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Rickettsiae Dr L ancy


Rickettsiae Small gram negative Intracellular bacteria Primary parasites found in the alimentary canal of arthropods-transmitted to humans by Lice/ flies /ticks and mites In humans – infect vascular endothelium and Reticuloendothelial cells Rickettsia named after HOWARD TAYLOR RICKETTS died of Typhus fever contracted during his studies Discovered spotted fever rickettsia (1906)

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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


CULTIVATION They are readily cultivated in the yolk sac of developing chick embryo They also grow on mouse fibroblast,HeLa,Hep2,Detroit-6 and other continuous cell lines but tissue cultures are not satisfactory for primary isolation Guinea pigs and mice are useful for the isolation of rickettsiae from patients


RESISTANCE Rickettsiae are readily inactivated by physical and chemical agents They are rapidly destroyed at 56 0 C and at RT when separated from host components. They can be preserved in skimmed milk or a suspending medium containing sucrose, potassium phosphate and glutamate(SPG medium)


Rickettsiae Family- Rickettsiae -three genera Rickettsia Orientia Ehrlichia Former members excluded Coxiella burnetti - Q fever Not athropod born Rochalimaea quintana Not an obligate intracellular parasite


Rickettsiae Genus recketsia Typhus fever group Epidemic typhus –R. prowazekii Endemic typhus – R.typhi

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Spotted fever group Tick borne ⁄mite borne R. ricketsii -rocky mountain spotted fever R. siberica-siberian tick typhus R. conori - indian tick typhus R. australis –Queensland tick typhus R. japonica- oriental spotted fever R. akari – Ricketsial pox


Rickettsiae Genus orientia Orientia tsutsugamushi – Scrub typhus Genus E hrlichia E. sennetsu-Ehrlichiosis resembling glandular fever E.chaffeenis – Human monocytic Ehrlichiosis E. equi - Human granulocytic Ehrlichiosis


Rickettsiae Genus Coxiella Coxiellla burnetti - Q fever Genus Bartonella B. bacilliformis – verruga peruvana Oroya fever /Carrion’s disease B. quintana – Trench fever (5 day fever ) Rochalimaea quintana B.henselae - cat scratch disease Bacillary angiomatosis Bacillary peliosis .

Epidemic typhus :

Epidemic typhus Louse borne typhus /classical typhus /gaol fever Epidemic during war and famine reported from all part of the world . Common in Russia and Eastern Europe Typhos = cloud / smoke Typhus =cloudy state of conciousness Incubation period -5-15 days

Epidemic typhus :

Epidemic typhus Starts with fever and chills Rash on 4 th or 5 th day – trunk  limbs(sparing palms and soles ) pt become stuporous and delirious during second week Case fatality rate 40%  with age In those who recover from disease , Rickettsia remain dorment for years in the lymphoid tissue or organs .Reactivation recrudescent typhus (Brill Zinsser disease )

Epidemic typhus :

Epidemic typhus Causative agent : R.prowazekii Named after Von Prowzek died of typhus fever while investigating the disease Humans are the only natural vertebrate host Reservoir hosts – squirrels Vector : Pediculus humanis corporis (body louse )

Epidemic typhus :

Epidemic typhus Lice infected by feeding on r ickettsiaemic patients , Rickettsiae multiply in the gut appear in the faeces after 3-5 days . Lice defecate while feeding . Infection transmitted when the contaminated louse faeces is rubbed through the minute abrasions caused by scratching . .

Epidemic typhus :

Epidemic typhus Other modes of transmission Aerosols and dried faeces through inhalation Through conjunctiva

Endemic typhus Murine or fleaborne typhus :

Endemic typhus Murine or fleaborne typhus Milder disease than epidemic 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 un affected but remain infectious for the rest of life

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Mode of transmission Through the bite of infected fleas .when their saliva /faeces rubbed in Through aerosols of dried faeces . Ingestion of food contaminated with rat urine /flea faeces Human infection is a dead end Man to man transmission does not occur .

NEILL-MOOSER REACTION tunica reaction:

NEILL-MOOSER REACTION tunica reaction Animal inoculation test to differentiate R.typhi and R.prowzekii Both are closely similar Blood sample collected from a patient Inoculated intra peritoneally Male guinea pigs Scrotal inflammation Scrotum becomes enlarged () Testes cannot be pushed back into the abdoman because of inflammatory adhesions between the layers of tunica vaginalis

Endemic typhus :

Endemic typhus If test is positivie  R.typhi If test is negative R.prowzekii

Tick typhus :

Tick typhus R.rickettsii  discovered by Ricketts in 1906 . First insect transmitted bacterial pathogen to be recognised Causative agent for Rocky mountain spotted fever Most serious type of spotted fever Prevalent in north/ south America Transmitted by ticks  Dermacentor andersoni

Rickettsial pox :

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 mouse Vector – mite R. akari has also been isolated from wild rodent in Korea The disease has also been reported from Eastern E urope and Korea .

Scrub typhus :

Scrub typhus Orientia tsutsugamushi – causative agent Formerly- R.tsutsugamushi - R.orientalis Tsutsugam =dangerous Mushi = insect /mite It is a place disease Found only in area with suitable climate plenty of moisture scrub vegetation

Scrub typhus:

Scrub typhus Vector – trombiculid mites Leptotrombidium L. akamushi – Japan L.deliensis - in India The mite inhabit sharply demarcated areas in the soil where the micro ecosystem is favourable . (Mite islands) Humans are infected while passing through these Mite islands. Bitten by mite larvae ( Chiggers) Chigger – borne typhus

Scrub typhus:

Scrub typhus The mite larvae feed on the serum of warm blooded animals only once during its cycle of development . Adult mites feed only on plants Resrviors –rodents and birds Scrub typhus originally found in scrub jungles sandy beaches, mountains ,deserts & equatorialrain forests. Zoonotic tetrad 4 factors essential for establishment of disease Orienta tsutsugamushi Chiggers Rats Transitional forms of vegetation Incubation period -1-3 weeks

Scrub typhus:

Scrub typhus Symptoms : fever , headache , conjunctival congestion A characteristic eschar over the site of mite bite Regional lymphadenopathy Maculo papular rash Pneumonia Encephalitis

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The disease is not a serious problem in civilian practice ,but assumes great importance in military medicine especially during jungle war fare

Ehrlichiosis :

Ehrlichiosis Three types of human infections identified . Resembling Glandular fever –endemic in japan E.sennetsu Human monocytic Erlichiosis - E.chaffeenis Human granulocytic Erlichiosis -E . equi - / E.phagocytophila E. sennetsu-Erlichiosis resembling –

Glandular fever type of Ehrlichiosis :

Glandular fever type of Ehrlichiosis Reported from Japan 1954 E.sennetsu - causative agent Endemic in Japan lymphoid hyperplasia Atypical lymphocytosis No arthropod vector Ingestion of fish carrying infected flukes –human infection

Human monocytic Ehrlichiosis:

Human monocytic Ehrlichiosis E.chaffeenis causative agent Vector amblyoma ticks Reservoir – deer and rodents Leucopenia ,thrombocytopenia ,and elevated liver enzymes Multisystem invovement Fatality rate high

Human granulocytic Ehrlichiosis:

Human granulocytic Ehrlichiosis E. equi - / E.phagocytophila is the causative agent Vector – ixodid tick Reservoir – deer,cattle ,sheep Leucocytopenia , thrombocytopenia Examination of blood film by giemsa stain – morula form of Ehrlichia Treatment : Doxycycline

‘Q’ fever:

‘Q’ fever 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

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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 ‘ Q’ fever

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Human disease Acute systemic infection –interstitial pneumonia Chronic infection – hepatitis ,meningitis , endocarditis 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

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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  Culture - yolk sac of chicken embryo cell cultures Serology – CFT,IFA Isolation of C oxiella from blood, sputum and other clinical specimens possible. But not recommended due to laboratory infection

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Vaccines Formalin killed whole cells trichloro acetic acid extracts live attenuated vaccine Treatment : Doxycycline Endocardits : combination therapy Tetracycline +Co- trimoxazole Tetracycline+ Rifampicin

Trench fever/5 day fever :

Trench fever/5 day fever During the first word war m ore than million cases occurred among soldiers fighting in the trenches in Europe Disease not fatal .Slow course and prolonged convalescence  considerable loss of man power Exclusively a human disease No animal reservoir Causative agent B. quintana / Rochalimaea quintana vector – body louse

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The faeces of lice become infectious 5-10 days after an infectious meal. The lice are unharmed but remain infective through out their life Vertical transmission does not occur in lice Culture B. quintana grows on blood agar –this is the only rickettsiae which can grow on artificial media The disease leads to chronic or latent infection

Oroya fever :

Oroya fever Causative agent: Bartonella . bacilliformis Outbreak of fever killed thousands of workmen in 1870 when the railway line from Lima to Oroya in PERU was built – oroya fever Some of the survivers developed nodular ulcerating skin lesions - Verruga peruvana The common etiology of these two condition established by a Peruvian medical student – Daniel carrion in 1885 who injected himself with the infected material obtained from a case of Verruga peruvana developed oroya fever and died – C arrions diseae

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Daniel carrion

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Clinical features Fever Progressive anaemia – bacterial invasion of erythrocytes Mortality high in untreated cases A late sequele in survivors or in those with asymptomatic infection B. bacilliformis seen inside in RBC and in skin lesions Pleomorphic gram negative rods Motile by a tuft of polar flagella Culture :semisolid agar with rabbit or human blood

Bartonella henselae:

Bartonella henselae Causative agent – cat scracth disease Immunodefifient pts (HIV)- Bacillary angiomatosis Bacillary peliosis Bacillary angiomatosis Vascular nodules / tumours appear on skin and mucosa Bacillary peliosis Affect liver and spleen sis Lymphnode biopsy- smear – staining Culture –blood agar – prolonged incubation

Weil –Felix reaction :

Weil –Felix reaction Serological diagnosis of Rickettsial disease Simple ,tube agglutination test – heterophile agglutination test Weil –Felix 1916 Sharing of an alkali stable carbohydrate antigen by some Rickettsia and by certain proteus (non motile ) Proteus vulgaris OX 19 & OX 2 Proteus mirabilis OX K Sera of patients mixed with proteus antigen produce agglutination in high titres 1:1000 1:5000 by the second week declines rapidly during convalescence . False positves  UTI, Typhoid fever ,liver disease

Weil –Felix Reaction Heterophyle Agglutination :

Weil –Felix Reaction Heterophyle Agglutination OX 19 OX 2 OX K Epidemic typhus +++ + - Endemic typhus +++ ± - Tick born spotted fever ++ ++ - Scrub typhus - - ++

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Weil –Felix reaction is not done for the diagnosis of Q fever which is caused by C oxiella burnetti

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