Fight Against Dengue Essays

Dengue fever (pronounced "DEN-gi") is an infectious disease caused by the dengue virus. People get the dengue virus from mosquitoes. Dengue fever is also called break-bone fever, because it can cause so much pain that people feel like their bones are breaking.

Most people with dengue fever can get better just by drinking enough. However, a small number of people get dengue hemorrhagic fever or dengue shock syndrome. These are medical emergencies and can kill a person if they do not get medical treatment.

There is no vaccine that can keep people from getting the dengue virus. There is also no treatment or cure for dengue fever. Doctors can only provide "supportive care," which means they can only treat dengue's symptoms.

Since the 1960s, many more people have been getting dengue fever. Since World War II, dengue has become a problem around the world. It is common in more than 110 countries. Every year, between 50 million and 100 million people get dengue fever.

Signs and symptoms[change | change source]

Most people who get the dengue virus (80%) have no symptoms, or have only mild symptoms (like a basic fever).[1][2][3] About 5% of infected people (or 5 out of every 100) get much sicker. A small number of these people have symptoms that could kill them.[1][3]

After a person gets the dengue virus from a mosquito, it takes between 3 and 14 days for them to get sick. (This is called the virus's incubation period.) Most often, people start to feel sick after 4 to 7 days.[4]

Often, when children have dengue fever, their symptoms are the same as gastroenteritis (stomach flu), like vomiting and diarrhea, or the common cold.[5] However, children are more likely to have bad complications from dengue fever.[6]

Dengue fever happens in three stages: febrile, critical, and recovery.[7]

The febrile stage[change | change source]

In the febrile stage, people with dengue usually have a high fever. ("Febrile" means that a person has a fever.) The fever is often over 40 degrees Celsius (104 degrees Fahrenheit). Sometimes the fever gets better, and then comes back.[8][9]

During the febrile stage, people may also have:[10][11][6]

The febrile stage usually lasts 2 to 7 days.[10][7] This stage ends when a person's high fever is gone.

The critical stage[change | change source]

In about 5% of people with dengue fever, the disease goes into a critical stage next.[6] ("Critical" means "very dangerous.") The critical phase usually lasts 1 to 2 days.[7]

During this stage, plasma (the liquid part of blood) leaks out of the body's small blood vessels. The plasma can build up in the chest and abdomen. This is a serious problem for a few reasons.

Plasma carries blood cells, glucose (sugar), electrolytes (salts), and many other important things to the whole body. Every part of the body needs these things to survive. If too much plasma leaks out of the blood vessels, there will not be enough left to carry these things to the body's most important organs.[7] Without these things, the organs cannot work normally. This is called dengue shock syndrome.

Plasma also carries platelets, which help the blood clot (they help stop bleeding). If a person does not have enough platelets, they can have dangerous bleeding. With dengue fever, this bleeding usually happens in the gastrointestinal tract.[6][7] When a person has bleeding, leaking plasma, and not enough platelets, they have dengue hemorrhagic fever. ("Hemorrhage" means "dangerous bleeding.")

The recovery stage[change | change source]

In the recovery stage, the plasma that leaked out of the blood vessels is taken back up into the bloodstream.[7] This stage usually lasts 2 to 3 days.[6]

During this stage, people with dengue often feel much better. ("Recovery" means "getting better.") However, they can have very bad itching and a slow heart rate.[6][7]

Serious problems can also happen during the recovery stage. If a person's body takes too much fluid back up into the bloodstream, it can cause "fluid overload." This can cause fluid to build up in the lungs, which causes breathing problems. Fluid overload can also cause seizures or an altered mental status (changes in a person's thinking and behavior).[6]

Complications[change | change source]

Every once in a while, dengue can affect other systems in the body.[7] For example, dengue can cause:

  • Altered mental status: This happens in 0.5% to 6% of people with very bad dengue fever. It can happen when the dengue virus causes an infection in the brain. It can also happen when important organs, like the liver, are not working correctly because of dengue.[5][9]
  • Neurological disorders: These are problems with the brain and the nerves, like Guillain–Barré syndrome[5] and Post-dengue acute disseminated encephalomyelitis.[12]
  • Infection of the heart, or sudden liver failure (these are very uncommon).[6][7]

Cause[change | change source]

Dengue fever is caused by the dengue virus. In the scientific system that classifies viruses, the dengue virus is part of the familyFlaviviridae and the genusFlavivirus. Other viruses that belong to the same family and can make humans sick include yellow fever virus, West Nile virus, Zika virus, Japanese encephalitis virus, and tick-borne encephalitis virus.[9] Most of these viruses are spread by mosquitoes or ticks.[9]

How dengue is spread[change | change source]

Dengue virus is spread mostly by mosquitoes from the Aedes genus, especially the Aedes aegyptispecies of mosquito.[2]Aides aegypti is the most likely type of mosquito to spread dengue, because it likes to live close to humans and feed off of people instead of animals.[13] A person can get the dengue virus from just one mosquito bite.[14]

Sometimes, mosquitoes can also get dengue from humans. If a female mosquito bites someone with dengue, the mosquito may get the dengue virus from the person's blood. After about 8 to 10 days, the virus spreads to the mosquito's salivary glands, which make saliva (or "spit"). Now the mosquito will make saliva that is infected with the dengue virus. When the mosquito bites a human, its infected saliva goes into the human and can give that person dengue.

A person can also get the dengue virus if they get a blood transfusion or organ donation from someone who has the virus.[15][16] In some countries where dengue is common, like Singapore, between 1.6 and 6 blood transfusions out of every 10,000 spread dengue.[17]

The dengue virus can also be spread from a mother to her fetusduring pregnancy, or when the child is born.[18] This is called vertical transmission.

Dengue is usually not spread in any other ways.[10]

Dengue virus in the human body[change | change source]

Once a person gets the dengue virus from a mosquito, the virus attaches to and enters the person's white blood cells. (The white blood cells are part of the immune system, which defends the body by fighting off threats, like infections.) As the white blood cells move around the body, the virus makes copies of itself. The white blood cells react by making many special proteins, like interferon, which tell the immune system to work harder because there is a threat in the body. These proteins cause the fever, flu-like symptoms, and severe pains that happen with dengue.

If a person has a bad infection, the virus makes copies of itself much more quickly inside the body. Because there is a lot more of the virus, it can affect many more organs (like the liver and the bone marrow). The virus can stop the bone marrow from making platelets normally. This makes very bad bleeding much more likely to happen.[19]

Risk factors[change | change source]

Babies and young children with dengue are more likely than adults to become very sick. Women are more likely than men to get very sick.[20] Dengue can be life-threatening in people with chronic (long-lasting) diseases, like diabetes and asthma.[20]

There are four different types of the dengue virus. Once a person has had one type of the virus, he usually is protected from that type for the rest of his life. However, he will only be protected against the other three types of the virus for a short time. If he later gets one of those three types of the virus, he will be more likely to have serious problems, like dengue shock syndrome or dengue hemorrhagic fever.[6][21]

Diagnosis[change | change source]

Usually, doctors diagnose dengue by examining the infected person and realizing that their symptoms match dengue.[1] However, when dengue is in its early stages, it can be difficult to tell the difference between this disease and other infections caused by viruses.[6]

The World Health Organization says that a person probably has dengue if:[7]

  1. He has a fever; AND
  2. He has two of these symptoms:
    1. Nausea and vomiting;
    2. A rash;
    3. Pain all over the body;
    4. A low number of white blood cells; or
    5. A positive tourniquet test. (To do this test, a doctor wraps a blood pressure cuff around a person's arm for five minutes, then counts any red spots on the skin. If the person has many spots, they are more likely to have dengue fever.)

The World Health Organization also says that in areas where dengue is common, any warning signs, plus a fever, usually signal that a person has dengue fever.[22]

Blood tests[change | change source]

Some blood tests show changes when a person has dengue fever. The earliest change is a low number of white blood cells in the blood. A low number of platelets can also signal dengue.[6] Special blood tests can look for the dengue virus itself; the virus's nucleic acids; or the antibodies that the immune system makes to fight off the virus.[20][23] However, these special tests are expensive.[23] Also, in many areas where dengue is common, most doctors and clinics do not have laboratories for blood tests or special machines.[1]

It can be difficult to tell the difference between dengue fever and chikungunya. Chikungunya is a similar viral infection that has many of the same symptoms of dengue, and happens in the same parts of the world.[10] Dengue can also have some of the same symptoms as other diseases, like malaria, leptospirosis, typhoid fever, and meningococcal disease. Often, before a person is diagnosed with dengue, their doctor will do tests to make sure they do not actually have one of these diseases instead.[6]

WHO classification systems[change | change source]

In 1997, the World Health Organization (WHO) created a system for describing the different types of dengue fever. Eventually, the WHO decided that this old way of dividing dengue needed to be simpler. It also decided that not everyone with dengue fever fit into the old categories.

In 2009, the WHO changed its system for classifying (dividing) dengue fever. However, the older system often is still used.[6][22][24]

The old system[change | change source]

The WHO's old system divided dengue into three categories:[24][22]

  1. Undifferentiated fever
  2. Dengue fever
  3. Dengue hemorrhagic fever. This was then divided into four stages, called grades I-IV:
    1. In Grade I, the person has a fever. He also bruises easily or has a positive tourniquet test.
    2. In Grade II, the person bleeds into the skin and other parts of the body.
    3. In Grade III, the person shows signs of circulatory shock. This is called dengue shock syndrome.
    4. In Grade IV, the person has shock so severe that his blood pressure and heartbeat cannot be felt. This is a more serious version of dengue shock syndrome.[24]

The new system[change | change source]

In 2009, the WHO created a simpler system which divided dengue fever into two types:[1][22]

  1. Uncomplicated: People who just have the febrile stage of dengue fever, and never go into the critical phase. They get better on their own or just need basic medical help.
  2. Severe: People who have symptoms that could kill them, or have serious complications from dengue.

Prevention[change | change source]

There are no vaccines that can keep people from getting the dengue virus.[1] The best ways to prevent dengue are to protect people from mosquito bites and to control the mosquito population.[25][25]


The best way to control the mosquito is to get rid of its (the places it lives) The best way to do this is to get rid of areas with standing water (water that does not move). Mosquitoes like standing water and often lay its eggs, to prevent getting bitten by mosquitoes, people can:

  • Wear clothing that fully covers their skin
  • Use bug spray
  • Use mosquito netting when they are resting.

Integrated Vector Control[change | change source]

The WHO suggests a program for preventing dengue (called an "Integrated Vector Control" program) that includes five different parts:[25]

  1. Advocacy, people working together, and legislation (laws) should be used to make public health organizations and communities stronger.
  2. All parts of society should work together. This includes the public sector (like the government), the private sector (like businesses and corporations), and the health care field.
  3. All ways of controlling disease should be brought together.
  4. Decisions should be make based on evidence. This will help make sure that the things that are done to address dengue are helpful.
  5. Areas where dengue is a problem should be given help, so that they can build their abilities to respond well to the disease on their own.

Treatment[change | change source]

There are no specific treatments for dengue fever.[1] No known anti-viralmedications (medicines which kill viruses) will kill the dengue virus. Health workers can give "supportive treatment" - treat dengue's symptoms to try to make patients feel better.

Different people need different treatments, depending on their symptoms. Some people can get better just by drinking fluids at home, and checking with their doctor to make sure they are getting better.

Treating dehydration is very important. Sometimes, people are so dehydrated that they need intravenous fluids - fluids given through a needle placed into a vein. Usually, people only need intravenous fluids for a day or two.[26]

Doctors can give medicines like acetaminophen (paracetamol) for fever and pain. Non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen and aspirin should not be used because they make bleeding more likely.[26]

People with bad dengue may need blood transfusions. Having extra blood will help a person if their blood pressure is getting very low (like it does in dengue shock syndrome) or if they do not have enough red blood cells in their blood (because they are bleeding from dengue hemorrhagic fever).[27]

When people reach the recovery stage of dengue, doctors usually stop giving intravenous fluids to prevent fluid overload (having too much fluid in the body). If a person gets fluid overload, doctors can give a type of medication called a diuretic, which will make the patient urinate out the extra fluid.[27]

Prognosis[change | change source]

Most people with dengue recover and don't have any problems afterward.[22]

Without treatment, 1% to 5% of infected people (1 to 5 out of every 100) die from dengue.[6] With good treatment, less than 1% die.[22] However, 26% of people with severe dengue die.[6]

Epidemiology[change | change source]

Dengue is common in more than 110 countries.[6] Every year, it infects 50 to 100 million people around the world. It also causes half a million hospitalizations[1] and about 12,500 to 25,000 deaths around the world each year.[5][28] However, the World Health Organization says that dengue fever is not taken as seriously as it should be. It calls dengue one of 16 "neglected tropical diseases" - diseases which do not get enough attention.[29] In every million people, dengue causes about 1600 years of life to be lost. This is about the same as other tropical and deadly diseases, like tuberculosis.[20] However, the WHO says the neglected tropical diseases, like dengue, do not get the attention and money that is needed to find treatments and cures.

Dengue is becoming much more common around the world. It is the most common viral disease that is spread by arthropods.[21] In 2010, dengue was 30 times more common than it was in 1960.[30] Scientists think dengue may be getting more common because:

  • More people are living in cities.
  • There are more people in the world. The world's population is growing.
  • More people are travelling internationally (between countries).
  • Global warming is thought to play a part in the increase in dengue.[1]

Dengue happens most around the equator. 2.5 billion people live in areas where dengue happens. 70% of these people live in Asia and the Pacific.[30] In the United States, 2.9% to 8% of people who come back from traveling in areas where dengue happens, and have a fever, were infected while traveling.[14] In this group of people, dengue is the second most common infection to be diagnosed, after malaria.[10]

History[change | change source]

Dengue fever is probably a very old disease. An ancient Chinese medical encyclopedia from the Jin Dynasty (which existed from 265 to 420 AD) talked about a person who probably had dengue. The book talked about a "water poison" that had to do with flying insects.[31][32]

Written records from the 17th century talk about what may have been epidemics of dengue (where the disease spread very quickly in a short time). The most likely early reports of dengue epidemics are from 1779 and 1780. These reports talk about an epidemic that spread across Asia, Africa, and North America.[32] From that time until 1940, there were not many more epidemics.[32]

In 1906, scientists proved that people were getting infections from Aedes mosquitoes. In 1907, scientists showed that a virus causes dengue. This was just the second disease that was shown to be caused by a virus. (The first was yellow fever.)[33] John Burton Cleland and Joseph Franklin Siler kept studying the dengue virus, and figured out the basics of how the virus spreads.[33]

Dengue began to spread much more quickly during and after World War II. Different types of dengue also spread to new areas. For the first time, people started to get dengue hemorrhagic fever. The first case of dengue hemorrhagic fever happened in the Philippines in 1953. By the 1970s, dengue hemorrhagic fever had become a major cause of death in children. It also spread to the Pacific and the Americas.[32] Dengue hemorrhagic fever and dengue shock syndrome were first reported in Central America and South America in 1981.

History of the word[change | change source]

It is not clear where the word "dengue" came from. Some people think that it comes from the Swahili phrase Ka-dinga pepo. This phrase talks about the disease being caused by an evilspirit.[31] The Swahili word dinga is thought to come from the Spanish word dengue, which means "careful." That word may have been used to describe a person having bone pain from dengue fever; that pain would make the person walk carefully.[34] However, it is also possible that the Spanish word came from the Swahili word, and not the other way around.[31]

Other people think that the name "dengue" comes from the West Indies. In the West Indies, slaves that had dengue were said to stand and walk like "a dandy." Because of this, the disease was also called "dandy fever."[35][36]

The name "breakbone fever" was first used by Benjamin Rush, a doctor and United States "Founding Father." In 1789, Rush used the name "breakbone fever" in a report about the 1780 dengue outbreak in Philadelphia. In his official report, Rush mostly used the more formal name "bilious remitting fever".[37][38]

The term "dengue fever" was not commonly used until after 1828.[36] Before that, different people used different names for the disease. For example, dengue was also called "breakheart fever" and "la dengue."[36] Other names were also used for severe dengue: for example, "infectious thrombocytopenic purpura", "Philippine," "Thai," and "Singapore hemorrhagic fever."[36]

Research[change | change source]

Scientists keep doing research on ways to prevent and treat dengue. People are also working on controlling mosquitoes,[39] creating a vaccine, and creating drugs to fight the virus.[25]

Many simple things have been done to control mosquitoes. Some of these things have worked. For example, guppies (Poecilia reticulata) or copepods can be put in standing water to eat the mosquito larvae (eggs).[39]

Scientists also keep working on creating antiviral drugs to treat attacks of dengue fever and keep people from getting severe complications.[40][41] They are also working on figuring out how the virus's proteins are structured. This may help them create medications that work well for dengue.[41]

Notes[change | change source]

  1. 1.01.11.21.31.41.51.61.71.8Whitehorn J, Farrar J (2010). "Dengue". Br. Med. Bull.95: 161–73. doi:10.1093/bmb/ldq019. PMID 20616106. 
  2. 2.02.1WHO (2009), pp. 14–16.
  3. 3.03.1Reiter P (2010-03-11). "Yellow fever and dengue: a threat to Europe?". Euro Surveil15 (10): 19509. PMID 20403310. http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19509. 
  4. ↑Gubler (2010), p. 379.
  5. 5.05.15.25.3Varatharaj A (2010). "Encephalitis in the clinical spectrum of dengue infection". Neurol. India58 (4): 585–91. doi:10.4103/0028-3886.68655. PMID 20739797. http://www.neurologyindia.com/article.asp?issn=0028-3886;year=2010;volume=58;issue=4;spage=585;epage=591;aulast=Varatharaj. 
  6. 6.006.016.026.036.046.056.066.076.086.096.106.116.126.136.146.15Ranjit S, Kissoon N (July 2010). "Dengue hemorrhagic fever and shock syndromes". Pediatr. Crit. Care Med.12 (1): 90–100. doi:10.1097/PCC.0b013e3181e911a7. PMID 20639791. 
  7. 7.07.17.27.37.47.57.67.77.87.9WHO (2009), pp. 25–27.
  8. Knoop KJ, Stack LB, Storrow A, Thurman RJ (eds.) (2010). "Tropical Medicine". Atlas of Emergency Medicine (3rd ed.). New York: McGraw-Hill Professional. pp. 658–9. ISBN 0071496181. 
  9. 9.09.19.29.3Gould EA, Solomon T (February 2008). "Pathogenic flaviviruses". The Lancet371 (9611): 500–9. doi:10.1016/S0140-6736(08)60238-X. PMID 18262042. 
  10. 10.010.110.210.310.4Chen LH, Wilson ME (October 2010). "Dengue and chikungunya infections in travelers". Curr. Opin. Infect. Dis.23 (5): 438–44. doi:10.1097/QCO.0b013e32833c1d16. PMID 20581669. 
  11. Wolff K, Johnson RA (eds.) (2009). "Viral Infections of Skin and Mucosa". Fitzpatrick's Color Atlas and Synopsis of Clinical Dermatology (6th ed.). New York: McGraw-Hill Medical. pp. 810–2. ISBN 9780071599757. 
  12. ↑Kamel MG, Nam NT, Han NHB, El-Shabouny A-E, Makram A-EM, Abd-Elhay FA-E, et al. (2017) Post-dengue acute disseminated encephalomyelitis: A case report and meta-analysis. PLoS Negl Trop Dis 11(6): e0005715. https://doi.org/10.1371/journal.pntd.0005715
  13. ↑Gubler (2010), pp. 377–78.
  14. 14.014.1Center for Disease Control and Prevention. "Chapter 5 – Dengue Fever (DF) and Dengue Hemorrhagic Fever (DHF)". 2010 Yellow Book. Retrieved 2010-12-23. 
  15. ↑Wilder-Smith A, Chen LH, Massad E, Wilson ME (January 2009). "Threat of Dengue to Blood Safety in Dengue-Endemic Countries". Emerg. Infect. Dis.15 (1): 8–11. doi:10.3201/eid1501.071097. PMC 2660677. PMID 19116042. https://www.cdc.gov/eid/content/15/1/8.htm. 
  16. ↑Stramer SL, Hollinger FB, Katz LM, et al. (August 2009). "Emerging infectious disease agents and their potential threat to transfusion safety". Transfusion49 Suppl 2: 1S–29S. doi:10.1111/j.1537-2995.2009.02279.x. PMID 19686562. 
  17. ↑Teo D, Ng LC, Lam S (April 2009). "Is dengue a threat to the blood supply?". Transfus Med19 (2): 66–77. doi:10.1111/j.1365-3148.2009.00916.x. PMC 2713854. PMID 19392949. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-3148.2009.00916.x/full. 
  18. ↑Wiwanitkit V (January 2010). "Unusual mode of transmission of dengue". Journal of Infection in Developing Countries4 (1): 51–4. PMID 20130380. http://www.jidc.org/index.php/journal/article/view/20130380. 
  19. ↑Martina BE, Koraka P, Osterhaus AD (October 2009). "Dengue Virus Pathogenesis: an Integrated View". Clin. Microbiol. Rev.22 (4): 564–81. doi:10.1128/CMR.00035-09. PMC 2772360. PMID 19822889. http://cmr.asm.org/cgi/content/full/22/4/564. 
  20. 20.020.120.220.3Guzman MG, Halstead SB, Artsob H, et al. (December 2010). "Dengue: a continuing global threat". Nat. Rev. Microbiol.8 (12 Suppl): S7–S16. doi:10.1038/nrmicro2460. PMID 21079655. http://www.nature.com/nrmicro/journal/v8/n12_supp/full/nrmicro2460.html. 
  21. 21.021.1Rodenhuis-Zybert IA, Wilschut J, Smit JM (August 2010). "Dengue virus life cycle: viral and host factors modulating infectivity". Cell. Mol. Life Sci.67 (16): 2773–86. doi:10.1007/s00018-010-0357-z. PMID 20372965. 
  22. 22.022.122.222.322.422.5WHO (2009), pp. 10–11.
  23. 23.023.1WHO (2009), pp. 90–95.
  24. 24.024.124.2WHO (1997). "Chapter 2: clinical diagnosis". Dengue haemorrhagic fever: diagnosis, treatment, prevention and control(PDF) (2nd ed.). Geneva: World Health Organization. pp. 12–23. ISBN 9241545003. 
  25. 25.025.125.225.3WHO (2009), pp. 59–60.
  26. 26.026.1WHO (2009), pp. 32–37.
  27. 27.027.1WHO (2009), pp. 40–43.
  28. WHO media centre (March 2009). "Dengue and dengue haemorrhagic fever". World Health Organization. Retrieved 2010-12-27. 
  29. Neglected Tropical Diseases. "Diseases covered by NTD Department". World Health Organization. Retrieved 2010-12-27. 
  30. 30.030.1WHO (2009), p. 3.
  31. 31.031.131.2Anonymous (2006). "Etymologia: dengue". Emerg. Infec. Dis.12 (6): 893. https://www.cdc.gov/ncidod/eid/vol12no06/pdfs/etymology.pdf. 
  32. 32.032.132.232.3Gubler DJ (July 1998). "Dengue and Dengue Hemorrhagic Fever". Clin. Microbiol. Rev.11 (3): 480–96. PMC 88892. PMID 9665979. http://cmr.asm.org/cgi/content/full/11/3/480. 
  33. 33.033.1

Picture showing the symptoms of dengue fever

Few people, unless they travel with an electron microscope, would ever notice the egg of an Aedes aegypti mosquito. But the insects follow us nearly everywhere we go. Aedes can breed in a teaspoon of water, and their eggs have been found in tin cans, beer bottles, barrels, jugs, flower vases, cups, tanks, tubs, storm drains, cisterns, cesspools, catch basins, and fishponds. They mate in the dew of spider lilies, ape plants, guava trees, palm fronds, in the holes of rocks formed from lava, and in coral reefs. More than any other place, perhaps, Aedes aegypti thrive in the moist, hidden gullies of used automobile tires.

As adults, the mosquitoes are eerily beautiful: jet black, with white spots on the thorax and white rings on their legs. Yet Aedes are among the deadliest creatures on earth. Before a vaccine was discovered in the nineteen-thirties, the mosquito transmitted the yellow-fever virus to millions of people, with devastating efficiency. During the Spanish-American War, U.S. troops suffered more casualties from yellow fever than from enemy fire. The mosquito also carries dengue, one of the most rapidly spreading viral diseases in the world. According to the World Health Organization, dengue infects at least fifty million people a year. For the fortunate, a case of dengue resembles a mild form of influenza. But more than half a million people become seriously ill from the disease. Many develop dengue shock syndrome or a hemorrhagic fever that leaves them vomiting and, often, bleeding from the nose, mouth, or skin. The pain can be so excruciating that the virus has a commonly invoked nickname: breakbone fever.

There is no vaccine or cure for dengue, or even a useful treatment. The only way to fight the disease has been to poison the insects that carry it. That means bathing yards, roads, and public parks in a fog of insecticide. Now there is another approach, promising but experimental: a British biotechnology company called Oxitec has developed a method to modify the genetic structure of the male Aedes mosquito, essentially transforming it into a mutant capable of destroying its own species. A few weeks ago, I found myself standing in a dank, fetid laboratory at Moscamed, an insect-research facility in the Brazilian city of Juazeiro, which has one of the highest dengue rates in the world. A plastic container about the size of an espresso cup sat on a bench in front of me, and it was filled with what looked like black tapioca: a granular, glutinous mass containing a million eggs from Oxitec’s engineered mosquito. Together, the eggs weighed ten grams, about the same as a couple of nickels.

Oxitec, which is short for Oxford Insect Technologies, has essentially transformed Moscamed into an entomological assembly line. In one tightly controlled, intensely humid space, mosquitoes are hatched, nurtured, fed a combination of goat’s blood and fish food, then bred. Afterward, lab technicians destroy the females they have created and release the males to pursue their only real purpose in life: to find females in the wild and mate with them. Eggs fertilized by those genetically modified males will hatch normally, but soon after, and well before the new mosquitoes can fly, the fatal genes will prevail, killing them all. The goal is both simple and audacious: to overwhelm the native population of Aedes aegypti and wipe them out, along with the diseases they carry.

The engineered mosquitoes, known officially as OX513A, lead a brief but privileged life. The entire process, from creation to destruction, takes less than two weeks. The eggs, oval spheres no longer than a millimetre, are milky white when laid. Within a couple of hours they harden, forming a protective cuticle and turning shiny and black. Looking around the lab, I saw long white sheets lining the shelves; each sheet was covered in tens of thousands of pin-sized dots and resembled some sort of computer code. The eggs can survive that way for a year; after four days, however, they are plunged into jam jars filled with water at twenty-seven degrees Celsius—a temperature that enables the eggs to hatch in less than an hour.

“These mosquitoes are relatively easy to breed and cost almost nothing to transport,’’ Andrew McKemey, Oxitec’s chief field officer, said as he led me around the lab. McKemey, a lanky man who was dressed in a green madras shirt and khaki cargo pants, spends much of his time in Brazil, teaching local scientists how to manufacture the company’s prize product. The lab churns out about four million mutant eggs a week, and will soon increase production to ten million. “That’s a start,’’ McKemey said. “In theory, we can build hundreds of millions of mosquitoes in this place.”

The field trial, which began a year ago, is a collaboration between Moscamed, Oxitec, and the University of São Paulo. Preliminary results have been impressive: the group recently collected a sample of eggs in two neighborhoods where the engineered mosquitoes had been released, and found that eighty-five per cent of them were genetically modified. With a large enough number of those eggs, the Aedes population would fall, and so would the incidence of dengue. “This is not a panacea,’’ Giovanini Coelho, who coördinates the Brazilian Ministry of Health’s National Program for Control of Dengue, told me. “I am not saying this alone will solve the problem or that there are no risks. There are always risks—that’s why we start with small studies in geographically isolated neighborhoods. But people are dying here, and this mosquito is resistant to many insecticides. We really do need something better than what we have.’’

In Juazeiro, where few families remain unaffected by dengue, the Moscamed team and its mosquitoes are treated with reverence. The researchers drive around in white vans that have pictures of mosquitoes and the word transgenico painted on the side. They try to visit every house in areas where they release mosquitoes, to explain that OX513A “are friendly bugs that protect you against dengue” and that, because the scientists are targeting Aedes aegypti where they live, under sofas and in back yards, the engineered mosquitoes can kill their brethren without harming any other plant or animal.

It’s an elegant approach to a health crisis that threatens much of the world, but it will take more than biological success to make it work. That’s because OX513A is not like other mosquitoes. In fact, it’s like nothing else on earth—a winged creature, made by man, then released into the wild. Despite the experiment’s scientific promise, many people regard the tiny insect as a harbinger of a world where animals are built by nameless scientists, nurtured in beakers, then set loose—with consequences, no matter how noble the intention, that are impossible to anticipate or control. “This mosquito is Dr. Frankenstein’s monster, plain and simple,’’ Helen Wallace, the executive director of the British environmental organization GeneWatch, said. “To open a box and let these man-made creatures fly free is a risk with dangers we haven’t even begun to contemplate.”

There are more than three thousand species of mosquito, but the vast majority take no interest in us; they feed mostly on rotting fruit and other sources of sugar. Only a few hundred species, including Aedes aegypti, need blood to survive. (The males never bite, but without a blood meal the females would be unable to nourish their eggs.) Mosquito mating habits can be brutal. “In the most successful encounters, the pair may become so tightly locked together that the male has some difficulty escaping in the end,’’ the late Harvard entomologist Andrew Spielman wrote in his 2001 book, “Mosquito: The Story of Man’s Deadliest Foe.” “An unfortunate few males manage to get away only by leaving their sex organs behind.” Yet Spielman also noted that the briefest exchanges can be highly productive: “A single minute or so of passion allows her to produce all the fertile eggs she will ever lay.’’

There has never been a more effective killing machine. Researchers estimate that mosquitoes have been responsible for half the deaths in human history. Malaria accounts for much of the mortality, but mosquitoes also transmit scores of other potentially fatal infections, including yellow fever, dengue fever, chikungunya, lymphatic filariasis, Rift Valley fever, West Nile fever, and several types of encephalitis. Despite our technical sophistication, mosquitoes pose a greater risk to a larger number of people today than ever before. Like most other pathogens, the viruses and parasites borne by mosquitoes evolve rapidly to resist pesticides and drugs. Many insecticides once used against Aedes aegypti are now considered worthless.

Aedes aegypti is an invasive species in the Americas. It most likely arrived on slave boats from Africa in the seventeenth century, along with the yellow fever it carried. The mosquitoes bred easily in the casks that provided drinking water on sailing ships. During the eighteenth century, a severe yellow-fever epidemic swept through New England and Philadelphia, as well as other American port cities; it took another century to discover that mosquitoes were the bearers of the disease.

Traditional mosquito control all but eradicated Aedes aegypti (and the diseases it carries) from the United States fifty years ago. But globalization has been good to mosquitoes, particularly species like Aedes aegypti, which travel easily and can lie dormant in containers for months. In recent years, the mosquito and dengue have returned to Texas, Hawaii, and Florida. The disease has also been transmitted for the first time in France and Croatia. “We have dragged mosquitoes around the world in billions of used tires,’’ Paul Reiter told me. Reiter, a professor of medical entomology at the Pasteur Institute, in Paris, is one of the world’s experts on the natural history of mosquito-borne diseases. Before moving to France, he spent more than two decades in the Dengue Branch of the Centers for Disease Control, devoting a surprising amount of his time to studying tires. He found that they are ideal incubators for mosquitoes: tires absorb heat, trap rainwater, and nurture bacteria in the puddles they create. The exponential growth of dengue fever—the number of cases reported to the World Health Organization has increased thirtyfold since 1965—can, at least in part, be attributed to the enormous increase in tire exports.

Aedes aegypti don’t fly far or live long; a major traveller would move a few hundred yards and, on average, survive as an adult for ten days. But it is a particularly wily insect. Most mosquitoes are noisy enough to wake a sleeping man and slow enough that one bite is all they’ll get before escaping or being crushed with an angry swat. Aedes aegypti feed during the day and strike in silence; they mostly stay low to the ground, preferring to bite people in the ankles or legs. The mosquito is highly sensitive to motion—as you move, it will, too, often stabbing its victim several times during each feeding, depositing pathogens with every bite and, in turn, increasing its chances of picking up dengue from infected people to pass along to others. (Unlike most mosquitoes, which can lay hundreds of eggs in a single raft the size of a grain of rice, Aedes aegypti usually deposits its eggs in multiple locations, thereby raising the odds that some will survive.)

Dengue has always been considered a tropical illness. But its mode of transport, the mosquito, rarely lives more than a hundred yards from the vector’s principal source of sustenance—us—and as our demographics have changed so have those of the mosquito. Aedes aegypti has adapted to the city with great dexterity. Even the most effective modern larvicides often miss the mosquito’s well-hidden urban breeding grounds. “Dengue is a terrible disease, just terrible,’’ Reiter said. “Its danger is impossible to exaggerate. And none of the methods used right now for dengue control are working. None.’’

It is not easy for an egg to become an OX513A. Most were originally modified in Oxitec’s laboratories, in the English countryside not far from Oxford, where scientists, working with glass needles so small they can be seen only under a powerful microscope, insert two genes into eggs no bigger than a grain of salt. One gene carries instructions to manufacture far too much of a protein required to maintain healthy new cells; the results are lethal. Scientists keep the gene at bay, and the mosquitoes alive, by placing the antibiotic tetracycline in the insects’ food. The drug latches on to the protein and acts as a switch that can turn it on or off. As long as tetracycline is present, the mosquitoes live and reproduce normally and can be bred for generations. Once they are released from the lab, however, the antidote is gone; the lethal gene goes unchecked. Within days the males, along with any eggs they help to create, will perish. In fact, Oxitec has already modified all the Aedes aegypti eggs the world may ever need.

The other gene is a fluorescent marker—the molecular version of a branding iron—that helps distinguish normal mosquitoes from modified ones. The naked eye sees nothing, but under the microscope the larvae give off a rich red glow, like a soft neon sign. Most of the altered eggs will die. Others will fail to incorporate the new genes into their DNA; these are useless, because the process succeeds only when the genes work their way into the critical germ cells the eggs need to reproduce. The task is difficult and tedious: the technicians can go through thousands of eggs to hit on just one that will pass the new genes to the next generation of mosquitoes. But once a sufficient number of eggs have been correctly modified they can, after many generations, produce millions of mutant mosquitoes.

OX513A are raised in the relative splendor of the laboratory. After they hatch, they are moved from petri dishes to plastic tanks the size of a home aquarium. Males are fed sugar; females, first lured by the smell of human sweat, feed on goat’s blood obtained weekly from a nearby abattoir. “Thank God for that place,’’ McKemey said with a laugh. “You can’t make mosquitoes without blood.” He stood in the close quarters of the rearing room as all around him eggs were morphing into larvae, hatching in the type of long trays bakers use to store loaves of bread. Across the room, in transparent, water-filled pails covered with cheesecloth, thousands of larvae, known to biologists as wrigglers, were frantically trying to work themselves out of their cases and emerge as pupae, the final stage before becoming an adult.

Adolescent mosquitoes have enormous heads and prominent eyes; under the microscope they look like sea horses or miniature versions of E.T. While the mosquitoes are still sheathed in their cases, their transparent wings are pinned behind their bodies. By this point, the mosquito has begun breathing through its syphon, a curling, segmented tube that pokes above the surface of the water like a snorkel. When the moment is right, the pupae inhale, expand their abdomens, burst their cases, and emerge head first as adults. “It’s thrilling to see,’’ McKemey said, as we watched the young mosquitoes take their first tentative flights. “I never tire of it.”

The Oxitec mosquito grew out of a pest-control method called sterile insect technique, or SIT, which has been used for decades. Billions of insects, all sterilized by intense bursts of radiation, have been reared in laboratories like Moscamed and released to mate in the wild. In 1982, SIT, which prevents the organism from reproducing, successfully eradicated the screwworm—a parasite that attacks the flesh of warm-blooded animals—from North America. But radiation is difficult to use properly on insects as small as mosquitoes. Administer too little and they remain virile; zap them too powerfully and the insects are left so weak that they are unfit to compete for mates.

In the early nineties, Oxitec’s chief scientist, Luke Alphey, was investigating the developmental genetics of Drosophila, the common fruit fly. One day, Alphey, now a visiting professor of zoology at Oxford, bumped into a colleague who was talking about sterile insect technique. Alphey, who knew little about the field, began to think about how to supplant radiation with the practices of modern molecular biology. Alphey is reserved, with a mop of brown hair and pensive eyes; one can practically see his brain in motion as he works out a scientific problem. His goal was not exactly to sterilize the males but to alter their genes so that any progeny would die. If he could do that without using radiation, he reasoned, the insects should be fit to compete sexually for wild females.

Alphey faced several scientific hurdles. He would have to engineer only males. (Female mosquitoes bite, so genetically modified females could, in theory, pass novel proteins to humans, with unknown consequences.) “I was trying to think of ways around the radiation issue,’’ he said. “I wondered, What if the engineered lethal system could be sex-specific? It turns out that, with Aedes aegypti, females are considerably larger than the males. That was a lucky break, because it means you can easily separate them on the basis of their size.”

Once released, the males would have to live long enough to impregnate females, and they would need to be healthy enough to compete with wild males for the right to do so. “You want the insect to breed successfully in the lab but to be dependent on an antidote that will no longer be available in nature,’’ Alphey said. “It was difficult to know how to do that.’’ But chance again intervened: he happened to attend a seminar at which researchers described using tetracycline as a switch to turn off a gene. “The molecule prevents the deadly gene from working,” Alphey said. “It was a perfect solution.”

In 2002, Oxitec was spun off as a company apart from the university. Alphey began to speak at tropical-disease meetings and in dengue-infested countries; he also gathered support from private investors and public-health philanthropies, including the Gates Foundation and the Wellcome Trust. In 2010, the company ran a series of field trials in the Cayman Islands, releasing 3.3 million genetically altered mosquitoes on sixteen hectares of land. OX513A became the first engineered mosquito set free on the planet.

The number of wild Aedes aegypti mosquitoes in the area fell by eighty per cent in two months. It was only a test of feasibility; no one knew how it might affect the local ecology or whether it would actually reduce the incidence of dengue. Environmental activists feared that the release of engineered insects could set off a cascade of events that nobody would be able to control.

“They don’t know how it will function in the real environment,” Silvia Ribeiro, the director in Latin America for an environmental organization called the ETC Group, said. “And once they release it they can’t take it back.” In 2010, Oxitec began a smaller trial in Malaysia. But the Brazilian experiment has been the biggest test so far, and it has laid the groundwork for Oxitec’s battle over entry into the world’s most significant market: the United States.

In 2009, Key West, Florida, suffered its first dengue outbreak in seventy-three years. There were fewer than thirty confirmed cases—a trifling number compared with the millions who are infected each year in South America, Africa, and Asia. There are just twenty thousand full-time residents in Key West, but, with more than two million visitors each year, the town is highly dependent on tourists. I was there during spring break, which is not the best time to visit unless you have a particular interest in keggers, tequila, or Eagles cover bands.

“They feed this town,’’ a woman who runs a cigar stand told me as we watched scores of sunburned students work their way down Truman Street and head toward Jimmy Buffett’s bar, Margaritaville, ground zero for the aggressively laid-back Key West life style. “Sometimes it’s a little gross out there,’’ she said. “But take the tourists away and we are just a bunch of taco stands, bars, and beach bums.”

Even a small dengue outbreak in Key West would send a troubling message. After 2009, the Florida Keys Mosquito Control District added ten inspectors to join the battle against Aedes aegypti. In 2010, there were twice as many cases. “Clearly, we have the potential for serious dengue outbreaks,’’ Michael S. Doyle told me. Doyle, an entomologist, is the district’s executive director. He moved to Key West in 2011, after spending five years at the Centers for Disease Control. “Part of our problem is the image of dengue,’’ he said. “A couple of hundred cases here could be devastating to the tourist economy.

“Think about it,’’ he continued. “Somebody in Milwaukee is cruising through Web sites and asks his wife, ‘Where should we go on vacation, honey, Key West or some place in the Caribbean?’ And the wife says, ‘Hey, didn’t I hear something about dengue in Key West?’ ” We were sitting in a café not far from Ernest Hemingway’s house, the city’s most heavily visited tourist site. Like many public buildings, the café has open windows and no screens; mosquitoes danced in the air beside us. “We live with open doors and windows,’’ Doyle said. “And they live with us. We are an ideal host.”

Doyle is a soft-spoken man with rimless eyeglasses and a neatly trimmed mustache. He pointed out that, when it comes to contracting dengue, the way people live is as important as where they live: from 1980 to 1999, Texas reported sixty-four cases of dengue along the Rio Grande, whereas there were more than sixty thousand cases in the Mexican states just across the river. “The population of Aedes aegypti was actually larger in Texas,” he said. But Texans have screens on their windows (and keep the windows closed), drive air-conditioned cars, and spend little time outdoors.

Doyle wanted to lower the risk of a dengue outbreak in Key West, but the district was already spending more than a million dollars a year on insecticide, and he was loath to dump more chemicals in people’s yards. Then a colleague attended a meeting of the American Society for Tropical Medicine and Hygiene and told him about OX513A. “I remember thinking that if this actually worked we would win in every possible way,’’ he said. “Other approaches are more costly and more environmentally challenging. The data looked solid, and certainly we need to think differently about mosquito control than we have in the past.”

In March, Doyle invited Luke Alphey, Oxitec’s founder, and Hadyn Parry, its chief executive, to explain their approach at a town meeting. It would be the first in a series of hearings intended to explore the possibility of testing the mosquitoes in one relatively isolated Key West neighborhood. “I don’t really know what to expect,’’ Alphey told me early on the day of the meeting. “But I hope the people of Key West understand that they have been lucky. Because they are living in a sea of dengue.”

Opponents mobilized within hours of receiving notice of the meeting. Boldly colored flyers, stating that the mosquito-control board was “planning on releasing and testing genetically modified (manmade) mosquitoes on you, your family and the environment,’’ were pasted onto half the city’s walls.

Before the meeting, I ran into Chris O’Brien, an artfully dishevelled woman with shoulder-length hair and searching blue eyes. She was dressed in the peaches and pinks one associates with southern Florida. She was also wearing combat boots. O’Brien is a “conch,” a term that describes people who are born, raised, and spend their lives in Key West. Her children and grandchildren are conchs, too.

“People live with mosquitoes here,’’ she said. “We always have. We have had no dengue for two years and maybe, at most, we will have a few cases. It’s not a huge deal. Certainly not big enough to bring in an unnatural insect about which we know so little. You are in much more danger of being hit by a car.”

It is impossible to predict the likelihood of a dengue outbreak based on the number of past infections. All it takes is the presence of the mosquito and the virus. Key West has plenty of the former; the rest is a matter of aggressive pest control—and chance. Once infectious mosquitoes start biting humans, an epidemic can erupt within weeks, as the virus moves from vector to host and back again. O’Brien, like many of her fellow-protesters, had been briefed by the Friends of the Earth about the concept of introducing man-made creatures into the local environment. “How do we know the females won’t breed and bite people?’’ she asked. “They would have enzymes in their bodies that don’t exist in real life. What would happen if they bit us? Getting rid of dengue would be wonderful, of course, but what would happen if we did succeed and these mosquitoes simply vanished from the earth? Isn’t there a food chain to worry about?”

Those are reasonable concerns. But ecologists are quick to note that Aedes aegypti have been in America for only two hundred years or so; that’s not enough time for a species to make an evolutionary impact. Many biologists argue that if Aedes aegypti, or, indeed, all mosquitoes, were to disappear, the world wouldn’t miss them, and other insects would quickly fill their ecological niche—if they have one. “More than most other living things, the mosquito is a self-serving creature,’’ Andrew Spielman has written. “She doesn’t aerate the soil, like ants and worms. She is not an important pollinator of plants, like the bee. She does not even serve as an essential food item for some other animal. She has no ‘purpose’ other than to perpetuate her species. That the mosquito plagues human beings is really, to her, incidental. She is simply surviving and reproducing.”

Not everyone agrees with Spielman’s assessment. “Genetic modification leads to both intended and unintended effects,” Ricarda Steinbrecher, of EcoNexus, a not-for-profit, public-interest research organization based in England, says. In a lengthy letter to government regulators in Malaysia, she stressed that there could be ancillary impacts “if the mosquitoes are eliminated altogether.” For instance, what would happen to those fish, frogs, other insects, and arthropods that feed on larval or adult mosquitoes? “What if their interactions with other organisms in the environment change?” she wrote. “There is also the question of what will fill the gap or occupy the niche should the target mosquitoes have been eliminated. Will other pests increase in number? Will targeted diseases be able to switch vectors? Will these vectors be easier or more difficult to control?”

It would be irresponsible to deploy transgenic insects widely without adequate answers to those questions, but most have been addressed in environmental-impact statements and by independent research. If the results were put to the vote of biologists, the overwhelming response would be: the potential benefits far outweigh the risks. There are no birds, fish, or other insects that depend solely on Aedes aegypti. It doesn’t pollinate flowers or regulate the growth of plants. It is not what entomologists call a “keystone” species in the United States.

“It is frankly difficult to see a downside,’’ Daniel Strickman, the national program leader in veterinary and medical entomology at the Agricultural Research Service, told me. “My job is to try and prevent human disease by modifying behavior and killing mosquitoes. So I come at it from that perspective. I am biased against mosquitoes. And Aedes aegypti cause immense damage. Raging epidemics of dengue would affect our economy badly. Go back to the days of yellow fever in this country and it had real demographic consequences. Whole towns died. Life expectancies in certain areas were reduced.” Strickman added, “I look at this new approach and there is nothing greener. It’s targeted at one species. If the sole question is what will happen if we kill off this single species of mosquito, it doesn’t seem like a close call.”

Mark Q. Benedict agrees. Benedict, an entomologist at the University of Perugia, has researched genetically modified insects for years and written about them extensively. “There are unanswered questions and there always will be,” he said. “But there are also unanswered questions about the effect of insecticides on children, and we use them every day to try and kill the very same mosquitoes. It’s important to remember: we’re already trying to wipe this species out, and for good reason. The risk involved in eliminating them is very, very small. The risk in letting them multiply is enormous.”

Environmentalists have expressed concern about what might happen if some of the modified females survived and, while biting people, injected them with an engineered protein. Oxitec separates males from females, but, with so many mosquitoes, a few genetically modified females inevitably slip by—Oxitec puts the number at about one in three thousand. “This is a nightmare scenario, and we don’t have any published data that answers this question,’’ Eric Hoffman, a food-and-technology policy campaigner for Friends of the Earth, told me. Hoffman has assiduously followed the Oxitec experiments. Reiter says that none of the protein introduced into transgenic mosquitoes enters its salivary glands—which means it couldn’t spread to the humans it bites. In addition, he has recognized nothing in the genetic structure of the modified mosquitoes that could cause humans harm. But he and others are eager to see papers published, by groups unconnected to Oxitec, that confirm those conclusions.

The biggest question raised by the creation of OX513A is who will regulate it and how. In Brazil, a single government body—the National Technical Commission on Biosafety—oversees the approval of all genetically modified organisms. In the United States, however, the regulatory structure is far more complex. It’s not clear whether engineered mosquitoes will be regarded as animals, under the jurisdiction of the Department of Agriculture, or as drugs, governed by the Food and Drug Administration.

“I would be so eager to have a clear regulatory situation in the United States,” Alphey told me, his frustration at the process barely held in check. “We do not want to move forward unless one is properly in place.” To the consternation of many, Oxitec recently applied to the F.D.A. for approval of its mosquito. “We are concerned that Oxitec has been less than forthcoming in their statements to the public,’’ Hoffman told me. “They are saying that these mosquitoes are sterile, but they are not sterile, since they impregnate females. They are genetically modified, and the public needs to know that.” Oxitec does call its mosquitoes sterile, but has not denied that they are genetically modified; almost all their literature says as much. “There is no layman’s term for ‘passes on an autocidal gene that kills offspring,’ ’’ Alphey said. “ ‘Sterile’ is the closest common term. OX513A is sterile in very much the same sense as radiation-sterilized insects are sterile.” Hoffman stops short of calling Alphey’s message deceptive, but he certainly doesn’t agree. “This country just doesn’t have the law or regulations necessary to move this project forward right now,’’ he said.

In Key West, the Oxitec scientists, along with Doyle and his team from the mosquito-control district, faced a packed room at the Harvey Government Center. It was a warm, sunny day, and many in the crowd had left work early to be there. Doyle explained how a small experiment might proceed; Oxitec made its case; then the floor was opened to the public. The meeting quickly became emotional and, at times, rancorous. Oxitec—a small company that had emerged from a zoology department—was portrayed as an international conglomerate willing to “play God” and endanger an American paradise. The insects were referred to as “robo-Franken mosquitoes.” More than a dozen people rose to speak; none defended the project or noted that, if successful, it would reduce a health threat and ease the county’s heavy reliance on insecticides. Overwhelmingly, the people with whom I spoke said they assumed that this decision had already been made; the meeting was taken up with accusations of lies and secrecy. But nothing had been decided. Every question asked, at the meeting or later, in writing, was forwarded to state regulators for their consideration.

“It breaks my heart to think that you guys have the nerve to come here and do this to our community,” one woman said. “Anything genetically modified should not be touched. I have a feeling that”—she pointed to Doyle and his colleagues on the dais—“your minds are made up. I know it. I can just sense it. I feel the vibe.” She concluded to thunderous applause. Another speaker, Rick Worth, was even more direct. “I, for one, don’t care about your scientific crap,” he said. “I don’t care about money you spend. You are not going to cram something down my throat that I don’t want. I am no guinea pig.”

One afternoon before leaving Brazil, I found myself inching along the rutted dirt roads of a neighborhood called Itaberaba, with Aldo Malavasi, the highly animated director of Moscamed. Itaberaba is only a few miles from the center of Juazeiro, and, as we drove, loudspeakers on the front of the car announced our arrival. “We are here to talk about the transgenic mosquito project,’’ the speakers said. “We are here to explain this program to you and answer your questions.” Malavasi, a large and charismatic man, said, “There is only one way to get people on your side: talk to them. This is a new technology. It is scary. But it also carries tremendous possibilities. People are not stupid. You just have to tell them all of that. Lay it out so they can decide.” Moscamed has spoken to nearly everyone living in the affected areas. When a team leaves a house, they etch the outlines of a mosquito on the doorframe, so that colleagues will know which houses still need to be visited.

Bahia is one of Brazil’s most important fruit-growing regions. We passed warehouses full of guavas, mangoes, limes, pineapples, and papayas. The scent of rotted fruit filled the humid air. People live in small, brightly painted cottages in these towns, and it seemed that at least one member of every family had had dengue. It isn’t as hard to explain to them the value of a modified mosquito as it is of, say, modified corn. “You tell people you are messing with soybeans or corn and they get suspicious,’’ Malavasi said. “This is different. They have suffered.”

When it comes to genetic engineering, acceptance clearly depends on the product. Opponents often invoke a one-sided interpretation of the “precautionary principle,’’ which argues against introducing activities into the environment that, in theory, could cause harm to human health. The sentiment is difficult to dispute, but so is the fact that dengue fever strikes tens of millions of people every year, that the threat is growing, and that there is no treatment or cure. The worry about theoretical risks tends to overwhelm any discussion of possible benefits. Many people, particularly in the rich Western world, object to modified food, but such complaints are almost never aired against the same scientific process when it is used to make insulin or heart medicine. “Sometimes I despair of these issues,’’ Paul Reiter, who has advised Oxitec, told me. “The objections so rarely have anything to do with the science or the safety of the research. It is an opposition driven by fear. I understand that, but this technology has been used in a different form for years.” He was referring to sterile insect technique. “The Oxitec approach is safer and more environmentally benign,” Reiter said. “If the phrase ‘genetically modified’ was not attached, I don’t think people would even mind.”

Malavasi shrugged when I brought up the opposition. “I know this sounds like science fiction,’’ he said. “And I am not naïve. But to get rid of the virus, we have to get rid of the mosquitoes. And, at least in this small experiment, it’s working.’’ He noted that the name of the program, the Projeto Aedes Transgenico—the Transgenic Aedes Project—was not accidental. “We put the word ‘transgenic’ right in the name of the program for everyone to see,’’ he said. “We hide nothing.”

We had stopped at a random spot on an unmarked road. The heat was oppressive as we emerged from the car; a small stream burbled by the roadside. “We are in mosquito heaven,’’ Malavasi said. As he spoke, a team from Moscamed began unloading several casserole-size Tupperware containers from the back of their van. The containers had white plastic lids, and one by one they were flipped open, releasing thousands of male mosquitoes. Each time a top was removed, scores of the tiny insects would alight, briefly, on the researchers’ bodies—not to bite but to orient themselves. It was the first time they had experienced freedom. For a moment, they seemed reluctant to fly away. Then, almost as a unit, they would lift off and, after hovering for a few seconds in the moist afternoon air, form a kind of flying carpet, and set off to fulfill their destiny. ♦

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