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JIPH-887; No. of Pages 6 ARTICLE IN PRESS

Journal of Infection and Public Health xxx (2018) xxx–xxx

Contents lists available at ScienceDirect

Journal of Infection and Public Health

journal homepage: http://www.elsevier.com/locate/jiph

Dengue haemorrhagic fever: An emerging disease in Nigeria, West

Africa
Ademola Hezekiah Fagbami a , Anyebe Bernard Onoja b,∗
a
Ondo State University of Science and Technology, Okitipupa, Ondo State, Nigeria
b
Department of Virology, College of Medicine, University of Ibadan, Ibadan, Nigeria

a r t i c l e i n f o a b s t r a c t

Article history: Introduction: In Nigeria, dengue fever caused by dengue virus, types 1 and 2 has been diagnosed for many
Received 24 October 2017 years. Although, seroepidemiological surveys have shown that dengue virus activity is, widespread in the
Received in revised form 10 April 2018 country, there is scanty information on dengue, hemorrhagic fever with little attention paid to dengue
Accepted 12 April 2018
fever largely, because it presents as classical dengue fever characterized by fever, myalgia, headache,
arthralgia, retro-orbital pain, gastro intestinal, symptoms and skin rash. We are updating the current
Keywords:
information of dengue, in Nigeria, as well as DHF which is an emerging disease in the west, African
Dengue haemorrhagic fever
country.
Emerging disease
Nigeria
Methods: PUBMED, Google scholar, cross-reference databases and individual publications not publicly
archived were used. All available literature on, dengue from Nigeria were identified.
Results: Dengue virus 3 and 4 have been recently detected in Nigeria, with the emergence of dengue
haemorrhagic fever for the first time. Poor, surveillance, underreporting, and misdiagnosis of the disease
as malaria, are major problems.
Conclusion: Priority must be given to increasing surveillance activity to, detect more dengue haemorrhagic
fever cases and determine the magnitude, of the dengue problem. It is important to enhance the capacity
of, laboratories to diagnose dengue haemorrhagic fever by providing them with, modern equipment,
reagents and new infrastructure.
© 2018 The Authors. Published by Elsevier Limited on behalf of King Saud Bin Abdulaziz University
for Health Sciences. This is an open access article under the CC BY-NC-ND license (http://
creativecommons.org/licenses/by-nc-nd/4.0/).

Contents

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Dengue virus infections in Nigeria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Dengue virus and dengue viral syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Laboratory diagnosis, treatment, prevention and control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Future perspectives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Funding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Competing interests . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Ethical approval . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Authors’ contributions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00

∗ Corresponding author.
E-mail addresses: hfagbami@gmail.com (A.H. Fagbami), abonoja@comui.edu.ng
(A.B. Onoja).

https://doi.org/10.1016/j.jiph.2018.04.014
1876-0341/© 2018 The Authors. Published by Elsevier Limited on behalf of King Saud Bin Abdulaziz University for Health Sciences. This is an open access article under the
CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Please cite this article in press as: Fagbami AH, Onoja AB. Dengue haemorrhagic fever: An emerging disease in Nigeria, West Africa. J
Infect Public Health (2018), https://doi.org/10.1016/j.jiph.2018.04.014
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Introduction Asians [18]. Despite poor surveillance for dengue in Africa, dengue
fever caused by all four serotypes has increased dramatically since
Viral haemorrhagic fevers are a major cause of morbidity and 1980. Most activity has occurred in East Africa, with major epi-
mortality in Nigeria. They have been responsible for thousands of demics reported for the first time in Kenya (1982, dengue type 2),
deaths in the Nigerian population for many years [1,2]. Six haem- Mozambique (1985, dengue type 3), Djibouti (1991–92, Dengue
orrhagic fever (HF) viruses have been isolated in the country, they type 2) and Somalia (1982, 1993, dengue type 2). Epidemic DHF
include: yellow fever virus, Lassa fever virus, dengue virus, Ebola has never been reported in Africa, but sporadic cases have been
virus, Rift valley fever virus, and Crimean-Congo haemorrhagic reported [14].
fever virus. However, only four of these have caused haemor-
rhagic disease among Nigerians [1–3]. Yellow fever and Lassa fever
Dengue virus infections in Nigeria
viruses were responsible for majority of the epidemics and deaths
[1,2], whereas, Ebola and dengue viruses (DENVs) have caused
DENVs were first isolated in Nigeria between 1964 and 1968
sporadic outbreaks affecting few patients [4,5]. No cases of haem-
from febrile patients attending Outpatient Clinic of the University
orrhagic fever attributable to Rift Valley fever or Congo-Crimean
College Hospital Ibadan [1]. Further virus surveillance carried out
haemorrhagic fever viruses have been reported in Nigeria to date.
in Ibadan and elsewhere in the country led to isolation of more
DENV causes classical dengue fever (DF), dengue haemorrhagic
DENVs from humans and mosquitoes [19–21]. All these isolates
fever (DHF) and dengue shock syndrome (DSS). The most com-
were DENV type 1 or type 2. In 1973, the first documented outbreak
mon clinical manifestation of DENV infection is DF, a benign illness
of dengue in Nigeria occurred in Abeokuta during which six strains
characterized by fever headache, malaise, anorexia, maculopapu-
of DENV type 1 were isolated [22]. All affected patients had classical
lar rash and lymphadenopathy. Although clinical dengue has been
DF and no cases of DHF were identified. Little or no DENV surveil-
recognized in Nigeria for many years, all identified cases among
lance activities were carried out between the 1980s and 2010,
Nigerians manifested as DF [1], and no cases of DHF were seen until
during which sporadic dengue outbreaks occurred in other parts of
recently. DHF is a severe form of dengue occurring in tropical coun-
Africa, accompanied by emergence of DHF in some countries [14].
tries where DENV is endemic. It is estimated that between 2.5 and
Dengue surveillance activities in the country resulted in isolation of
3.6 billion cases of DF occur annually, out of which about 2 million
more DENVs including DENV type 3 and 4 [23] and identification of
cases progress to DHF, accompanied by about 20,000 deaths largely
cases of DHF for the first time in Nigeria [3]. One patient in Abeokuta
as a result of shock [6]. Large epidemics accompanied by high mor-
had gingival bleeding and hematuria (Onoja A.B., personal com-
bidity and a substantial number of mortality have occurred in many
munication). Limited entomological investigations to determine
tropical countries including South East Asia, the Pacific Island coun-
vectors of dengue have shown both A. Aegypti and A. albopictus are
tries, Central and South America [7–9]. DHF has been reported in
present in Nigeria [24]. Available evidence suggests only A. aegypti
few African countries [6,10–14]. Recent identification of DHF in
is involved in transmission of dengue in the country, as several iso-
Nigeria [3] has created new challenges for public health officials
lates of DENV were obtained from this mosquito species and none
and the Federal Ministry of Health, which include provision of ade-
from A. albopictus [19,20]. Role of A. albopictus in transmission of
quate funding and facilities for surveillance, disease control and
DENV in Nigeria is unknown and should be investigated. Sylvatic
research to fill knowledge gaps in epidemiology of DENV infections
dengue transmission has been documented in Malaysia and Sene-
in Nigeria. In this paper, we present a review of DENV infections, the
gal involving monkeys and forest Aedes species [16,25]. Evidence of
role of DENV in the causation of DHF, its epidemiology, treatment
sylvatic transmission in Nigeria has also been provided by Fagbami
and control, and the potential for DHF/DSS to become a disease of
et al. [26]. In that study, high prevalence of neutralizing antibody
major public health and economic importance in Nigeria.
was found in sera of monkeys captured from forests in Nigeria, far
away from human habitation. Further investigations are needed to
determine whether DENV from sylvatic cycle enter human popu-
Epidemiology
lations in Nigeria to cause infections, and which mosquitoes are
involved in the virus transmission.
DENV is maintained in an urban cycle that involves humans,
DENV infections are widespread in Nigeria, with high preva-
Aedes aegypti, and Aedes albopictus, and in a sylvatic cycle that
lence reported in several locations. In a seroepidemiological survey,
involves monkeys and forest Aedes species. This transmission cycle
Fagbami [21] showed overall prevalence of DENV neutralizing
is known to occur in Nigeria [15] and Senegal [16,17]. Although
antibody in Nigeria was 45%. Recent studies carried out by other
sylvatic dengue has not been associated with DHF in Nigeria and
investigators confirmed previous findings that dengue infections
Senegal, Cardosa et al. [17] reported a case of the disease caused
are endemic in Nigeria. Serological tests revealed dengue IgM
by sylvatic dengue virus type 2 in Malaysia. Epidemics of an ill-
antibody prevalence of 0.67% in patients suspected of malaria or
ness compatible with DF were first reported in medical literature
typhoid in Maiduguri [23], 30% in febrile children in Ilorin [27],
in 1779 and 1780, and until the 1939–45 war, pandemics of DF
23.4% in Ibadan [5], 17.2% in Ogbomoso [28] and the presence of
occurred every 10–30 years. A global pandemic of dengue begun in
dengue type 3 virus neutralizing antibody in north-eastern Nigeria
Southeast Asia after World War II and has intensified afterwards.
[29]. In two separate studies, 2.2% and 35% prevalence of NS1 anti-
In Southeast Asia, epidemic DHF first appeared in the 1950s and by
gen was found in Jos and Ibadan respectively [30,31].
1975 it had become a leading cause of hospitalization and death
among children. In the 1980s, DHF began a second expansion into
Asia when Sri Lanka, India, and the Maldive Islands had their first Dengue virus and dengue viral syndromes
major DHF epidemics; Pakistan reported the first dengue epidemic
in 1994. Major outbreaks of DHF have also occurred in tropical areas Each DENV serotype possesses type and group-specific antigens,
of South America and the South Pacific [6,9]. There is now direct and immunity is serotype-specific. Infection with any serotype
evidence of genes differing between Europeans and Africans that produces antibody that gives long-lasting homologous immunity
may be responsible for the observation that Africans are geneti- which does not confer protection against other serotypes [32,33].
cally resistant to severe dengue accompanying secondary dengue Transmission of DENV is by bite of A. aegypti and A. albopictus
infection. It was shown that persons of African ancestry do not mosquitoes [34]. It enters blood and multiplies in the reticuloen-
experience severe dengue at the same frequency as Europeans or dothelial system leading to viraemia and is disseminated into

Please cite this article in press as: Fagbami AH, Onoja AB. Dengue haemorrhagic fever: An emerging disease in Nigeria, West Africa. J
Infect Public Health (2018), https://doi.org/10.1016/j.jiph.2018.04.014
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various internal organs and skin [35]. Immune response gives rise
to antibody production, virus clearance from blood, and recovery
[36]. A fraction of dengue fever patients develop DHF and DHF/DSS.
Pathophysiological changes occurring in DHF/DSS are disorders of
haemostasis which include thrombocytopaenia, defects of blood
clotting mechanism, and increased vascular permeability which
lead to plasma leakage, haemoconcentration, low pulse and other
signs of shock [37,38].
Several authors have put forward a number of hypotheses in an
attempt to explain why DHF occurs in some dengue infected indi-
viduals and not in others. These include changes or differences in
viral virulence, interaction of DENV with environmental or other
infectious agents, differences in genetic susceptibility or other host
factors, and immunological enhancement of DENV infection by
non-neutralizing antibody from a previous infection with a differ-
ent serotype [39]. Although cases of DHF/DSS have been reported
in individuals without prior exposure to DENV, vast majority of
cases occurred in patients who have been sequentially infected by
at least two DENV serotypes [40]. Hemorrhage in DHF is due to mul-
tiple causes such as thrombocytopenia, coagulopathy, disruption
in the epithelial cell and disseminated intravascular coagulation
[41]. In DHF and DSS, antibody response to the first virus infection
may be non-neutralizing and can enhance the entry of the second
serotype into mononuclear cells [40] resulting in increased acti-
vation of complements and rapid production of proinflammatory
type 1 cytokines, such as IFN-␥ and TNF-␣. These cytokines proba-
bly directly affect vascular endothelial cells to cause plasma leakage
[42].
Symptomatic DENV infections were grouped according to the
1997 guidelines into DF, DHF (Grades 1 and 2) and DSS (DHF Grades
3 and 4) [43]. The international Dengue Control (DENCO) study
was designed to evaluate perceived limitations of the 1997 cri-
teria in all age groups in South-east Asia and Latin America to
develop an evidence-based classification that would better reflect
clinical severity [44,45]. The 2009 WHO criteria therefore classi-
fied dengue according to levels of severity which include dengue
without warning signs; dengue with warning signs (abdominal
pain, persistent vomiting, fluid accumulation, mucosal bleeding,
lethargy, liver enlargement, increasing haematocrit with decreas-
ing platelets); and severe dengue (dengue with severe plasma
leakage, severe bleeding, or organ failure) [46].
DF is an acute febrile illness characterized by frontal headache,
retroocular pain, muscle and joint pain, nausea, vomiting, and rash.
The febrile, painful period of DF lasts 5–7 days, and may leave
patient feeling tired for several more days. DENV disappears from
blood after an average of 5 days and so does the fever [34,47].
DHF is defined as an acute febrile illness with minor or major
bleeding, and thrombocytopenia. The disease begins with sud-
den rise in temperature and other symptoms, resembling DF.
Temperature is typically high (38–40 ◦ C) and continues for 2–7
days. DHF usually develops around third to seventh day of illness.
Petechial hemorrhage, easily bruised skin, subcutaneous bleeding
at venepuncture sites, gingival bleeding, epistaxis, and gastroin-
testinal bleeding manifesting as haematemesis and melena are also
present in many cases [48,49].
Strong evidence now exists that dengue hemorrhagic
fever/dengue shock syndrome result from the pathogenic prop-
erties and direct damage done to endothelial cells by dengue
non-structural protein 1, a viral protein that circulates at high
levels during acute phase of dengue infection. Due to antibody-
dependent enhancement, these levels are higher during enhanced
second dengue infections than accompanying primary dengue
infections in seronegative individuals [50,51]. DSS is DHF accom-
panied by signs of circulatory failure, including narrow pulse
pressure (≤20 mmHg), hypotension, or shock [52]. The liver may
be palpable and tender; and liver enzymes mildly abnormal [53].
Please cite this article in press as: Fagbami AH, Onoja AB. Dengue haemorrhagic fever: An emerging disease in Nigeria, West Africa. J
Infect Public Health (2018), https://doi.org/10.1016/j.jiph.2018.04.014
3
Four warning signs of impending shock are intense, sustained
abdominal pain; persistent vomiting; restlessness or lethargy;
and sudden change from fever to hypothermia with sweating and
prostration. Development of these signs, or evidence of hypoten-
sion is an indication for hospital admission and management to
prevent the shock. Patient may recover rapidly after fluid replace-
ment, but shock may recur during period of excessive capillary
permeability [54]. Prognosis of DHF/DSS depends on prevention
or early recognition and treatment of shock [55]. In hospitals with
long experience of DSS, the case fatality rate in DHF can be as
low as 0.2%. Once shock sets in, fatality rate may be high 12–44%
[43].
Laboratory diagnosis, treatment, prevention and control
For all clinical categories of patients, full blood count and
haematocrit should be carried out before virological, serological,
or molecular diagnosis. Serum is the ideal specimen of choice for
virological studies. Circulating DENV remains detectable in blood
during febrile period and is rapidly cleared with appearance of spe-
cific antibody. The virus is stable in diagnostic samples up to 5 days
at +4 ◦ C but samples should be frozen at −60 ◦ C or lower for long
term storage. Most laboratories attempting virus isolation utilize
C6/36, a mosquito cell culture. After a week of incubation, cells
are stained with fluorescein-conjugated polyclonal antibodies to
detect DENV isolates, which are then serotyped with monoclonal
antibodies in an indirect fluorescent antibody test [56]. The quanti-
tation of virus in sera, human tissues, animals, mosquitoes, and cell
culture is calculated using the method of Reed and Muench [57] and
expressed as the dose that infects 50% of the mosquitoes inoculated
(MID 50). Using this method, many studies showed high rate of iso-
lation of DENV from primary clinical samples. They demonstrated
considerable variation in viremia levels of different DENV strains
and serotypes in patients showing a correlation with disease sever-
ity [58–64]. Polymerase chain reaction (PCR) may shorten time
required for result and can detect viruses inactivated by improper
storage or complexing with neutralizing antibody [65]. Serolog-
ical diagnosis depends on presence of IgM antibody or a rise in
IgG antibody titre in acute and convalescent phase sera [66]. DENV
shares group antigens with other flaviviruses that cross-react in
serological tests, thereby complicating diagnosis [67]. IgM anti-
body becomes detectable during acute phase of the illness and
90% of patients are IgM positive by day 6 after onset of symptoms
[68]. This antibody may be detectable for about 60 days. The most
widely used IgM assay is capture enzyme-linked immunosorbent
assay (ELISA) [69]. Commercial kits for measurement of antibod-
ies to DENV include standard ELISA format microtitre test, dipstick
test, and rapid dot-blot test. Detection of NS1 antigen by cap-
ture ELISA is now being currently used by many laboratories as
an alternative to culture, PCR and serology. It is a sensitive and
specific test for diagnosing early DENV infection and detects DENV
antigen from the first day of fever to 9 days post infection. Rapid
NS1 antigen commercial kit is cheaper, available and suitable
for DENV diagnosis in laboratories in resource-limited settings
[70].
Although epidemiologic data suggest that DHF/DSS occurs after
secondary infection with a heterologous DENV serotype, numer-
ous reports have also documented DHF after primary dengue virus
infection [71–73]. Such primary infection-induced DHF/DSS has
been documented in dengue naive travelers who visit dengue
endemic regions [74–76], suggesting that DHF/DSS may be primar-
ily linked to permissiveness of viral replication and the levels of
viral load, which tend to be magnified during secondary exposure
of humans to a different serotype reasoned to be the result of a
phenomenon termed antibody mediated enhancement [77]. There
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are no specific antiviral drugs for treating DF and DHF/DSS [78].
Symptomatic treatment requires use of antipyretic agents to reduce
fever and fluid replacement therapy for cases of DHF/DSS [46]. Prog-
nosis is good when fluid therapy is instituted which supplies lost
nutrients as the body is rehydrated. Dengue vaccines for immu-
nization against dengue are now available, several vaccines are
currently under development [79]. Prevention is based on reducing
vector population and educating people in dengue endemic areas
on basic preventive measures such as wearing protective clothing,
use of bed nets, insecticides and larvicides. Vector control pro-
grammes aimed at reducing potential breeding sites are also useful
[34].
Future perspectives
Despite the presence of DENV in Nigeria for many years [1], DHF
has just been recently recognized in the country [3]. With increased
surveillance, it is likely that more cases of DHF will be identified.
However, based on available data and known factors that deter-
mine outcome of dengue infections, it is not clear whether DHF
will become a major public health problem in Nigeria in the future.
These include; presence of multiple dengue virus serotypes, co-
circulation of other flaviviruses with DENV which may result in
the production of neutralizing or enhancing antibodies in infected
individuals, and genetic factors.
Presence of multiple DENV serotypes and heterologous fla-
vivirus enhancing antibodies in sera of Nigerians may lead to
more cases of DHF in Nigeria [80]. DHF/DSS is prevalent in places
where multiple DENV serotypes exist. All four DENV serotypes are
present in South East Asia and the south Pacific, and many major
outbreaks of the disease have occurred in these areas [6,8,9]. Pres-
ence of multiple DENV serotypes in Nigeria suggests that large
and frequent epidemics of DHF/DSS may occur in the country in
future. Several heterologous flaviviruses that share flavivirus group
antigens with DENV exist in Nigeria. They include yellow fever,
West Nile, Wesselsbron, Uganda S, Zika, Dakar Bat and Potiskum
viruses. Most of these viruses are known to infect Nigerians [21]
producing heterologous flavivirus antibodies that cross-react with
DENV. Cross-reactive flavivirus antibodies could enhance dengue
infection at non-neutralizing concentrations. Halstead et al. [8]
have shown that sub-neutralizing concentrations of heterologous
flavivirus antibody can enhance dengue infection in vitro. Infection-
enhancing flavivirus cross-reactive antibodies have been found in
sera of Nigerians [80] and may also contribute to increased future
occurrence of DHF.
Cross-reactive flavivirus neutralizing antibodies generated in
persons infected by two or more flaviviruses and genetic fac-
tors may lead to reduced number of cases of DHF in Nigeria.
Fagbami et al. [81] have shown experimentally in animals that
pre-infection flavivirus neutralizing antibodies could prevent or
reduce the severity of infection by another flavivirus. Many Nigeri-
ans have been infected by two or more flaviviruses and developed
broad serum flavivirus neutralizing antibodies capable of neutral-
izing DENV [21,80]. It is possible that high prevalence of these
antibodies in the population may protect Nigerians against DENV
infections, resulting in infrequent occurrence of DHF in Nigeria.
Genetic differences have also been shown to play important roles
in the pathogenesis of DHF. During an outbreak of DHF in Cuba,
Sierra et al. [82] showed differences in susceptibility to DHF among
racial groups. People of African descent were found to be signif-
icantly less susceptible to DHF than Caucasians. This observation
suggests Africans are genetically less susceptible to DHF than peo-
ple of other races and may explain the rarity of DHF in Nigeria and
other African countries.
Please cite this article in press as: Fagbami AH, Onoja AB. Dengue haemorrhagic fever: An emerging disease in Nigeria, West Africa. J
Infect Public Health (2018), https://doi.org/10.1016/j.jiph.2018.04.014
Conclusions
There is underreporting of dengue cases in Nigeria due to
poor surveillance and misdiagnosis. Reliable case reporting will
facilitate determination of magnitude of DHF in the country and
collection of data for health planning including budgeting for diag-
nosis, treatment, and control. Capacity building for surveillance and
emergency response systems, laboratory diagnosis and infrastruc-
ture should be given top priority by the Federal government to
facilitate prompt and accurate identification of the causative agent
and control of DHF outbreaks. At present, only few laboratories in
the country have facilities and manpower to carry out laboratory
diagnosis of dengue. There is need to strengthen these laborato-
ries, build new ones and provide state-of-the-art facilities including
modern equipment, test reagents and adequate manpower in them.
If major outbreaks of DHF occur in Nigeria, it will be neces-
sary to create awareness on danger DENV poses and how to avoid
being infected. Workshops should be organized for health per-
sonnel especially physicians on clinical diagnosis, collection and
handling of specimens for laboratory diagnosis and management
of clinical cases. Awareness activities should include lectures in
schools, churches, mosques and social clubs. Epidemics of DHF in
other parts of the world often stretch health services to their limits.
In the event of major DHF outbreaks, there will be increase in the
number of hospital admissions. Therefore, national health services
should be prepared to face a variety of challenges such as short-
age in number of hospital beds, medications, hospital supplies and
laboratory reagents and supplies. Research activities that will fill
knowledge gaps in epidemiology of DENV, and strategies for pre-
vention and control should be supported. Priority should be given to
research projects that will provide answers to questions on sylvatic
transmission of DENV, role of A. albopictus in dengue transmission
in Nigeria, and public health and economic impact of DHF.
Funding
No funding sources.
Competing interests
None declared.
Ethical approval
Not required.
Authors’ contributions
FHA and OAB reviewed literature, wrote, revised and approved
the final draft.
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