This document discusses several arboviral diseases prevalent in India, with a focus on dengue. It provides information on the following:
1) Arboviruses are transmitted by arthropod vectors like mosquitoes and ticks. Over 40 arboviruses have been detected in India, with more than 10 known to cause human disease.
2) Important arboviral diseases discussed include dengue, Japanese encephalitis, chikungunya, yellow fever, and Kyasanur Forest disease. Details are provided on their transmission cycles, clinical features, diagnosis and prevention.
3) Dengue is transmitted by Aedes aegypti and Aedes albopictus mosquitoes. It
Arthropods form a major group of disease vectors with mosquitoes, flies, sand flies, lice, fleas, ticks and mites transmitting a huge number of diseases.
Chikungunya (chik-un-GUN-yuh) is a viral illness transmitted by mosquitoes that causes the sudden onset of fever and severe joint pain. Other signs and symptoms may include fatigue, muscle pain, headache and rash. Signs and symptoms of chikungunya usually appear within two to seven days after being bitten by an infected mosquito.
This lecture presentation contains description of arbovirus particularly detailing Dengue virus infections. Lecture outlined general characteristics of Arbovirus, classification of Arboviruses, salient features of Dengue virus, dengue pathogenesis, clinical course, laboratory diagnosis, complications of secondary dengue and some recent aspect of dengue vaccine preparation.
Arthropods form a major group of disease vectors with mosquitoes, flies, sand flies, lice, fleas, ticks and mites transmitting a huge number of diseases.
Chikungunya (chik-un-GUN-yuh) is a viral illness transmitted by mosquitoes that causes the sudden onset of fever and severe joint pain. Other signs and symptoms may include fatigue, muscle pain, headache and rash. Signs and symptoms of chikungunya usually appear within two to seven days after being bitten by an infected mosquito.
This lecture presentation contains description of arbovirus particularly detailing Dengue virus infections. Lecture outlined general characteristics of Arbovirus, classification of Arboviruses, salient features of Dengue virus, dengue pathogenesis, clinical course, laboratory diagnosis, complications of secondary dengue and some recent aspect of dengue vaccine preparation.
Rabies is an acute viral infection of the nervous system that primarily affects dogs and can also be transmitted to humans. It is a zoonotic infectious disease caused by a virus. The word Rabies originated about 3000BC from the word Rabha, which means, “violence”
Arthropods form a major group of disease vectors with mosquitoes, flies, sand flies, lice, fleas, ticks and mites transmitting a huge number of diseases.
Many such vectors are haematophagous, which feed on blood at some or all stages of their lives.
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
How to Give Better Lectures: Some Tips for Doctors
Arbovirsues with special emphasis on dengue
1. ARBOVIRAL DISEASE PREVALENCE IN INDIAARBOVIRAL DISEASE PREVALENCE IN INDIA
WITH SPECIAL EMPHASIS ON DENGUEWITH SPECIAL EMPHASIS ON DENGUE
DR. KUMAR VIKRAMDR. KUMAR VIKRAM
MD (MICROBIOLOGY)MD (MICROBIOLOGY)
IGIMS, PATNAIGIMS, PATNA
2. Arthropod-borne viruses (arboviruses) are viruses that can be
transmitted to man by arthropod vectors.
WHO definition
Arboviruses are viruses that are maintained in nature principally, or to an
important extent, through biological transmission between susceptible
vertebrate host by hematophagous arthropods; they multiply in the tissues
of arthropods, and are passed on to new vertebrates by the bites arthropod
after a period of extrinsic incubation.
3. Arboviruses are worldwide in distribution .
More numerous in the tropical than in temperate zones.
Over 500 viruses have been listed
Most cause silent infections in rodents and other wild mammals
100 of them can infect humans
In India , over 40 arboviruses have been detected, of which more
than 10 are known to produce human disease
GEOGRAPHICAL DISTRIBUTIONGEOGRAPHICAL DISTRIBUTION
4. Many different factors can contribute to the emergence of arboviral disease.
These include:
(1)virological determinants such as mutation, recombination, reassort- ment, natural
selection, fitness adaptation, and evolutionary progression
(2)Individual host determinants such as specific risk behaviors, innate resistance,
acquired immunity, and physiological factors such as age, nutritional status, and pregnancy
(3)Host population determinants such as community, behavioral, societal, transport,
commercial, and iatrogenic factors;
(4)Environmental determinants such as ecological and zoonotic influences;
(5)viruses intentionally used for harm – the threat of bioterrorism
EMERGING/ RE-EMERGING ARBOVIRAL DISEASE
5.
6. General propertiesGeneral properties
The arboviruses share some common biological properties:
1. All members produce fatal encephalitis in suckling mice after intracerebral inoculation
2. They possess haemagglutinin and agglutinate erythrocytes of goose
or day-old chicks
3. They can be grown in yolk sac or chorioallantoic membrane of chick embryo,in tissue cultures of
primary cells like chick embryo fibroblasts or continuous cell lines like vero, and in cultures of
appropriate insect tissues.
4. In general, arboviruses are readily inactivated at room temperature
and by bile salts, ether and other lipid solvents.
7. Arthropod Vectors
Mosquitoes
Japanese encephalitis, dengue, yellow fever, Rift valley fever
St. Louis encephalitis, EEE, WEE, VEE etc
Ticks
Crimean-Congo haemorrhagic fever, Kyasanur forest disease
and various tick-borne encephalitis etc.
Sandflies
Sicilian sandfly fever
8. Examples of Arthropod VectorsExamples of Arthropod Vectors
Aedes aegyptiAedes aegypti
Ixodid Ticks
Phlebotomine SandflyCulex Mosquito
9. Animal ReservoirsAnimal Reservoirs
In many cases, the actual reservoir is not known. The following animals areIn many cases, the actual reservoir is not known. The following animals are
implicated as reservoirsimplicated as reservoirs
BirdsBirds Japanese B encephalitis, St Louis encephalitis,
EEE, WEE
PigsPigs Japanese B encephalitis
MonkeysMonkeys Yellow FeverYellow Fever
RodentsRodents VEE, Russian Spring-Summer encephalitisVEE, Russian Spring-Summer encephalitis
10. Diseases CausedDiseases Caused
Fever with or without rash -- this is usually a non-specific illness resembling a number of
other viral illnesses such as influenza, rubella, and enterovirus infections. The patients
may go on to develop encephalitis or haemorrhagic fever
Encephalitis - e.g. EEE, WEE, St Louis encephalitis, Japanese B encephalitis- e.g. EEE, WEE, St Louis encephalitis, Japanese B encephalitis
Haemorrhagic fever - e.g. yellow fever, dengue, Crimean-Congo haemorrhagic fever- e.g. yellow fever, dengue, Crimean-Congo haemorrhagic fever
All arbovirus infections occur with varying degree of severity, subclinical infections being
common
11. Virus Reservoir Vector Disease
Chikungunya Monkeys Mosquito Chikungunya fever
Dengue Monkeys, Man Mosquito Dengue haemorrhagic fever
Japanese B
encephalitis
Wild birds, pigs Mosquito Encephalitis
Kyasanur forest
disease
Forest birds,
animals
Tick Haemorrhagic fever
Sindbis - Mosquito Sindbis fever
Arboviruses prevalent in India
12. virus first isolated from patients and mosquitoes during an epidemic in Tanzania in
1952-53
Outbreak in kolkata in 1963-64
In 1965 outbreak in chennai gave rise to 3,00,000 cases .
Virus was not active since 1965.
REAPPEARENCE after 41 years
During 2006, there was a large outbreak of chikungunya in India with 1.39 million
officially reported cases spread over 16 states.
First noticed in Andhra pradesh and subsquently spread to Tamil nadu, kerala ,
karnataka and then northwards as far as Delhi
Other states involved were: Maharashtra, Madhya pradesh, Gujarat, Rajasthan,
Pondicherry, Goa, Orissa, west bengal, U.P, Andaman and Nicobar islands.
14. Chikungunya virus
Chickungunya is the native word for the disease in which the
patient lies ‘doubled up’ due to severe joint pain.
The virus is transmitted by Aedes aegypti
There is no animal reservoir for the virus
Incubation period – 4-7 days
The disease is chracterised by fever, crippling joint pains,
lymphadenopathy, conjunctivitis and rash
Migratory polyarthritis mainly affects the small joints of the hands
and wrists
The fever is typically biphasic with a period of remission after
1-6 days
15. A maculopapular rash is common and most intense on the trunk
and limbs that may desquamate
Haemorrhagic manifestations are seen in some patients
DIAGNOSIS
Virus isolation – intracerebral inoculation in suckling mice or VERO cell
serological diagnosis – haemagglutination inhibition, serum neutralisation, CFT, ELISA
RT-PCR
CONTROL
• VECTOR CONTROL
•VACCINE – no vaccine has been developed
16. GEOGRAPHICAL DISTRIBUTION
Leading cause of viral encephalitis in Asia and occurs in almost all
Asian countries.
The disease has been recognised in Japan since 1871 and was
named Japanese B encephalitis to distinguish from encephalitis A.
Virus was first isolated in Japan during epidemic in 1935.
As a result of immunisation, its incidence has been declining in japan ,
the Korean peninsula and in some of regions of china.
The disease is increasingly reported from Bangladesh, India, Nepal,
Pakistan, northern Thailand, and Vietnam.
17. PROBLEM IN INDIA
•Recognition of JE was first made in 1955 in Tamil nadu when the virus was isolated
from culex vishnui.
•Remained confined to southeastern parts of India till 1973 when it caused large
outbreak in West Bengal
•From 1976, there have been periodic outbreaks in various parts of India –
Dibrugarh(Assam) in the east, Gorakhpur (UP) and Haryana in the north and Goa
and Maharashtra in the west.
•Endemic in 14 states.
•Assam, Bihar, Haryana, UP, Karnataka, and Tamil nadu report outbreaks every year
and contribute to 80% of cases and deaths .
•About 300 million people are at risk.
18.
19.
20. Epidemiology
Vector –culicine mosquitoes like culex tritaeniorhynchus, c. vishnui, c. gelidus
and some anophelines
breeding place – rice fields, shallow ditches, pools
Reservoir host – herons, egrets
Amplifier host – pigs
Human infection is a incidental “dead end’ event.
21. Clinical features
Most human infections are subclinical: the inapparent to clinical
cases is 500-1000:1
Incubation period: 5-15 days
The course of the disease in man may be divided into three stages
1.Prodromal stage
2.Acute encephalitic stage
3.Late stage and sequelae
22. Prodromal stage
The onset of illness is usually acute and symptoms include fever,
headache and vomiting
Acute encephalitic stage
After 1-6 days, signs of encephalitis characterised by neck rigidity,
convulsions, altered sensorium and coma appear
Late stage and sequelae
Convalescence may be prolonged and residual neurological deficits
may not be uncommon
Case fatality rate varies between 20-40%, but it may reach 58% and
over in some epidemics
Residual neurological damage may persist in about 50% of survivors
23. The disease is usually diagnosed by serology
No specific therapy is available
Prevention
Preventive measures include mosquito control and establishment
of piggeries away from residential areas
VACCINES:
1.Formaline inactivated mouse brain vaccine
• Based on Nakayama or Beijing strains
• Dose-0.5 ml for children< 3yrs and 1 ml for children more than
1 yr
• Route- subcutaneously
• Administration – 2 primary doses 4 weeks apart and booster doses
after 1 year and subsquently at 3 year interval until the age of
10-15 yrs.
24. 2. Live attenuated vaccine
Based on SA 14-14-2 strain
dose – 0.5 ml
Route - subcutaneously
Single dose followed by a single booster given at an interval of 1 year
26. Yellow FeverYellow Fever
Yellow fever is a mosquito-borne acute febrile illness accompanied by hepatic necrosisYellow fever is a mosquito-borne acute febrile illness accompanied by hepatic necrosis
It occurs mainly in tropical Africa and Latin AmericaIt occurs mainly in tropical Africa and Latin America
It does not exist in IndiaIt does not exist in India
The name has been derived from ‘yellow quarantine flag’ usedThe name has been derived from ‘yellow quarantine flag’ used
by the ships during 17by the ships during 17thth
century to warn the presence, on boardcentury to warn the presence, on board
of this infectionof this infection
Yellow fever occurs in 2 major forms: urban and jungle (sylvatic) cycleYellow fever occurs in 2 major forms: urban and jungle (sylvatic) cycle
27. In the urban cycle, man serves both as reservoir and as definitive
host, the virus being transmitted by Aedes aegypti mosquito
In the forest or sylvatic cycle, wild monkeys act as reservoirs and several species
of forest mosquitos (Haemagogus spegazzinnii in south America and Aedes
africanus and A. simpsoni in Africa) are vectors. Human cases occur only when
humans trespass into the forest or when monkeys raid villages.
28. India is a yellow fever “receptive area” that is “ an area in which yellow fever
does not exist, but where conditions would permit its development if
introduced”
The population of india is unvaccinated and susceptible to yellow fever.
The vector, Aedes aegypti is found in abundance
The climatic conditions are favourable in most parts of india for its
transmission
The only missing link is the virus of yellow fever which does not seem
to occur in india
29. Clinical features
After an incubation period of 3-6 days, patient develops fever with
chills, headache, myalgia and vomiting
Most cases are mild in nature, especially in the endemic areas, in
whom the disease may present as undifferentiated fever without
jaundice
The pulse is usually slow despite a high temperature
In 15-20% of cases, the disease progresses to a more serious form
with jaundice, albuminuria, renal failure and haemorrhagic
manifestations and the patient may die of hepatic and renal failure
30. Prophylaxis
There is no antiviral drug against yellow fever
The control of urban yellow fever can be achieved by eradicating
the vector mosquito
vaccine
17D vaccine was developed by Theiler in 1937 by passaging the
Asibi strain.
Given subcutaneously
Mandatory for travel to or from endemic areas.
Valid for 10 years beginning 10 days after vaccination.
31. Kyasanur Forest Disease (KFD)
oKyanasur forest disease is a febrile disease associated with haemaorrhages transmitted to man
by bite of infective ticks.
HISTORY
first recognised in 1957 in Shimoga district of karnataka state .
Local inhabitants called it “monkey disease”
Later named after the locality – kyanasur forest
PROBLEM STATEMENT
Remained confined to the areas contiguous to its original focus in the Sagar, Sorab and
Shikarpur taluks of Shimoga district for many years.
Between 1972 and 1975 , another foci developed in adjacent areas in north Kanara.
In 1982, appearance of epizoonotic and epidemic in Belthangadi taluk in south kanara.
The ecological disturbance caused by clear felling of virgin forest is believed to have
activated a silent enzoonotic focus of the virus.
32.
33. Epidemiology
NATURAL HOST AND RESERVOIR
Reservoir- small mammals particularly rats and squirrels, birds and bats
Monkeys- amplifying host
VECTORS
Haemaphysalis spinigera
H. turtura
INCUBATION PERIOD – between 3 and 8 days
CLINICAL FEATURES
Sudden onset of fever, headache and sever myalgia
Gastrointestinal disturbances and haemorrhages from nose, gums , stomach
and instestine in severe cases
Case fatality rate – 5-10 %
34. Control
Control of ticks
The population at risk should be vaccinated with killed KFD vaccine
Personnel protection – protection of individuals by adequate clothing
and insect repellents
35.
36. HISTORY
Dengue virus was isolated in Japan in 1943 by inoculation of serum of patients in
suckling mice and at Calcutta (now Kolkata) in 1944 from serum samples of US
soldiers.
The first epidemic of clinical dengue-like illness was recorded in Madras (now
Chennai) in 1780 and the first virologically proved epidemic of DF in India occurred
in Calcutta and Eastern Coast of India in 1963-1964.
The first major epidemic of the DHF occurred in 1953-1954 in Philippines
followed by a quick global spread of epidemics of DF/DHF.
The DHF started simmering in various parts of India since 1988.
The first major wide spread epidemics of DHF/DSS occurred in India in 1996
involving areas around Delhi and Lucknow13 and then it spread to all over the
country
37. PROBLEM STATEMENT
oDengue is the most rapidly spreading mosquito-borne viral disease in the world.
o In the last 50 years, incidence has increased 30-fold with increasing geographic expansion
to new countries and, in the present decade, from urban to rural settings.
o An estimated 50 million dengue infections occur annually and approximately 2.5 billion
people live in dengue endemic countries.
o5,00,000 people with DHF require hospitalisation each year.
o 90% of them are childern less than 5 years and about 2.5 % of those affected die.
o Dengue is endemic in more than 100 countries.
o The south – east asia and western pacific regions are the most seriously affected.
38. An Epidemic, Endemic& Hyper Endemic
South- East Asia is divided into 3 Categories:
Cat A: India, Bangladesh, Myanmar, Sri Lanka, Indonesia, Thailand,
Maldives
Cat B: Bhutan, Nepal
Cat C: DPR Korea
39. INDIAN SCENARIO
Increased risk in recent years due to
Rapid urbanisation
Lifestyle changes
Deficent water management
Seasonal pattern – cases peak after monsoon
Perennial transmission in southern states and Gujarat
Endemic in 31 states/UTs.
All the serotypes have been isolated in India.
At present DENV-1 and DENV-2 serotypes are widespread.
40. Epidemiological studies where dengue virus was identified
Year Region where study was conducted Type of dengue virus
detected
1964 Vellore, Tamil Nadu DV-2
NA South India DV-3
1966 Vellore, Tamil Nadu DV-3
1968 Vellore, Tamil Nadu DV- 1,2,3 & 4
1968 Kanpur, Uttar Pradesh DV-4
1969 Kanpur, Uttar Pradesh DV-4 and DV-2
1970 Hardoi, Uttar Pradesh DV-2
NA NA DV- 1,2,3 & 4
1983 Kolkata, West Bengal DV-3
1985 Jalore town, South-West
Rajasthan
DV-3
NA Chikalthana, Pimpalgaon and
Waloor villages in Parbhani
district of Maharashtra.
DV-1 & 2
1988 Delhi DV-2
1990 Calcutta, West Bengal DV-3
1988 Rural and urban areas of Gujarat DV-2
1993 Mangalore, Karnataka DV-2
NA Assam and Nagaland DV-2
1996 Ludhiana, Punjab DV- 1,2,3 & 4
1996 Lucknow DV-2
1996 Delhi DV-2
1996 Delhi DV-2
1997 Delhi DV-1
1996 Delhi DV-2 (Genotype IV)
NA Ahmedabad, Gujarat DV-2
1997 Delhi DV-1
NA Delhi DV-2 (Genotype IV)
1996 Rural areas of Haryana DV-2
2001 Dharmapuri district, Tamil Nadu DV-2
NA Andaman and Nicobar Islands DV-2
2001 Gwalior, Madhya Pradesh DV-2
NA Northern India DV-2 (Genotype IV)
2001 Chennai, Tamil Nadu DV-3
2003 Northern India (Delhi & Gwalior) DV-3
2005 Kolkata, West Bengal DV-3
2003 Kanyakumari district, Tamil Nadu DV-3
2003-04 Delhi DV-3 (subtype III)
2003-05 Delhi 2003 - DV - 1,2,3 & 4
2005 - D - 3
2006 Delhi DV-3
2006 Delhi DV-1 & 3
2001-07 North India (Delhi and Gwalior
region)
DV-1 (Genotype III)
2006 Delhi DV-1,3 & 4
2008 Delhi region DV-1,2 & 3
44. The AgentThe Agent
Arbovirus (ss RNA Virus)
Genus Flavivirus
Family Flaviviraede
4 serotypes- DENV 1, DENV 2, DENV 3 & DENV4
Antigenic similarity but infection with one serotype does not
provide lifelong immunity for other serotypes (Cross Immunity
lasts only a few months),
…Instead prior immune sensitization worsens the disease
scenario
45. Denv Has…Denv Has…
A lipoprotein envelope
3 structural protein genes encoding: {CME}
– Nucleocapsid or core protein (C),
– Membrane- associated protein (M),
– Envelope protein (E), and
7 non-structural protein (NS) genes including, envelope glycoprotein,
NS 1
NS 1 is of diagnostic and pathological importance.
It is associated with viral haemagglutination and neutralization activity.
46.
47. The HostThe Host
Infective Stage: 1 day before onset of fever to day 5
Intrinsic Incubation Period: 4- 6 days
High Risk Patients:
– Extremes of Age
– Pregnancy
– Any condition prone to heavy blood loss: Peptic ulcer disease;
menstruation; haemolytic anaemia; G- 6PD deficiencies;
thalassemia; patients on steroids, NSAIDS
– Any chronic condition: DM, HTn, Asthma, Cirrhosis, IHD, CRF
48. Remember… “Prior immune sensitization
worsens the disease scenario”
1st
Infectio
n with
DENV-
1
Asymptomatic/
Non specific
manifestations/
DF
2nd
Infection
with
DENV- 2, 3
or 4
DHF/
DSS/
Severe
Disease
Secondary Infection with DENV 2 or multiple infections with different
serotypes causes Severe Disease (DHF/ DSS)
DENV 1/ DENV 2 Sequence is the worst
50. The EnvironmentThe Environment
Tropical& Sub- tropicalTropical& Sub- tropical
Urban, Peri urban;Urban, Peri urban; RuralRural
Rapid Unplanned uncontrolledRapid Unplanned uncontrolled urbanizationurbanization,,
Transportation:Transportation: human movement and congregationhuman movement and congregation
Poor water storage and managementPoor water storage and management
Seasonal Pattern:Seasonal Pattern: Post Monsoon (But Perennial in Gujarat&Post Monsoon (But Perennial in Gujarat&
South India)South India)
51. Global WarmingGlobal Warming
2 degree rise in temp-2 degree rise in temp-
– Shortens extrinsic IP- more infected mosquitos to furtherShortens extrinsic IP- more infected mosquitos to further
spread DENVspread DENV
– Enhances the life cycle of AedesEnhances the life cycle of Aedes
– Shortens the size of the mosquitoShortens the size of the mosquito
– Rise in temp- mosquito bites more frequently due toRise in temp- mosquito bites more frequently due to
“dehydration”- further spreads DENV“dehydration”- further spreads DENV
52. The VectorThe Vector
Ae albopictusAe albopictus Eggs Survive Sub Freezing TempEggs Survive Sub Freezing Temp
Ae aegyptiAe aegypti-- Cosmo tropical species between latitudes 45°N and 35°SCosmo tropical species between latitudes 45°N and 35°S
Vector CompetencyVector Competency
Vector CapacityVector Capacity
Transovarial SpreadTransovarial Spread
Endophagic, EndophilicEndophagic, Endophilic
16- 35 °C, 60- 80% Relative Humidity16- 35 °C, 60- 80% Relative Humidity
53. Vector CompetencyVector Competency
– High susceptibility to infecting virus
– Ability to replicate the virus
Ability to transmit the virus to another host
Both Ae. aegypti and Ae. albopictus carry high vectorial
competency for dengue viruses.
54. VectorialVectorial CapacityCapacity: Depends on the: Depends on the
Environmental and BiologicalEnvironmental and Biological
characteristics of the Vectorcharacteristics of the Vector
Ae. aegyptiAe. aegypti
Highly domesticated
Strongly anthropophilic
Nervous feeder (i.e. it bites more
than one host to complete one blood
meal) and
Discordant species (i.e. it needs
more than one feed for the
completion of the gonotropic cycle)
These habits epidemiologically result
in the generation of multiple cases
and the clustering of dengue cases
in cities.
Ae. albopictusAe. albopictus
Feral
Feeds on both humans and animals
Aggressive feeder (i.e. it can complete
its blood meal in one go on one
person)
Concordant species (does not require
a second blood meal for the
completion of the gonotropic cycle)
So, Ae. albopictus has poor vectorial
capacity.
55.
56. Undifferentiated FeverUndifferentiated Fever
Primary dengue infection
May develop a simple fever indistinguishable from other viral
infections.
Maculopapular or rubelliform rashes on face, neck and chest may
accompany the fever or may appear during defervescence (Day 3-5)
URTI and GI symptoms are common
57. Dengue FeverDengue Fever
Older children, adolescents and adults
Acute (Sudden, sharp) rise in temperature (39°C- 40°C) for 5- 7 days
Biphasic fever with severe headache, myalgia, arthralgia and bone pains
(break-bone fever), particularly in adults
Rashes, flushed face, retro-orbital pain on eye movement or eye pressure,
photophobia
Altered taste sensation, Anorexia, Sore throat, Dragging pain in inguinal region
Leukopenia and thrombocytopenia- mild
Occasionally, Haemorrhage such as gastrointestinal bleeding, hyper
menorrhea, massive epistaxis (DF with Hmrgh)
58. Dengue Haemorrhagic Fever (DHF)Dengue Haemorrhagic Fever (DHF)
Children less than 15 years of age in hyper endemic areas, in association with repeated
dengue infections (secondary dengue infection). Incidence of DHF in adults is increasing
Rarely DHF may occur in Primary infections with DENV-1 and DENV-3 as well as in infants.
Signs and symptoms similar to DF in the early febrile phase.
Positive tourniquet test (TT), petechiae on extremities, easy bruising and/or GI haemorrhage
Abnormal haemostasis and plasma leakage are the main pathophysiological hallmarks of
DHF
Thrombocytopenia and rising haematocrit/haemo concentration before the subsidence of
fever/ onset of shock.
59. COURSE AND CLINICAL FEATURES
3 PHASES
FEBRILE PHASE
Sudden high grade fever
accompanied by facial flushing, skin erythema, generalised
body ache, myalgia, arthralgia, retro-orbital eye pain,
photophobia
Sore throat, injected pharynx, conjunctival injection
Anorexia, nausea and vomiting – common
Mild haemorrhagic manifestations – petechiae, mucosal
bleeding
Last for 2-7 days
Progressive decrease in total white cell count
60. CRITICAL PHASECRITICAL PHASE
Warning signs
Condition worsen around the time of deferevescence
On 3-8 days of illness
Progressive leucopenia
Rapid decrease in platelet
Increase in heamatocrit severity of plasma leakage
Haemorrhagic manifestation – easy bruising and bleeding at venepuncture site
Profound shock
hypoperfusion metabolic acidosis, organ impairement,
DIC severe haemorrhage decrease heamatocrit
61. WARNING SIGNSWARNING SIGNS
Between 3-7 days of illness
Abdominal pain and tenderness
Persistent vomiting
Clinical fluid accumulation
Mucosal bleed
Lethargy, restlessness
Liver enlargement > 2cm
Increase in Hct with rapid decrease in platelet count
62. RECOVERY PHASERECOVERY PHASE
Gradual reabsorption of extravascular fluidGradual reabsorption of extravascular fluid
Improvement inImprovement in
– General well beingGeneral well being
– ApetiteApetite
– GI symptomsGI symptoms
– Hemodynamic statusHemodynamic status
Isles of white in the sea of redIsles of white in the sea of red
Haematocrit stabilisesHaematocrit stabilises
Rise of WBC countRise of WBC count
Recovery of platelet countRecovery of platelet count
63. Dengue Shock Syndrome (DSS)Dengue Shock Syndrome (DSS)
Hypovolemic shock due to plasma leakage
Pleural effusion, Ascites (plasma leakage to pleural& peritoneal cavities)
Hypothermia- Cold clammy skin
Fulminant hepatic failure
Optimal fluid management is important- Avoid over hydration
70. CONTROL MEASURES
MOSQUITO CONTROL
– ANTI-LARVAL MEASURES
– ANTI- ADULT MEASURES
VACCINES
– NO SATISFACTORY VACCINE
OTHER MEASURES
– Bed-nets
– Wearing full sleeve shirts, full pants
– Mosquito repellent creams
– Environmental measures
Elimination of mosquito breeding places
Management of roof tops
Proper covering of stored water
Editor's Notes
Hyperendemicity: All 4 strains present in the community
Cat A:
If PSM guys teach “dengue” in your country then you are in Cat A,
Dengue is leading cause of hospitalizations& deaths among children
Hyperendemicity
Spreading to Rural Areas
Cat B: 2004
Uncertain Endemicity
Cat C: Non endemic