with renal syndrome (HFRS), infectious
mononucleosis, HIV seroconversion, septicemia (especially typhoid),
and malaria are important differential diagnoses . Laboratory diagnosis of scrub typhus is difficult. Culture (requiring
BSL3 facilities) is 100% specific, but has low sensitivity. Immunofluorescence
(IFA) and immunoperoxidase IgM and IgG antibody tests
have been commonly used, but these are expensive, rarely accessible
and are bedevilled by subjectivity of interpretation and uncertainty as
to the most appropriate cut-off titers in different communities [10].
Ideally, they should be interpreted by comparing titers between paired
acute and convalescent samples , The Weil-Felix OXK test is still commonly used
in Asia, but has low sensitivity. Conventional and quantitative realtime
PCR assays for the detection of O. tsutsugamushi in blood, eschar
tissue, and CSF have been developed [11, 12]. However, there remain
great difficulties in the accessibility of the diagnosis of scrub typhus
in rural endemic areas. Mixed infections may occur with, for example,
leptospirosis but, given the persistence of antibodies, distinguishing
these from serial infections without culture or PCR techniques is
difficult. Given the difficulties of making a timely laboratory diagnosis and the
significant minority who develop severe disease, empirical treatment
should be considered for all cases with scrub typhus in the differential
diagnosis. The diversity of O. tsutsugamushi suggests it is unlikely that
one treatment regimen will be appropriate across the wide distribution
of this organism. Chloramphenicol- and doxycycline-resistant
scrub typhus have been described in northern Thailand [13], but there
are no subsequent published data on this clinical problem. Given the difficulties of making a timely laboratory diagnosis and the
significant minority who develop severe disease, empirical treatment
should be considered for all cases with scrub typhus in the differential
diagnosis. The diversity of O. tsutsugamushi suggests it is unlikely that
one treatment regimen will be appropriate across the wide distribution
of this organism. Chloramphenicol- and doxycycline-resistant
scrub typhus have been described in northern Thailand [13], but there
are no subsequent published data on this clinical problem. There are few data to guide the antibiotic treatment of severe disease
โ parenteral or nasogastric doxycycline or chloramphenicol are potential
options. Appropriate supportive care is essential. The treatment
of scrub typhus in pregnancy is problematic โ chloramphenicol
(although contraindicated in the last trimester), azithromycin, and
rifampicin have been used. In children, the risks of short-course doxycycline
are almost certainly exceeded by the benefit of effective cure.
In a retrospective analysis of children with scrub typhus, no significant
differences in fever clearance times were found between doxycycline,
chloramphenicol, or roxithromycin therapy [21].
Mortality is very variable, ranging from 0โ60% in untreated patients,
for reasons that are unclear. Delayed administration of doxycycline
has been associated with major organ dysfunction and prolonged
In south american countries,40% pts suspected of dengue but lacking dengue antibodies were diagnosed with SFG rickettsioses
In areas with amblyomma species ticks-antibodies against SFG group are very common in africa
C. burnetiiย infection of pregnant women can provoke placentitis and often lead to premature birth, growth retardation, spontaneous abortion, or fetal death The disease is usually benign, but mortality occurs in 1 to 11% of patients with chronic Q fever
The poor sensitivity and low specificity of the Weil-Felix test is,PCR also low sensitivity .
IgM Elisa now well demonstrated for the diagnosis of Rocky mountain spotted fever (RMSF), Murine typhus, epidemic typhus and scrub typhus.
Although a good correlation between the results of the Weil-Felixtest and detection of IgM antibodies by an IFA is often
observed, with the development of techniques that are used to grow rickettsiae, this test should be used only as a first line of testing in rudimentary hospital laboratories. the Weil Felix test still serves as a useful and cheapest available tool for the laboratory diagnosis of rickettsial diseases.
A four-fold rise in agglutinin titres in paired sera is diagnostic for infection with these febrile agents.9
