This document provides information on herpes infections caused by herpesviruses. It begins by classifying herpesviruses as large, enveloped viruses that establish latent infections in hosts. There are three subfamilies of herpesviruses: alphaherpesviruses which establish latency in neurons (including HSV-1 and HSV-2), betaherpesviruses which establish latency in secretory glands and kidneys (including CMV), and gammaherpesviruses which establish latency in lymphoid cells (including EBV). The replication cycle is described along with pathogenesis. Clinical presentations of HSV-1 and HSV-2 are also summarized, including primary infection, recurrent infection, and infections in
The Epstein–Barr virus (EBV), also called human herpesvirus 4 (HHV-4), is one of eight known human herpesvirus types in the herpes family, and is one of the most common viruses in humans.
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The herpes simplex is a contagious disease and it carries ability to reoccur again after ever few months. The ultimate herpes protocol works to help get rid of herpes in a natural way. The methods are based on ancient natural techniques, so they are completely safe to use.
Syphilis is a sexually transmitted infection caused by the bacterium Treponema pallidum subspecies pallidum. The signs and symptoms of syphilis vary depending in which of the four stages it presents (primary, secondary, latent, and tertiary).
The Epstein–Barr virus (EBV), also called human herpesvirus 4 (HHV-4), is one of eight known human herpesvirus types in the herpes family, and is one of the most common viruses in humans.
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The herpes simplex is a contagious disease and it carries ability to reoccur again after ever few months. The ultimate herpes protocol works to help get rid of herpes in a natural way. The methods are based on ancient natural techniques, so they are completely safe to use.
Syphilis is a sexually transmitted infection caused by the bacterium Treponema pallidum subspecies pallidum. The signs and symptoms of syphilis vary depending in which of the four stages it presents (primary, secondary, latent, and tertiary).
If someone says the word “Herpes”, everyone cringes. Surprisingly, about 2/3 of you reading
this now, may have had HSV 1 (the type that causes cold sores), and about 20% of you may
have had the genital type of Herpes (HSV2).
describes the etiopathogenesis , clinical features, investigations, differential diagnosis and management and prophylaxis of all important viral lesions affecting the oral cavity
herpes simplex virus is a double stranded DNA virus causing many symptoms all over the body. it affects globally all over the world .
neonatal hsv attacks even the baby and made them to a fatal conditions.
A type of virus that causes herpes infections and has DNA as its genetic material. There are two types of human herpesviruses. Infections with type 1 viruses cause cold sores on the lips or nostrils. Infections with type 2 viruses cause sores on the genitals (external and internal sex organs and glands).
There are nearly 100 viruses of the herpes group that infect many different animal species.
Official name of herpesviruses that commonly infect human is Humans herpesvirus (HHV)
herpes simplex virus types 1 (HHV 1)
Herpes simplex virus type 2 (HHV 2)
Varicella-zoster virus (HHV 3)
Epstein-Barr virus, (HHV 4)
Cytomegalovirus (HHV 5)
Human herpesvirus 6 (HHV 6)
Human herpesvirus 7 (HHV 7)
Human herpesvirus 8 (HHV 8) (Kaposi's sarcoma-associated herpesvirus).
Herpes B virus of monkeys can also infect humans
hELMINTHS#corona virus#Aspergillosis#BUGANDO#CUHAS#CUHAS#CUHAS
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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.
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
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!
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
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
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
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.
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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3. INTRODUCTION
A. Herpesviridae - large, enveloped dougle
stranded DNA viruses; morphologically alike;
share a common mode of replication.
B. Herpesviruses - ubiquitous and cause
infections ranging from painful skin ulcers to
chickenpox to encephalitis.
4. C. An outstanding property - the ability to
establish latent infections, to persist
indefinitely in infected hosts, and to periodically
become reactivated.
D. With all these viruses, immunocompromised
patients, especially those with altered cellular
immunity, have more frequent and severe
infections, including severe disease from
reactivation of the virus
E. Effective antiviral drugs available to treat
these infections.
5. CLASSIFICATION
A. Alphaherpesviruses are fast growing,
cytolytic viruses that establish latent infections
in neurons. Herpes simples virus type 1 and
2 (HSV-1 and HSV- 2) and Varicella- zoster virus
(VSV) are members of this subfamily. These
three viruses produce vesicular rashes both in
their primary infections and in reactivation.
6. B. Betaherpesviruses include the slow growing
Cytomegalovirus (CMV) - so named because it
causes the cells it infects to become cytomegalic –
become massively enlarged. These viruses become
latent in secretory glands and kidneys. This
subfamily also includes the newly identified human
Herpesviruses 6 and 7.
• Human herpesvirus 6 causes a common
childhood illness – sixth disease – roseola
infantum.
• Human herpesvirus 7 – is closely related to
human herpesvirus 6, but is not firmly associated
with human disease.
7. C. Gammaherpesviruses, exemplified by Epstein
Barr virus (EBV) infect and become latent in
lymphoid cells. A new herpesvirus – also called
Kaposi's sarcoma associated herpesvirus has
been detected in over 90% of Kaposi's sarcomas
and a rare type of B cell lymphoma from AIDS
patients.
12. Replication Cycle
• 1. Virus attaches to the cell receptors
(heparan sulfate moiety of cellular
proteoglycans) via glycoprotein spikes.
• 2. Enters the cell after pH independent fusion
with the cell membrane.
• 3. Tegument proteins are released, one of
which shuts down cellular protein synthesis.
13. • 4. The nucleocapsid is transported along the
cytoskeleton to a nuclear pore where viral
DNA is released, enters the nucleus, and
circularizes.
• 5. Viral gene expression is tightly regulated,
with three classes of mRNA's, alpha, beta, and
gamma, being transcribed in an ordered
sequence by cellular RNA polymerase II.
14. • 6. The virus buds through the nuclear
membrane.
• 7. Enveloped virions accumulate in
endoplasmic reticulum and the mature virions
are released by exocytosis. The length of the
replication cycle varies from 18h (HSV) to over
70h (CMV).
15.
16. Pathogenesis
Entry by skin or mucous membranes
viral multiplication
sensory nerve
lysis of cells
root ganglia
vesicles
latency
ulcers
REACTIVATION
COLD
FEVER
SURGERY
UNKNOWN
17. HOW IS LATENCY MAINTAINED?
Not fully understood.
If interested read about HHV Latency Associated Transcript
19. Course of the Disease
• The incubation period for herpes - 2 to 7 days.
• Persons with primary herpetic lesions are
infectious for about 7 to 12 days.
• Genital, rectal, or oral herpes recurs in 60 to
80% of persons whose primary infection was
symptomatic.
• These recurrent episodes of herpes are milder
and of shorter duration than the initial
outbreak.
20. Epidemiology
• HSV-1 and 2 infections are life-long.
• The virus is found in the lesions on the skin
but can be present in body fluids including
saliva and vaginal secretions.
• As a result of poor hygiene in underdeveloped
countries, HSV-1 antibodies are found in more
than 90% of children.
21. Epidemiology 2
• HSV-2 is normally spread sexually and is found in the
anus, rectum and upper alimentary tract as well as
the genital area.
• An infant can be infected at birth by a genitallyinfected mother.
• The infant can also be infected in utero if the
mother’s infection spreads.
• Because of the infant’s underdeveloped immune
system, the resulting infection can be very severe
and sometimes be deadly.
22. Definitions of Infection Types
First Clinical Episode
• Primary infection
– First infection ever with either HSV-1 or HSV-2
– No antibody present when symptoms appear
– Disease is more severe than recurrent disease
• Non-primary infection
– Newly acquired HSV-1 or HSV-2 infection in an
individual previously seropositive to the other
virus
– Symptoms usually milder than primary infection
– Antibody to new infection may take several
weeks to a few months to appear
22
23. Definitions of Infection Types
Recurrent symptomatic infection
• Antibody present when symptoms appear
• Disease usually mild and short in duration
Asymptomatic infection
• Serum antibody is present
• No known history of clinical outbreaks
23
24. Types of Infection
Infection Type
Lesions/
Symptoms
Type-specific
antibody at time of
presentation
HSV-1
HSV-2
First episode, Primary
(Type 1 or 2)
+/Severe,
bilateral
-
-
First episode, Non-primary
Type 2
+/Moderate
+
-
First episode, Recurrence
Type 2
+/Mild
+/-
+
Symptomatic, Recurrence
Type 2
+/Mild,
unilateral
+/-
+
Asymptomatic, Infection
Type 2
-
+/-
+
24
25. Transmission
a. HSV-1- usually transmitted in saliva (kissing,
sharing of glasses, etc.)
b. HSV-2 transmitted by
• 1. sexual contact (HSV-2 can infect genitalia,
anorectal tissues, or the orpharynx)
• 2. autoinoculation
• 3. during pregnacy and labour
c. Both types can cause oral and genital lesions.
26. Special “at risk” groups:
• Neonates
• Immunocompromised
• Physicians, nurses, dentists, etc. in
contact with oral and genital secretions.
27. Immunity
a. During primary infection, interferon and natural killer cells limit the
progression of the infection.
b. Antibody directed against envelope glycoproteins can neutralize
extracellular viruses and help limit their spread. Antibody can also
participate in ADCC. Viruses can escape antibody neutralization and
clearance by:
• (1) Direct cell-to cell spread- limiting their time spent outside the
cell.
• (2) Latent infections of the neurons
• (3) Binding the antibody “upside down” with Fc receptors and/or
inhibiting C3b
c. Cell mediated immunity is essential for controlling and resolving HSV
infections. Without functional cell mediated immunity, the virus may
disseminate to vital organs and the brain
ADCC-Antibody-dependent cellular cytotoxicity
28. Clinical Presentations
• The classical presentation of HSV-1 and 2 is
the lesion – a clear vesicle on an
erythematous base – “the dewdrop on a rose
petal”- which then progresses to pustular
lesions, ulcers, and crusted lesions.
29.
30. • Primary herpes infection may be
asymptomatic or symptomatic.
• In women, the primary infection is usually
more severe than in men.
• lymphadenopathy, as well as flu-like
symptoms including fever, headache, malaise,
and muscle aches during the first few weeks
of infection.
31. Recurrent oral infection is more common with HSV-1
infections than with HSV-2.
Symptoms typically progress in a series of eight stages
• Latent (weeks to months incident-free): The
remission period; After initial infection, the
viruses move to sensory nerve ganglia
(Trigeminal ganglion), where they reside as
lifelong, latent viruses. Asymptomatic
shedding of contagious virus particles can
occur during this stage.
32. • Prodromal (day 0–1): Symptoms often
precede a recurrence. Symptoms typically
begin with tingling (itching) and reddening of
the skin around the infected site. This stage
can last from a few days to a few hours
preceding the physical manifestation of an
infection and is the best time to start
treatment.
33. • Inflammation (day 1): Virus begins
reproducing and infecting cells at the end of
the nerve. The healthy cells react to the
invasion with swelling and redness displayed
as symptoms of infection.
34. • Pre-sore (day 2–3): This stage is defined by the
appearance of tiny, hard, inflamed papules
and vesicles that may itch and are painfully
sensitive to touch. In time, these fluid-filled
blisters form a cluster on the lip (labial) tissue,
the area between the lip and skin (vermilion
border), and can occur on the nose, chin, and
cheeks.
35. • Open lesion (day 4): This is the most painful
and contagious of the stages. All the tiny
vesicles break open and merge to create one
big, open, weeping ulcer. Fluids are slowly
discharged from blood vessels and inflamed
tissue. This watery discharge is teeming with
active viral particles and is highly contagious.
Depending on the severity, one may develop a
fever and swollen lymph glands under the jaw.
36. • Crusting (day 5–8): A honey/golden crust starts to
form from the syrupy exudate. This yellowish or
brown crust or scab is not made of active virus
but from blood serum containing useful proteins
such as immunoglobulins. This appears as the
healing process begins. The sore is still painful at
this stage, but, more painful, however, is the
constant cracking of the scab as one moves or
stretches their lips, as in smiling or eating. Virusfilled fluid will still ooze out of the sore through
any cracks.
37. • Healing (day 9–14): New skin begins to form
underneath the scab as the virus retreats into
latency. A series of scabs will form over the sore
(called Meier Complex), each one smaller than
the last. During this phase irritation, itching, and
some pain are common.
• Post-scab (12–14 days): A reddish area may linger
at the site of viral infection as the destroyed cells
are regenerated. Virus shedding can still occur
during this stage.
41. Herpes labialis
(fever blisters or cold sores)
• a milder, recurrent form of infection
characterized by crops of vesicles, usually at
the mucocutanous junction of the lips or nose.
Reoccurs frequently at the same site usually
with less severe symptoms.
42.
43.
44. Oral Herpes :
Herpetic Gingivostomatitis
• an infection of the oral mucosa characterized
by redness of oral tissues, formation of
multiple vesicles, painful ulcers and fever.
Occurs primarily in children characterized by
fever, irritability and vesicular mouth lesions.
Primary disease is more severe and lasts
longer than recurrences. Lesions heal
spontaneously in 2-3 weeks. Many children
have asymptomatic primary disease and
produce neutralizing antibody.
45. Symptoms
The symptoms can be mild or severe and may
include:
• Not able to chew or swallow
• Sores on the inside of the cheeks or gums
• Fever
• General discomfort, uneasiness, or ill feeling
• Very sore mouth with no desire to eat
• Halitosis (bad breath)
46.
47.
48. Herpetic whitlow
• A herpetic whitlow is a lesion (whitlow) on a
finger or thumb caused by the herpes simplex
virus.
• Herpes whitlow can be caused by infection by
HSV-1 or HSV-2.
• HSV-1 whitlow is often contracted by health care
workers that come in contact with the virus; it is
most commonly contracted by dental workers
and medical workers exposed to oral secretions.
49.
50.
51. Herpes gladiatorum
• Individuals that participate in contact sports such
as wrestling, rugby, and soccer sometimes
acquire a condition caused by HSV-1 known as
herpes gladiatorum, scrumpox, wrestler’s herpes,
or mat herpes, which presents as skin ulceration
on the face, ears, and neck.
• Symptoms include fever, headache, sore throat
and swollen glands. It occasionally affects the
eyes or eyelids.
52.
53. Eczema herpeticum
• Eczema herpeticum is a rare but severe
disseminated infection that generally occurs at
sites of skin damage produced by, for example,
atopic dermatitis, burns, long term usage of
topical steroids or eczema.
• It is also known as Kaposi varicelliform eruption,
Pustulosis varioliformis acute and KaposiJuliusberg dermatitis.
• This infection affects multiple organs, including
the eyes, brain, lung, and liver, and can be fatal.
55. • Keratoconjunctivitis is inflammation of the
cornea and conjunctiva.
• Primary infection typically presents as swelling
of the conjunctiva and eyelids
(blepharoconjunctivitis), accompanied by
small white itchy lesions on the surface of the
cornea. The effect of the lesions varies, from
minor damage to the epithelium (superficial
punctate keratitis), to formation of dendritic
ulcers.
56. Herpes esophagitis
• Herpes esophagitis is a viral infection of the
esophagus caused by Herpes simplex virus.
• While the disease most often occurs in
immunocompromised patients, including
post-chemotherapy, immunosuppression with
organ transplants and in AIDS.
57. • Patients with herpes esophagitis experience
odynophagia, or painful swallowing and
dysphagia.
• Other symptoms can include food impaction,
hiccups, weight loss, fever and on rare
occasions upper gastrointestinal bleeding and
tracheoesophageal fistula.
58.
59.
60. Herpesviral encephalitis
• Herpes simplex encephalitis (HSE) is a rare,
but severe viral infection of the human central
nervous system. It is estimated to affect at
least 1 in 500,000 individuals per year.
• The majority of cases of herpes encephalitis
are caused by herpes simplex virus-1 (HSV-1)
• About 10% of cases of herpes encephalitis are
due to HSV-2, which is typically spread
through sexual contact.
61. • About 1 in 3 cases of HSE result from primary
HSV-1 infection, predominantly occurring in
individuals under the age of 18;
• 2 in 3 cases occur in seropositive persons, few
of whom have history of recurrent orofacial
herpes.
• Approximately 50% of individuals that
develop HSE are over 50 years of age.
62. Pathophysiology
• HSE is thought to be
caused by the
retrograde
transmission of virus
from a peripheral site
on the face following
HSV-1 reactivation,
along a nerve axon, to
the brain.
63.
64. • HSE results in rapid death in approximately
70% of cases.
• survivors suffer severe neurological damage.
• Only a small population of survivors (2.5%)
regain completely normal brain function.
• Earlier treatment (within 48 hours of symptom
onset) improves the chances of a good
recovery.
65. Genital Herpes
• painful vesicular lesions of the male and
female genitals and anal area.
• Lesions more severe and protracted in primary
disease than in recurrence.
• Asymptomatic infections occur in both men
and women.
• Many infections are asymptomatic – many
people have antibody to HSV-2 but have no
history of disease.
66. How common is genital herpes?
• CDC estimates that, annually, 776,000 people
in the United States get new herpes infections.
• Nationwide, 16%, or about one out of six,
people aged 14 to 49 years have genital HSV-2
infection.
• Over the past decade, the percentage of
persons with genital herpes infection in the
United States has remained stable.
67. • Transmission from an infected male to his
female partner is more likely than from an
infected female to her male partner.
• Because of this, genital HSV-2 infection is
more common in women (approximately one
out of five women aged 14 to 49 years) than in
men (about one out of nine men aged 14 to
49 years).
68. symptoms of genital herpes
• Most individuals infected with HSV-1 or HSV-2
experience either no symptoms or have very
mild symptoms that go unnoticed or are
mistaken for another skin condition. Because
of this, most people infected with HSV-2 are
not aware of their infection. When symptoms
do occur, they typically appear as one or more
blisters on or around the genitals, rectum or
mouth. The blisters break and leave painful
sores that may take two to four weeks to heal.
69. • Itching or burning feeling in the genital or anal
area
• Flu-like symptoms, including fever
• Swollen glands
• Pain in the legs, buttocks, or genital area
• Vaginal discharge
78. Neonatal herpes simplex
• Neonatal herpes simplex is a rare but serious
condition, usually caused by vertical
transmission of herpes simplex virus from
mother to newborn.
79. Transmission
• The majority of cases (85%) occur during birth
when the baby comes in contact with infected
genital secretions in the birth canal, most
common with mothers that have newly been
exposed to the virus,
• an estimated 5% are infected in utero, and
approximately 10% of cases are acquired
postnatally. Detection and prevention is difficult
because transmission is asymptomatic in 60% 98% of cases.
80.
81.
82. FACTORS INFLUENCING TRANSMISSION
•
•
•
•
•
Type of maternal infection (primary/recurrent)
Maternal antibody status
Duration of rupture of membranes
Integrity of mucocutaneous barriers
Mode of delivery (C-section/vaginal)
83. INCIDENCE OF NEONATAL DISEASE
• 2/1000 mothers are HSV culture + at delivery
asymptomatic
• 50-70% affected infants born to women
asymptomatic at the time of delivery
• Antepartum cultures are not useful in
assessing risk of neonatal infection
• Increased risk w/ primary vs recurrent
infection
• Incidence from 1/2000 to 1/5000 live births
and increasing
84. RISK OF NEONATAL HSV INFECTION
• 50% risk: Infants born to women w/ primary
infection near the time of delivery
• 30% risk: Infants born to mothers with first
episode, non-primary infection (antibody to
type 1, new acquisition type 2 and vice versa)
• 1 to 3% of infants born to mothers w/
recurrent infection
• Passive immunity protects against infection ,
but has little effect on the severity of disease
85. TIMES OF TRANSMISSION
•
HSV of the newborn is acquired during one
of three distinct time intervals:
1. Intrauterine (in utero 5%)
2. Peripartum (perinatal 85%)
3. Psotpartum (postnatal 10%)
86. DISEASE CLASSIFICATION
• Disease localized to the skin, eyes and mouth
SEM disease accounting for 45% of cases
• Encephalitis w/ or w/out CNS involvement
accounting for 30%
• Disseminated infection including CNC, lungs,
etc. accounting for 25%
• This classification is predictive of morbidity
and mortality
87. DIAGNOSTIC TESTS
• Cultures from skin lesions, mouth,
nasopharynx, conjunctiva, urine, stool/anorectum and CSF.
• Positive cultures at more than 48 hrs are
consistent w/ viral replication as opposed to
colonization
• Serologic tests should not be relied on
• PCR testing for CSF HSV DNA is the diagnostic
method of choice for HSV encephalitis
88. TREATMENT AND FOLLOW UP
•
•
•
•
Acyclovir is the treatment of choice
SEM 14 days of treatments
CNS and disseminated disease 21 days
Oral acyclovir contraindicated in neonates for
HSV treatment
• Ocular involvement requires trifluridine
89.
90. Diagnosis
HSV Diagnosis
• Clinical diagnosis is insensitive and nonspecific
• Clinical diagnosis should be confirmed by
laboratory testing:
– Virologic tests
– Type-specific serologic tests
90
91. Diagnosis
Virologic Tests
•
Viral culture (gold standard)
–
–
–
–
–
•
Preferred test if genital ulcers or other mucocutaneous lesions are present
Highly specific (>99%)
Sensitivity depends on stage of lesion; declines rapidly as lesions begin to
heal
Positive more often in primary infection (80%–90%) than with recurrences
(30%)
Cultures should be typed
Polymerase Chain Reaction (PCR)
–
–
More sensitive than viral culture; has been used instead of culture in
some settings; however PCR tests are not FDA-cleared or widely available
Preferred test for detecting HSV in spinal fluid
91
92. Diagnosis
Virologic Tests
(continued)
• Antigen detection (DFA or EIA)
– Fairly sensitive (>85%) in symptomatic shedders
– Rapid (2-12 hours)
– May be better than culture for detecting HSV in
healing lesions
• Cytology (Tzanck or Pap)
– Insensitive and nonspecific and should not be relied
on for HSV diagnosis
92
93. Diagnosis
Type-specific Serologic Tests
• Type-specific and nonspecific antibodies to HSV
develop during the first several weeks to few months
following infection and persist indefinitely
• Presence of HSV-2 antibody indicates anogenital
infection
• Presence of HSV-1 does not distinguish anogenital
from orolabial infection
93
94. Diagnosis
Uses of Type-specific Serologic Tests
• Type-specific serologic assays might be
useful in the following scenarios:
– Recurrent or atypical genital symptoms with
negative HSV cultures
– A clinical diagnosis of genital herpes without
laboratory confirmation
– A sex partner with herpes
– As part of a comprehensive evaluation for STDs
among persons with multiple sex partners, HIV
infection, and among MSM at increased risk for
HIV acquisition
94
95. Diagnosis
Evaluation of Genital Ulcer
• All patients with genital ulcers should be
evaluated with a serologic test for syphilis and
a diagnostic evaluation for genital herpes
• In settings where chancroid is prevalent, a test
for Haemophilus ducreyi should also be
performed
95
96. Management
• There is no method to eradicate herpes virus
from the body, but antiviral medications can
reduce the frequency, duration, and severity
of outbreaks.
• Analgesics such as ibuprofen and
acetaminophen can reduce pain and fever.
• Topical anesthetic treatments such as
prilocaine, lidocaine, benzocaine or tetracaine
can also relieve itching and pain
97. Antiviral
There are several antivirals that are effective for
treating herpes including:
• aciclovir (acyclovir),
• valaciclovir (valacyclovir),
• famciclovir,
• and penciclovir.
98. Management
CDC-Recommended Regimens for First
Clinical Episode
• Acyclovir 400 mg orally 3 times a day for 7-10 days,
or
• Acyclovir 200 mg orally 5 times a day for 7-10 days,
or
• Famciclovir 250 mg orally 3 times a day for 7-10 days,
or
• Valacyclovir 1 g orally twice a day for 7-10 days
98
99. Management
CDC-Recommended Regimens for
Suppressive Therapy
•
•
•
•
Acyclovir 400 mg orally twice a day, or
Famciclovir 250 mg orally twice a day, or
Valacyclovir 500 mg orally once a day, or
Valacyclovir 1 g orally once a day
99
100. Management
CDC-Recommended Regimens for
Episodic Therapy
• Acyclovir 400 mg orally 3 times a day for 5 days, or
• Acyclovir 800 mg orally twice a day for 5 days, or
• Acyclovir 800 mg orally 3 times a day for 2 days, or
• Famciclovir 125 mg orally twice a day for 5 days, or
• Famciclovir 1000 mg orally twice a day for 1 day, or
• Valacyclovir 500 mg orally twice a day for 3 days, or
• Valacyclovir 1 g orally once a day for 5 days
100
101. Management
Severe Disease
• IV acyclovir should be provided for patients with
severe disease or complications requiring
hospitalization
• CDC-Recommended Regimen:
– Acyclovir 5-10 mg/kg IV every 8 hours for 2-7 days or until
clinical improvement
– Follow with oral antiviral therapy to complete at least 10
days total therapy
101
102. Management
Allergy, Intolerance, and Adverse
Reactions
• Allergic and other adverse reactions to acyclovir,
valacyclovir, and famciclovir are rare
• Desensitization to acyclovir is described by Henry
RE, et al., Successful oral acyclovir desensitization.
Ann Allergy 1993; 70:386-8
102
103. Management
Herpes in HIV-Infected Persons
• HIV-infected persons may have prolonged,
severe, or atypical episodes of genital,
perianal, or oral herpes
• HSV shedding is increased in HIV-infected
persons
103
104. Management
CDC-Recommended Regimens for
Daily Suppressive Therapy in
HIV-Infected Persons
• Acyclovir 400-800 mg orally twice a day or
three times a day, or
• Famciclovir 500 mg orally twice a day, or
• Valacyclovir 500 mg orally twice a day
104
105. Management
CDC-Recommended Regimens for Episodic
Infection in
HIV-Infected Persons
• Acyclovir 400 mg orally 3 times a day for 5-10
days, or
• Famciclovir 500 mg orally twice a day for 5-10
days, or
• Valacyclovir 1 g orally twice a day for 5-10
days
105
106. Management
Genital Herpes in Pregnancy
• Majority of mothers of infants who acquire neonatal
herpes lack histories of clinically evident genital
herpes
• Risk for transmission to neonate is high (30%-50%)
among women who acquire genital herpes near the
time of delivery
• Risk is low (<1%) in women with histories of recurrent
herpes at term or who acquire genital HSV during the
first half of pregnancy
106
107. Management
Genital Herpes in Pregnancy (continued)
• Prevention of neonatal herpes depends on:
✓ avoiding acquisition of HSV during late pregnancy
✓ avoiding exposure of the infant to herpetic lesions during
delivery
• All pregnant women should be asked whether they
have a history of genital herpes
107
108. Management
Genital Herpes in Pregnancy (continued)
• At the onset of labor:
– All women should be questioned carefully about
symptoms of genital herpes, including prodromal
– All women should be examined carefully for herpetic
lesions
• Women without symptoms or signs of genital herpes
or its prodrome can deliver vaginally
108
109. Management
Genital Herpes in Pregnancy (continued)
• Safety of acyclovir, valacyclovir, famciclovir in
pregnancy not definitively established, but no
clear evidence for increased birth defects
• Oral acyclovir may be given for first-episode or
severe recurrent herpes; IV acyclovir should be
used for severe infection
• Suppressive acyclovir late in pregnancy reduces
frequency of cesarean sections in women with
recurrent genital herpes; many specialists
recommend it
109
111. Prevention
Patient Counseling and Education
• Goals
– Help patients cope with the infection
– Prevent sexual and perinatal transmission
• Counsel initially at first visit
• Education on chronic aspects may be beneficial after
acute illness subsides
• HSV-infected persons may express anxiety about
genital herpes that does not reflect the actual clinical
severity of their disease
111
112. Prevention
Patient Counseling and Education
• Counseling should include:
–
–
–
–
Natural history of the infection
Treatment options
Transmission and prevention issues
Neonatal HSV prevention issues
• Emphasize potential for recurrent episodes,
asymptomatic viral shedding, and sexual
transmission
112
113. Prevention
Counseling: Natural History
•
Recurrent episodes likely following a first
episode; with HSV-2 more than HSV-1
–
–
–
•
Frequency of outbreaks may decrease over time
Stressful events may trigger recurrences
Prodromal symptoms may precede outbreaks
Asymptomatic viral shedding is common and
HSV transmission can occur during
asymptomatic periods
113
114. Prevention
Counseling: Treatment
• Suppressive therapy available and effective in
preventing symptomatic recurrences
• Episodic therapy sometimes useful in shortening
duration of recurrent episodes
• When and how to take antiviral medications
• Recognition of prodromal symptoms to know
when to begin episodic therapy
114
115. Prevention
Counseling: Transmission and Prevention
• Inform current and future sex partners about genital
herpes diagnosis
• Abstain from sexual activity with uninfected partners
when lesions or prodrome present
• Correct and consistent use of latex condoms might
reduce the risk of HSV transmission
• Valacyclovir suppressive therapy decreases HSV-2
transmission in heterosexual couples in which source
partner has recurrent herpes
115
116. Prevention
Counseling: Neonatal Herpes
Prevention
• Risk of neonatal HSV infection should be explained
to all patients, including men
• Pregnant women should inform their
prenatal/perinatal providers that they have genital
herpes
• Pregnant women without HSV-2 infection should
avoid intercourse during third trimester with men
who have genital herpes
• Pregnant women without HSV-1 infection should
avoid oral sex from a partner with oral herpes
116
117. Prevention
Counseling for Asymptomatic Persons
• Give asymptomatic persons diagnosed with
HSV-2 infection the same counseling messages
as symptomatic persons
• Teach the common manifestations of genital
herpes, as many patients will become aware
of them with time
117
118. Prevention
Partner Management
• Symptomatic sex partners
– Evaluate and treat in the same manner as patients
who have genital lesions
• Asymptomatic sex partners
– Ask about history of genital lesions
– Educate to recognize symptoms of herpes
– Offer type-specific serologic testing
118