This document discusses several types of hepatitis viruses. It covers hepatitis A virus, hepatitis B virus, hepatitis C virus, hepatitis D virus, and hepatitis E virus. For each virus, it describes key aspects such as transmission, pathogenesis, clinical manifestations, diagnosis, and prevention. Hepatitis viruses can cause liver inflammation and damage, and some may lead to chronic infection or liver cancer if not addressed. Vaccines exist to prevent hepatitis A and B.
The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).
The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).
The genus Shigella exclusively infects human intestine.
Shigella dysenteriae is the causative agent of bacillary dysentery or shigellosis in humans.
It is a diarrheal illness which is characterized by frequent passage of blood stained mucopurulent stools.
The four important species of the genus Shigella are:
Shigella dysenteriae
Shigella flexneri
Shigella sonnei
Shigella boydii.
Cholera is a serious bacterial disease that usually
causes severe diarrhea and dehydration. The disease is typically spread through contaminated water.
Modern sewage and water treatment have effectively eliminated cholera in most countries. It’s still a problem in countries like Asia, America and Africa. Mostly in India.
Countries affected by war, poverty, and natural disasters have the greatest risk for a cholera outbreak.
Taxonomy:
class : Gamma Proteobacteria
Order: Vibrionales
Family: Vibrionaceae
Genus: Vibrio
Species: v.cholerae, v.parahaemolyticus,
v. vulnificus, v. alginolyticus
MORPHOLOGY:
Gram negative, actively motile, short, rigid curved bacilli
Resembling letter “V”
about 34 genus
most common in water
1.5µ X 0.2 -0.4 µ in size
polar flagellum , strongly aerobic
Smear – fish in stream appearance
PATHOGENESIS:
Source: Ingestion of contaminated water, food,
fruits and vegetables etc.,
Incubation periods: 1-5 days
Symptoms: Watery diarrhoea, vomiting, thirst, dehydration, muscle cramps
Complications: muscular pain, renal failure, pulmonary edema, cardiac arrhythrnias
DIAGNOSIS:
Specimen: stool sample, water sample(envt)
Microscopy: a) Hanging drop : +ve
b) Gram stain :-ve
Culture: Mac conkey Agar :colourless to light pink
TCBS : yellow colonies
Serology: serological tests are no diagnostic value
TREATMENT:
Adequate replacement of fluids and electrolytes.
Oral tetracycline reduces the period of vibrio excreation.
PREVENTION:
Drink and use bottled water
Frequent washing
Sanitary environment
Defecate in water
Cook food thoroughly
A picornavirus is a virus belonging to the family Picornaviridae, a family of viruses in the order Picornavirales. Vertebrates, including humans, serve as natural hosts. Picornaviruses are nonenveloped viruses that represent a large family of small, cytoplasmic, plus-strand RNA viruses with a 30-nm icosahedral capsid.
This powerpoint contains slides describing types of hepatitis viruses, pathogenesis, clinical course, laboratory diagnosis, treatment and prevention against hepatitis viruses. This presentation is intended to use by medical students, nurses, paramedics in the learning on virology. The slided could also be resource materials for the academicians.
Adenoviridae is a group of medium sized, non-enveloped, double stranded DNA viruses that replicate and produce disease in the eye and in the respiratory, gastrointestinal and urinary tracts;
The genus Shigella exclusively infects human intestine.
Shigella dysenteriae is the causative agent of bacillary dysentery or shigellosis in humans.
It is a diarrheal illness which is characterized by frequent passage of blood stained mucopurulent stools.
The four important species of the genus Shigella are:
Shigella dysenteriae
Shigella flexneri
Shigella sonnei
Shigella boydii.
Cholera is a serious bacterial disease that usually
causes severe diarrhea and dehydration. The disease is typically spread through contaminated water.
Modern sewage and water treatment have effectively eliminated cholera in most countries. It’s still a problem in countries like Asia, America and Africa. Mostly in India.
Countries affected by war, poverty, and natural disasters have the greatest risk for a cholera outbreak.
Taxonomy:
class : Gamma Proteobacteria
Order: Vibrionales
Family: Vibrionaceae
Genus: Vibrio
Species: v.cholerae, v.parahaemolyticus,
v. vulnificus, v. alginolyticus
MORPHOLOGY:
Gram negative, actively motile, short, rigid curved bacilli
Resembling letter “V”
about 34 genus
most common in water
1.5µ X 0.2 -0.4 µ in size
polar flagellum , strongly aerobic
Smear – fish in stream appearance
PATHOGENESIS:
Source: Ingestion of contaminated water, food,
fruits and vegetables etc.,
Incubation periods: 1-5 days
Symptoms: Watery diarrhoea, vomiting, thirst, dehydration, muscle cramps
Complications: muscular pain, renal failure, pulmonary edema, cardiac arrhythrnias
DIAGNOSIS:
Specimen: stool sample, water sample(envt)
Microscopy: a) Hanging drop : +ve
b) Gram stain :-ve
Culture: Mac conkey Agar :colourless to light pink
TCBS : yellow colonies
Serology: serological tests are no diagnostic value
TREATMENT:
Adequate replacement of fluids and electrolytes.
Oral tetracycline reduces the period of vibrio excreation.
PREVENTION:
Drink and use bottled water
Frequent washing
Sanitary environment
Defecate in water
Cook food thoroughly
A picornavirus is a virus belonging to the family Picornaviridae, a family of viruses in the order Picornavirales. Vertebrates, including humans, serve as natural hosts. Picornaviruses are nonenveloped viruses that represent a large family of small, cytoplasmic, plus-strand RNA viruses with a 30-nm icosahedral capsid.
This powerpoint contains slides describing types of hepatitis viruses, pathogenesis, clinical course, laboratory diagnosis, treatment and prevention against hepatitis viruses. This presentation is intended to use by medical students, nurses, paramedics in the learning on virology. The slided could also be resource materials for the academicians.
Adenoviridae is a group of medium sized, non-enveloped, double stranded DNA viruses that replicate and produce disease in the eye and in the respiratory, gastrointestinal and urinary tracts;
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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
The presentation is about the disease, hepatitis, its causing agent, symptoms, treatment and cure. the presentation focusses on the virus causing the disease, its morphology and life cycle. It has also discussed the different types of hepatitis disease and the virus causing them
Hepatitis B virus HBV infection in detailsHassn Aljubory
Presentation
serological markers
Laboratory test
vaccinations
Chronic hepatitis B
Approach
Harrison
Davidsons
Step up medicine
Mksap
Notes & notes
Gastrointestinal disease
Hepatology
Risk group
Management
Hepatitis in pregnancy
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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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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
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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 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
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2. Hepatitis viruses
The causes of hepatitis are varied and include viruses,
bacteria, and protozoa, as well as drugs and toxins (eg,
isoniazid, carbon tetrachloride, and ethanol). The
clinical symptoms and course of acute viral hepatitis
can be similar, regardless of etiology, an determination
of a specific cause depends primarily on the use of
laboratory tests.
3. Hepatitis viruses
Hepatitis may be caused by at least five different
viruses
Non-A, non-B hepatitis is a term previously used to
identify cases of hepatitis not due to hepatitis A or B
With the discovery of the hepatitis viruses C, E, and G,
virtually all the viral etiologies of non-A, non-B disease
can be specifically identified
Other viruses, such as Epstein–Barr virus and
cytomegalovirus, can also cause inflammation of the
liver, but hepatitis is not the primary disease caused by
them
4. Hepatitis A Virus
Hepatitis A virus is an unenveloped, single-stranded
RNA virus with cubic symmetry
Hepatitis A Viruses is classified in a separate genus
(hepatovirus) of picornaviruses
5. Hepatitis A transmission
Hepatitis A virus is spread by the fecal–oral route, and
outbreaks may be associated with contaminated food
or water
6. Pathogenesis & Clinical manifestation
The virus is believed to replicate initially in the enteric
mucosa
Multiplication in the intestines is followed by a period
of viremia with spread to the liver
The response to replication in the liver consists of
lymphoid cell infiltration, necrosis of liver
parenchymal (Hepatocytes) cells, and proliferation of
Kupffer cells
The extent of necrosis often coincides with the severity
of disease
7. Pathogenesis & Clinical manifestation cont…
It can be demonstrated in feces for 10 to 14 days before
onset of disease
In most patients with symptoms of the disease, virus is
no longer found in fecal specimens
Contagion is greatest 10–14 days before symptoms
appear
8. Pathogenesis & Clinical manifestation cont…
In hepatitis A virus infection, an incubation period of
10 to 50 days is usually followed by the onset of fever;
anorexia (poor appetite); nausea; pain in the right
upper abdominal quadrant; and, within several days,
jaundice
The liver is enlarged and tender, and serum
aminotransferase and bilirubin levels are elevated as a
result of hepatic inflammation and damage
Recovery occurs in days to weeks
9. Lab Diagnosis
Antibody to hepatitis A virus can be detected during early
illness, and most patients with symptoms or signs of acute
hepatitis A already have detectable antibody in serum
Early antibody responses are predominantly IgM, which can be
detected for several weeks or months
During convalescence, antibody of the IgG class predominates.
10. Hepatitis B Virus
Hepatitis B virus is an enveloped DNA virus belonging to
the family Hepadnaviridae
The complete virion is a spherical particle that
consists of an envelope around a core. The core comprises a
nucleocapsid that contains the DNA genome
Other components of the core are a hepatitis B core antigen
(HBcAg) and the hepatitis B e antigen (HBeAg), which is a
low-molecular-weight glycoprotein
The envelope of the virus contains the hepatitis B surface
antigen (HBsAg)
11.
12. Transmission
It has become clear that the major mode of acquisition
is through close personal contact with body fluids of
infected individuals
HBsAg has been found in most body fluids, including
saliva, semen, and cervical secretions
Under experimental conditions, as little as 0.0001 mL
of infectious blood has produced infection
Transmission is therefore possible by vehicles such as
inadequately sterilized hypodermic needles or
instruments used in tattooing and ear piercing
13. Pathogenesis and clinical manifestation cont…
The clinical picture of hepatitis B is highly variable
The incubation period may be as brief as 7 days or as long
as 160 days (mean, approximately 10 weeks)
Liver injury appears to occur from a cell-mediated immune
system attack on HBV. Viral antigens on the surface of
infected hepatocytes are targets for cytotoxic T-cells
Immune complexes of antibody and HBsAg can deposit in
tissues and activate the immune system, resulting in
arthritis, as well as skin and kidney damage
Patients who have immunosuppressed states, such as
malnutrition, AIDS, and chronic illness, are more likely to
be asymptomatic carriers because their immune system
does not attack
14. Pathogenesis and clinical manifestation cont…
HBV can cause acute and chronic hepatitis
The following are disease states caused by HBV:
1) Acute hepatitis
2) Fulminant hepatitis: Severe acute hepatitis with rapid destruction
of the liver
3) Chronic hepatitis:
a) Asymptomatic carrier: The carrier patient never develops
antibodies against HBsAg (anti-HBsAg) and harbors the virus without
liver injury. There are an estimated 200 million carriers of HBV in the
world
b) Chronic-persistent hepatitis: The patient has a low-grade
"smoldering" hepatitis
c) Chronic active hepatitis: The patient has an acute hepatitis state
that continues without the normal recovery (lasts longer than 6-12
months)
15. Pathogenesis and clinical manifestation cont…
Acute hepatitis B is usually manifested by the gradual
onset of fatigue, loss of appetite, nausea and pain, and
fullness in the right upper abdominal quadrant
With increasing involvement of the liver, there is
increasing cholestasis and, hence, clay-colored stools,
darkening of the urine, and jaundice
16. Complications
Primary hepatocellular carcinoma: With chronic
infection the HBV DNA becomes incorporated into
the hepatocyte DNA and triggers malignant growth.
There is a 200X increase in the risk of developing
primary hepatocellular carcinoma in HBV carriers as
compared to non carriers.
Cirrhosis: Infection with HBV can result in
permanent liver scarring and loss of hepatocytes
17. Lab Diagnosis
Many antigens and antibodies are simpler than they
seem, as follows:
1) HBsAg: The presence of HBsAg always means
there is LIVE virus and infection, either acute, chronic,
or carrier. When anti-HBsAg develops, HBsAg
disappears and the patient is protected and immune.
a) HBsAg = DISEASE (chronic or acute)
b) Anti-HBsAg = IMMUNE, CURE, NO ACTIVE
DISEASE!!!
18. Lab Diagnosis
2) HBcAg: Antibodies to HBcAg are not protective
but we can use them to understand how long the
infection has been ongoing
With acute illness we will see IgM anti-HBcAg
With chronic or resolving infection IgG anti-HBcAg
will develop
a) IgM anti-HBcAg = NEW INFECTION
b) IgG anti-HBcAg = OLD INFECTION
19. Lab Diagnosis
3) HBeAg: The presence of HBeAg connotes a high
infectivity and active disease
Presence of anti-HBeAg suggests lower infectivity
a) HBeAg = HIGH INFECTIVITY, virus going wild!
b) anti-HBeAg = LOW INFECTIVITY
21. Prevention
Safe sex practices and avoidance of needle stick injuries or
injection drug use are approaches to diminishing the risk of
hepatitis B infection
Serologic tests on donor blood to remove HBV contaminated
blood from the donor pool
Active immunization: The vaccine is a recombinant vaccine. The
gene coding for HBsAg is cloned in yeast and used to produce
mass quantities of HBsAg, used as vaccine. There is no risk of
developing disease from the vaccine because it contains only the
surface envelope and proteins (HBsAg = no DNA or capsid)
The HBV vaccine is now given to all infants at birth, 2, 4, and 15
months
It is also given as 3 injections to adolescents and high-risk adults
(health care workers, IV drug users, etc.)
22. Prevention
Administration of HBIG soon after exposure to the
virus greatly reduces the development of symptomatic
disease
Post exposure prophylaxis with HBIG should be
followed by active immunization with vaccine
23. Delta Hepatitis (Hepatitis D)
Hepatitis D is found only in hepatitis B–infected
persons
HDV uses HBsAg for assembly
Hepatitis D virus is a small single-stranded RNA virus
with helical nucleocapsid
Infection occurs in 2 ways:
1) Co-infection: HBV and HDV both are transmitted
together parenterally (IV drug use, blood transfusions,
sexual contact, etc.) and cause an acute hepatitis
similar to that caused by HBV. Antibodies to HBsAg
will be protective against both, ending the infection
24. Delta Hepatitis (Hepatitis D)
2) Super infection: HDV infects a person who has
chronic HBV infection (like the 200 million worldwide
HBV carriers)
This results in acute hepatitis in a patient already
chronically infected with HBV. This HDV infection is often
severe, with a higher incidence of fulminant hepatitis,
cirrhosis, and a greater mortality (5-15%)
Diagnosis is made most commonly by demonstrating IgM
or IgG antibodies, or both, to the delta antigen in serum
IgM antibodies appear within 3 weeks of infection and
persist for several weeks. IgG antibodies persist for years
25. Hepatitis C Virus
Hepatitis C virus is an RNA virus in the flavivirus
family
There are at least six major genotypes, with multiple
subtypes
The genotypes have different geographic distributions
and may be associated with differing severity of
disease as well as response to therapy
26. Hepatitis C Disease
Hepatitis C is an insidious disease in that it does not
usually cause a clinically evident acute illness
Instead, its first manifestation (in 25% of those
infected) may be the presence of smoldering chronic
hepatitis that may ultimately lead to liver failure. Its
transmission is less well understood than for hepatitis
A, B, and D
27. Pathogenesis and clinical manifestation
The transmission of hepatitis C by blood is well
documented: indeed, until screening blood for
transfusions was introduced, it caused the great
majority of cases of posttransfusion hepatitis
Hepatitis C may be sexually transmitted but to a much
lesser degree than hepatitis B. Needle sharing accounts
for up to 40% of cases
28. Pathogenesis and clinical manifestation
The incubation period of hepatitis C averages 6–12
weeks
The infection is usually asymptomatic or mild and
anicteric but results in a chronic carrier state in up to
85% of adults of patients
The average time from infection to the development of
chronic hepatitis is 10–18 years
Cirrhosis and hepatocellular carcinoma are late
sequelae of chronic hepatitis
29. Lab Diagnosis
Antigens of hepatitis C are not detectable in blood, so
diagnostic tests attempt to demonstrate antibody
Unfortunately, the antibody responses in acute disease
remain negative for 1 to 3 weeks after clinical onset and
may never become positive in up to 20% of patients
with acute, resolving disease
Quantitative assays of hepatitis C RNA may be used for
diagnosis
30. Hepatitis E
Hepatitis E is a small, single-strand, non-enveloped RNA
virus that is similar to but distinct from caliciviruses
Transmission is by the faecal–oral route.
Outbreaks occur after contamination of water supplies or
food
It is found in Asia, Africa and Central America.
It usually causes a self-limiting hepatitis of varying severity
Diagnosis is by IgM or NAAT.
Infection is prevented by hygiene measures.
31. Hepatitis G
Hepatitis G is an RNA virus similar to hepatitis C and members of the
flavivirus family
An antibody assay can detect past, but not present, infection, and
detection of acute infection with hepatitis G requires a PCR assay for
viral RNA in serum.
Up to 2% of volunteer blood donors are seropositive for hepatitis G
RNA, which is a blood-borne virus
In addition to being closely related to hepatitis C, data suggest that the
majority of patients infected by hepatitis C are also infected by
hepatitis G. Given this association, it has been difficult to ascertain the
contribution of hepatitis G to clinical disease
Patients infected with both viruses do not appear to have worse disease
than those infected by hepatitis C virus only
Currently, there is no useful serologic test and no therapy is established