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RICKETTSIAL DISEASES Dr. BHUWAN SHARMA Asst. Professor (Grant Govt. Medical College)
RICKETTSIAE Rickettsiae are obligate intracellular gram negative parasites. Most are zoonoses spread to humans by arthropods (except Q fever).
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
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
DISEASES RICKETTSI INSECT MAMMALIAN AL AGENT VECTOR RESERVOIR TYPHUS GROUPa) Epidemic R. prowazekii Louse Humantyphusb) Murine R. typhi Flea Rodentstyphus(Endemic typhus)c) Scrub R. Mite Rodentstyphus tsutsugamushi
DISEASES RICKETTSI INSECT MAMMALIAN AL AGENT VECTOR RESERVOIR SPOTTED FEVER GROUPa) Indian tick R. conorii Tick Rodent, Dogtyphusb) Rocky R. rickettsii Tick Rodents, Dogsmountainspotted feverc) Rickettsial R. akari Mite Micepox
DISEASES RICKETTSI INSECT MAMMALIA AL AGENT VECTOR N RESERVOIR OTHERSa) Q fever C. burnetti Nil Cattle, sheep,goatsb) Trench Rochalimaea Louse Humanfever quintana
Rickettsial diseasesEpidemic 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 oneschar) – all eschar) •Lymphadeno- wrist andover body Trunk> pathy ankle.except palm extremitiessole & face. •Milder form of illness.
Rickettsial diseases Rocky Mountain Rickettsial Spotted Pox Fever •Mild Illness•Fever •Fever•Headache •Headache•Rash (No •Vesicular Rasheschar) – first with escharappear on wrist & •Lymphadenopathankle y•Palms & soles •Resemblance toinvolved chicken pox•SystemicComplications –R/S, CVS, CNS,Renal, Hepatic
Among the major group of rickettsioses, the commonly reported diseases in India are Scrub typhus Murine (Endemic) typhus Indian tick typhus Q fever
SCRUB TYPHUS IS CONSIDERED IN SOMEDETAIL … 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.
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
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
CLINICAL FEATURES: Fever Chills Gen. Lymphadenopathy ESCHAR – A punched out ulcer covered with a blackened scab which indicates the location of the mite bite.
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.
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
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 .
CLINICAL FEATURES• Low grade Fever• Myalgia• Headache• Rash (No eschar) Trunk> extremities• Milder form of illness than epidemic typhus.
‘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.
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 IngestionPerson to person transmission is rareTicks are not important in human infection
Human disease 1. Acute systemic infection –interstitial pneumonia 2. Chronic infection – hepatitis ,meningitis , endocarditis 3. Spontaneous recovery is usualCoxiella burnetti is an obligate intracellularpathogen primarily affect monocytes –macrophage cellsRemain dormant after recovery in the tissue ofthe patient for 2-3 years latent infection
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
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.
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 .
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.
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.
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
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.
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.
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.
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.
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.
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.
CONTROL Vector control. Clearing the vegetation where rats and mice live. Rodent control
Q1. VECTOR FOR SCRUB TYPHUS ?• R. Prowazekii• R. Typhi• R. tsutsugamushi• R. conorii
Q.2 INCUBATION PERIOD OF SCRUB TYPHUS 8-10 days 10-12 days 3-5 weeks None