RECENT ADVANCES IN CHICKEN POX

A SEMINAR

PRESENTED BY
NDUAGU JACINTA CHISOM

20121828185

SUPERVISED BY

DR.O.I OGUOMA

SUBMITTED TO

DEPARTMENT OF SCIENCE LABORATORY TECHNOLOGY

SCHOOL OF PHYSICAL SCIENCE
FEDERAL UNIVERSITY OF TECHNOLOGY, OWERRI

IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE

AWARD OF BACHELOR OF TECHNOLOGY (B. TECH) DEGREE IN
SCIENCE LABORATORY TECHNOLOGY

JUNE, 2018

i
DEDICATION
This seminar is dedicated to God Almighty, the giver of life.

ii
ACKNOWLEDGEMENT
I appreciate Almighty God, the creator of my life, the Father of wisdom and

strength and the giver of knowledge and inspiration.

I am grateful to my H.O.D. Dr E.C Nwogu for academic guidance, my

supervisor Dr.O.I Oguoma for his tolerance, guidance and contributions to

ensure that this work is completed. My Course Advicer Mr Dioha

Emmanuel for his constant support and other lecturers for their immense

contribution towards my education from my first year till now.

I am grateful to God for my parents Mr and Mrs Nduagu for their endless

support and contributions.

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ABSTRACT

Chickenpox is extremely contagious. More than 90% of unvaccinated people

will become infected during their lifetime, but infection occurs at different

ages in different parts of the world. It is usually a mild and self-limiting

disease, but it can be severely complicated by pneumonitis or disseminated

disease in some individuals, particularly neonates and those who are

immunocompromised.in this seminar, the preventive measure was

thoroughly explain and potent treatment strategies proffered. Moreover, the

risk factors like age se and immunity were also explained.

iv
CHAPTER ONE

INTRODUCTION

Chickenpox, also known as varicella, is a highly contagious disease caused

by the initial infection with varicella zoster virus (VZV) (Anthony and
Dirk;2012). The disease results in a characteristic skin rash that forms small,
itchy blisters, which eventually scab over (Abro et al;2009) It usually starts
on the chest, back, and face then spreads to the rest of the body. Other
symptoms may include fever, tiredness, and headaches. Symptoms usually
last five to seven days. Complications may occasionally include pneumonia,
inflammation of the brain, and bacterial skin infections (Baren et
al;1996).The disease is often more severe in adults than in children.[7]
Symptoms begin 10 to 21 days after exposure to the virus.

Chickenpox is an airborne disease which spreads easily through the coughs

and sneezes of an infected person. It may be spread from one to two days
before the rash appears until all lesions have crusted over. It may also spread
through contact with the blisters (Anderson et al;1994). Those with shingles
may spread chickenpox to those who are not immune through contact with
the blisters. The disease can usually be diagnosed based on the presenting
symptom; however, in unusual cases it may be confirmed by polymerase
chain reaction (PCR) testing of the blister fluid or scabs. Testing for
antibodies may be done to determine if a person is or is not immune.[7]
People usually only get chickenpox once. Although reinfections by the virus
occur, these reinfections usually do not cause any symptoms.

1
The varicella vaccine has resulted in a decrease in the number of cases and
complications from the disease. It protects about 70 to 90 percent of people
from disease with a greater benefit for severe disease. Routine immunization
of children is recommended in many countries (Anderson et al;1994).
Immunization within three days of exposure may improve outcomes in
children. Treatment of those infected may include calamine lotion to help
with itching, keeping the fingernails short to decrease injury from scratching,
and the use of paracetamol (acetaminophen) to help with fevers. For those
at increased risk of complications antiviral medication such as aciclovir are
recommended(Anderson et al;1994).

Chickenpox occurs in all parts of the world. In 2013 there were 140 million
cases of chickenpox and herpes zoster worldwide.[12] Before routine
immunization the number of cases occurring each year was similar to the
number of people born. Since immunization the number of infections in the
United States has decreased nearly 90%. In 2015 chickenpox resulted in
6,400 deaths globally – down from 8,900 in 1990 (Atkinsonand
William;2011) Death occurs in about 1 per 60,000 cases. Chickenpox was
not separated from smallpox until the late 19th century. In 1888 its
connection to shingles was determined. The first documented use of the
term chicken pox was in 1658. Various explanations have been suggested
for the use of "chicken" in the name, one being the relative mildness of the
disease (Domino and Frank;2007).

2
CHAPTER TWO

SIGNS AND SYMPTOMS

The early (prodromal) symptoms in adolescents and adults are nausea, loss
of appetite, aching muscles, and headache. This is followed by the
characteristic rash or oral sores, malaise, and a low-grade fever that signal
the presence of the disease. Oral manifestations of the disease (enanthem)
not uncommonly may precede the external rash (exanthem). In children the
illness is not usually preceded by prodromal symptoms, and the first sign is
the rash or the spots in the oral cavity. The rash begins as small red dots on
the face, scalp, torso, upper arms and legs; progressing over 10–12 hours
to small bumps, blisters and pustules; followed by umbilication and the
formation of scabs (Domino and Frank;2007).

At the blister stage, intense itching is usually present. Blisters may also occur
on the palms, soles, and genital area. Commonly, visible evidence of the
disease develops in the oral cavity and tonsil areas in the form of small ulcers
which can be painful or itchy or both; this enanthem (internal rash) can
precede the exanthem (external rash) by 1 to 3 days or can be concurrent.
These symptoms of chickenpox appear 10 to 21 days after exposure to a
contagious person. Adults may have a more widespread rash and longer
fever, and they are more likely to experience complications, such as varicella
pneumonia(Domino and Frank;2007).

Because watery nasal discharge containing live virus usually precedes both
exanthem (external rash) and enanthem (oral ulcers) by 1 to 2 days, the
infected person actually becomes contagious one to two days before

3
recognition of the disease. Contagiousness persists until all vesicular lesions
have become dry crusts (scabs), which usually entails four or five days, by
which time nasal shedding of live virus ceases.

The condition usually resolves by itself within a couple of weeks. The rash
may, however, last for up to one month. Chickenpox is contagious starting
from one to two days before the appearance of the rash and lasts until the
lesions have crusted (Gnann and John;2007)

Chickenpox is rarely fatal, although it is generally more severe in adult men

than in women or children. Non-immune pregnant women and those with a
suppressed immune system are at highest risk of serious complications.
Arterial ischemic stroke (AIS) associated with chickenpox in the previous year
accounts for nearly one third of childhood AIS (Heuchan and Isaac;2001).
The most common late complication of chickenpox is shingles (herpes
zoster), caused by reactivation of the varicella zoster virus decades after the
initial, often childhood, chickenpox infection.

4
Pathophysiology

Exposure to VZV in a healthy child initiates the production of host

immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A
(IgA) antibodies; IgG antibodies persist for life and confer immunity. Cell-
mediated immune responses are also important in limiting the scope and the
duration of primary varicella infection. After primary infection, VZV is
hypothesized to spread from mucosal and epidermal lesions to local sensory
nerves. VZV then remains latent in the dorsal ganglion cells of the sensory
nerves. Reactivation of VZV results in the clinically distinct syndrome of
herpes zoster (i.e., shingles), postherpetic neuralgia, and sometimes Ramsay
Hunt syndrome type II. (Mazzella et al;2003). Varicella zoster can affect the
arteries in the neck and head, producing stroke, either during childhood, or
after a latency period of many years.

Diagnosis

The diagnosis of chickenpox is primarily based on the signs and symptoms,

with typical early symptoms followed by a characteristic rash. Confirmation
of the diagnosis is by examination of the fluid within the vesicles of the rash,
or by testing blood for evidence of an acute immunologic response.

Vesicular fluid can be examined with a Tzanck smear, or by testing for direct
fluorescent antibody. The fluid can also be "cultured", whereby attempts are

5
made to grow the virus from a fluid sample. Blood tests can be used to
identify a response to acute infection (IgM) or previous infection and
subsequent immunity (IgG) (Mazzella et al;2003).

Prenatal diagnosis of fetal varicella infection can be performed using

ultrasound, though a delay of 5 weeks following primary maternal infection
is advised. A PCR (DNA) test of the mother's amniotic fluid can also be
performed, though the risk of spontaneous abortion due to the
amniocentesis procedure is higher than the risk of the baby's developing
fetal varicella syndrome.

Prevention

The disease menace can be prevented through;

Hygiene measures

The spread of chickenpox can be prevented by isolating affected individuals.

Contagion is by exposure to respiratory droplets, or direct contact with
lesions, within a period lasting from three days before the onset of the rash,

6
to four days after the onset of the rash The chickenpox virus is susceptible
to disinfectants, notably chlorine bleach (i.e., sodium hypochlorite). Like all
enveloped viruses, it is sensitive to desiccation, heat and detergents.

Vaccine

The varicella vaccine is recommended in many countries. Some countries

require the varicella vaccination or an exemption before entering elementary
school. A second dose is recommended five years after the initial
immunization. A vaccinated person is likely to have a milder case of
chickenpox if they become infected (Mohsen and Mckendrick;2003).
Immunization within three days following household contact reduces
infection rates and severity in children.

It is part of the routine immunization schedule in the US. Some European

countries include it as part of universal vaccinations in children, but not all
countries provide the vaccine due to its cost. In the UK as of 2014, the
vaccine is only recommended in people who are particularly vulnerable to
chickenpox. In populations that have not been immunized or if immunity is
questionable, a clinician may order an enzyme immunoassay. An
immunoassay measures the levels of antibodies against the virus that give
immunity to a person. If the levels of antibodies are low (low titer) or
questionable, reimmunization may be done.

7
Treatment

Treatment mainly consists of easing the symptoms. As a protective measure,

people are usually required to stay at home while they are infectious to avoid
spreading the disease to others. Cutting the nails short or wearing gloves
may prevent scratching and minimize the risk of secondary infections.

8
Although there have been no formal clinical studies evaluating the
effectiveness of topical application of calamine lotion (a topical barrier
preparation containing zinc oxide, and one of the most commonly used
interventions), it has an excellent safety profile. It is important to maintain
good hygiene and daily cleaning of skin with warm water to avoid secondary
bacterial infection. Scratching may also increase the risk of secondary
infection (Tebruegge;2006).

Paracetamol (acetaminophen) but not aspirin may be used to reduce fever.

Aspirin use by someone with chickenpox may cause the serious, sometimes
fatal disease of the liver and brain, Reye syndrome. People at risk of
developing severe complications who have had significant exposure to the
virus may be given intra-muscular varicella zoster immune globulin (VZIG),
a preparation containing high titres of antibodies to varicella zoster virus, to
ward off the disease.

Prognosis

The duration of the visible blistering caused by varicella zoster virus varies
in children usually from 4 to 7 days, and the appearance of new blisters
begins to subside after the fifth day. Chickenpox infection is milder in young
children, and symptomatic treatment, with sodium bicarbonate baths or

9
antihistamine medication may ease itching. Paracetamol (acetaminophen) is
widely used to reduce fever. Aspirin, or products containing aspirin, should
not be given to children with chickenpox, as it can cause Reye's
Syndrome(Pino et al;2006).

In adults, the disease is more severe, though the incidence is much less
common. Infection in adults is associated with greater morbidity and
mortality due to pneumonia (either direct viral pneumonia or secondary
bacterial pneumonia), bronchitis (either viral bronchitis or secondary
bacterial bronchitis), hepatitis, and encephalitis. In particular, up to 10% of
pregnant women with chickenpox develop pneumonia, the severity of which
increases with onset later in gestation. In England and Wales, 75% of deaths
due to chickenpox are in adults. Inflammation of the brain, or encephalitis,
can occur in immunocompromised individuals, although the risk is higher
with herpes zoster. Necrotizing fasciitis is also a rare complication.

Varicella can be lethal to adults with impaired immunity. The number of

people in this high-risk group has increased, due to the HIV epidemic and
the increased use of immunosuppressive therapies. Varicella is a particular
problem in hospitals, when there are patients with immune systems
weakened by drugs (e.g., high-dose steroids) or HIV.

Secondary bacterial infection of skin lesions, manifesting as impetigo,

cellulitis, and erysipelas, is the most common complication in healthy
children. Disseminated primary varicella infection usually seen in the
immunocompromised may have high morbidity. Ninety percent of cases of
varicella pneumonia occur in the adult population. Rarer complications of

10
disseminated chickenpox include myocarditis, hepatitis, and
glomerulonephritis.

Hemorrhagic complications are more common in the immunocompromised

or immunosuppressed populations, although healthy children and adults
have been affected. Five major clinical syndromes have been described:
febrile purpura, malignant chickenpox with purpura, post infectious purpura,
purpura fulminans, and anaphylactoid purpura. These syndromes have
variable courses, with febrile purpura being the most benign of the
syndromes and having an uncomplicated outcome. In contrast, malignant
chickenpox with purpura is a grave clinical condition that has a mortality rate
of greater than 70%. The cause of these hemorrhagic chickenpox syndromes
is not known (Parmet et al;2004).

Epidemiology

Primary varicella occurs in all countries worldwide. In 2013 the disease

resulted in 7,000 deaths – down from 8,900 in 1990.

11
In temperate countries, chickenpox is primarily a disease of children, with
most cases occurring during the winter and spring, most likely due to school
contact. It is one of the classic diseases of childhood, with the highest
prevalence in the 4–10-year-old age group. Like rubella, it is uncommon in
preschool children. Varicella is highly communicable, with an infection rate
of 90% in close contacts. In temperate countries, most people become
infected before adulthood, and 10% of young adults remain susceptible.

In the tropics, chickenpox often occurs in older people and may cause more
serious disease. In adults, the pock marks are darker and the scars more
prominent than in children.

In the United States, the Centers for Disease Control and Prevention (CDC)
does not require state health departments to report infections of chickenpox,
and only 31 states currently volunteer this information. However, in a 2013
study conducted by the social media disease surveillance tool called
Sickweather, anecdotal reports of chickenpox infections on Facebook and
Twitter were used to measure and rank states with the most infections per
capita, with Maryland, Tennessee and Illinois in the top three.

12
CHAPTER THREE

RECENT ADVANES IN THE TREATMENT OF CHICKEN POX

The following drugs are used recently in the treatment of chicken pox;

Acyclovir and valacyclovir

Acyclovir, an acyclic analogue of guanosine, is a selective inhibitor of VZV

and HSV replication (Whitley and Gnann, 1992). The drug is converted to
acyclovir monophosphate by virus-encoded thymidine kinase (TK), a reaction
that does not occur to any significant extent in uninfected cells. Cellular
enzymes catalyze the subsequent diphosphorylation and triphosphorylation
steps which yield high concentrations of acyclovir triphosphate in VZV-
infected cells. Acyclovir triphosphate inhibits viral DNA synthesis by
competing with deoxyguanosine triphosphate as a substrate for viral DNA
polymerase. Incorporation of acyclovir triphosphate into viral DNA results in
obligate chain termination since the molecule lacks the 3-hydroxyl group
required for further DNA chain elongation. Viral DNA polymerase is tightly
associated with the terminated DNA chain and is functionally inactivated.
Viral DNA polymerase has a much higher affinity for acyclovir triphosphate
than does cellular DNA polymerase, resulting in little incorporation of
acyclovir triphosphate into cellular DNA. The median inhibitory concentration
of acyclovir necessary to reduce VZV plaque counts by 50% (IC50) is
approximately 3 µg/ml.

13
After oral administration, acyclovir is slowly and incompletely absorbed with
bioavailability of about 15–30%. Following oral administration of multiple
doses of 200 mg or 800 mg of acyclovir, mean plasma peak concentrations
at steady state are approximately 0.6 and 1.6 µg/ml, respectively. Plasma
protein binding is less than 20%. Acyclovir penetrates well into most tissues,
including the CNS. About 85% of an administered acyclovir dose is excreted
unchanged in the urine via glomerular filtration and tubular secretion. The
terminal plasma half-life of acyclovir is 2–3 hours in adults and 3–4 hours in
neonates with normal renal function, but is extended to about 20 hours in
anuric patients.

Valacyclovir is an orally administered prodrug of acyclovir that overcomes

the problem of poor oral bioavailability and exhibits improved
pharmacokinetic properties (Acosta and Fletcher, 1997). Valacyclovir, the L-
valine ester of acyclovir, is well absorbed from the gastrointestinal tract via
a stereospecific transporter and undergoes essentially complete first pass
conversion in the gut and liver to yield acyclovir and L-valine. Using this
prodrug formulation, the bioavailability of acyclovir is increased to about
54%, yielding peak plasma acyclovir concentrations that are three- to
fivefold higher than those achieved with oral administration of the parent
compound. Oral valacyclovir doses of 500 mg or 1000 mg produce peak
plasma acyclovir concentrations of 3–4 and 5–6 µg/ml, respectively.
Following administration of valacyclovir at a dose of 2 g orally four times
daily, plasma acyclovir area-under-the-curve (AUC) values approximate
those produced by acyclovir given intravenously at a dose of 10 mg/kg every
8 hours. Acyclovir AUC values after oral valacyclovir dosing are slightly higher

14
in elderly individuals when compared with younger control groups,
presumably due to declines in creatinine clearance associated with aging.

Acyclovir is cleared primarily by renal mechanisms so dosage modification

for both acyclovir and valacyclovir are required for patients with significant
renal dysfunction. The mean elimination half-life of acyclovir after a single 1
gram dose of valacyclovir is about 14 hours in patients with end-stage renal
disease. Acyclovir is readily removed by hemodialysis, but not by peritoneal
dialysis. No specific dosage modification for these drugs is required for
patients with hepatic insufficiency. Acyclovir and valacyclovir are not
approved for use in pregnancy, but have been widely use to treat serious
HSV and VZV infections in pregnant women without evidence of maternal or
fetal toxicity (Reiff-Eldridge et al., 2000).

Acyclovir is an extremely safe and well-tolerated drug. Local inflammation

and phlebitis may occur following extravasion of intravenous acyclovir. Renal
dysfunction resulting from accumulation of acyclovir crystals in the kidney
has been observed following rapid intravenous infusion of large doses of
acyclovir, but is uncommon and usually reversible. Acyclovir-related
neurotoxicity (including agitation, hallucinations, disorientation, tremors, and
mild clonous) has been reported, most often in elderly patients with
underlying CNS abnormalities and renal insufficiency (Hellden et al., 2003).
Oral acyclovir therapy is rarely associated with either neurotoxicity or
nephrotoxocity. Studies of patients receiving long-term acyclovir for chronic
suppression of genital herpes have revealed no cumulative toxicity (Tyring
et al., 2002).

15
At standard doses, valacyclovir is also a very safe and well-tolerated drug
(Acosta and Fletcher 1997). A syndrome of thrombotic microangiopathy
(characterized by fever, microangiopathic hemolytic anemia,
thrombocytopenia, and renal dysfunction) was observed in AIDS patients
receiving high dose valacyclovir (8 grams per day) in a clinical trial. However,
this syndrome has not been observed in immunocompetent patients
receiving valacyclovir at standard doses (up to 3 grams per day). There is
no contraindication to using valacyclovir at approved doses in HIV-infected
patients. Clinically significant interactions between acyclovir or valacyclovir
and other drugs are extremely uncommon.

Acyclovir is available in topical, oral, and intravenous formulations. The

dermatologic preparation consists of 5% acyclovir in a cream or polyethylene
glycol ointment base. Topical acyclovir is intended for treatment of minor
mucocutaneous HSV infections and plays no role in treatment of VZV. Oral
acyclovir preparations include a 200 mg capsule, 400 and 800 mg tablets,
and a liquid suspension (200 mg per 5 ml). Acyclovir sodium for intravenous
infusion is supplied as a sterile water-soluble powder that must be
reconstituted and diluted to a concentration of 50 mg/ml. The approved dose
of oral acyclovir for chickenpox is 200 mg/kg (up to a maximum of 800 mg)
4–5 times daily for 5 days. Adults with herpes zoster can be treated with oral
acyclovir at a dose of 800 mg five times daily. The recommended dose of
intravenous acyclovir for VZV infections is 10 mg/kg every 8 hours, although
higher doses (12–15 mg/kg) are sometimes used for life-threatening
infections, especially in immunocompromised patients. Dosage reduction is
required in patients with renal insufficiency. Valacyclovir is available as 500

16
mg and 1000 mg tablets. The recommended dose for immunocompetent
adults with varicella or herpes zoster is 1000 mg three times daily for 7 days.
Because a suspension formulation of valacyclovir is not available, clinical
experience with this drug in children with chickenpox is limited.

Penciclovir and famciclovir

Penciclovir is an acyclic guanine derivative that resembles acyclovir in

chemical structure, mechanism of action, and spectrum of antiviral activity
(Perry and Wagstaff, 1995). Like acyclovir, penciclovir is first
monophosphorylated by viral TK, then further modified to the triphosphate
form by cellular enzymes. Penciclovir triphosphate blocks viral DNA synthesis
through competitive inhibition of viral DNA polymerase. Unlike acyclovir
triphosphate, penciclovir triphosphate is not an obligate chain terminator and
can be incorporated into the extending DNA chain. Intracellular
concentrations of penciclovir triphosphate are higher then those seen with
acyclovir triphosphate. In VZV infected cells, the half-life values for
penciclovir triphosphate and acyclovir triphosphate are 7 hours and 1 hour,
respectively. However, this potential advantage is offset by the lower affinity
of penciclovir triphosphate for viral DNA polymerase. The median IC50 of
penciclovir for VZV in MRC-5 cells is 4.0 µg/ml. Because penciclovir is very
poorly absorbed, famciclovir (the diacetyl ester of 6-deoxy-penciclovir) was
developed as the oral formulation. The first acetyl side chain of famciclovir
is cleaved by esterases found in the intestinal wall and the second acetyl
group is removed on first pass through the liver. Oxidation catalyzed by
aldehyde oxidase occurs at the six position, yielding penciclovir.

17
When administered as the famciclovir prodrug, the bioavailability of
penciclovir is about 77%. Following a single oral dose of 250 mg or 500 mg
of famciclovir, peak plasma penciclovir concentrations of 1.9 and 3.5 µg/ml
are achieved at 1 hour. The pharmacokinetics of penciclovir are linear and
dose dependent over a famciclovir dosing range of 125–750 mg. Penciclovir
is not metabolized, but is eliminated unchanged in urine, with an elimination
half-life of about 2 hours after intravenous administration. Penciclovir for
intravenous administration has not been commercially marketed. Famciclovir
is available as 125 mg, 250 mg, and 500 mg tablets. In the United States,
the recommended dose of famciclovir for uncomplicated herpes zoster is 500
mg three times daily. Famciclovir doses of 250 mg three times daily and 750
mg once daily are approved for treatment of shingles in some countries and
appear to be comparable with respect to cutaneous healing of herpes zoster
(Shafran et al., 2004). Adjustment of the famciclovir dose is required in
patients with creatinine clearance of <60 ml/min. The adverse effects most
frequently reported by patients participating in clinical trials of famciclovir
were headache and nausea, although these symptoms did not differ
significantly between famciclovir and placebo recipients.

Brivudin

Brivudin (bromovinyl deoxyuridine) is a highly potent thymidine nucleoside

analogue with selective activity against HSV-1 and VZV (Keam et al., 2004).
The mechanism of action of brivudin appears to be inhibition of the viral DNA
polymerase. The drug is well-absorbed after oral administration and has a
favorable pharmacokinetic profile which permits once-daily dosing. Brivudin

18
is generally well-tolerated; nausea is the most frequently reported adverse
event. Because of concerns about the safety profile of the drug, commercial
development of brivudin was halted in the United States. The drug is
available in several countries as a 125 mg tablet and as a 0.1% ointment for
ophthalmologic use.

Foscarnet

Foscarnet (phosphonoformic acid) is a pyrophosphate analogue that

functions as an inhibitor of viral DNA polymerase by blocking the
pyrophosphate binding site (Wagstaff and Bryson, 1994). Unlike the
nucleoside analogues discussed above, foscarnet does not require
intracellular activation by TK, therefore, TK-deficient HSV and VZV isolates
that are resistant to acyclovir and related drugs remain susceptible to
foscarnet. Foscarnet is administered only by the intravenous route and 80%–
90% of an administrated dose is excreted unchanged in the urine. The
appropriate dose of foscarnet for treatment of acyclovir-resistant VZV
infections has not been assessed systematically, but doses ranging from 40
mg/kg every 8 hours to 100 mg/kg every 12 hours have been used
successfully. The most important adverse effect associated with foscarnet
therapy is nephrotoxicity. Dose limiting renal toxicity was noted in 15%–20%
of patients treated with foscarnet for CMV retinitis. Loading the patient with
intravenous saline prior to foscarnet infusion can help reduce the risk of
nephrotoxicity. Foscarnet can also induce a variety of electrolyte and
metabolic abnormalities, most notably hypocalcemia. Foscarnet-induced
electrolyte disturbances can predispose the patient to cardiac arrhythmias,

19
tetany, altered mental status, or seizures. To avoid serious adverse effects
that can result from bolus infusion, foscarnet must be administered with an
infusion pump over a duration of at least one hour. Serum creatinine levels
should be checked at least three times weekly in patients receiving foscarnet
and the dosage adjusted according to the manufacturer’s guidelines.

Vidarabine

Vidarabine (adenine arabinoside) was the first intravenous antiviral drug

accepted for widespread clinical use and was shown to be effective for VZV
infections in immunocompromised patients. Vidarabine has now been
replaced by more effective and less toxic antiviral drugs.

Interferon

Administration of alpha-interferon to immunocompromised patients with

herpes zoster reduces the risk of viral dissemination, but has little impact on
dermatomal rash healing or pain. Interferon therapy was associated with
significant adverse events and has been supplanted by more specific antiviral
drugs.

20
CHAPTER FOUR

CONCLUSION AND RECOMMENDATION

Chickenpox is an airborne disease which spreads easily through the coughs

and sneezes of an infected person. It may be spread from one to two days

before the rash appears until all lesions have crusted over. It may also spread

through contact with the blisters. Those with shingles may spread

chickenpox to those who are not immune through contact with the blisters.[2].

The
disease is often diagnosed by preventing the symptom. Recent advances

in the treatment of the disease have proven to be more efficacious that the

later approaches.

The treatment encourages protective measures like staying at home during

the infection, cutting of the nails short to avoid scratching and wearing of

gloves.

21
RECOMMENDATION

From the work, the following recommendations were made;

i. Greater efforts should be made to disseminate information about

chickenpox disease and its prevention.

ii. Important misconceptions regarding vaccine efficacy need to be

addressed, especially among medical students who represent future

generations of doctors.

iii. Further research is required to objectively assess disease burden,

cost-effectiveness of the vaccine, and physician preferences in

influencing chickenpox vaccine uptake.

iv. Chickenpox vaccine should be to incorporate chickenpox vaccine into

the national Immunization schedule as part of an effective public

health programme.

v. Further research should be encouraging to unravel the mysteries

behind the chicken pox virus.

22
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