This talks about the HAV, HBV and HCV , intro, properties, epidemiology and transmission, pathogenesis , clinical findings , laboratory diagnosis, and prevention
Dr Paba Palihawadana, Chief Epidemiologist, World Hepatitis Day symposium was organized by the Sri Lanka College of Venereologists on world hepatitis day on 28. July 2015 at BMICH
Hepatitis C
Hepatitis C is a liver disease caused by the hepatitis C virus (HCV): the virus can cause both acute and chronic hepatitis, ranging in severity from a mild illness lasting a few weeks to a serious, lifelong illness.
Polio: flaccid paralysis, major and minor
disease, fecal-oral
Coxsackievirus A: vesicular diseases,
meningitis; coxsackievirus B (body):
pleurodynia, myocarditis
Other echovirus and enteroviruses: like
coxsackievirus
Rhinoviruses: common cold, acid labile, does
not replicate above 33° C
Biology, Virulence, and Disease
• Small size, icosahedral capsid, positive RNA
genome with terminal protein
• Genome is sufficient for infection
• Encodes RNA-dependent RNA polymerase,
replicates in cytoplasm
Enteroviruses
• Capsid virus resistant to inactivation
• Disease due to lytic infection of important
target tissue
• Polio: cytolytic infection of motor neurons of
anterior horn and brainstem, paralysis
• Coxsackievirus A: herpangina, hand-foot-
and-mouth disease, common cold,
meningitis
• Coxsackievirus B: pleurodynia, neonatal
myocarditis, type 1 diabetes
Rhinoviruses
• Acid labile and cannot replicate at body
temperature
• Restricted to upper respiratory tract
• Common cold
Epidemiology
• Enteroviruses transmitted by fecal-oral route
and aerosols
• Rhinoviruses transmitted by aerosols and
contact
Diagnosis
• Immune assays (ELISA) or RT-PCR genome
analysis of blood, CSF, or other relevant
sample
Treatment, Prevention, and Control
• OPV and IPV polio vaccines
P
icornaviridae is one of the largest families of viruses and
includes some of the most important human and animal
viruses (Box 46-1). As the name indicates, these viruses are
small (pico) ribonucleic acid (RNA) viruses that have a
naked capsid structure. The family has more than 230
members divided into nine genera, including Enterovirus,
Rhinovirus, Hepatovirus (hepatitis A virus; discussed in
Chapter 55), Cardiovirus, and Aphthovirus. The enterovi-
ruses are distinguished from the rhinoviruses by the stabil-
ity of the capsid at pH 3, the optimum temperature
for growth, the mode of transmission, and their diseases
Viral hepatitis is the leading cause of liver cancer and the most common reason for liver transplantation
In the United States, an estimated 1.2 million Americans are living with chronic Hepatitis B and 3.2 are living with chronic Hepatitis C
Many do not know they are infected
Each year an estimated 21,000 persons become infected with Hepatitis A; 35,000 with Hepatitis B, and 17,000 with Hepatitis C
Hepatitis A – fecal/oral, contaminated food, vaccine available
Hepatitis B – blood, semen, vertical (mother-child), vaccine available
Hepatitis C – blood (IV drug use, transfusion, organ donation, unsterile injecting equipment, sexual intercourse)
Hepatitis D – survives only in cells co-infected with hepatitis B
Hepatitis E* – contaminated food or water, fecal/oral
*causes short-term disease and is not a chronic carrier state
Dr Paba Palihawadana, Chief Epidemiologist, World Hepatitis Day symposium was organized by the Sri Lanka College of Venereologists on world hepatitis day on 28. July 2015 at BMICH
Hepatitis C
Hepatitis C is a liver disease caused by the hepatitis C virus (HCV): the virus can cause both acute and chronic hepatitis, ranging in severity from a mild illness lasting a few weeks to a serious, lifelong illness.
Polio: flaccid paralysis, major and minor
disease, fecal-oral
Coxsackievirus A: vesicular diseases,
meningitis; coxsackievirus B (body):
pleurodynia, myocarditis
Other echovirus and enteroviruses: like
coxsackievirus
Rhinoviruses: common cold, acid labile, does
not replicate above 33° C
Biology, Virulence, and Disease
• Small size, icosahedral capsid, positive RNA
genome with terminal protein
• Genome is sufficient for infection
• Encodes RNA-dependent RNA polymerase,
replicates in cytoplasm
Enteroviruses
• Capsid virus resistant to inactivation
• Disease due to lytic infection of important
target tissue
• Polio: cytolytic infection of motor neurons of
anterior horn and brainstem, paralysis
• Coxsackievirus A: herpangina, hand-foot-
and-mouth disease, common cold,
meningitis
• Coxsackievirus B: pleurodynia, neonatal
myocarditis, type 1 diabetes
Rhinoviruses
• Acid labile and cannot replicate at body
temperature
• Restricted to upper respiratory tract
• Common cold
Epidemiology
• Enteroviruses transmitted by fecal-oral route
and aerosols
• Rhinoviruses transmitted by aerosols and
contact
Diagnosis
• Immune assays (ELISA) or RT-PCR genome
analysis of blood, CSF, or other relevant
sample
Treatment, Prevention, and Control
• OPV and IPV polio vaccines
P
icornaviridae is one of the largest families of viruses and
includes some of the most important human and animal
viruses (Box 46-1). As the name indicates, these viruses are
small (pico) ribonucleic acid (RNA) viruses that have a
naked capsid structure. The family has more than 230
members divided into nine genera, including Enterovirus,
Rhinovirus, Hepatovirus (hepatitis A virus; discussed in
Chapter 55), Cardiovirus, and Aphthovirus. The enterovi-
ruses are distinguished from the rhinoviruses by the stabil-
ity of the capsid at pH 3, the optimum temperature
for growth, the mode of transmission, and their diseases
Viral hepatitis is the leading cause of liver cancer and the most common reason for liver transplantation
In the United States, an estimated 1.2 million Americans are living with chronic Hepatitis B and 3.2 are living with chronic Hepatitis C
Many do not know they are infected
Each year an estimated 21,000 persons become infected with Hepatitis A; 35,000 with Hepatitis B, and 17,000 with Hepatitis C
Hepatitis A – fecal/oral, contaminated food, vaccine available
Hepatitis B – blood, semen, vertical (mother-child), vaccine available
Hepatitis C – blood (IV drug use, transfusion, organ donation, unsterile injecting equipment, sexual intercourse)
Hepatitis D – survives only in cells co-infected with hepatitis B
Hepatitis E* – contaminated food or water, fecal/oral
*causes short-term disease and is not a chronic carrier state
Hepatitis is inflammation of the liver tissue.[3][5] Some people or animals with hepatitis have no symptoms, whereas others develop yellow discoloration of the skin and whites of the eyes (jaundice), poor appetite, vomiting, tiredness, abdominal pain, and diarrhea.[1][2] Hepatitis is acute if it resolves within six months, and chronic if it lasts longer than six months.[1][6] Acute hepatitis can resolve on its own, progress to chronic hepatitis, or (rarely) result in acute liver failure.[7] Chronic hepatitis may progress to scarring of the liver (cirrhosis), liver failure, and liver cancer.[3]
Hepatitis
Alcoholic hepatitis.jpg
Alcoholic hepatitis as seen with a microscope, showing fatty changes (white circles), remnants of dead liver cells, and Mallory bodies (twisted-rope shaped inclusions within some liver cells). (H&E stain)
Specialty
Infectious disease, gastroenterology, hepatology
Symptoms
Yellowish skin, poor appetite, abdominal pain[1][2]
Complications
Scarring of the liver, liver failure, liver cancer[3]
Duration
Short term or long term[1]
Causes
Viruses, alcohol, toxins, autoimmune[2][3]
Prevention
Vaccination (for viral hepatitis),[2] avoiding excessive alcohol
Treatment
Medication, liver transplant[1][4]
Frequency
> 500 million cases[3]
Deaths
> One million a year[3]
Hepatitis is most commonly caused by the virus hepatovirus A, B, C, D, and E.[2][3] Other viruses can also cause liver inflammation, including cytomegalovirus, Epstein–Barr virus, and yellow fever virus. Other common causes of hepatitis include heavy alcohol use, certain medications, toxins, other infections, autoimmune diseases,[2][3] and non-alcoholic steatohepatitis (NASH).[8] Hepatitis A and E are mainly spread by contaminated food and water.[3] Hepatitis B is mainly sexually transmitted, but may also be passed from mother to baby during pregnancy or childbirth and spread through infected blood.[3] Hepatitis C is commonly spread through infected blood such as may occur during needle sharing by intravenous drug users.[3] Hepatitis D can only infect people already infected with hepatitis B.[3]
Hepatitis A, B, and D are preventable with immunization.[2] Medications may be used to treat chronic viral hepatitis.[1] Antiviral medications are recommended in all with chronic hepatitis C, except those with conditions that limit their life expectancy.[9] There is no specific treatment for NASH; physical activity, a healthy diet, and weight loss are recommended.[8] Autoimmune hepatitis may be treated with medications to suppress the immune system.[10] A liver transplant may be an option in both acute and chronic liver failure.[4]
Worldwide in 2015, hepatitis A occurred in about 114 million people, chronic hepatitis B affected about 343 million people and chronic hepatitis C about 142 million people.[11] In the United States, NASH affects about 11 million people and alcoholic hepatitis affects about 5 million people.[8][12] Hepatitis results in more than a million deaths a year.
Triaging patients with suspected pulmonary embolismKhaled AlKhodari
This lecture aims to guide the way to deal with patients with suspected pulmonary embolism and to classify them according to risk scores.
Additionally it helps in the decision of thrombolysis
How to read ECG systematically with practice strips Khaled AlKhodari
This lecture simplifies the steps of reading ECG systematically. It starts with a simple heart anatomy and the logical steps that should be followed to perfect ECG reading without missing any abnormality. Finally, there are some practice ECG strips that include but not only MI, STEMI, Wellens syndrome, Pulmonary embolism, LVH, arrhythmias... and others
This simplified lecture gives an account of how to approach a patient with a neck mass. Moreover, it shows hoe master thyroid gland history taking and examination and general examination.
Additionally, the lecture is supported by many real-life scenarios to cover the topics from a clinical point of view.
This lecture covers the basics of suturing i.e wound healing, indications and contraindications of suturing, wound assessment, wound aftercare, suture and needle types, suturing techniques, knot types.
This lecture shows the recently updated guidelines for the management of hypertension in primary health care clinics. Moreover, it talks about secondary and resistant hypertension.
This presentation explains in detail the definition, pathophysiology, signs & symptoms, management, and prognosis of intestinal obstruction, ileus, and volvulus.
this lecture explains Syncope which is a transient loss of consciousness from many points: the definition, causes, next step, history and physical examination from evidence based resources as the UpToDate and the European society of cardiology guidelines 2018.
INTRODUCTION — Normal bone growth and mineralization require adequate calcium and phosphate, the two major constituents of the crystalline component of bone. Deficient mineralization can result in rickets and/or osteomalacia. Rickets refers to deficient mineralization at the growth plate, as well as architectural disruption of this structure. Osteomalacia refers to impaired mineralization of the bone matrix. Rickets and osteomalacia usually occur together as long as the growth plates are open; only osteomalacia occurs after the growth plates have fused.
rickets is a nutritional deficiency disease that involves mainly calcium, vitamin d, or phosphate resulting in decreased bone stability and strength, Delayed closure of the fontanelles,Parietal and frontal bossing. Craniotabes (soft skull bones).
Enlargement of the costochondral junction visible as beading along the anterolateral aspects of the chest (the "rachitic rosary") . Formation of Harrison sulcus (or groove),Widening of the wrist and bowing of the distal radius and ulna, Progressive lateral bowing of the femur and tibia and causes defects in teeth.
there is two types of rickets: phosphopenic and calcipenic.
pathogenesis: Growth plate thickness is determined by two opposing processes: o chondrocyte proliferation and hypertrophy on the one hand. o vascular invasion of the growth plate followed by conversion into primary bone spongiosa on the other. • Vascular invasion requires mineralization of the growth plate cartilage and is delayed or prevented by deficiency of calcium or phosphorus growth plate cartilage accumulates and the growth plate thickens. • In addition, the chondrocytes of the growth plate become disorganized, losing their columnar orientation with characteristic expansion of the hypertrophic zone. • In the bone tissue below the growth plate (metaphysis), the mineralization defect leads to the accumulation of osteoid.
Involuntary movements- dyskinesia are abnormal involuntary motor movements associated with many diseases
Here I try to show some common movements in a simple way
this show talks about some new technologies in medicine including visual reality , some mobile medical apps , and few about databases
this focuses more on the pharmacology.
Benign prostatic hyperplasia is a disease affects men older than 40 years , it means increase in prostate to a level can obstruct urination or making icfections to urinary tract.
Main reference is Robbins basic pathology 9the ed and others
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
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
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.
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
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.
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.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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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.
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
4. Hepatitis A is an acute infectious disease of the liver caused by
the Hepatitis A virus
There are Five medically important viruses infect the liver
1- HAV
2- HBV
3- HCV
4- HDV
5- HEV
4
6. *- HAV is a typical enterovirus related to picornavirus family , it has
a single strand RNA genome and a nonenveloped icosahedral
nucleocapsid and replicates in the cytoplasm
*-Has one serotype, and there is no antigenic relationship to
HBV or other hepatitis viruses
6
8. *- HAV is transmitted by the fecal–oral route and viruses appear in the stool
2 weeks before the appearance of symptoms,
*- Children are the most common infected group . And mostly occurs in
summer camps and boarding schools
*- Sources of this virus arise from fecally contaminated water and eating raw
foods .. (( it is unlike HBV & HCV )
*- 50 – 75 % of the adults in the united states are infected by this virus
8
9. *-pathogenesis of HAV isn't completely understood and infected hepatocytes usually
produce no cytopathic effects . ( it occurs by the attack of the cytotoxic T cells )
*- No chronic infection after Hepatitis A ensues
*-The immune response consists initially of IgM antibody which is detectable
at the time of jaundice
*- appearance of IgM is followed 1 to 3 weeks later by the production of
IgG antibody which provides lifelong protection
9
10. The clinical manifestations of hepatitis are virtually the same . It includes
Fever, anorexia, nausea, vomiting, and jaundice are typical
*-Dark urine, pale feces, and elevated transaminase levels are seen
*-Most cases resolve spontaneously in 2 to 4 weeks , and it has an
incubation period of (3–4 weeks(
*-There is no predisposition to hepatocellular carcinoma
10
12. 1- The detection of IgM antibody is the most important test
2- A four-fold rise in IgG antibody titer can also be used.
3-isolation of the virus in cell culture is possible but not available
in the clinical laboratory.
12
13. 1-active immunization with a vaccine containing inactivated HAV
is available.
.
2-passive immunization should be given to provide immediate protection
and the vaccine given to provide long-term protection
3-vaccine is also effective in post-exposure prophylaxis if given within
2 weeks of exposure.
4-Twinrix vaccine can be given
5-proper hygiene (e.g sewage disposal and handwashing
13
18. HEPATITIS B VIRUS
Disease
HBV causes hepatitis B.
Important Properties
1-HBV is a member of the Hepadnavirus family.
(DNA enveloped virus )
2-It is an enveloped virion with an icosahedral nucleocapsid
core containing a partially double-stranded circular DNA
genome
18
Hepatitis B Virion : Also known as a Dane particle (named for
the scientist who first published electron micrographs of the
virion).
19. Figure 41–1
19
FIGURE 41–2 Hepatitis B
virus—electron
micrograph. Long
arrow points to a typical
virion of hepatitis B virus.
Short arrow points
to a small sphere (just left
of arrowhead) and a long
rod (just right of
arrowhead), both
composed only of HB
surface antigen
20. MCQ :
Which of these organisms is also called Dane particle :
1-infectious HAV
2-infectious HBV
3-infectious HDV
4-infectious HCV
5-1+2+3
6-4+3+1
7-None of the above
8-all of the above
20
22. HEPATITIS B VIRUS
((Electron microscopy of a patient’s serum reveals three
different types of particles:
a few virions and many spheres and long filaments which
are composed of surface antigen (Figure 41–2). HBV is the
only human virus that produces these spheres and filaments
in such large numbers in the patient’s blood. The ratio of
filaments and small spheres to virions is 1000:1))
22
23. HEPATITIS B VIRUS
The envelope contains a protein called the surface antigen (HBsAg), which is important
for laboratory diagnosis and immunization.
The genome contains four genes that encode five proteins <<:
1- the S gene encodes the surface antigen,
2- the C gene encodes the core antigen and the e antigen,
3- the P gene encodes the polymerase,
4- and the X gene encodes the X protein.
The X protein is an activator of viral RNA transcription.
23
HBsAg was known as Australia antigen because it was first found in the
serum of an Australian aborigine.
24. HEPATITIS B VIRUS
In addition to HBsAg, there are two other important antigens: the core
antigen (HBcAg) and the e antigen (HBeAg).
The core antigen, as the name implies, forms the nucleocapsid core of
the virion,
the e antigen is secreted from infected cells into the blood. The e
antigen is an important indicator of transmissibility. )
24
25. HEPATITIS B VIRUS
For vaccine purposes, HBV has one serotype based on HBsAg.
The specificity of HBV for liver cells is based on two properties:
1-virus-specific receptors located on the hepatocyte cell membrane
(facilitate entry)
2-transcription factors found only in the hepatocyte that enhance
viral mRNA synthesis
Humans are the only natural hosts of HBV.
There is no animal reservoir.
25
26. Transmission & Epidemiology
The three main modes of transmission are:
1- blood
2- sexual intercourse,
3- perinatally from mother to newborn.
The observation that needle-stick injuries can transmit the virus
indicates that only very small amounts of blood are necessary.
HBV infection is especially prevalent in addicts who use intravenous
drugs.
Screening of blood for the presence of HBsAg has greatly decreased
the number of transfusion-associated cases of hepatitis B
26
27. However, because blood transfusion is a modern procedure, there must
be another, natural route of transmission. It is likely that sexual
transmission and transmission from mother to child during birth or breast
feeding are the natural routes.
Note that enveloped viruses, such as HBV, are more sensitive to the
environment than nonenveloped viruses and hence are more efficiently
transmitted by intimate contact (e.g., sexual contact).
Nonenveloped viruses, such as HAV, are quite stable and are
transmitted well via the environment
(e.g., fecal–oral transmission).
27
28. Hepatitis B is found worldwide but is particularly prevalent in Asia.
Globally, more than 300 million people are chronically infected
with HBV, and about 75% of them are Asian.
There is a high incidence of hepatocellular carcinoma
(hepatoma) in many Asian countries.
Immunization against HBV has significantly reduced the
incidence of hepatoma in children. It appears that the HBV
vaccine is the first vaccine to prevent a human cancer.
28
31. Pathogenesis & Immunity
After entering the blood, the virus infects hepatocytes, and viral antigens are
displayed on the surface of the cells.
Cytotoxic T cells mediate an immune attack against the viral antigens,
inflammation and necrosis occur.
Immune attack against viral antigens on infected hepatocytes is mediated by
cytotoxic T cells.
The pathogenesis of hepatitis B is probably the result of this
cell-mediated immune injury, because HBV itself does not cause a cytopathic effect.
Antigen–antibody complexes cause some of the early symptoms (e.g., arthralgias,
arthritis, and urticaria) and some of the complications in chronic hepatitis
(e.g., glomerulonephritis, cryoglobulinemia, and vasculitis).
31
33. Pathogenesis & Immunity
About 5% of patients with HBV infection become chronic carriers; in contrast,
there is no prolonged carrier state in patients with HAV infection.
A chronic carrier is someone who has HBsAg persisting in
their blood for at least 6 months.
The chronic carrier state is attributed to a persistent infection of the
hepatocytes, which results in the prolonged presence of HBV and HBsAg in
the blood. The main determinant of whether a person clears the infection or
becomes a chronic carrier is the adequacy of the cytotoxic T-cell response.
HBV DNA exists primarily as an episome in the cytoplasm of persistently
infected cells; a small number of copies of HBV DNA are integrated into cell
DNA.
33
34. What is ( episome ?)
extra-chromosomal genetic
material that may replicate
autonomously or become
integrated into the chromosome
34
35. Pathogenesis & Immunity
A high rate of hepatocellular carcinoma occurs in chronic carriers. The
HBV genome has no oncogene, and hepatocellular carcinoma appears
to be the result of persistent cellular regeneration that attempts to
replace the dead hepatocytes. Alternatively, malignant transformation
could be the result of
insertional mutagenesis, which could occur when the HBV genome
integrates into the hepatocyte DNA. Integration of the HBV DNA could
activate a cellular oncogene, leading to a loss of growth control.
35
36. Pathogenesis & Immunity
Chronic carriage is more likely to occur when infection
occurs in a newborn than in an adult, probably because
a newborn’s immune system is less competent than that
of an adult’s. Approximately 90% of infected neonates
become chronic carriers. Chronic carriage resulting from
neonatal infection is associated with a high risk of
hepatocellular carcinoma.
36
37. Pathogenesis & Immunity
Lifelong immunity occurs after the natural infection and is
mediated by humoral antibody against HBsAg. Antibody
against HBsAg (HBsAb) is protective because it binds to
surface antigen on the virion and prevents it from interacting
with receptors on the hepatocyte. (HBsAb is said to neutralize
the infectivity of HBV.)
Note that antibody against the core antigen (HBcAb) is not
protective because the core antigen is inside the virion and
the antibody cannot interact with it.
37
39. The window period lies between the
end of detecting of surface antigen
and the beginning of detecting the
surface antigen -antibody
39
40. In window period ,, the amount of the surface
antigens equal the amount of the surface
antibody and u can not detect them in the
blood
40
LOOK FOR HBC-AB
44. Laboratory Diagnosis
The most important laboratory test for the
detection of early HBV infection is the
immunoassay for HBsAg. HBsAg appears during
the incubation period and is detectable in most
patients during the prodrome and acute disease
44
45. It falls to undetectable levels during convalescence in most cases; its
prolonged presence (at least 6 months) indicates the carrier state and the risk
of chronic hepatitis and hepatic carcinoma.
HBsAb is not detectable in the chronic carrier state. Note that HBsAb is, in
fact, being made but is not detectable in the laboratory tests because it is
bound to the large amount of HBsAg present in the blood. HBsAb is also being
made during the acute disease but is similarly undetectable because it is
bound in antigen–antibody complexes.
45
46. Note that there is a period of several weeks when HBsAg has
disappeared but HBsAb is not yet detectable. This is the window phase.
At this time, the HBcAb is always positive and can be used to make the
diagnosis.
HBcAb is present in those with acute infection and chronic infection, as
well as in those who have recovered from acute infection. Therefore, it
cannot be used to distinguish between acute and chronic infection. The
IgM form of HBcAb is present during acute infection and disappears
approximately 6 months after infection. The test for HBcAg is not readily
available.
46
47. HBeAg arises during the incubation period and is present during the
prodrome and early acute disease and in certain chronic carriers. Its
presence indicates a high likelihood of transmissibility, and, conversely,
the finding of HBeAb indicates a lower likelihood, but transmission can
still occur.
DNA polymerase activity is detectable during the incubation period
and early in the disease, but the assay is not available in most clinical
laboratories. The detection of viral DNA (viral load) in the serum is strong
evidence that infectious virions are present.
47
51. Prevention
(1) The vaccine (e.g., Recombivax) contains HBsAg produced in yeasts by
recombinant DNA techniques. The vaccine is highly effective in preventing
hepatitis B and has few side effects. The seroconversion rate is
approximately 95% in healthy adults. It is indicated for people who are
frequently exposed to blood or blood products, such as certain health care
personnel (e.g., medical students, surgeons, and dentists), patients
receiving multiple transfusions or dialysis, patients with frequent sexually
transmitted disease, and abusers of illicit intravenous drugs. Travelers who
plan a long stay in areas of endemic infection, such as many countries in
Asia and Africa, should receive the vaccine. The U.S. Public Health Service
recommends that all newborns and adolescents receive the vaccine
51
52. Prevention
Seroconversion is the term used to describe
the finding of antibody to a virus (or any
microbe) in a patient’s serum when the
patient previously had no antibody
52
53. Prevention
At present, booster doses after the initial three-dose regimen are not
recommended. However, if antibody titers have declined in immunized
patients who are at high risk, such as dialysis patients, then a booster
dose should be considered.
Widespread immunization with the HBV vaccine has significantly
reduced the incidence of hepatocellular carcinoma in children.
A vaccine called Twinrix that contains both HBsAg and inactivated
HAV provides protection against both hepatitis B and hepatitis A.
53
54. Prevention
(2) Hepatitis B immune globulin (HBIG)
contains a high titer of HBsAb. It is used to
provide immediate, passive protection to
individuals known to be exposed to HBsAg
positive blood (e.g., after an accidental
needle-stick injury).
54
55. Prevention
Precise recommendations for use of the vaccine and HBIG are
beyond the scope of this book. However, the recommendation
regarding one common concern of medical students, the
needle-stick injury from a patient with HBsAg-positive blood, is
that both the vaccine and HBIG be given (at separate sites).
This is true even if the patient’s blood is HBeAb positive. Both
the vaccine and HBIG should also be given to a newborn
whose mother is HBsAg-positive. These are good examples of
passive–active immunization, in which both immediate and
long-term protection are provided.
All blood for transfusion should be screened for HBsAg. No one
with a history of hepatitis (of any type) should donate blood,
because non-A, non-B viruses may be present.
55
58. NON-A, NON-B HEPATITISVIRUSES-NANBH
Describe the cases of hepatitis for which
existing serologic tests had ruled out all
known viral causes.
The term is not often used because
namely ,HCV, has been identified.
58
59. NANBH
HCV was identified in 1989 after isolation of a viral RNA from a chimpanzee infected
with blood from a person with NANBH.The viral RNA obtained from blood was
converted to DNA with reverse transcriptase, its proteins were expressed, and
antibodies from people with NANBH were then used to detect the viral proteins.
These studies led to the development of ELISA and genomic and other tests for
detection of the virus, which still cannot be grown in tissue culture
59
61. IMPORTANT PROPERTIES
A member of the flavivirus family.
Enveloped virion.
Genome (9100 nucleotides) encodes 10 proteins,
Single-stranded
Positivepolarity RNA.
It has no virion polymerase.
61
62. IMPORTANT PROPERTIES
At least six genotypes + multiple subgenotypes
Based on differences in the genes that encode one of its two envelope glycoproteins
“hypervariable” region in the envelope glycoprotein.
Hypervariablety due to:
The high mutation rate in the envelope gene
The absence of a proofreading function in the virion-encoded RNA polymerase.
So multiple subspecies (quasispecies) often occur in the blood of an infected
individual at the same time.
Genotypes 1a and 1b are the most common in the united states. 62
63. TRANSMISSION
Humans are the reservoir for HCV.
Transmitted primarily via blood.
At present, injection drug use accounts for almost all new HCV infections.
Transmission via blood transfusion rarely occurs?
Transmission via needle-stick injury occurs, but the risk is < for HBV.
Sexual transmission and transmission from mother to child occur but are inefficient
modes.
63
71. TRANSMISSION & EPIDEMIOLOGY
HCV is the most prevalent blood-borne pathogen in the U.S.
In the nationally reported incidence HCV ranks below HIV and HBV as a blood-
borne pathogen, but it is estimated that HCV is more prevalent.
~ 4 million people in the US (1%–2% of the population) are chronically infected with
HCV.
Unlike yellow fever virus, there is no evidence for an insect vector for HCV.
Worldwide, it is estimated that 180m people are infected with HCV.
71
72. TRANSMISSION & EPIDEMIOLOGY
In the united states, about 1% of blood donors have antibody to HCV.
People who share needles when taking intravenous drugs are very commonly
infected.
Commercially prepared immune globulin preparations are generally very safe,
but several instances of the transmission of HCV have occurred.
This is the only example of an infectious disease transmitted by immune globulins.??
72
73. PATHOGENESIS
Infects hepatocytes primarily-how?-, no evidence for a cytopathic effect on it.
Death of the hepatocytes is probably caused by immune attack by cytotoxic T cells.
Strongly predisposes to hepatocellular carcinoma:
But there is no evidence for:
An oncogene in the viral genome
Insertion of a copy of the viral genome into the DNA of the cancer cells.
This supports the idea that the cancer is caused by prolonged liver damage and the consequent rapid
growth rate of hepatocytes as the cells attempt to regenerate rather than by a direct oncogenic effect
of HCV.
Alcoholism greatly enhances the risk
Patients with cirrhosis of any origin, not just alcoholic cirrhosis, have an increased risk
73
74. IMMUNITY
Antibodies against HCV are made, but approximately 75% of patients are chronically
infected and continue to produce virus for at least 1 year.
Chronic carriage of HCV is much higher than the rate of chronic carriage of
HBV.
Chronic active hepatitis and cirrhosis occur in approximately 10% of these patients.
For patients who clear the infection, it is not known whether reinfection can occur
or whether there is lifelong immunity.
74
75. CLINICAL FINDINGS
Acute infection with HCV is milder than infection with HBV.
Fever, anorexia, nausea, vomiting, and jaundice are common.
Dark urine, pale feces, and elevated transaminase levels are seen.
Hepatitis C resembles hepatitis B as far as the ensuing
chronic liver disease, cirrhosis, and the predisposition to hepatocellular carcinoma
are concerned.
Chronic carrier state occurs more often with HCV infection than with HBV.
75
76. CLINICAL FINDINGS
Liver biopsy is often done in patients with chronic infection to evaluate the
extent of liver damage and to guide treatment decisions.
Many infections with HCV ,including both acute and chronic infections, are
asymptomatic and are detected only by the presence of antibody.
The mean incubation period is 8 weeks.
Cirrhosis resulting from chronic HCV infection is the most common indication
for liver transplantation.
76
79. CLINICAL FINDINGS
HCV infection also leads to significant autoimmune reactions, including vasculitis,
arthralgias, purpura, and membranoproliferative glomerulonephritis.
The main cause of essential mixed cryoglobulinemia.
composed of HCV antigens and antibodies.
79
80. LABORATORY DIAGNOSIS
Detecting antibodies to HCV in an ELISA: ///What is known Ag or Ab ??
The antigen in the assay is a recombinant protein formed from three immunologically stable HCV
proteins and does not include the highly variable envelope proteins.
The test does not distinguish between IgM and IgG
Does not distinguish between an acute, chronic, or resolved infection.
False-positive results can occur in the ELISA.
Confirmatory test= RIBA (recombinant immunoblot assay)
+ PCR that detects the presence of viral RNA (viral load) in the serum to determine whether
active disease exists
Isolation of the virus from patient specimens is not done.
80
82. LABORATORY DIAGNOSIS
A chronic infection is characterized by:
Elevated transaminase levels
A positive RIBA
Detectable viral RNA
For at least 6 months.
82
83. PREVENTION
Blood found to contain antibody is discarded prevented virtually all cases of transfusion-
acquired HCV infection since 1994, when screening began.
There is no vaccine.
Hyperimmune globulins are not available.
Pooled immune serum globulins are not useful for postexposure prophylaxis.
There is no effective regimen for prophylaxis following needle-stick injury; only monitoring
is recommended.
83
84. PREVENTION HEPATOCELLULAR CARCINOMA
Pt advised to reduce or eliminate their consumption of alcoholic beverages.
Pt should be monitored with alpha-fetoprotein tests and liver sonograms.
Pt with liver failure due to HCV infection can receive a liver transplant,
but infection of the graft with HCV typically occurs.
84
The virus probably replicates in the gastrointestinal tract and spreads to the liver via the blood.
The infection is cleared and the damage is repaired
Uusually used in the lab diagnosis
in contrast to that of HBV which is 10- 12 weeks هنا اقصد ال incubation period
in contrast to that of HBV which is 10- 12 weeks هنا اقصد ال incubation period
Two doses, an initial dose followed by a booster
6 to 12 months later, should be given. No subsequent booster
dose is recommended.
وهذا مثال ع passive- active immuinzation
given to traveler to developing countries , to children between 2-18
and for men who have sex with men
أهم ماركر للدلالة على وجود كرونيك انفكشين هو السيرفيس أنتجين بي اللي ضل لمدة ست شهور لكن كيف نميز بين الكرونيك و الكرونيك آكتيف ؟ عن طريق e-antigen
Ab for e-antigen
ازا كان عندك سيجيفيكانت إي أنتيجين مع البي يعني كرونيك اكتيف إي أنتي بادي يعني دخلت في كرونيك الكور أنتيجين بيعلي في الأكيوت و الكرونيك مش هيفيدك كتيرwindow : the amount of the surface antigens equal the amount of the surface antibody and u can not detect them in the blood في الويندو بيريود ,, بتروح تفحص للمريض ,, الأنتي كور , انت فحصت السيرفيس أنتيجين و السيرفيس أنتي بادي و لقيتهم نورمال و قلت للمريض متخافش يا حج ,, انت بخير يا غالي في الأكيوت هيباتايتيس , أول اتنين برتفعو هم : سيرفيس أنتيجين ,, و الإي انتيجين , و بيرتفع أيضاً الأنتي كور أنتي بادي في الأكيوت هيباتايتيس ما بتقدر تطلع لا على السيرفيس أنتيجين و لا على الأنتي بادي سيرفيس , بتطلع على الأنتي كور في الاكيوت هيباتايتيس , لما يظهر عندنا الأنتي سيرفيس أنتجين يعني انت في الكافاري موود هلأ في الكرونيك رحنا فحصنا السيرفس أنتجين و لقيناهم كانو مرتفعين خلال الست شهور اللي فاتت خلاص انت كرونيك للتمييز بين الكرونيك آكتيف و الكرونيك حاف بنطلع على الإي أنتيجين ,, في الكرونيك لا يوجد أنتي بادي للسيرفيس أنتجين لكن يوجد أنتي بادي للكور أنتيجين و يوجد أنتي بادي ل الإي أنتجين و كلاهما ما لهم غير اهمية واحدة و هي انو انت معك كرونيك هيباتايتس بي
Within the core is a DNA-dependent DNA polymerase. The genome contains four genes (four open reading frames) that encode five proteins, namely, the S gene encodes the surface antigen, the C gene encodes the core antigen and the e antigen, the P gene encodes the polymerase, and the X gene encodes the X protein. The X protein is an activator of viral RNA transcription. The DNA polymerase has both RNA-dependent (reverse transcriptase) and DNA-dependent activity
يوجد عندنا إيرلي ستيج لصناعة البروتين و ليت ستيج , هلأ هادا الفايروس بيستخدم الدي أن إيه ديبيندانت بولي ميريز عشان يروح يكمل الديفيكتيف بارتكل تبعون و يصير كومبليت دابل ستراند ,, و بعدها يتم تصنيع بروتين , من ضمن البروتينات اللي بيتم تصنيعها في المرحلة الاولى هي بروتين إكس , بعدها هادا البروتين بيحفز تكوين البروتيانات الاخرى في الليت فيز
However, for epidemiologic purposes, there are four serologic subtypes of HBsAg based on a group-specific antigen, “a,” and two sets of mutually exclusive epitopes, d or y and w or r. This leads to four serotypes—adw, adr, ayw, and ayr—which are useful in epidemiologic studies because they are concentrated in certain geographic areas.
the main cause of non-A, non-B hepatitis,
out
The viral RNA-dependent RNA polymerase is error prone and generates mutations in the glycoprotein and other genes.
because donated blood containing antibody to HCV is discarded
cdc
3.234
binds to CD81 (tetraspanin) surface receptors, which is expressed on hepatocytes and B lymphocytes,
and can also coat itself with LDL / VLDL and then use the lipoprotein receptor to facilitate uptake into hepatocytes.
aNonicteric hepatitis is common in children.bAmong the age group 15–29 years, hepatitis B and C are often associated with drug abuse or promiscuous sexual behavior. Patients with transfusion-associated hepatitisB or C virus are generally older than age 29 years.