Dr. Kumar Himanshu presents information on scrub typhus, a bacterial infection caused by Orientia tsutsugamushi and transmitted by chigger mites. Some key points include:
- Scrub typhus is endemic to parts of Asia and Northern Australia and is a major cause of undifferentiated fever in India.
- Clinical features include fever, eschar (painless skin lesion) at the site of the mite bite, rash, and lymphadenopathy. Complications can involve multiple organ systems.
- Diagnosis is challenging as symptoms are non-specific. Serological tests like Weil-Felix, IgM ELISA and PCR on blood/eschar are used but
Its all about the Scrub typhus or bush typhus caused byintracellular parasite Orientia tsutsugamushi , a Gram-negative alpha proteobacterium of family Rickettsiaceae
Scrub typhus is a mite-borne disease caused by Orientia tsutsugamushi (formerly Rickettsia tsutsugamushi). Symptoms are fever, a primary lesion, a macular rash, and lymphadenopathy. (See also Overview of Rickettsial and Related Infections.) Scrub typhus is related to rickettsial diseases.
Its all about the Scrub typhus or bush typhus caused byintracellular parasite Orientia tsutsugamushi , a Gram-negative alpha proteobacterium of family Rickettsiaceae
Scrub typhus is a mite-borne disease caused by Orientia tsutsugamushi (formerly Rickettsia tsutsugamushi). Symptoms are fever, a primary lesion, a macular rash, and lymphadenopathy. (See also Overview of Rickettsial and Related Infections.) Scrub typhus is related to rickettsial diseases.
Scrub typhus, also known as bush typhus, is a disease caused by a bacteria called ORIENTIA TSUTSUGAMUSHI.
Scrub typhus is spread to people through bites of infected chiggers (larval mites).
Most cases of scrub typhus occur in rural areas of Southeast Asia, Indonesia, China, Japan, India, and northern Australia. Anyone living in or travelling to areas where scrub typhus is found could get infected
Scrub typhus is not transmitted directly from person to person; it is only transmitted by the bites of vectors
Chiggers are abundant in locales with high relative humidity (60%–85%), low temperature (20°C–30°C), low incidence of sunlight, and a dense substrate-vegetative canopy.
Occupational risk is higher in farmers (aged 50–69 years), females.
Chikungunya- a short PPT.
This tells in brief about the infection.
The neurological complications is the main focus.
The management and other related issues are also discussed.
SYNOPSIS
Etiology of scrub typhus
Clinical features
Laboratory diagnosis
Treatment
Prevention
Aka Japanese River fever
caused by Orientia tsutsugamushi
Mode of Infection
Bite of infected trombiculid mites of genus leptotrombidium.
Chiggerosis
EPIDEMIOLOGY
World scenario:
Japan,China, Philippines, and South -East Asia, including India.
Indian Scenario:
Assam and West Bengal during the Second World War.
Widespread in many parts of India, including Puducherry
Zoonotic tetrad:
Four elements are essential to maintain 0. tsutsugamushi in nature-
1. Trombiculid mites
2. Small mammals
3. Secondary scrub vegetations or forests.
4. Wet season
CLINICAL MANIFESTATIONS
Triad
Eschar (at the site of bite),
Regional lymphadenopathy
Maculopapular Rashad
Complications such as encephalitis and interstitial pneumonia- rarely
LABORATORY DIAGNOSIS
Serology – Main stay of diagnosis
Non specific Tests-
Weil Felix Test
Specific Tests
Indirect Immunofluorescence Assay
Complement Fixation Test
IgM Capture ELISA
Latex Agglutination Test
Isolation:
Rickettsiae cannot be cultivated in cell free media
cell lines (Vero,primary chick embryo, Wl-38, HeLa),
egg (yolk sac inoculation), or
animal inoculation (guinea pig) in Biosafety level III facilities
PCR-detecting 16S rRNA or Omp genes
TREATMENT
Doxycycline is the drug of choice - 100 mg twice a day orally for 1-5 days.
Chloramphenicol - alternative.
PREVENTION
• Vector control strategies- insecticides
• Control of rodents and other animals
• Improvement of personal hygiene.
No vaccine is available at present against rickettsial infections.
SUMMARY
Scrub typhus – produced by Orientia tsutsugamushi
Mode of Infection – Bite of Trombiculid mite
Zoonotic tetrad
Clinical Manifestations - Triad
Laboratory diagnosis- Weil Felix and IFA
Treatment- Doxycycline
Please find the power point on Typhus and its managemen. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
japenese encephalitis is an important vector borne disease which carries a high mortality as well as high disability. it is a preventable disease and an effective vaccine is available for it.the vaccine is an important part of universal immunization program in india. Environmental modification and control of vector will go long way in the control of this disease.
Scrub typhus, also known as bush typhus, is a disease caused by a bacteria called ORIENTIA TSUTSUGAMUSHI.
Scrub typhus is spread to people through bites of infected chiggers (larval mites).
Most cases of scrub typhus occur in rural areas of Southeast Asia, Indonesia, China, Japan, India, and northern Australia. Anyone living in or travelling to areas where scrub typhus is found could get infected
Scrub typhus is not transmitted directly from person to person; it is only transmitted by the bites of vectors
Chiggers are abundant in locales with high relative humidity (60%–85%), low temperature (20°C–30°C), low incidence of sunlight, and a dense substrate-vegetative canopy.
Occupational risk is higher in farmers (aged 50–69 years), females.
Chikungunya- a short PPT.
This tells in brief about the infection.
The neurological complications is the main focus.
The management and other related issues are also discussed.
SYNOPSIS
Etiology of scrub typhus
Clinical features
Laboratory diagnosis
Treatment
Prevention
Aka Japanese River fever
caused by Orientia tsutsugamushi
Mode of Infection
Bite of infected trombiculid mites of genus leptotrombidium.
Chiggerosis
EPIDEMIOLOGY
World scenario:
Japan,China, Philippines, and South -East Asia, including India.
Indian Scenario:
Assam and West Bengal during the Second World War.
Widespread in many parts of India, including Puducherry
Zoonotic tetrad:
Four elements are essential to maintain 0. tsutsugamushi in nature-
1. Trombiculid mites
2. Small mammals
3. Secondary scrub vegetations or forests.
4. Wet season
CLINICAL MANIFESTATIONS
Triad
Eschar (at the site of bite),
Regional lymphadenopathy
Maculopapular Rashad
Complications such as encephalitis and interstitial pneumonia- rarely
LABORATORY DIAGNOSIS
Serology – Main stay of diagnosis
Non specific Tests-
Weil Felix Test
Specific Tests
Indirect Immunofluorescence Assay
Complement Fixation Test
IgM Capture ELISA
Latex Agglutination Test
Isolation:
Rickettsiae cannot be cultivated in cell free media
cell lines (Vero,primary chick embryo, Wl-38, HeLa),
egg (yolk sac inoculation), or
animal inoculation (guinea pig) in Biosafety level III facilities
PCR-detecting 16S rRNA or Omp genes
TREATMENT
Doxycycline is the drug of choice - 100 mg twice a day orally for 1-5 days.
Chloramphenicol - alternative.
PREVENTION
• Vector control strategies- insecticides
• Control of rodents and other animals
• Improvement of personal hygiene.
No vaccine is available at present against rickettsial infections.
SUMMARY
Scrub typhus – produced by Orientia tsutsugamushi
Mode of Infection – Bite of Trombiculid mite
Zoonotic tetrad
Clinical Manifestations - Triad
Laboratory diagnosis- Weil Felix and IFA
Treatment- Doxycycline
Please find the power point on Typhus and its managemen. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
japenese encephalitis is an important vector borne disease which carries a high mortality as well as high disability. it is a preventable disease and an effective vaccine is available for it.the vaccine is an important part of universal immunization program in india. Environmental modification and control of vector will go long way in the control of this disease.
lecture for MBBS students
Rickettsia named after HOWARD
TAYLOR RICKETTS died of Typhus fever contracted during his studies
Discovered spotted fever rickettsia (1906)
Obligate intracellular parasite
Gram negative pleomorphic rods
Parasite of arthropods – fleas, lice, ticks and mites.
No Human to human transmission.
Rickettsia are transmitted to humans by the bite of infected arthropod vector.
Multiply at the site of entry and enter the blood stream.
Localise in the vascular endothelial cells and multiply to cause thrombosis lead to rupture & necrosis
Hydropericardium syndrome(inclusion body hepatitis)Sumeet Jyoti
This presentation has been uploaded to share knowledge about hydropericardium syndrome. various references has been taken for this presentation and it is mainly focused in nepalese context.
Thank you!!!
Epidemiology and control measures for Yellow fever AB Rajar
It is an acute infectious disease of short duration, with sudden
onset,fever,headache,prostration,nausea,epistaxis,buccal bleeding,hematemesis,malena and jaundice
Introduction, epidemiology, global trends, Indian setting, pathogenesis, life cycle, clinical manifestations, investigations, treatment regimen, prevention.
In this presentation you will find about the zoonotic potential of rabies virus, its impact in terms of DALYs.
Epidemiology and geographical distribution of rabies.
You will learn about the reservoir and source of rabies, transmission of rabies virus.
You will also learn about the virology of rabies virus inculding its family, genus, its structure, its different protein and the replication cycle of rabies virus.
It will also put light on the pathogenesis of rabies virus and different stages of rabies virus infection.
Then it will discuss about the laboratory diagnosis of rabies virus infection in humans as well as in animals including specimen collection, culturing, microscopy, animal inoculation and molecular diagnosis.
After that, you will get information about the prevention and control of rabies and different successful control strategies adopted by several countries of the world.
In the end it will discuss the status of rabies in Pakistan and specially WHO responses to rabies control in pakistan.
DETAILED DISCUSSION OF NECROTIZING FASCIITIS.
A SOFT TISSUE INFECTION. USUALLY CALLED AS FLESH EATING BACTERIAL INFECTION. CAUSED BY BACTERIA. AFFECTS THE SOFT SKIN TISSUES
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
3. SCRUBTYPHUS-Introduction
• Also known as -Japaneseriver fever
• known in Japanese folk to be associated with the jungle mite or
chigger, termed ‘tsutsugamushi’ inJapanese.
(tsutsuga =disease,harm, noxious and mushi =bug)
• isa zoonosis,with humansbeing accidental,dead end hosts.
4. Historical Perspective
• Rickettsial infection hasbeen one of the great scourges of mankind,
occurring in devastating epidemics during times of war and famine.
• Hippocrates in 460 bc used the termtyphus,
meaning ‘smoke’, to describe the ‘confused
state of the intellect – atendency to stupor’
associated with highfevers.
5. • Napoleon’s retreat fromMoscow
wasforced by rickettsial disease
breaking out among histroops.
• Lenin is said to have remarked, in
reference to rickettsial disease during
Russianrevolution,“either socialism will
defeat the louse or the louse will defeat
the socialism”
6. • Its impact on immunologically naive Allied
troops between 1942 and 1945 resulted in
18000 cases and 639 deaths (4.0%), as
well as an estimated 20000 cases in
Japanese troops.
• First batch of scrub typhus vaccine
used to inoculate human subjects was
dispatched to India for use by the
Allied Land Forces, South-East Asia
Command, in June 1945.
• Leading cause of pyrexia of unknown
origin (PUOs) in forces of USA during
the Vietnam conflict.
9. Indian Scenario
• In India, the disease had occurred among troops
during the Second World War in Assam and West
Bengal, and in the 1965 Indo-Pak war.
• There was a resurgence of the disease in 1990 in a
unit of an army deployed at the Pakistan border of
India.
• Occurrence reported from several states in India
including Jammu and Kashmir, Himachal
Pradesh, Uttarakhand, Bihar, West Bengal,
Meghalaya, Rajasthan, Maharashtra, Karnataka,
Tamil Nadu and Kerala.
• Scrub typhus accounts for upto 50% of
undifferentiated fever presenting to hospitals
and It remains a major uderdiagnosed
(suspected) cause of undifferentiated fever.
10. Agent of Scrub Typhus
Budding of O. tsutsugamushi on the cellular surface
• Gram-negative, rod-shaped (cocco-bacillus) bacterium
Orientia (Rickettsia) tsutsugamushi.
• wide phenotypic and genotypicdiversity
• reported serotypes are
Karp, Kato, Gilliam, Boryong,Kawazaki
• does not have a vacuolar membrane and
hence it grows freely in the cytoplasm of
infected cells.
• Cell wall lackslipopolysaccharide and
peptidoglycan and doesnot haveanouter
slime layer
11. Vector - PrimaryReservoir
• Transmitted by bite of infected larvae of the trombiculid mite
Leptotrombidium deliense (“chiggers”)
• feeds on lymph and tissue fluid rather than blood.
• bite of the mite leaves a characteristic black eschar
12. Earlier it was thought that
rodents were the natural
reservoir of infection,but it is
now believed that mites are
both the vector and the
reservoir.
Natural Reservoir
13.
14. Grasslands
Areas Around Houses
Rice Fields
The term scrub of
scrub typhus came
from the type of
vegetations (terrain
between woods &
clearings) that harbor
the vectors.
Moist Areas: Swamp & Bog
Chigger’s Habitats
16. ClinicalPresentation– Eschar
…a pathognomonicsign
• Apainless papule occurs at the bite site, later ulcerates, & transforms into
a black crust or ‘eschar’in a variable proportion of patients, the border of
the eschar is surrounded by reddisherythema.
• Difficult tospot in darker individuals; moist intertriginous surfacesmay be
missed if not looked intocarefully
18. Onset:Appears at the end of the 1st week, lasts
3~7days.
Location: Chest, abdomen, whole trunk, or upper
and lower limbs. rarely involves the face, palms
and soles.
Initially rash is in the form of pink, blanching,
discrete maculae which subsequently becomes
maculopapular, petechial or hemorrhagic.
Maculopapular Rash
19. Lymphadenopathy
• Regional lymphadenopathy:
•occurs at the end of the 1st week.
•localize: the draining lymph node around the primary
eschar
•characterized by tenderness and enlargement
• Generalized lymphadenopathy: appears 2-3 days later.
21. ClinicalPresentation- Complications
• More virulent strains of O.tsutsugamushi can cause
Respiratory
• interstitial
pneumonitis
• overwhelming
pneumonia with ARDS
Cardiac
•Toxic myocarditis
Hematological
• Thrombocytopenia
• Pancytopenia
• disseminated
intravascular
coagulation (DIC)
Neuropsychiatric
• Meningitis, Encephalitis
• Cochlear component of 8th nerve
involvement
• Transverse Myelitis
Abdominal
• acute hepatic failure
• acute renal failure
• GI bleeding
• para-aortic, portahepatic and the
splenic hilar lymphadenopathy
22. DDx– “typhus-like illness”
Typhus
(SFG, TG and/or STG)
distinguished only by specific serological tests with
acute and convalescent samples (IFA, IIP, ELISA, RFD) or
PCR assays tests, same treatment for all
Malaria by stained blood films, antigen detection assays
Arbovirus infections
(e.g. dengue, chikungunya)
serological methods (NS1, IgM, IgG assays). Dengue rash
is finer and more erythematous than scrub typhus and
with marked thrombocytopenia
Leptospirosis PCR (full blood) or culture (blood, CSF)
Relapsing fever
(lice or ticks)
demonstration of Borrelia in blood smears, serology or
PCR
Meningococcal disease blood and CSF cultures
Typhoid blood and bone marrow cultures
Viral fevers with macular rash, for example Epstein–Barr virus,
infectious mononucleosis, and primary HIV infection,
distinguished serologically
24. TheProblems faced by us..
• Diagnosis is greatly hampered by the lack of accurate andaccessible
laboratory diagnosis.
• Given the large populations of India and China, the numbers
potentially exposed areenormous.
• With the growth of ecotourism in Asia, more travellers are returning
to non-endemic areas with thisdisease.
25. LABORATORY DIAGNOSIS
Weil-Felix test
ELISA based tests, particularly immunoglobulin M
(IgM) capture assays
Molecular diagnosis byPCR
Indirect ImmunoperoxidaseAssay(IPA)
ImmunofluorescenceAssay(IFA) GOLD STANDARD
26. WEILFELIX TEST
• Sharing of the antigens between rickettsia and proteus is the basis of
this heterophile antibodytest.
• Demonstrates agglutinins to Proteus vulgaris strain OX19,OX2
and Proteus mirabilis OXK..
• Though this test lacks high sensitivity and specificity but still
serves as a useful and inexpensive diagnostic tool for
laboratory diagnosis of rickettsial disease.
• Should be carried out only after 5-7 days of onset of fever.
27. IgM and IgG ELISA
• ELISA techniques, particularly immunoglobulin M (IgM) capture
assays for serum, are probably the most of sensitive tests
available for rickettsial diagnosis.
• In cases of infection with O. tsutsugamushi,
• a significant IgM antibody titre is observed at the end of
1st week,
• IgG antibodies appear at the end of 2nd week.
28. Polymerase ChainReaction (PCR)
• a rapid and specific test for diagnosis, available only at few
centres in India.
• can be used to detect rickettsial DNA in whole blood and
eschar samples.
• P C R is targeted at the gene encoding the major 56 Kda
and/or 47 KdHTRa surface antigen gene.
• The results are best within first week for blood samples
because of presence of rickettsemia in first 7-10 days.
29. Immunufluoroscence Assay(IFA)
• This is a reference serological method for
diagnosis of Rickettsial Diseases
• considered serological ‘gold standard’; however, cost
and requirement of technical expertise limit its wide
use.
• IFA slide presents antigens from only 3 serotypes
namely Karp, Kato and Gilliam
• Therefore, it is recommended only for research
and in areas where sero-prevalence of rickettsial
diseases has been established
30. Immunoperoxidase Assay(IPA)
• is amodification of IFAtechnique that
replaces the fluorochrome with
peroxidase.
• Slide is observed using abright-field
microscope.
• Staining reaction is positive whenO.
tsutsugamushi particles stain light
brown. Control Infected
31. Supportive laboratoryInvestigations
• ChestX-Rayshowing infiltrates, mostly
bilateral
• WBCcount may become elevated tomore
than 11,000 / cu. mm.
• Thrombocytopenia (i.e. <1,00,000/ cu.mm)is
seenin majority ofpatients.
Before admission
• RaisedTransaminaselevels are commonly
observed
After treatment
32. Suspected/Clinical case
• Acute undifferentiated febrile illness of 5 days or more
with or without eschar – suspect Rickettsial infection.
• If eschar is present, fever of less than 5 days duration should
be considered as scrub typhus.
• Other presenting features: headache and rash,
lymphadenopathy, multi-organ involvement like liver, lung and
kidney involvement.
33. Probablecase
Points to consider as positive for typhus and spotted fever
groups of Rickettsiae.
A suspected clinical case
titres of 1:80 or above in OX2, OX19 and OXK
antigens by Weil Felix test
optical density (OD) > 0.5 for IgM by ELISA
34. TREATMENT
• Without waiting for laboratory confirmation of the Rickettsial
infection, antibiotic therapy should be instituted when
rickettsial disease is suspected.
• Preantibiotic era -- Mortality was variable.
• Antibiotic therapy brings about prompt disappearance of the
fever and dramatic clinical improvement.
35. Primary Health CentreLevel
• Lesssevere cases.....
ADULT CHILDREN IN PREGNANCY
Doxycycline 200 mg/day in
two divided doses for 7
days
Or
Azithromycin 500 mg in a
single oral dose for 5
days.
Doxycycline 4.5 mg/kg
body weight/day in two
divided doses for 7 days
Or
Azithromycin 10mg/kg body
weight in a single oral dose
for 5 days.
Azithromycin 500 mg in a
single oral dose for 5
days.
36. Primary Health CentreLevel
If presents with Complications
• Refer to secondary or tertiary centre - ARDS, acute renal
failure, meningo encephalitis, multi-organ dysfunction.
• Doxycycline should be initiated before referring the patient.
• In addition to recommended management of community
acquired pneumonia, Doxycycline is to be initiated
whenscrub typhus is considered likely.
37. Secondary and Tertiary Care
I.V Doxycycline
• (wherever available) 100mg twice daily in 100 ml normal saline to be
administered as infusion over half an hour initially followed by oral
therapy to complete 7-15 days of therapy.
I.V Azithromycin
• in the dose of 500mg IV in 250 ml normal saline over 1 hour once daily
for 1-2 days followed by oral therapy to complete 5 days of therapy.
I.V Chloramphenicol
• 50-100 mg/kg/d 6 hourly doses to be administered as infusion over 1
hour initially followed by oral therapy to complete 7-15 days of
therapy.
38. Prophylaxis
• Recommended under special circumstances where disease is
endemic.
• Oral chloramphenicol or tetracycline given once every 5
days for thirty-five days or weekly doses of doxycycline during
and for 6 weeks after exposure have both been shown to be
effective regimens.
• Resistance to antibiotics has been noted in several areas,
therefore prophylaxis with antibiotics cannot be guaranteed.
39. Vaccine against scrub typhus?
• There is enormous antigenic variation in Orientia
tsutsugamushi strains, and immunity to one strain does
not confer immunity to another…
• A vaccine developed for one locality may not be protective in
another locality, because of antigenic variation.
• This complexity continues to hamper efforts to produce a
viable vaccine against O.tsutsugamushi.
40. PREVENTION
• Protective clothing.
• Insect repellents containing dibutyl phthalate, benzyl
benzoate, diethyl toluamide etc applied to the skin and
clothing to prevent chigger bites.
• Do not sit or lie on bare ground or grass.
• Clearing of vegetation and chemical treatment of the soil may
help to break up the cycle of transmission from chiggers to
humans to other chiggers.
42. Public
Education
Take home message:-
Scrub typhus is a re-emerging disease in India.
an important cause of community acquired undifferentiated febrile illness in India.
It has to be considered in the differential diagnosis of sepsis and multiorgan dysfunction
syndrome.
Failure of early diagnosis is associated with significant mortality and morbidity and also leads to
expensive PUO workup.
Search for an eschar in hidden areas of body.
Screening by Weil-Felix & Diagnosis is done by IgM scrub typhus ELISA
Drug of choice - - - - Doxycycline.
43. REFERENCES-
Public
Education
•PARK’S TEXTBOOK OF PREVENTIVE AND SOCIAL MEDICINE
-23RD EDITION
•COMMUNITY MEDICINE WITH RECENT ADVANCES
-BY A.H.SURYAKANTHA ; 4TH EDITION
•HARRISON’S MANNUAL OF INTERNAL MEDICINE -19TH EDITION
•DAVIDSON’S PRINCIPLES AND PRACTICE OF MEDICINE-21ST EDITION
•WIKIPEDIA AND GOOGLE FOR WEB REFERENCES