Dengue Fever

Causative Agent: Aedes Aegypti

Incubation Period: 4-5 days and maximum of 12 days
Pathognomonic Sign: Hermans sign. It appears on the upper and lower extremities, purplish or
violaceous red with blanched areas about 1 cm or less in size.
Dengue fever is a mosquito-borne disease that occurs in tropical and subtropical areas of the
world. Mild dengue fever causes high fever, rash, and muscle and joint pain. A severe form of dengue
fever, also called dengue hemorrhagic fever, can cause severe bleeding, a sudden drop in blood pressure
(shock) and death.
Millions of cases of dengue infection occur worldwide each year. Dengue fever is most common in
Southeast Asia and the western Pacific islands, but the disease has been increasing rapidly in Latin
America and the Caribbean.
Researchers are working on dengue fever vaccines. For now the best prevention is to reduce mosquito
habitat in areas where dengue fever is common.
Causes
Virology
The virus of dengue fever belongs to the family flaviviridae. It is the RNA virus. Other member of the
Flaviridae virus is the virus of yellow fever, virus of West Nile, virus of encephalitis of St. Louis, virus of
Japanese encephalitis, virus of encephalitis of Tick-bone, virus of disease Kyasanur forest and last but not
least the virus of fever omsk hemorrhagic. It is found that most of the disease is transmitted by ticks or
mosquitoes, commonly known as anthropods and also referred by the name of arboviruses, is the virus of
anthropod-borne.
The genome of the dengue virus lies between the range of 11000 bases of nucleotide which become the
code for the other three types of different molecules of protein (E, C, prM) which help in making the
particles of virus and even help in the formation of seven other types of molecules of protein (NS5, NS4a,
NS2b, NS1, NS2a, NS3, NS4b) that are mostly found in the cells of infected host and which are needed
for virus to get replicated.
Transmission
It is known that dengue fever is caused by the bite of female Aedes mosquito commonly known as A.
aegypti. It is found that these types of mosquitoes live in the area of 35 degree from south and 35 degree
north from the latitude which is below in the angle of elevation 1000 metres (3,300 ft). Aedes mosquitoes
mainly attack during the morning time and evening time.
Aedes is the mosquitoes that have its many species transmitting disease are A.scutellaris, A.albopictus and
last but not least is A.polynesiensis. Humans are known for the host of virus but it is found that virus also
circulates in the primates of non human. The infection from Aedes can be transmitted on a single bite. It is

stated that female Aedes also get infected while sucking the blood of a person who is infected with
dengue fever. Dengue is the fever which is also transmitted through the blood products which is infected
and also through the donation of an organ.
The risk of dengue fever in the countries like Singapore lies between the range of 1.6 and the transfusion
of dengue is 6 per 10000. During the time of pregnancy, there has been transmission from mother to the
born child. It is found that there is also transmission of the virus directly from person to person.
Predisposition
Babies and the children who are in young stage are more prone to the diseases of various types. Children
are very well nourished in contrast to various infections. Other factors which are very risky are from sex
of female and the index of weighted body. Each serotype is responsible for the disease to get spectrum
which in turn become the risky factor of virus strain. There are four types of serotypes as we already
know and it is also known that the one serotype can only give lifelong immune capacity to the type which
is similar to it but cannot give good immune capacity to other serotypes.
Polymorphism is known for creating the link with increase in complications of dengue virus. There are
certain examples which contain the code for the various genes of proteins. They are DC-sign, TGF,
TNFa, PLCe1 and lectin of mannan-binding and there is some other forms leukocyte antigen of human
from the variations of the genes of HLA-B.
Pathophysiology
Pathogenesis is linked to the host immune response, which is triggered by infection with the
dengue virus. Primary infection is usually benign in nature; however, secondary infection with a different
serotype or multiple infections with different serotypes may cause severe infection that can be classified
as either dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS), depending on the clinical
signs.
Non-neutralizing, cross-reactive antibodies elicited by a previous primary infection are involved in the
phenomenon of antibody-dependent enhancement (ADE), which causes a heavy viral burden. Cells of the
monocyte-macrophage lineage are the major sites of viral replication, but the virus can infect other tissues
in the body such as the liver, brain, pancreas, and heart.
Antigen-presenting dendritic cells, the humoral immune response, and the cell-mediated immune
response are involved in the pathogenesis. Proliferation of memory T cells and the production of proinflammatory cytokines leads to vascular endothelial cell dysfunction, which results in plasma leakage.
There is a higher concentration of cytokines such as interferon-gamma, tumor necrosis factor (TNF)alpha, and interleukin-10, as well as reduced levels of nitric oxide and some complement factors. NS1 is a
modulator of the complement pathway and plays a role in low levels of complement factors. After
infection, specific cross-reactive antibodies, as well as CD4+ and CD8+ T cells, remain in the body for
years.
Vascular leak is the hallmark of DHF and DSS, and causes an increase in hematocrit, hypoalbuminaemia,
and the development of pleural effusions or ascites. Preliminary data suggest that transient dysfunction of

the endothelial glycocalyx layer leads to vascular leak. There is also a tendency towards haemorrhage
associated with severe thrombocytopenia and coagulation disorders.
In severe infection, loss of intravascular fluid leads to tissue hypoperfusion, resulting in lactic acidosis,
hypoglycemia, hypocalcaemia, and, finally, multiple organ failure. Multiple organ dysfunction including
myocarditis, encephalopathy, and liver cell necrosis can also result from direct viral damage to, and
subsequent inflammation in, tissues.
Infants can develop severe dengue infection during a primary infection (which is usually benign in nature)
due to transplacental transfer of maternal antibodies from an immune mother, which subsequently
amplifies the infant's immune response to the primary infection.
Diagnostic Procedure
1. Viral isolation and serotype identification
Specimens for virus isolation should be collected early in the course of the infection,
during the period of viraemia (usually before day 5). Virus may be recovered from serum, plasma
and peripheral blood mononuclear cells and attempts may be made from tissues collected at
autopsy (e.g. liver, lung, lymph nodes, thymus, bone marrow). Because dengue virus is heatlabile, specimens awaiting transport to the laboratory should be kept in a refrigerator or packed in
wet ice. For storage up to 24 hours, specimens should be kept at between +4 C and +8 C. For
longer storage, specimens should be frozen at -70 C in a deep-freezer or stored in a liquid
nitrogen container. Storage even for short periods at 20 C is not recommended.
Cell culture is the most widely used method for dengue virus isolation. The mosquito cell
line C6/36 (cloned from Ae. albopictus) or AP61 (cell line from Ae. pseudoscutellaris) are the
host cells of choice for routine isolation of dengue virus. Since not all wild type dengue viruses
induce a cytopathic effect in mosquito cell lines, cell cultures must be screened for specific
evidence of infection by an antigen detection immune fluorescence assay using serotype-specific
monoclonal antibodies and flavivirus group-reactive or dengue complex-reactive monoclonal
antibodies. Virus isolation followed by an immune fluorescence assay for confirmation generally
requires 12 weeks and is possible only if the specimen is properly transported and stored to
preserve the viability of the virus in it.Virus antigen is detected in mouse brain or mosquito head
squashes by staining with anti-dengue antibodies.
2. Nucleic Acid detection
RNA is heat-labile and therefore specimens for nucleic acid detection must be handled
and stored according to the procedures described for virus isolation.
3. Antigen Detection
Detection of dengue antigens in acute-phase serum was rare in patients with secondary
infections because such patients had pre-existing virus-IgG antibody immune complexes. New
developments in ELISA and dot blot assays directed to the envelop/membrane (E/M) antigen and

the non-structural protein 1 (NS1) demonstrated that high concentrations of these antigens in the
form of immune complexes could be detected in patients with both primary and secondary
dengue infections up to nine days after the onset of illness.
The NS1 glycoprotein is produced by all flaviviruses and is secreted from mammalian
cells. NS1 produces a very strong humoral response. Many studies have been directed at using the
detection of NS1 to make an early diagnosis of dengue virus infection.
Fluorescent antibody, immune peroxidase and avidin-biotin enzyme assays allow
detection of dengue virus antigen in acetone-fixed leucocytes and in snap-frozen or formalinfixed tissues collected at autopsy.
Serological Tests
1. IgM ELISA
For the IgM antibody-capture enzyme-linked immune sorbent assay (MAC-ELISA) total
IgM in patients' sera is captured by anti- chain specific antibodies (specific to human IgM)
coated onto a microplate. Dengue-specific antigens, from one to four serotypes (DEN-1, -2, -3,
and -4), are bound to the captured anti-dengue IgM antibodies and are detected by monoclonal or
polyclonal dengue antibodies directly or indirectly conjugated with an enzyme that will transform
a non-coloured substrate into coloured products. The optical density is measured by
spectrophotometer.
Serum, blood on filter paper and saliva, but not urine, can be used for detection of IgM if
samples are taken within the appropriate time frame (five days or more after the onset of fever).
Serum specimens may be tested at a single dilution or at multiple dilutions. Most of the antigens
used for this assay are derived from the dengue virus envelope protein (usually virus-infected cell
culture supernatants or suckling mouse brain preparations). MAC-ELISA has good sensitivity and
specificity but only when used five or more days after the onset of fever..
Cross-reactivity with other circulating flaviviruses such as Japanese encephalitis, St
Louis encephalitis and yellow fever, does not seem to be a problem but some false positives were
obtained in sera from patients with malaria, leptospirosis and past dengue infection. These
limitations have to be taken into account when using the tests in regions where these pathogens
co-circulate. It is recommended that tests be evaluated against a panel of sera from relevant
diseases in a particular region before being released to the market. It is not possible to use IgM
assays to identify dengue serotypes as these antibodies are broadly cross-reactive even following
primary infections.
2. IgM Rapid Test
3. IgM/IgG ratio
A dengue virus E/M protein-specific IgM/IgG ratio can be used to distinguish primary
from secondary dengue virus infections. IgM capture and IgG capture ELISAs are the most
common assays for this purpose.

Hematologic Test
Platelets and hematocrit values are commonly measured during the acute stages of dengue
infection. These should be performed carefully using standardized protocols, reagents and equipment.
A drop of the platelet count below 100 000 per L may be observed in dengue fever but it is a
constant feature of dengue hemorrhagic fever. Thrombocytopenia is usually observed in the period
between day 3 and day 8 following the onset of illness.
Hemoconcentration, as estimated by an increase in hematocrit of 20% or more compared with
convalescent values, is suggestive of hypovolaemia due to vascular permeability and plasma leakage.
Pharmacologic Management
No specific treatment for dengue fever exists. Drink plenty of fluids to avoid dehydration from vomiting
and high fever. Acetaminophen (Tylenol, others) can alleviate pain and reduce fever. Avoid pain relievers
that can increase bleeding complications such as aspirin, ibuprofen (Advil, Motrin IB, others) and
naproxen sodium (Aleve, others).
If you have severe dengue fever, you may need:
-

Supportive care in a hospital

Intravenous (IV) fluid and electrolyte replacement
Blood pressure monitoring
Transfusion to replace blood loss

Nursing Diagnosis
1.
2.
3.
4.
5.

Imbalanced Nutrition: Less than body requirements related to nausea, vomiting, and no appetite.
Increased body temperature related to the process of dengue virus infection.
Risk for bleeding related to thrombocytopenia.
Deficient Fluid Volume related to increased capillary permeability, bleeding, vomiting and fever.
Deficient Knowledge: about the disease process related to a lack of information.

Nursing Intervention
1.
2.
3.
4.
5.
6.
7.
8.

Assess the general state and condition of the patient

To determine if there is signs of dehydration and Hermans sign
Assess for the vital signs (temperature, pulse, respiratory rate)
Assess for signs of dehydration
Assess drip infusion and intravenous needle insertion site
Balance of fluid (the fluid input and output)
To be able to determine if there is fluid retention
Encourage patients to drink a lot approximately 1500 to 2000 cc per day.
To prevent dehydration and to replace fluid loss
Instruct the patient's family to replace the patient's clothing is wet with sweat.
Collaboration with doctors in the provision therapy

Republic of the Philippines

Mariano Marcos State University
College of Health Sciences
DEPARTMENT OF NURSING
Batac, Ilocos Norte

DENGUE
SUBMITTED BY:
WYOGYHNA QUIDILLA
BSN III A