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Tuesday, June 19 2018 @ 10:39 AM EDT

Dengue Fever in Panama

Healthcare Dengue (DF) and dengue hemorrhagic fever (DHF) are caused by one of four closely related, but antigenically distinct, virus serotypes (DEN-1, DEN-2, DEN-3, and DEN-4), of the genus Flavivirus. Infection with one of these serotypes provides immunity to only that serotype for life, so persons living in a dengue-endemic area can have more than one dengue infection during their lifetime. DF and DHF are primarily diseases of tropical and sub tropical areas, and the four different dengue serotypes are maintained in a cycle that involves humans and the Aedes mosquito. However, Aedes aegypti, a domestic, day-biting mosquito that prefers to feed on humans, is the most common Aedes species. Infections produce a spectrum of clinical illness ranging from a nonspecific viral syndrome to severe and fatal hemorrhagic disease. Important risk factors for DHF include the strain of the infecting virus, as well as the age, and especially the prior dengue infection history of the patient. Background: Dengue fever (DF) describes the symptom complex produced by infection with 1 of the 4 serotypes of dengue virus. Dengue infection may be asymptomatic, result in a nonspecific febrile illness, or produce classic DF. A small percentage of persons with dengue infection develop bleeding complications, a syndrome termed dengue hemorrhagic fever (DHF). A subset of patients with DHF develop shock (dengue shock syndrome, DSS) and/or die.

DF-like illnesses have been described in Chinese medical writings dating as early as 265 AD. Outbreaks of febrile illnesses compatible with DF have been recorded throughout history. In 1789, Benjamin Rush, MD published an account of a probable DF epidemic in Philadelphia in 1780. Dr. Rush coined the term breakbone fever from a description of the symptoms by one of his patients. Probable epidemics of DF occurred sporadically every 10-30 years until after World War II. The socioeconomic disruptions caused by World War II resulted in increased spread of dengue viruses throughout the world.

The first epidemic of DHF was described in Manila in 1953. After that, outbreaks of DF became more common. A pattern developed in which DF epidemics occurred with increasing frequency and were associated with occasional DHF cases. Subsequently, DHF epidemics occurred every few years. Eventually, DHF epidemics occurred yearly, with major outbreaks occurring approximately every 3 years. This pattern has repeated itself as DF has spread to new regions. Initially, epidemics were confined to large urban centers, but with increasing spread of dengue viruses, suburban and rural areas have been involved in epidemics. Dengue has spread from Southeast Asia westward into India and Sri Lanka and eastward into China and several Western Pacific islands, including Tahiti. Currently, DHF is one of the leading causes of hospitalization and death in children in many Southeast Asian countries.

Less information is available on the epidemiology of DF in Africa. DF is known to be present in 19 countries on the African continent. In a 1993 epidemic in the Comoros, an estimated 60,000 persons were infected with dengue. No major DHF epidemics have occurred in Africa, but all 4 dengue serotypes are known to be circulating in the continent.

In the Americas, dengue epidemics were rare throughout the 1950s, 1960s, and most of the 1970s because Aedes aegypti mosquitoes had been eradicated from most of the region through coordinated international efforts. The systematic elimination of A aegypti mosquitoes was halted in the early 1970s. By the 1990s, A aegypti mosquitoes had repopulated most of the countries from which they had been eliminated. The first DHF epidemic in the Americas occurred in Cuba in 1981. During the Cuban epidemic, 24,000 cases of DHF, 10,000 cases of DSS, and 158 deaths occurred. Since then, increasing numbers of cases of DF and DHF have occurred. Dengue is now endemic and hyperendemic in countries from which it had been eradicated for many years.

The potential for further global spread of dengue exists. Factors believed to be responsible for part of the spread include explosive population growth, unplanned urban growth, poor mosquito control measures, increased international travel, and decay in public health systems. All of these factors need to be addressed to control the spread of dengue and other mosquito-borne infections.

Pathophysiology: Dengue infection is caused by 1 of 4 related, but distinct viruses named dengue virus 1 (DENV-1), dengue virus 2 (DENV-2), dengue virus 3 (DENV-3), and dengue virus 4 (DENV-4), which were speciated by Albert Sabin in 1944. Dengue viruses are small, spherical, single-stranded RNA viruses with an envelope and are from the family Flaviviridae (70 species, type species yellow fever), genus Flavivirus.

Dengue viruses are transmitted to humans by the bite of an infected mosquito. A aegypti mosquitoes are by far the predominant vectors for dengue infection, but Aedes albopictus mosquitoes and other Aedes species also are able to transmit dengue with varying degrees of efficiency.

The United States has 2 competent vectors for this virus, A albopictus and A aegypti. These mosquito species have adapted well to human habitation, often breeding around dwellings in small amounts of water found in old tires or other small containers discarded by humans. Aedes mosquitoes are daytime feeders and, being easily disturbed, often interrupt meals, which makes them efficient vectors. Entire families developing infection within a 24- to 36-hour period, presumably from the bites of a single infected vector, is not an unusual occurrence.

The mosquitoes acquire the virus when they feed on a viremic human. The mosquito is capable of transmitting dengue if it immediately bites another host or after 8-12 days of viral replication in its salivary glands (extrinsic incubation period). The mosquito remains infected for the remainder of its 15- to 65-day lifespan. Vertical transmission of dengue virus in mosquitoes has been documented. The eggs of Aedes mosquitoes are able to withstand long periods of desiccation, reportedly as long as 1 year.

Although some lower primates can be infected with dengue viruses, humans are by far the predominant host. Once inoculated into a host, dengue has an incubation period of 3-14 days. Following incubation, a 5- to 7-day acute febrile illness ensues. Recovery usually is complete by 7-10 days. Infection with one dengue serotype provides lifelong protection from reinfection with that same serotype but only partial and short-lived protection from infection with other dengue serotypes.

DHF or DSS usually develops around the third to seventh day of illness, approximately at the time of defervescence. The major pathophysiological abnormalities that occur in DHF and DSS are plasma leakage and bleeding. Plasma leakage is caused by increased capillary permeability and is manifested as pleural effusion, ascites, and hemoconcentration. The bleeding tendency is caused by capillary fragility and thrombocytopenia and can present in a variety of ways, ranging from petechial skin hemorrhages to life-threatening gastrointestinal bleeding.

Most patients who develop DHF or DSS have had prior infection with one or more dengue serotypes. Nonneutralizing antibodies to one dengue serotype, when bound by macrophage Fc receptors, have been proposed to result in increased viral replication in macrophages and increased cytokine production and complement activation. This phenomenon is called antibody-dependent enhancement. Also, certain dengue strains, particularly those of DEN-2, have been proposed to be more virulent, in part because more epidemics of DHF have been associated with DENV-2 than with the other serotypes.


In the US: In 1998, 90 confirmed or probable cases of DF were imported into the United States, resulting in one fatal case. The true number of DF cases is believed to be higher because most US physicians are not aware of dengue or its manifestations. Travel histories obtained from 35 (39%) of these patients indicated recent travel to the Caribbean Islands. DF also has been acquired domestically in 1980, 1986, 1995, and 1997. Most of these cases occurred in southern Texas.

In 1999, more than 300 cases of DF were reported from Nuevo Laredo, Tamaulipas, Mexico. Nuevo Laredo lies directly across the Rio Grande River from Laredo, Texas. No cases had been reported from Laredo in more than 12 years. A aegypti mosquitoes are present in both cities. The Texas Department of Health reviewed 494 patient records from 5 outpatient sites and was able to confirm 11 cases of DF. Mosquito abatement measures were instituted in Laredo, and health care providers were notified of the DF cases. In the latter half of 1999, Laredo-area health care providers identified 161 suspected DF cases and 18 were confirmed. This underscores the need for health care providers to be aware of DF and its manifestations and to test for it in appropriate cases.
Internationally: An estimated 2.5-3 billion people live in areas throughout the world in which they are at risk for dengue infection. Yearly, 20-100 million people are infected with dengue, and DHF develops in 250,000-500,000 of these individuals. Worldwide, approximately 24,000 deaths are attributed to dengue annually. Pan American Health Organization (PAHO) member states reported 741,794 cases of DF or DHF in 1998, which was more than double the number of cases reported in 1997.

Recovery from dengue infection usually is complete. Even patients who meet strict criteria for DHF or DSS typically recover without sequelae.
The fatality rate for DSS varies by country from 12-44%. In a 1997 Cuban epidemic of DF, the fatality rate for patients who met criteria for DHF or DSS was approximately 6%. The mortality rate of DF is less than 1%.
Data from the 1997 Cuban epidemic indicate that for every clinically apparent case of DF, 13.9 cases of dengue infection went unrecognized due to minimal or absent symptoms.

Dengue affects all races.

Dengue viruses affect both sexes.

Dengue affects people of all ages. In Southeast Asia, where dengue is hyperendemic, DHF usually affects children younger than 15 years. However, in the Americas, where dengue is becoming progressively hyperendemic, DHF shows no age predilection.

CLINICAL Section 3 of 10
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Fever in symptomatic DF may be as high as 41°C. The fever typically lasts 5-7 days. Occasionally, the fever abates for a day, only to return, a pattern that has been called saddleback fever. Patients are at risk for development of DHF or DSS at approximately the time of defervescence.
Headache usually is generalized. Retroorbital pain is common.
Patients may report nausea and vomiting.
Patients may have a truncal scarlatinalike rash.
Patients may have severe myalgias/arthralgias.
Hemorrhagic manifestations may range from small amounts of bleeding from the nose or gums to melena or hematemesis.
Abdominal pain is reported.
Patients also report malaise.

Fever is present.
Rash is discussed as follows:
The rash of DF may be present in as many as half the patients.
The rash is variable and may be scarlatiniform or maculopapular.
Petechiae and purpura may develop as hemorrhagic manifestations.
Conjunctival injection can be seen in approximately one third of patients with DHF.
Pharyngeal injection is seen in almost 97% of patients with DHF.
Generalized lymphadenopathy is observed.
Hepatomegaly is present more often in DSS than in milder cases. Very mild elevations of hepatic transaminases may occur.
Hemorrhagic manifestations include the following
Petechiae and bleeding at venipuncture sites are most common.

Results from a tourniquet test often are positive. This test is performed by inflating a blood pressure cuff on the upper arm to midway between diastolic and systolic blood pressures for 5 minutes. The results are considered positive if more than 20 petechiae per square inch are observed on the skin of the arm.
Other hemorrhagic manifestations include nasal or gingival bleeding, melena, or hematemesis.
DF presents in a nonspecific manner and may not be distinguishable from other viral or bacterial illness. The PAHO has developed the following case definitions for the diagnosis of DF and DHF or DSS:
The clinical description of DF is an acute febrile illness of 2-7 days duration associated with 2 or more of the following:

Severe headache

Retroorbital pain

Severe myalgias


Characteristic rash

Hemorrhagic manifestations

Laboratory criteria for diagnosis include one or more of the following:

Isolation of the dengue virus from serum, plasma, leukocytes, or autopsy samples

Demonstration of a 4-fold or greater change in reciprocal immunoglobulin G (IgG) or immunoglobulin M (IgM) antibody titers to one or more dengue virus antigens in paired serum samples

Demonstration of dengue virus antigen in autopsy tissue by immunohistochemistry or immunofluorescence or in serum samples by enzyme immunoassay (EIA)

Detection of viral genomic sequences in autopsy tissue, serum, or cerebral spinal fluid (CSF) samples by polymerase chain reaction
Cases are classified as suspected if they are compatible with the clinical description.
Cases are classified as probable if they are compatible with the clinical definition and satisfy one or more of the following criteria:

Supportive serology (reciprocal hemagglutination-inhibition antibody titer greater than 1280, comparable IgG EIA titers, or positive IgM antibody test in late acute or convalescent-phase serum specimen)

Occurrence at the same location and time as other confirmed cases of DF
A confirmed case is one that is compatible with the clinical definition and is confirmed by the laboratory.
Criteria for the diagnosis of DHF include a probable or confirmed case of dengue infection and hemorrhagic tendencies as evidenced by one or more of the following:

A positive result from the tourniquet test

Petechiae, ecchymoses, or purpura

Bleeding from the mucosa, gastrointestinal tract, injection sites, or other sites

Hematemesis or melena and thrombocytopenia (<100,000 cells/mm3) and evidence of plasma leakage due to increased vascular permeability manifested by one or more of the following: greater than 20% rise in average hematocrit level for age and sex, greater than 20% drop in hematocrit level following volume replacement compared to baseline, or signs of plasma leakage (eg, pleural effusion, ascites, hypoproteinemia)
DSS is diagnosed in cases meeting all of the above criteria plus evidence of circulatory failure, such as the following:

Rapid, weak pulse

Narrow pulse pressure (<20 mm Hg)


Cool, clammy skin

Altered mental status
Causes: Dengue infection is caused by 1 of the 4 dengue viruses (ie, DENV-1, DENV-2, DENV-3, DENV-4) and is transmitted to humans by the bite of an infected mosquito. DIFFERENTIALS Section 4 of 10
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Ebola Virus
Hepatitis, Viral
Lymphocytic Choriomeningitis
Meningococcal Infections
Rocky Mountain Spotted Fever
Sepsis, Bacterial
Septic Shock
Yellow Fever

Other Problems to be Considered:

Chikungunya virus
Mayaro fever
Ross River fever
Sindbis virus
Hemorrhagic fever viruses

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Ebola Virus

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Sepsis, Bacterial

Septic Shock


Yellow Fever

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WORKUP Section 5 of 10
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Lab Studies:

Complete blood cell count findings include the following:
Leukopenia is observed near the end of the febrile phase of illness. Lymphocytosis, with atypical lymphocytes, commonly is seen before defervescence or shock.
A rise in hematocrit greater than 20% is a sign of hemoconcentration and precedes shock. The hematocrit level should be monitored every 3-4 hours in severe cases of DHF or DSS.
Platelet count less than 100,000 is seen in DHF or DSS and occurs before defervescence and the onset of shock.
Basic metabolic panel findings include the following:
Hyponatremia is the most common electrolyte abnormality observed in patients with DHF or DSS.
Metabolic acidosis is observed in those with shock, and it must be corrected rapidly.
Elevated BUN is observed in those with shock.
Liver function test findings include the following:
Mild elevations in transaminase levels may be seen.
Low albumin is a sign of hemoconcentration.
Coagulation studies may help guide therapy in patients with severe hemorrhagic manifestations. Findings are as follows:
Prothrombin time is prolonged.
Activated partial thromboplastin time is prolonged.
Low fibrinogen and elevated fibrin degradation product levels are signs of disseminated intravascular coagulation.
Typing and crossmatching of blood should be performed in cases of severe DHF or DSS because blood products may be required.
Serum specimens should be sent to the laboratory for diagnosis. Because the signs and symptoms of DF are nonspecific, attempting laboratory confirmation of dengue infection is important.
Cultures of blood, urine, CSF, and other body fluids should be performed as necessary to exclude or confirm other potential causes of the patients' condition.
Imaging Studies:

Chest radiograph: Right-sided pleural effusion is typical. Bilateral pleural effusions are common in patients with DSS.
Other Tests:

Arterial blood gas determinations should be performed in severe cases to assess pH, oxygenation, and ventilation.

Intravenous catheter - For fluid administration
Central venous catheter
For fluid administration
For central venous pressure measurement
Arterial catheter
For continuous blood pressure measurement
For serial arterial blood gas measurement
Urethral catheterization - May be useful to strictly monitor urine output
TREATMENT Section 6 of 10
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Medical Care:

DF usually is a self-limited illness, and only supportive care is required. Acetaminophen may be used to treat patients with symptomatic fever.
Patients with known or suspected DF should have their platelet count and hematocrit measured daily from the third day of illness until 1-2 days after defervescence. Those patients with a rising hematocrit or falling platelet count should have intravascular volume deficits replaced. Those patients who improve can continue to be monitored in an outpatient setting. Those patients who do not improve should be admitted to the hospital for continued hydration.
Patients who develop signs of DHF warrant closer observation. Patients who develop signs of dehydration, such as tachycardia, prolonged capillary refill time, cool or mottled skin, diminished pulse amplitude, altered mental status, decreased urine output, rise in hematocrit, narrowed pulse pressure, or hypotension, require admission for intravenous fluid administration.
Intravascular volume deficits should be corrected with isotonic fluids such as sodium chloride solution or Ringer solution. Boluses of 10-20 mL/kg should be given over 20 minutes and may be repeated. If this fails to correct the deficit, the hematocrit value should be determined, and, if it is rising, limited clinical information suggests that a plasma expander may be administered. Dextran 40 or albumin 5% at a dose of 10-20 mL/kg may be used. If the patient does not improve after this, blood loss should be considered. Patients with internal or gastrointestinal bleeding may require transfusion.
After patients with dehydration are stabilized, they usually require intravenous fluids for no more than 24-48 hours. Intravenous fluids should be stopped when the hematocrit level falls below 40% and adequate intravascular volume is present. At this time, patients reabsorb extravasated fluid and are at risk for volume overload if intravenous fluids are continued. Do not interpret a falling hematocrit value in a clinically improving patient as a sign of internal bleeding.

Patients who are resuscitated from shock recover rapidly. Patients with DHF or DSS may be discharged from the hospital when they meet the following criteria:
Afebrile for 24 hours without antipyretics

Good appetite, clinically improved condition

Adequate urine output

Stable hematocrit

At least 48 hours have passed since recovery from shock

Absence of respiratory distress

Platelet count greater than 50,000
Surgical Care: No specific surgical intervention is necessary in patients with DF, DHF, or DSS.


Consultation with an infectious diseases specialist may be helpful in guiding decisions regarding diagnosis and treatment.
Consultation with a critical care medicine specialist may be helpful when treating patients with DHF or DSS and severe hemorrhagic manifestations or shock.

No specific diet is necessary for patients with DF.
Patients may become dehydrated from fever, lack of oral intake, or vomiting. Patients who are able to tolerate oral fluids should be encouraged to drink oral rehydration solution, fruit juice, or water to prevent dehydration.
Return of appetite after DHF or DSS is a sign of recovery.
Activity: Bedrest is recommended for patients with symptomatic DF, DHF, or DSS.
MEDICATION Section 7 of 10
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No specific antiviral medication currently is available to treat dengue infections. Single-dose methylprednisolone showed no mortality benefit in the treatment of DSS in a prospective, randomized, double-blind, placebo-controlled trial.

Acetaminophen (paracetamol) is recommended for treatment of pain and fever. Aspirin, other salicylates, and nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided.

Drug Category: Analgesics/antipyretics -- The treatment of DF is symptomatic and supportive in nature. Bedrest and mild analgesic-antipyretic therapy often are helpful in relieving lethargy, malaise, and fever associated with the disease.Drug Name
Acetaminophen (Tylenol, Feverall) -- Reduces fever by acting directly on hypothalamic heat-regulating centers, which increases dissipation of body heat via vasodilation and sweating. Used in dengue infections to relieve pain and lower temperature when fever is thought to contribute to patient discomfort.
Adult Dose 325-650 mg PO/PR q4-6h or 1000 mg tid/qid; not to exceed 4 g/d
Pediatric Dose 15 mg/kg PO/PR q4h prn; not to exceed 2.6 g/d
Contraindications Documented hypersensitivity
Interactions Rifampin can reduce analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity; chronic use may potentiate effects of warfarin
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Hepatotoxicity possible in those with chronic alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; APAP is contained in many OTC products, and combined use with these products may result in cumulative APAP doses exceeding recommended maximum dose
Drug Category: Volume expanders -- Plasma volume expanders are used in the treatment of intravascular volume deficits or shock to restore intravascular volume, blood pressure, and tissue perfusion.Drug Name
Lactated ringers with isotonic sodium chloride solution -- Used to expand intravascular volume. Both fluids are essentially isotonic and have equivalent volume restorative properties. Although some differences exist between metabolic changes seen with administration of large quantities of either fluid, for practical purposes and in most situations, differences are clinically irrelevant. Importantly, no demonstrable difference in hemodynamic effect, morbidity, or mortality exists between resuscitation using either product.
Adult Dose 10-20 mL/kg IV initially administered rapidly, over 20 min; followed by reassessment of hemodynamic response; repeat prn
Pediatric Dose Administer as in adults
Contraindications Major complication of isotonic fluid resuscitation is interstitial edema; edema of extremities is unsightly, but not a significant complication; edema in brain or lungs is potentially fatal; major contraindication to isotonic fluid resuscitation is pulmonary edema; added fluid promotes more edema and may lead to the development of ARDS
Interactions None reported
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Caution in CHF; caution admixing other agents (monitor for incompatibilities)
Drug Name
Dextran 40 (Macrodex, LMD) -- Polymer of glucose. When infused, it increases intravascular volume, blood pressure, and capillary perfusion. Used to restore intravascular volume when isotonic crystalloid use fails.
Adult Dose Variable; not to exceed 20 mL/kg on d 1 or 10 mL/kg thereafter
Pediatric Dose Administer as in adults
Contraindications Documented hypersensitivity; pulmonary edema
Interactions Caution when administering parenteral fluids to patients receiving corticosteroids or corticotropin, especially if the solution contains sodium ions; can interfere with blood cross-matching and measuring serum glucose and bilirubin levels (draw blood for laboratory testing prior to administration)
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions May cause nausea, which also may occur with hypoglycemia; IV dextrose solutions may result in dilution of serum electrolyte concentrations or overhydration when fluid overload is present; caution in patients experiencing congested states or pulmonary edema; hypertonic dextrose given peripherally may cause thrombosis (administer instead through central venous catheter); caution in subclinical diabetes mellitus or carbohydrate intolerance
Increased risk of inducing significant hyperglycemia or hyperosmolar syndrome if solution is administered rapidly, especially in patients with chronic uremia or carbohydrate intolerance; concentrated solutions should not be administered SC or IM; rates of dextrose infusion faster than 0.5 g/kg/h may produce glycosuria; at infusion rates of 0.8 g/kg/h, the incidence of glycosuria is 5%; monitor fluid balance, electrolyte concentrations, and acid-base balance closely; dextrose administration may produce vitamin B complex deficiency
Drug Name
Albumin (Albuminar-5, Buminate) -- Human albumin is a sterile solution of albumin (major plasma protein responsible for colloid oncotic pressure of blood). Pooled from blood, serum, plasma, or placenta from healthy donors. Infusion of albumin results in a shift of fluid from extracellular space into circulation, thereby decreasing hemoconcentration and blood viscosity.
May be administered wide open when treating shock. Patient response must be assessed before repeating dose.
Adult Dose 25 g IV; not to exceed 250 g/48 h
Pediatric Dose <37 weeks' gestation: 1 g/kg
Infants and children: 25-50% of adult dose
Contraindications Documented hypersensitivity; pulmonary edema; protein load of 5% albumin
Interactions None reported
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Caution in poor left ventricular systolic function (monitor central venous pressure during infusion)
FOLLOW-UP Section 8 of 10
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Further Inpatient Care:

Report known or suspected cases of DF or DHF/DSS to public health authorities. Such reports should include patient demographics, case classification, date of onset of illness, whether or not hospitalization was necessary, outcome, and recent travel history. When multiple patients are involved, reports should include the number of cases of DF and DHF/DSS stratified by age, number of confirmed cases and serotypes, and number of hospitalizations and deaths.
Draw serum specimens for diagnosis as soon as possible after the onset of illness or hospitalization and at the time of death or discharge from the hospital. Immediately place specimens on wet ice and send to the laboratory.
Evaluate and treat patients appropriately for other possible conditions until the diagnosis of DF or DHF/DSS is established.
Further Outpatient Care:

Draw a serum specimen 7-21 days after the acute-phase serum specimen was drawn. Ideally, draw the convalescent-phase serum specimen 10 days after the acute-phase specimen. Immediately place the specimen on wet ice, and send it to the laboratory.
In/Out Patient Meds:

No specific medications are needed for patients with DF or DHF/DSS. In general, patients should continue to take any medications necessary for the treatment of other medical conditions. However, use diuretics and antihypertensives with caution in patients with DHF because these medications may exacerbate the pathophysiologic derangement associated with DHF. Review the risks and benefits of each medication, and make individualized decisions regarding whether the medication should be continued.
The differential diagnosis of DF and DHF/DSS includes many conditions that are treatable with specific medications, such as antibiotics. Until such conditions are excluded, they should be treated.

Transfer patients with DF or DHF/DSS when necessary monitoring and treatment cannot be provided in the current unit or facility. Treat patients with DSS in intensive/critical care units.

No vaccine is available for the prevention of dengue infection. Immunogenic vaccines have been developed and are being tested. Because immunity to a single dengue strain is the major risk factor for DHF and DSS, a vaccine must provide high levels of immunity to all 4 dengue strains to be clinically useful.
The only way to prevent dengue virus acquisition is to avoid being bitten by a vector mosquito. This can be accomplished in several ways, as follows:
Avoid travel to areas where dengue is endemic. This is not an ideal strategy because it would require a person to avoid most tropical and subtropical regions of the world, and many of these regions are popular travel destinations.
Wear mosquito repellant.
Wear protective clothing.
Remain in well-screened or air-conditioned places.
Use mosquito netting.
Eliminate the mosquito vector using indoor sprays.
Eliminate the breeding ground of the mosquitoes by not allowing them access to small accumulations of water around human habitats. Such accumulations can be found in pots, old tires, or any vessel capable of holding water.

Neurologic manifestations such as seizures and encephalitis/encephalopathy have been reported in rare cases of dengue infection. Some of these cases did not manifest other typical features of dengue infection. Other neurological complications associated with dengue infection include neuropathies, Guillain-Barré syndrome, and transverse myelitis.
Liver failure has been associated with DHF/DSS epidemics. Whether this is a viral effect or a product of prolonged liver hypoperfusion remains unclear.
Overhydration is a well-recognized complication of DF and DHF/DSS.

The prognosis of patients with DF is excellent, with complete recovery being the norm. Patients with DHF or DSS who do not die usually recover without sequelae.
Patient Education:

Educate patients who recover from DF to avoid mosquito bites when traveling to dengue-endemic areas. Current evidence suggests that those with a history of DF are at highest risk for DHF or DSS if they are infected with a different dengue strain.
MISCELLANEOUS Section 9 of 10
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Medical/Legal Pitfalls:

Failure to suspect dengue infection in febrile patients with a history of travel to dengue endemic areas within 2 weeks of the onset of illness
Failure to suspect, identify, and treat other possible diseases such as meningitis
Failure to admit patients with signs and symptoms of intravascular volume loss for intravenous hydration
Failure to administer adequate fluids to patients with DHF or DSS
Failure to notify public health authorities about suspected cases of dengue infection
Special Concerns:

Older patients, particularly those with congestive heart failure, must not be given excessive amounts of intravenous fluids.
Rare cases of vertical dengue transmission have been reported. Dengue should be suspected in pregnant patients with compatible clinical features. The potential for a neonate to be born with signs and symptoms of DF should be anticipated.
BIBLIOGRAPHY Section 10 of 10
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