CHAPTER ONE

INTRODUCTION

Hepatitis B virus (HBV) infections is still one of the most important causes of liver disease, with

2 billion people infected worldwide and more than 600, 000 deaths each years, caused in 94% of

cares by chronic infection related cirrhosis and hepatic cellular carcinoma (HCC). The world

health organization (WHO) estimates more than 360 million organized people being chronic

carries worldwide (6% of the world population). The indicate of HBV infection has been

declining over the last two decades thanks to the introduction of universal immunization

programs and the implementation of blood- donor screening. Nevertheless, a significant number

of adults and children are still infected each year, the letter often developing chronic infection

and requiring an appropriate follow-up. In spite of a rather being course of chronic disease

during childhood and adolescence, HBV chronic carries have a lifetime risk of developing HCC

up to 25% and an incidence of cirrhosis of 2.3% per years safe and partially effective antiviral

therapies are available but few are licensed for use in s and accurate selection of subjects to treat

and of the right timing for treatment is needed to optimized efficacy and reduce viral resistance.

2012 European association for the study of liver published by Elsevier B U right reserved.

Epidemiology HBV is transmitted by percutaneous and mucous membranes

exposure to infections blood, semen,vaginal secretion and solve the extreme resilience of HBV,

allowing its survival for more than a week on dry surfaces, explains the increase risk for

horizontal intramilian transmission and the need of carriers counseling and household members

vaccination nonetheless after 20 years from the introduction of immunization programs most

infants and children are protected against HBV and chronic carries should not be isolated in

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school or prevented from practicing sports. Transmission occurs rarely in childcare setting but

the risks is higher in detention centers, where adolescents are less likely to be immunized and

have high-risk behaviors in highly endemic areas, with mother to child transmission accounting

for more than half of chronic infection. After exposure, the risk for developing is indeed higher

for newborns (90%) than for infants and children 5 years of age or adolescents and adult (5%) to

further reduce mother to child transmission, who recommends the administration of both the

vaccine and hepatitis B immunoglobins (HBIG) to newborn of Hbc Ag- negative mothers does

not overall protection rate but decreases the risk of fulminate hepatitis higher in this group

providing to the cost-effective. Newborns of highly viremic HB Ag-positive mother are at

increased risk of HBV infection despite proper immunization (break through infection),

compared to babies born to HBC Ag-negative mothers (16.8% vs 1.6%) and are at increased risk

for chronicity break through infection is more likely to occur in newborns of mothers with

genotypes c, who have higher viral loads. Vaccination programs are therefore changing the HBV

genotype distribution intrauterine infection. Hypo responsiveness to vaccines, and vaccine

escapes mutants could play a role as well the risk of mother- child transmission also depends on

maternal serum HBS Ag titer and mode of delivery 10.5% per elective cesarean section vs. 20%

for vaginal delivery vertical transmission can be further reduced by treating highly viremic

mothers dunngs the list trimester of pregnancy with either lamivudine, telbivudine or tenofovir

(1-2% risk reduction for lamivudines and 8% for telbinudine HBs Ag and HBV DNA can be

detected in breast milk of chronic carries, but no increased risk of transmission to a breast fed

infants has been shown and breastfeeding is currently recommended after proper infants

immunization . who has recommended universal HBV vaccination since 1991, with the first dose

to be admitted within 24hours from birth, followed by at least two doses at land 6 months of life.

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By the end of 2010, 179 of the 193 who member states had implemented a nationwide childhood

HBV immunization program and global HBV vaccine coverage was estimated at 75% in

countries where such programs have been implemented, prevalence of HBV infection decreased

dramatically (38-40) many countries with high HBs Ag sero prevalence (7.8%) before

vaccination programs (like china and Taiwan) are now considered at intermediate (2-7%) or low

prevalence (<2%) in Taiwan prevalence of HBs Ag. In children younger than 15 years of aged

decreased from 9.8% to 0.5% after 20 years of vaccination. In china HBVs Ag prevalence in

children aged 1-14 years decreased by 83% (from 8% in1992 to 1.36%) in 2006 are not study,

4.6% of the total population of the units states has been exposure to HBV ( past or chronic

infection, with up to a 50 – fold variation as age ethnicity and country of birth vary. HBs Ag

Sero prevalence in children and adolescent aged 6-12 years and 13-17 years is 0.03%,

respectively prevalence of both exposure and chronic carries state is higher among people

coming from high or intermediate prevalence countries and among those with lower family

income or with high-risk behavior.

Although among children born in Western Europe and north amenea prevalence of HBV

infection is low, pediatacian and hematologist are confronted within increasing number of

children adopted from higher prevalence countries (table 1). Between 2% and 5% of all

internationally adopted children all international adopted children, all coming from 7-2%

prevalence areas, are still infected with HBV CDC and American academy of predicates

recommend screening all children adopted from these countries for HBV (HBs Ag, HBs Ab HBs

>m/u ml) or diagnose a previously unknown infection and processed to immunization of

household contacts. Ten genotypes (A-g) and several subtypes have been described for HBV,

with a distinctive geographic distribution although in most of Europe and north America,

3
genotypes A is predominant, many of the children coming from high or intermediate endemicity

countries are infected with genotypes B, C, D or F (table1) are at increased risk of complications

and many have a worse response to therapy

1.1BACKGROUND

Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) with affects the liver it

can cause both acute and chronic infections. Many people have no symptoms during the initial

infection, some develop a rapid onset of sickness, with vomiting yellowish skin, feeling tired,

dark urine and abdominal pain (world health organization (who), 2014. Also these symptoms last

a few weeks and rarely does the initial infection result in dead (Rapheal et al, 2008). It may take

30 180days for symptom to begin (who, 2014) in those who get infected around the time of birth,

90% develop chronic hepatitis B while less than 10% of those infected after the age of five do

(centre for disease control (cdc) 2011). Most of those with chronic hepatitis B have no system.

However, arrhosis and liver cancer may eventually develop (chang et al 2007). These

complication result in the death of 15% to 25% of those with chronic disease (who, 2010), the

virus transmitted when blood, semen or any other body fluid from a person infected with the

hepatitis B virus get in contact with the body fluid of someone who is not infected. Infection

around the time of birth or from contact with other people blood during childhood is the more

frequent method by which hepatitis B is acquired in area where the disease is common. In areas

where the disease is rar, intravenous (iv) drugs infection (who. 2014) other risk factors include

working in health care, blood transfusion, living with an infected person, travelling into countries

where the infection rate is high (CDC, 2011). Tattooing and acupuncture led to a significant

number of cases in the 1980s; however, this has become less common with improve eternity

(Thomas he, 2013).

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It is estimated but about a third of the world population has been infected at one point in their

lives, including 240 million to 350 million who have chronic infections (schisky 2013). Over

750, 000 peopledie of hepatitis B each year (who 2010), about 360, 000 of these are (global

burden of disease (GBD) collaborators 2014 the infection has been preventable by vaccination

since 1982 (pungpagong et al. 2007). Vaccination is recommended by world health organization

in the first day of life if possible, two or three more doses are required at a later time to full

effect. This vaccines works about 95% of the time (who, 2014), about 180 countries gave the

vaccine as part of national programs as of 2006 (Williams, 2006). Early record of an epidemic

caused by hepatitis B virus was made by lurman in 1885 (lurmanet, al, 1885).

The record was made by when an outbreak of small pox occurred in Bremen in 1883 and 1, 289

shipyard employed were vaccinated with lymph from other people. after several weeks and und

skin to eight month later, 191 of vaccinated works become ill with young dice, the yellow

discoloring of the eye and skin which is a common symptoms of hepatitis B infection other

employee who have been inoculated with different batches of lymph remained healthy. Lumens

paper now regarded as a classical example of an epidemiological study proved that contaminated

lymph was the source of the outbreak. Later, numerous similar outbreaks were reported

following the introduction in 1909, of hypodermic needles that were used, and more importantly

re-used for administering salvers for the treatment of syphilis. The virus was not discovered until

1966 when brunch blub erg, then working at the national institutes of health (who, and currently

at the fox chase cancer centre, discovered the Australia antigen (later known as hepatitis B

surface antigen, or HBs Ag) in the blood of aboriginal people (alter et al 1966). Although a virus

has been suspected since the research by McCollum in 1947 (McCollum, 1947), D.S dane and

others (1970) discovered the viral practices in 1970 by electoral microscopy (dane et al, 1970).

5
By the early (1980s the gnome of the virus has been sequenced (galabert et al, 1979) and the first

vaccines where been tested (lancet, 1980).

Chronic hepatitis B virus infection affects approximately 350 million people worldwide, half of

whom acquired the infection from pre-natal transmission or in early childhood (janas, 2009 and

lavanchy, 2004). Currently over two billion people have evidence of previous HBV infection and

350 million have become chronic carries of the virus, 60 million of them residing Africa

(department of health, 2006). Here seem to be differing risks for HCC by geographical location,

with higher risk recorded in countries in sub-sahara Africa and Asia compared to Europe

(woinbaum et al, 2008).

Thus, sub-saharan Africa including Nigeria has been reported as a region of high endemicity

with an average carries rate of 10-20% among the general population. They further added that

about 70-95% of adult carrier in sub-sahara Africa posses at least one HBV maker

(tmechebeGoetal, 2009).

According to emechebe et al, (2009), an estimated 5-10% of infected ult become chronic carries

while the rest most often dominate without sequalee, the virus from their body they further added

that an estimated one quarter of chronic carries often die due to hepatic complications, of few

remain lifelong carrier while others at varying intervals clear the infections.

This study was aimed to determine the prevalence of hepatitis B amongst young children on 1-5

years attending Murtala Muhammad Specialist Hospital Kano.

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Hepatitis B virus:

The virus is much smaller than a human cell hepatitis B virus is a sphencal particle with

adimeters of 42 nonometers (inm= 0.000000001meter).

Hepatitis B is a DNA virus of the epadnavidae family of viruses. Once inside a host cells, it takes

over the cells normal functions and uses the cells resources to produce more viruses, a process

called replication. The hepatitis B virus primarily infects liver cells and other cells of the body,

including white blood and other tissue, can harbor the HBV.

The virus is composed of an outer coat or surfaces protein, called the surface antigen (HBs- Ag,

previously known as the Australia antigen). The surface protein coat or surround. The inner care

(machinery) of the virus that contains the genetic material (genes made of DNA) of the virus and

some enzymes that are essential for the reproductive process of the HBV. This surface coat is

made in abundance and is shed into the blood this is the marker for the surface antigen test.

The virus infects a person when blood or certain body fluid such as semen- carrying the virus

enters a person. Infection can occur through a break or abrasion in the skin or when the blood

borne virus comes into contact with a mucus membrane such as the thin lining inside the mouth,

around the eye balls or inside the or inside the nose.

Once in the bloodstream, it is easy for the virus to come into contact with the liver, the largest

internal organ in the body. If the hepatitis virus make it past the body immune system and

encounters a liver cells (known as hepatogyte), the virus outer coat sticks to the liver cell

surfaces and the virus core genetic material inserts itself into the liver cell.

7
The longer the hepatitis B virus replicates in the liver, especially in those infected as children, the

more entrenched the virus becomes within the structure of the liver cells. Researchers suspect

that over a period of years or decade the hepatitis B DNA locks itself into the genetic material

(DNA) of the liver cell- a process called integration which makes it harder for the immune

system to target and fight the

Infected cells, may make the liver cell more prone to becoming cancerous.

An estimated one-third of the world population about 2 billion have been exposed to the hepatitis

B virus (HBV) through contact with infected blood or body fluid, according to the world health

organization (who). Such infections may occur during the birthing process, white sharing

contaminated needles or during transfusion with infected blood.

When teens and adults with healthy immune system are exposed to the virus, more than 90

percent will successfully fight off the infection and clear the virus.

Those acute and short- lived brushes with HBV infection typically cause only minor, flu-like

symptoms if any symptoms at all.

But when newborns and very young children are infected their immune system often fail to

recognized and vanquish the virus. As a result, about 90 percent babies will develop the virus or

long- term infection.

The virus begins by silently replicating in their livers, under undeterred by the young immune

system over years and even decades, the infection can cause extensive damage before their

immune systems finally recognized the virus and attack the liver cells where their virus resides,

possibly resulting in cirrhosis or even liver cancer.

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1.2 STATEMENT OF THE PROBLEM

The difficulties faced by young children in controlling can lead to the development of argosies

and this Larcaranoma in chronic carries. Thus, diagnosing and treating the development of

arrhosis and hepatitis cellular carcinoma. This therefore motivated the researcher to carry out this

process to assess the prevalence of HBV amongst youth children attending Murtala Muhammad

Specialist Hospital Kano

1.3 RESEARCH QUESTION

• What is the prevalence of the hepatitis B amongst young children (1-5 years) attending

the Murtala Muhammad Specialist Hospital, Kano?

• What is the prevalence of hepatitis B amongst young children classified according to

age?

• What is the prevalence of hepatitis B amongst young children classified according to sex?

• What is the factors that Predispose children 8 to hepatitis B infection?

1.4 OBJECTIVES OF THE STUDY

• To determine the prevalence of hepatitis B amongst youths children attending the Murtala

Muhammad Specialist Hospital Kano.

• To determine the prevalence of hepatitis B amongst young children classified according

to age.

• To determine the prevalence of hepatitis B amongst young children

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 • Classified according to sex.

• To determine risk factors of hepatitis B amongst young adults attending the Murtala

Muhammad Specialist Hospital, Kano.

1.5 RATIONATE OF THE STUDY

Little or no work has been in the Murtala Muhammad Ladan on the prevalence of Haepatitis B

amongst young adults, so this work is going to sensitize the community on the prevalence of

hepatitis B and how to prevent the transmission of the virus.

This work is going to help the ministry of public priority on hepatitis B infection.

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 CHAPTER TWO

LITERATURE REVIEW

2.1 Scientific classification of hepatitis B virus.

Group: group vii (ds DNA RT)

Family: Hepadnavind GB

Genus: Orthohepadnavirus

Species: hepatitis B virus (hunt Richard, 2007)

2.2.1 Morphology of hepatitis B virus surfaces antigens (HBsAg)

• Hepatitis B surfaces Antigens (HBsAg)

The virus surface proteins are called the hepatitis B surface antigen and it is commonly referred

to as aHBsAg. The presence of the surface antigen in a blood test indicates a current HBV

infection (either acute or chronic) and that the person may be capable of transmitting the

infections to other.

When a virus replicates in a liver cells these surfaces proteins chump together into rods and

spheres in the blood stream. In completely for red viruses capable of infecting liver cells, the

surfaces proteins encapsulate the core proteins and DNA particles.

Te excesses spheres and rods of the surfaces antigen either the blood stream in large number and

when presents they indicate an active NBV infection that can be either acute (shot lived the body

cannot quickly eradicate it).

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White only a small portion of surface antigen combines with the viral core products to form a

complete virus anyone with the surface antigen in his or her blood stream should be considered

infectious to other.

Laboratory test can usually find the surfaces antigen about four week after infection with the

virus but detection in some may range from one to twelve weeks after infection detection of the

surfaces antigens can precede. The on set of symptoms such as jaundice and elevation of liver

emzymes (which indicates liver cells are injured) by one to seven weeks. (WHO 2009, 2010).

2.2.2 Morphology of Hepatitis B Core Antigen (Hbcag)

HBcAg (figure 1) is the major structural proteins of the core particles and it is a (21kd) is the

product of indication from the more internal start codon. The HBcAg is the more conserved

polypeptide among the mammalian hepdna viruses with 68% homology between hbv AND Gstu

and WHv (who, 2009)

• Hepatitis B core antibodies (anti HBcAb)

• Hepatitis B virus DNA (HBv DNA)

Hepatitis B virus (HBv DNA) is the geneticmmaternals that carries the replication blueprint of

the virus. DNA is one of the first things that can be detected as soon as one week after infection,

if sensitive test are used to detect the genetic materials measuring HBV DNA has led to the

recognition of low level viremia (HBv DNA) in many patient of the who have no apparent liver

injury “noted the authors of the national academy of clinical biochemistry laboratory medicine

practices guideline for screening, diagnosis and monitory of disease of liver disease.

12
Generally, HBv DNA levels indicates how fast the virus is replicating high levels indicates

ongoing replication of the virus. Low or undetectable levels indicate the infection is in a less

active phase.

HBv DNA is a detected by genetic engineering using a techniques called the paymerase chain

reactions (PCR) test, this is the most sensitive testing method or assay for measuring DNA level

the PCR creates copies of specific DNA fragments to detect and measure the HBv DNA.

Therefore, HBv DNA measure the “copies” or number of viruses in a blood sample per formed

as a standard test tomoneter infection.

Hepatitis B X protein (HBX protein)

Hepatitis B virus

2.2.3. Morphology of Hepatitis e antigen (HBeAg)

HBeAg (Figure 1) (16-18kD) is one of the serum markers for Hepatitis B virus infection and

correlates with high infectivity. Being a non structural protein produced by actively replicating

HBV, HBeAg is detectable in the serological course after exposure to HBV, usually after first

Month of infection (WHO, 2009).

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Figure 1: structure of the hepatitis B virus

2.3. Life Cycle of Hepatitis B Virus

According to Inan&Tabak (2015), Hepadnaviruses, including human hepatitis B virus (HBV),

replicate through reverse transcription of an RNA intermediate, the Pregenomic RNA (pgRNA).

They also reported that the first step in HBV replication and life cycle is the reversible non-

energy requiring binding to a host structure or cell surface. Hepatitis B virus infects and

multiplies within the hepatocytes through several stages ranging from binding to cell receptors to

the release of the virus particles (Urban S. et al., 2010). In addition, Urban et al. (2010) further

reported that the binding of the virus particles to the hepatocytes involves non reversible and

reversible specific attachment to the receptors - cell associated heparan sulfate proteoglycans and

hepatocyte-specific preS1- receptor, respectively. The entry mechanisms into the cell are via two

major mechanisms: endocytosis which leads to the release of nucleocapsids from the endocytic

vesicles and fusion of the viral envelope with the plasma membrane (Inan&Tabak 2015). Within

the hepatocytes, the nucleocapsids is transported through the microtubules to the nucleus. The

interaction of the accumulated Capsids with the adaptor proteins of the nuclear pore complex

degrade the viral nucleocapsids and ensure the release of the relaxed circular DNA (rcDNA) into

the nucleoplasm though the mechanism via which the degradation occurs is not known. It is

reported that the RDNA is repaired by the cellular enzymes through the removal of the viral

polymerase and short RNA-primer used for the DNA plus strand synthesis from the 5’-end of the

minus strand DNA. He added that the propagation of the viral DNA is enhanced by the

formation of CCCDNA which occurs via the ligation of both DNA strands. Production of viral

RNAs for protein synthesis and viral replication is mediated by the host cell’s transcription

factors (CCAAT/enhancer-binding protein(C/EBP) and hepatocyte nuclear factors (HNF) as well

14
as viral proteins (core, the regulatory X-protein) which also plays a vital role in gene expression.

The major mRNA produced in this stage is processed, stabilized and exported by the host factor

La RNA binding protein (Urban S. et al., 2010; Beck J and Nassal M. 2007). According to

Levrero et al. (2009), the translation process involves formation of viral core proteins and

polymerase as well as subsequent formation of a complex of core proteins, polymerase and

assembly of a nucleocapsid containing RNA. The RNA is then reversed transcripted to a plus

strand DNA followed by maturation and release of the virons from the nucleus into the

cytoplasm (Urban S. et al., 2010; Levreroet al., 2009).

Figure 2: Lifecycle of hepatitis B Virus

From: http://www.globalserve.net/~harlequin/HBV/hbvcycle.htm

2.4. Pathogenesis and Immunity of Hepatitis B Virus

Following HBV infection, there is an initial hepatitis that may or may not be symptomatic.

Successful clearance and resolution of infection depends on the age and immune status of the

individual with most infections of immune competent adults being self-limiting. Persistent or
15
chronic infection is more likely to occur following vertical transmission (from mother to child)

or horizontal transmission to children or to immune compromised adults (Mason et al.., 1991).

The immune determinants of successful clearance of HBV are not fully understood but both

cellular and humoral immune responses are important (Webster et al., 2000). At the same time,

however, liver inflammation and disease are also believed to be largely immune-mediated.

Therefore, a complex interaction exists between HBV and the host in the initial clearance of

HBV, the long-term persistence of HBV and the pathogenesis of HBV liver disease.

Immune responses against HBV and effects of chronic HBV, infection Control of HBV infection

requires the combined action of both the innate immune response and the humoral and cellular

arms of the adaptive immune response. There are several mechanisms that have been associated

with persistent or chronic HBV infection. Chronic HBV infection is associated with reduced

ability of DCs to prime T-cells and produce cytokines as well as reduced expression of TLR2 on

peripheral monocytes (Zhenget al., 2004). CD4+ T-cells are skewed toward a Th2 CD4+ T-cells

phenotype (Beckebaumet al., 2003). In addition, an increase in activity of regulatory T-cells, or

CD25+ CD4+ T-cells further increases production of IL-10(Franzeseet al.., 2005). The remaining

Th1 CD4+ T-cells have reduced proliferative capacity and impaired production of antiviral

cytokines (Boniet al., 2003). Reduced function of Th1 CD4+ T-cells and reduced priming from

DCs both impair the function and number of HBV-specific CD8 + T-cells. These anergic HBV-

specific CD8+ T-cells may have elevated PD-1 expression (Boettleret al., 2006). Liver damage

may still occur in the liver and is largely mediated by infiltration of HBV-nonspecific CD8 + T-

cells (Mainiet al., 2000).

The study of the pathogenesis of HBV has been limited by the lack of available animal models

and cell lines that support HBV infection. HBV can infect chimpanzees that only acquire a self-

16
limiting acute hepatitis. Other animal models include infection of ducks with Duck HBV and

woodchucks with Woodchuck HBV. More recent developments in transgenic mouse models

have allowed for a better understanding of the relative contribution of the different arms of the

immune system to clearance of HBV, in particular the contribution of the early innate immune

response (Isogawaet al., 2005).

2.5. STAGES OF HBV INFECTION

Remarkable progress has been made in the understanding of the three (3) main natural stages of

the HBV infection in hosts: acute infection, chronic asymptomatic and chronic symptomatic

stages (AASLD, 2007). However, not all HBV-infected patients go through all the three stages.

The risk to develop liver–related complications, such as cirrhosis and hepatocellular carcinomas

increases as patient progresses from acute to chronic stage of the infection. Indeed, most HBV

infections end up at the acute stage (~ 90%) with a few progressing on to the chronic stage.

2.5.1. Acute HBV infection

This is the initial stage of the infection and every HBV- infected patient goes through this, even

though not all patients transit beyond this stage. Early phases of this stage of the infection are

characterized serologically by the presence of HBsAg, high serum HBV DNA, HBeAg, and

normal level of serum aminotransferase level (ALT), and minimal or insignificant inflammation

on liver biopsy (Altiparmaket al., 2005). A later phase, also called immunity phase, is marked by

increased serum titres of anti-HBsAgIgG (HBsAb), anti-HBcAgIgG, lowered or disappearance

of HBsAg and HBV DNA, normal liver histology. This is true for those who recover fully from

the infection after attaining full and permanent immunity through exposure. The duration of

either phase differs among patients but generally lasts between 5 - 8 months (AASLD, 2007).

However, those patients who fail to mobilize adequate immune response factors to combat the

17
infection end up with the fate of living with the disease their entire lifetime. In this case, it is said

the disease has become chronic. The physical signs and symptoms, such as jaundice, fever, dark-

urine formation, nausea, among others, would occur, even though they will last shortly after

which they get resolved following recovery. Generally, transition from the acute stage to the

chronic stage depends on several factors including: age, gender, viral genotype, and host immune

competence.

2.5.2. Chronic HBV infection

This occurs as a progression of the early phase of the acute HBV infection due to the host‘s

failure to mount the necessary immune stimulus to ensure total viral clearance and consequent

resolution of the disease. It is serologically marked by relative rise in serum anti-HBcAgIgG,

disappearance or lower titers of anti-HBsAgIgG, and either normal or significant liver damage as

shown by ultrasonography (WHO, 2008). Also, this stage of the disease may be characterized by

normal or elevated serum aminotransferase levels (aspartateaminotransferase (AST) and alanine

amino transferase (ALT)) (AASLD, 2007). Chronic HBV infected patients fall into one of the

two pathologically progressive forms, namely:

A. chronic asymptomatic, marked by:

• Presence of HBsAg in serum

• Anti-HBsAgIgG (HBsAb ) positive

• Normal liver histology indicated by apparently normal ALT levels

• Relatively lower viral load (<103 copies/ml) (AASLD, 2007)

B. Chronic symptomatic, marked by;

• Presence of HBsAg in serum

• Anti-HBsAgIgG (HBsAb ) positive

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 • Relatively higher viral load (>103 copies/ml),

• Significant damage on liver histology, showed by elevated ALT levels (AASLD, 2007).

Patients at the chronic symptomatic stage may show mild to severe liver cirrhosis. Terminal

stage of liver damage is accompanied by complications such as hepatomegaly, lower abdominal

bleeding, elevated serum endogenous mercaptans, hepatic encephalopathy, hepatic coma,

membranous glomerulonephritis, etc. (Lok and Mahon, 2007).

The serological presence of HBeAg is real in all stages of the disease. The presence of this

antigen together with elevated viral load (HBV DNA > 10 3copies/ml) and higher ALT (>

60IU/l) is a strong indication of viral activity, replication, and infectivity (WHO, 2008). Patients

with such manifestations are put on retrovirals. A key event in the natural history of HBeAg –

positive CHB patients is HBeAgseroconversion (Sharma et al., 2005). It is believed that

seroconversion of HBeAg to HBeAb is accompanied with cessation of HBV replication and

remission of liver disease. Several studies have shown that seroconversion with a marked

reduction in HBV replication is associated with biochemical and histological remission of

inflammatory activity in the majority of patients (Sharma et al., 2005,Elghouhariet

al,2008.McMahon, 2005). Some studies showed that the mean annual rate of spontaneous

HBeAgseroconversion ranges from 8% - 15% in children or adults with an elevated ALT level

(Sharma et al., 2005; McMahon, 2005). Although the ALT level is normal in most Asian

children, their spontaneous HBe Agseroconversion rate is less than 2% during the first3 years of

age and then increases to 4%-5%. In some cases, spontaneous recurrence of hepatitis is not

frequently recognized because it is usually asymptomatic. Since subsequent HBe Agsero

conversion would not occur in such situations of hepatitis, it can thus be viewed as an abortive

attempt at seroconversion. However, regression of fibrosis occurs several months or years after

19
HBeAgseroconversion (McMahon et al., 1990). The recurrence of hepatitis may precede the

disappearance of HBeAg and development of HBeAg antibody, culminating in the remission of

hepatitis activity (Furusyoet al., 2002; Chan et al., 1999).Absence of HBeAg could rather be

indicative of viral dormancy/hibernation (Tsai et al., 1992). Although a high serum DNA level in

patients with liver disease with minimal or no inflammation is considered as a sequela to

immune tolerance to HBeAg, it has been shown that HBeAg may promote HBV chronicity by

functioning as an immunoregulatory protein (Milich and Liang, 2003). Such a mechanism may

be responsible for the high chronic HBV infection rate (~ 90%) observed in babies infected by

their HBeAg – positive mothers, accounting for theeinability of infants to clear perinatal HBV

infection. HBeAg can also enter thymus. It has been reported that HBeAg specific Th2-like cells

can preferentially survive tolerance production to a greater extent than HBeAg – specific Th1-

like cells (Huang et al., 2006). Therefore, chronicity resulting from vertical transmission of

HBV, characterized by the predominance of HBeAg -specific Th2-like cells and secretion of

anti-inflammatory cytokines, such as IL-4, IL-5, and IL-10, can enhance antibody production,

and viral persistence would characterize the HBeAg specific T-cell response. Presence of

HBeAg and absence of the HBeAb increases a patient‘s risk of developing liver – related

complications, such as cirrhosis, fibrosis, carcinoma, etc.

2.5.3. Occult HBV infection

Recent investigations into the serologic and pathological distinctions among the various stages of

HBV infections have led to the discovery of a new form, though rare, called occult HBV

infection (HBI). Occult HBI is defined as the existence of HBV DNA in serum marked with

absence of HBsAg (Torbenson and Thomas, 2002; Conjeevaram and Lok, 2001). In addition to a

symptomatic and serologically evident infection, occult persistent HBV carriage has been

20
identified since nucleic acid amplification assay enhances its sensitivity to hepadnaviral genomes

and their replicative intermediates. There is evidence that occult HBV infection is a common and

long-term consequence of acute hepatitis B resolution. This form of residual infection is termed

as secondary occult infection (SOI) (Conjeevaram and Lok, 2001).

2.6. Signs and Symptoms of the infection

Some studies have revealed that hepatitis B virus infection could either be acute or chronic

depending on factors including the duration of its incubation and persistence in the bloodstream

as well as the age and immune status of the person involved (Janahi EM. 2010). Acute infections

could either be asymptomatic or symptomatic with signs and symptoms appearing faster

compared to the chronic form most often observed in adults. The incubation period of acute

hepatitis B virus has been reported to range from one to three months and present symptoms

including nausea, tiredness, fever, loss of appetite, diarrhea, abdominal pain, aches and pains,

dark urine and as well as jaundice (Ansari AS. et a., 2010). In rare scenarios, acute liver failure

which often leads to death has been reported in some patients with acute hepatitis (Janahi EM.

2010). In most cases, infection with HBV could be chronic (continued existence of HBsAg in

blood for more than six months); causing chronic liver infection that often develops into cirrhosis

and cancer of the liver (Janahi EM. 2010)). According to Liang (2009), most chronically infected

persons exhibit mild liver diseases with short term morbidity whereas in others, infection may

progress to cirrhosis and hepatocellular carcinoma. Chronic infections have also been reported

mostly among children (Inan N, Tabak F. 2015). McMahon (2009) added that cirrhosis often

become visible once depreciation of the immune system occurs, enabling the development of

more apparent symptoms usually indicative of cirrhosis.

21
According to McMahon (2009), the development of chronic hepatitis B infection occurs in three

basic phases including; immune tolerant phase, the immune active phase and the inactive phase.

2.7. Complications of chronic Hepatitis B

Patients with chronic Hepatitis B (CHB) are at increased risk of cirrhosis, hepatic decomposition

and hepatocellular carcinoma (HCC) (Liaw, 2009). Longitudinal studies of patients with CHB

indicate that, after diagnosis, the 5 years cumulative incidence of cirrhosis is from 8 to 20%, and

once cirrhosis has developed, the annual risk of HCC is 2–5% (EASL, 2009). It has been

estimated that HBV infection is responsible for 50–80% of HCC cases worldwide (Venooket al.,

2010). The risk of cirrhosis is highest in those with chronic active hepatitis (HBeAg-positive

CHB or HBeAg-negative CHB), whereas the risk in those who remain in the low explicative or

HBsAg-negative phase approaches that of the background uninfected population. The majority

of cases of HCC occur in individuals who have already developed cirrhosis, although recent

studies have shown that HCC can still occur in the low explicative and the HBsAg-negative

phases in patients with seemingly normal liver architecture (Liaw, 2009). The risk of cirrhosis

and HCC is increased in males, older age, family history of HCC, high viral load, persistently

raised ALT, co-infection with HCV or HIV and HBV Genotypes C and F (Liaw, 2009).

2.8. Epidemiology of Hepatitis B virus

Hepatitis B is an infection of the liver caused by the HBV, a double-stranded DNA virus of the

hepadnaviridae family. The virus is transmitted via percutaneous or permucosal exposure to

infected blood or body fluids and has an incubation period ranging from 40 to 160 days (average

60–90 days) (Ottet al.., 2012). Transmission can occur vertically from infected mother to child,

horizontally (e.g. child-to-child transmission within a household), sexually or parent rally (e.g.

via injecting drug use, sharps injury or contaminated blood products).

22
The majority of acute HBV infections are asymptomatic. In adults, approximately 30% will

present with jaundice and hepatitis and 0.1–0.5% develops fulminant liver failure (Alter et al.,

1990). During acute infection, hepatitis B surface antigen (HBsAg) and hepatitis B e antigen

(HBeAg) can be detected in the serum and there are high levels of IgM antibodies to the viral

core antigen (IgM anti-HBc) (Kowdley, et al.,2012). A successful host immune response to the

virus leads first to clearance of HBeAg (and appearance of antibody to HBeAg) and subsequent

clearance of HBsAg (and appearance of antibody to HBsAg). The appearance of antibodies to

HBsAg indicates recovery from acute infection (Kowdley et al., 2012). The persistence of

HBsAg for >6 months from its first detection denotes chronic hepatitis B (CHB) infection. The

likelihood of developing CHB varies with the age at which the infection is acquired, the risk

being lowest in adults (<5%) and greatest in neonates whose mothers are HBeAg positive

(approximately 90%) (Tassopouloset al, 1987). The prevalence of HBV infection varies

geographically and can be categorized into areas of high (>8%), intermediate (2–8%) and low

(<2%) endemicity (Ottet al.., 2012). The principal mode of HBV transmission also varies

geographically. In low prevalence areas such as Northern Europe and North America, HBV

infection is primarily acquired in adulthood through sexual contact or injecting drug use, whereas

in high prevalence areas, HBV infection is most commonly acquired prenatally or in early

childhood (Stevens et al., 1975). Hepatitis B prevalence is highest in sub-Saharan Africa and

East Asia, where between 5–10% of the adult population is chronically infected.

High prevalence areas include: China, South East Asia, sub-Saharan Africa, parts of South

America and Alaska. Intermediate prevalence areas include: parts of South America, North

Africa, and Eastern Europe, parts of Southern Europe, the Eastern Mediterranean area and the

23
Indian subcontinent. Low prevalence areas include: most of North America, Australia, Northern

Europe and most of Western Europe.

In a recent review conducted by the European Centre for Disease Prevention and Control (CDC,

2009), population prevalence of CHB was found to vary widely between European countries

ranging from 0.1% in Ireland and the Netherlands to >7% in the eastern part of Turkey. The

review also found that in all the countries for which data were available, the estimated

prevalence of CHB infection was higher among migrant groups than in the general population.

Similarly, immigration of individuals with CHB from countries of intermediate and high HBV

prevalence has been estimated to account for >95% of the estimated annual incidence of CHB

infections in England (Ly et al., 1990).

2.9. Modes of transmission

The virus is a blood-borne virus and any contact with contaminated blood or bodily fluids

containing infected blood through the mucous membranes or broken skin could potentially result

into transmission (Harrison, Dusheiko and Zuckerman 2009).

2.9.1 Vertical transmission

The virus can be transmitted from mother to child either in utero or during delivery and shortly

after birth through the close contact between the infected mother and the neonate (perinatally).

Although in utero transmission is rare, its occurrence is significantly associated with high

maternal viral loads (Wood and Isaacs 2012), a history of threatened preterm labour (Tran 2012),

acute infection during the third term of pregnancy (Wood and Isaacs 2012) and can occur by the

infection of endothelial cells of placenta capillaries and by cellular transfer from cell to cell (Xu

D et al., 2002). Polymorphisms in cytokine genes have also been correlated with a susceptibility

of intra-uterine HBV infection (Jonas 2009). This mode of transmission commonly results in

24
infection of the neonate despite vaccination at birth (Lee et al., 1986) and is associated with the

mother’s viral load irrespective of e-antigen status (Burk et al., 1994).

Transmission at birth is possible when the baby is exposed to the blood and the genital secretions

of the mother in the birth canal (Ranger-Rogez and Denis 2004). Breast-feeding is not contra-

indicated in mothers infected with HBV except if there is a possibility of exposure to maternal

blood through cracked and bleeding nipples (Tran 2012). Although the virus is detected in breast

milk, this has not been shown to result in HBV transmission (Hill et al., 2002; Wang et al.,

2003).

2.9.2 Horizontal transmission in childhood

Horizontal transmission is thought to be the most common route of transmission of HBV in

childhood in sub Saharan Africa either from sibling to sibling or between playmates (Whittle et

al., 1983). Horizontal transmission in children is transmission which does not occur vertically or

through sexual or parenteral routes (Davis, Weber and Lemon 1989). The routes of horizontal

transmission have not yet been clearly identified although several potential routes have been

investigated.

One of the possible vehicles of transmission is saliva, which would explain how children

transmit the virus from one another. Although saliva has been shown in gibbons to be infectious

if injected (Bancroft et al., 1977), and high levels of HBV DNA have been found in the saliva of

chronic carriers including children (Van Der Eijket al., 2005), no studies have yet shown that

oral exposure to saliva causes transmission of the virus. Transmission through bites from an

infected person has been shown to occur (Stornelloet al., 1991, Huiet al., 2005). This mode of

transmission could be explained by the exposure of the blood of the uninfected person to the

saliva of a chronic carrier known to carry a high viral load. Butler et al. (2010) showed that the

25
mucosal surfaces and broken skin of children are commonly exposed to the saliva of their

caregivers through various means including premastication of food and cleaning a cut/scrape on

the children’s bodies with saliva.

Other bodily fluids containing high levels of HBV DNA in infected individuals, including urine

and sweat, have also been investigated but these have not been associated with transmission

(Knutsson and Kidd-Ljunggren 2000; Van Der Eijket al., 2005). A recent study showed that

tears from a chronically infected baby could cause HBV infection in chimera mice (Komatsu et

al., 2012).

In Africa, other modes of horizontal transmission could include ritual scarification and

circumcision performed by a ‘witch-doctor’ or a traditional healer using unsterilized instruments

(Kew et al., 1973). HBV virus is a sturdy virus capable of existing on surfaces for more than a

week in the absence of visible blood, and still be infectious (Bond et al., 1981, Faveroet al.,

1974). Bedbugs have also been implicated as possible vehicles of transmission (Mayans et al.,

1990).

2.9.3 Contact with infected bodily fluids

In areas of low endemicity, the virus is mostly transmitted in the adult population, between drug

users sharing needles and through sexual contact with an infected person (Alter 2003).

Nosocomial infections are also possible especially among patients undergoing haemodialysis

(Alter 2003). Improper sterilization of needles and reuse of disposable needles are also possible

modes of transmission in hospital settings (Alter 2003).

2.10. Risk Factors of Hepatitis B Virus

• The still born foetus whose mother is infected with the virus.

• Health care workers.

26
 • Laboratory workers who do not handle suspected specimens in the right way.

• Sex workers who practice unsafe sexual intercourse and those who have many sex

partners (WHO, 2013).

• Persons living in regions or travelling to regions with endemic hepatitis B.

• Sexually active heterosexuals.

• Patients and employees in haemodialysiscentres (CDC, 1998).

• Injection drug users sharing unsterile needles

• Other individuals at risk include; embalmers, morticians and prison service staff.

2.11. Diagnosis of Hepatitis B Virus

The tests, or assays, for detection of hepatitis B virus infection involve serum or blood tests that

detect either viral antigens (proteins) or antibodies produced by the host. Interpretation of these

assays is complex (Boninoet al., 1987). The first step in identifying patients with chronic HBV

infection is to screen those with risk factors. Screening is focused on patients in high-risk groups,

such as persons born in endemic areas, patients engaged in high-risk sexual behaviours, injection

drug users, dialysis patients, HIV-infected and other immune suppressed patients, pregnant

women, and persons with occupational exposure, as well as family/household members and

sexual contacts of HBV-infected persons. The hepatitis B surface antigen (HBsAg) is most

frequently used to screen for the presence of this infection. Testing for antibody to hepatitis B

core (anti-HBc), and antibody to hepatitis B surface antigen (anti-HBs) indicate whether an

individual has been previously exposed to HBV. The HBV DNA levels are not required for

preliminary screening for the HBV-infection.

27
The HBsAg is the first detectable viral antigen to appear during infection. However, the length of

time within which detectable amount of HBsAg may persist in host depends on efficiency of host

immune function at clearing the virus-infected hepatocytes and establishing enduring immunity

(AASLD, 2007). This antigen may persist when infection has become chronic stage of the

infection. The molecular mechanism underlying this adaptation remains yet unknown. The

infectious virion contains an inner "core particle" enclosing viral genome. The icosahedral core

particle is made of 180 or 240 copies of core protein, alternatively known as hepatitis B core

antigen, or HBcAg. During this 'window' in which the host remains infected but is successfully

clearing the virus, IgM antibodies to the hepatitis B core antigen (anti-HBcIgM) may be the only

serological evidence of disease.

Individuals who remain HBsAg positive for at least six months are considered to be hepatitis B

carriers (Lack and McMahon, 2007). Carriers of the virus may have chronic hepatitis B, which

would be reflected by elevated serum alanine aminotransferase levels and inflammation of the

liver, as revealed by biopsy. Carriers who have seroconverted to HBeAg negative status,

particularly those who acquired the infection as adults, have very little viral multiplication and

hence may be at little risk of long-term complications or of transmitting infection to others (Chu

and Liaw, 2007). Additionally, polymerase chain reaction (PCR) tests have been developed to

detect and measure the amount of viral nucleic acid in clinical specimens. These tests measure

viral loads and are used to assess a person's infection status and to monitor treatment (Zoulim,

2006).

2.12. Prevention of Hepatitis B virus

The hepatitis B vaccine is the mainstay of hepatitis B prevention. WHO recommends that all

infants receive the hepatitis B vaccine as soon as possible after birth, preferably within 24 hours.

28
The birth dose should be followed by 2 or 3 doses to complete the primary series. In most cases,

one of the following two options is considered appropriate:

• A 3-dose schedule of hepatitis B vaccine, with the first dose (monovalent) being given at

birth and the second and third (monovalent or combined vaccine) given at the same time

as the first and third doses of diphtheria, pertussis (whooping cough), and tetanus (DTP)

vaccine; or

• 4 doses, where a monovalent birth dose is followed by three monovalent or combined

vaccine doses, usually given with other routine infant vaccines.

The complete vaccine series induces protective antibody levels in more than 95% of infants,

children and young adults. Protection lasts at least 20 years and is probably lifelong. Thus, WHO

does not recommend booster vaccination for persons who have completed the 3 dose vaccination

schedule?

All children and adolescents younger than 18 years-old and not previously vaccinated should

receive the vaccine if they live in countries where there is low or intermediate endemicity

(WHO, 2002). In those settings it is possible that more people in high-risk groups may acquire

the infection and they should also be vaccinated. They include:

• People who frequently require blood or blood products, dialysis patients, recipients of

solid organ transplantations (Dodd, 2000).

• Persons who inject drugs (Des Jarlaiset al., 2003).

• Household and sexual contacts of people with chronic HBV infection (Thompson et al.,

2009).

29
 • Health-care workers and others who may be exposed to blood and blood products

through their work (Buster et al., 2003).

• Travellers who have not completed their hepatitis B vaccination series, who should be

offered the vaccine before leaving for endemic areas.

The vaccine has an excellent record of safety and effectiveness. Since 1982, over 1 billion doses

of hepatitis B vaccine have been used worldwide (WHO 2002). In many countries where 8–15%

of children used to become chronically infected with the hepatitis B virus, vaccination has

reduced the rate of chronic infection to less than 1% among immunized children.

As of 2013, 183 Member States vaccinate infants against hepatitis B as part of their vaccination

schedules and 81% of children received the hepatitis B vaccine. This is a major increase

compared with 31 countries in 1992, the year that the World Health Assembly passed a

resolution to recommend global vaccination against hepatitis B. Furthermore, as of 2013, 93

Member States have introduced the hepatitis B birth dose vaccine.

In addition, implementing of blood safety strategies, including quality-assured screening of all

donated blood and blood components used for transfusion, can prevent transmission of HBV

(Chung et al., 1993). Safe injection practices, eliminating unnecessary and unsafe injections, can

be effective strategies to protect against HBV transmission. Furthermore, safer sex practices,

including minimizing the number of partners and using barrier protective measures (condoms),

also protect against transmission (Ahmed et al., 2008).

30
 CHAPTER THREE

METODOLOGY

3.0 The materials that were used are: - dry cotton wool, syringe, and cotton, socket in 70%

alcohol, anticoagulant tubes, tourniquet, serum or plasma, HBSAg strip.

3.1 Study Area

The study will be carried out at Murtala Muhammad Specialist Hospital Kano (MMSH).

3.2 Facility for the study

The study will be carried out in Kano Metropolis Kano state Nigeria.

3.4 Study Design

The study was a cross- sectional analytical study which comprises all adults who come to the

laboratory requested by the physician and who agreed to sign the informed consent form.

3.5 Study population

The study involved of both sexes of the age range 15-24 years all patient who come to the

laboratory requested by the doctor were included in the study.

3.5.1 Study sample

The research involved adults of age range 15-24 years who come to the laboratory requested by

the physicians and who have their consent and wish to participation in the research.

31
3.6 Inclusion criteria

The study involved all individuals in the adult age that come to the laboratory for laboratory that

come to the laboratory for lab rest requested by the physicians who falls in the age range 15-24

years and who gave their content and filled the questionnaire.

3.7 Exclusion criteria

All those who refused to fill the questionnaire and sign the informed consent form and who did

not fall in the age range 15-24 years were excluded from the study.

3.8 Sample collection

Data was collected through questionnaires which were self administered to the participant who

filled them with pens or pencil, data were collected three a week throughout the study period.

Diagnosis test for HBs Ag was also used to collected data based on participant section to HBs

Ag.

3.9 Venous blood collection

The test tube was label the upper arm the patient was tied with tourniquet and he was asked to

make a fist. An ante-cubital vein was collected on the patient’s arms. The area was wiped with

cotton soaked in 70% alcohol the ball of the needle was adjusted and a veniponoture was made

and about 2ml of blood was collected the tourniquet was released and the patient was asked to

avoid haemolysis. The blood was centrifuge at 3000rpm for serious to obtain plasma (chees

brought, 2005).

32
3.10 HBs Ag serology

The strip was removed from the sealed packed and placed on the dry tissue paper on the working

bench using a pipete. Son (one drop) of plasma was placed on the test spot of the strip and

allowed for 2mins after two minutes the result were read and recorded if just the control line

appeared then the test was recorded as positive (checbrough 2005).

3.11 Data Analysis

The data was input a microscope excel page tabs were used to analyze the data.

3.12 Ethical considered

33
 CHAPTER FOUR

RESULT

4.1 Demographic Data

The study involved 70 patients of varied ages and both sex, 54 (77%) of the participants were

male, while 16 (22.9%) were females, the ages of the participants ranged from 15-24 years, the

highest numbers of participants were in the age group 19-20 years as shown in table 1.

Table 1: Distribution of study population according to ages

S/N AGE FREQUENCY PERCENTAGE (%)

1 15-16 7 10

2 17-18 12 17.1

3 19-20 20 28.6

4 21-22 13 18.6

5 23-24 18 25.7

6 Total 70 100

4.2 Total Prevalence of Hepatitis B

From the study carried out, the total numbers of positive were 28 (40%) and total numbers of

were 45 (60%) as shown on table 2:

34
Table 2: Total prevalence of hepatitis B

S/N NUMBER PERCENTAGE (%)

1 Positive 28 40

2 Negative 42 60

3 Total 70 100

4.3 Total prevalence of hepatitis B According to age

From the study carried out, hepatitis B was more prevalence amongst the age group 23-24 years

followed by age group 19-20 years as shown I table 3

Table 3: Prevalence of hepatitis B according to age

S/N AGE(YRS) POSITIVE CASES (N) PERCENTAGE (%)

1 15-16 2 7.1

2 17-18 3 10.7

3 19-20 9 32.1

4 21-22 4 14.3

5 23-24 10 35.7

6 Total 28 100

4.4 Prevalence of hepatitis B according to sex

According to the study carried out, hepatitis B was more prevalence amongst males (78.5%) than

females (21.4%) as shown in table 4

35
Table 4: prevalence of hepatitis B according to sex

S/N FREQUENCY POSITIVE (N) PERCENTAGE (%)

1 Male 22 78.5

2 Female 16 21.4

3 Total 70 100

4.5 predisposing factors of hepatitis B infection

From the study, the predisposing factors of hepatitis B include family history, unprotected sex,

unawareness and negligence as shown in table 5

Table 5: predisposing factors of hepatitis B amongst youths

36
 CHAPTER FIVE

5.1 Discussion

The results of the study indicate that the general prevalence of hepatitis B amongst youth adults

was 40%. This is strongly more in line with whom, 2013 that reported the prevalence of hepatitis

B to be greater in areas of sub-Sahara Africa, Asia and Latin America with a prevalence of 28%.

Nigeria as one of the countries in sub-Sahara Africa and this may be due to poverty, lack of

appropriate medical facilities and due to negligence which causes the rates of hepatitis B to be

high in this local government.

The observed high prevalence of HBsAg among blood youths is in conformity with earlier

reports from community and hospital based studies in some part of Nigeria with prevalence of

HBsAgranging from 14.3% 26.0% (Ekpo, m.et at, 1995).

According to the study hepatitis B was more prevalent amongst the age group 23-24 (35.7%).

The probable reason for this high prevalence is because most of the participants are in this age

group so the probability of having more positive cases in this group is high some indicated on the

questionnaire that they were born already with hepatitis B infected and this was confirmed by the

test which showed positive.

Since youth in this age did not reported any unprotected sex but were infected based on the

responses given on the questionnaire we realized that many of them are aware of the infection

but neglected the infection because according to them using condoms reduces their sexual

pleasure some of the youths in this age group said they don’t actually like to expose themselves

but their boyfriends insist on having direct sexual contact and most of them were entry excited

37
about life so they don’t actually considered that their actions can cause harm to them, the next

age group with a high prevalence was the age group 19-20 in which 20 participate were involved

and nine had hepatitis B, giving a prevalence of 32.1% the positive case happens to the due to un

awareness and one happened to be due to family history.

According to the study hepatitis B infection among youth was more prevalent in males (78.5%)

than in females (21.4%). This is probably due to the reason that males are more involved in the

study than female. Also males are more susceptible to the infections than males due to their life

style.

Using a structured questionnaire the predisposing factor identified were family history of

hepatitis B, unprotected sex, UN awareness and negligence majority of participants both males

and female affirmed that they have un protected sex or have had unprotected sex for the past six

months and according to who, 2013, this is more often the rules by which hepatitis B, is spread.

Some group of participants who were unaware about hepatitis B and virus ended being positive.

They said in the questionnaire that they have heard about hepatitis B and the vaccine but to them

all those things are lies to scare people and those sicknesses are western illnesses.

Most of the work reviewed showed that sexual activity increased the carriage of HBsAg (tablet

2) ola et al, 2002-2008 found that butchers from Ibadan had higher infection rate and showed

high risk of behavior which may lead to the spread of infection in slaughter houses in Nigeria

belo (2000) showed a higher prevalence of HBV infection among surgeons in Lagos than the

general public belo, A.C (2000).

The prevalence rate for HIV/HBV co- infection was high (27%) in a study conducted in 2aria the

higher value could be because HIV and HBV share similar made of transmission and risk factors

38
many HIV positive individual have also been exposed to HBV. Studies suggest that as many as

70-90% HIV positive people have evidence of past or current HBV infection. Since majority of

patients spontaneously clear HBV without treatment however the rate active infection is much

lower.

The persistent high prevalence in Nigeria could be attributed in part to the fact that through who

adopted HBV immunization as part EPI in 1991 it was not until 2003 that it was incorporated

into Np1and and it was mostly not available until recently. It was also noted that HBV infection

is not commonly perceived problem in Africa. This is because infections are often sub-clinical

and there is long interval before the consequences of chronic carriage manifest.

5.2 Conclusion

the mean prevalence of 10.7% in this review that Nigeria is higher endemic for HBV infection

which is cause for alarm such as higher prevalence question the effectiveness of the Nigeria

HBV vaccination program therefore there is a need for health promotion awareness campaign to

educate the general public, mode of transmission and the risk factors associated with HBV

infection especially among youth population.

Based on this study, the following conclusion can be made.

• The prevalence of hepatitis B amongst youth adults attending the general Muhammad

specialist hospital Kano is 40%.

• Males are more infected with hepatitis B than their female counter part.

• hepatitis B is more prevalent amongst youth adult of the age group 23-24 followed by

those of 19-20 years

39
 • The factors that predisposal youth adults in the local government were negligence and

unprotected sex, family history and unawareness.

5.3 Recommendations

i. Health talks should be given in the hospital and schools especially to young adults about

the spread of hepatitis B and its prevention.

ii. Medicalscreaming should be done at schools to screen young adult on hepatitis B and

treat those infected in order to control spread.

iii. The government should provide free test and vaccine to the community.

iv. Parents should caution specially by sharing razor blade at their various home.

v. Hypatetis drugs should be sold at subsidy price at the government hospital.

vi. Blood should be well screen before transfusion.

40
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 APPENDIX I

CONSENT FORM

I am muhammad abdulkadir danladi, a level three Student of Aminu dabo College

52
 APPENDIX II
Demographic Data:

Serial number.........................................................

Sex: Male Female

Age...........................................................................

Occupation..............................................................

Marital status: Married Single Divorced

Residence..............................................................

Clinical Data:

Do you have family history of Hepatitis B? Yes No

If yes, who? ............................................................

How many sex partners do you have?

1 2 more than 2

Have you had unprotected sexual intercourse, or in the past 6months? Yes No

If yes, why? ..............................................................

Have you ever gone for Hepatitis B screening before? Yes No

Are you aware of the spread of Hepatitis B amongst youths? Yes No

Do you take any preventive measures against the disease? Yes No

53
If yes, what preventive measure do you take?

Specify..................................................................

Do you take intravenous drugs? Yes No

If yes, do you share needles with other drug users? Yes No

Are you a homosexual? Yes No

Have you ever gone for tattooing? Yes No

Have you ever been pierced by any suspected contaminated sharp object?

Yes No

54
APPENDIX III

55