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Rickettsiae
Rickettsial diseases are difficult to diagnose clinically and often go unrecognized, leading to significant morbidity and mortality. They are caused by intracellular bacteria from the Rickettsia genus that are typically spread by arthropod vectors like ticks, fleas and mites. Some of the most common rickettsial diseases found in India include scrub typhus, murine typhus, Indian tick typhus and Q fever. Diagnosis relies on clinical suspicion combined with serology. Treatment involves doxycycline. Prevention focuses on vector control and improving hygiene.
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Rickettsiae
- 1. DR . SHAANAHMED JR ,Community Medicine, NMCH RICKETTSIAL DISEASES
- 2. Introduction:- Rickettsial diseasesare 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 – Significant morbidity & mortality.
- 3. History:- Hippocrates in460 BC used the term Typhus, meaning ‘smoke’ 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 typhuswas 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 hostcell 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:
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- 8. 1812-1813: Napoleonsuffers 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/ Classicaltyphus 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
- 10. Symptoms: Acute febrileillness Headache Myalgia Neurologic manifestations- Stupor, delirium Vasculitis Gangrene Rash : 40-80% macular, centrifugal spread, spare palms and soles
- 11. Brill –Zinsser disease/Recrudescenttyphus (or these days “jail fever”) 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 – BHC, Malathion Rodent control measures in infested areas
- 16. Scrub typhus Rickettsialagent : 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 :- Acuteonset with chills and Fever, headache, myalgia, Dry cough with Escher- the punched out ulcer covered with black scab –indicates a site of the bite Macular rash appears around the 5th day of the bite Lymphadenopathy Lymphocytosis Cardiac and cerebral involvement
- 18. An Eschar ofScrub Typhus 17 Feb 2016 18
- 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.
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- 22. Rocky mountain spottedfever 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 symptomsof 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
- 25. Rickettsial pox Benign febrileillness with vesicular rashes resembling chickenpox. Vector:- Liponyssoides sanguineus Reservoir:- Domestic mouse (Mus musculus) Self-limiting, non-fatal.
- 26. Q FEVER (QUERYFEVER)
- 27. Q fever Etiology: Coxiellaburnetti 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 RickettsialDiseases 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.
- 31. 17 Feb 2016 Oldertechniques Newer techniques Giemsa Staining Technique Immunological Assays 1. Indirect Immuno-Peroxidase / Immunoflouroscent assay 2.ELISA 3.PCR Rapid Detection Kits 1.Dip-S-Ticks 2.Scrub typhus RCT 3.Scrub typhus IgM / IgG Rapid Immunochromatographic Assay Multitest Weil-Felix Proteus Agglutination Test Diagnostic Techniques
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- 33. When you Suspectsooner ….. Treatment is easier ……. 1.Clinically 2.Tick exposure 3.Epidemiological data 4.Lab features 5.Rapid defervescence with proper antibiotics
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Editor's Notes
- #7 Q fever is excluded from the rickettsiaceae family as it doesn’t 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.
- #10 R. prowazekii requires an arthropod vector to infect the human host. In this case, the vector is the body louse, Pediculus humanus humanus (more commonly known as Pediculus humanus corporis):
- #11 Non specific symptom gangrene of extremities , Untreated cases, I.P. :- 5-21 days ,8 Case fatality :- 15 to 70%
- #13 Who surveillance 1 louse born typhus 2 Malaria 3 Polio 4 Rabies 5 Human influenza RMPTIR 6 Salmonella typhoid’ 7 Relapsing fever
- #14 Synonyms: flea-borne typhus, endemic typhus Xenopsylla chaeopsis Disease outcome: usually favorable – low rate of complications and mortality
- #16 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.
- #19 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 6–14 days. Ten to fifty percent of patients may have an eschar – 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-Barré 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 11–88% 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 – parenteral or nasogastric doxycycline or chloramphenicol are potential options. Appropriate supportive care is essential. The treatment of scrub typhus in pregnancy is problematic – 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 0–60% in untreated patients, for reasons that are unclear. Delayed administration of doxycycline has been associated with major organ dysfunction and prolonged
- #23 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
- #28 C. burnetii 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
- #32 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
- #33 cdc