Vector-borne plagues of the twenty-first century.

Robert Gwadz1


Many of the vector borne diseases which now affect the human race were present as zoonotic infections before our ancestors were recognizable as human. Many more remained as diseases of animals until they and their vectors expanded their range of pathogenicity. Three of the most feared, malaria, bubonic plague and epidemic typhus had extraordinary influence on the evolution of the human race and all have had important roles in human history [1].


The most devastating of the ongoing pandemics is malaria (Figure 1) [2, 3]. It was suggested by Baruch Blumberg, the Nobel Laureate, that “as many as half of all human deaths since the beginning of time could be attributed to malaria” and today it is estimated that somewhere in the world a child dies of malaria every 30 seconds. Malaria is a disease caused by infection with single-celled protozoa of the genus Plasmodium. There are four species of the parasite that infect humans, P. falciparum, P. vivax, P. ovale and P. malariae. A fifth species, P. knowlesi, a parasite found in monkeys in South East Asia, has recently been identified as a significant infection in humans. P. falciparum is the most pathogenic of the malarias and responsible for most deaths.


Figure 1. Malaria – key affected areas (map created using http://www.worldmalariareport.org/)
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Malaria is transmitted from person to person through the bites of infected mosquitoes of the genus Anopheles. This is a large and varied group of mosquitoes with a complex array of habits and behaviours. Every region has its own group of anopheline vectors with varying degrees of man biting and vector efficiency (Figures 2, 3). There is a wide range of antimalarial drugs which can protect from or cure malaria. The first antimalarial drug was quinine, an extract of the bark of the South American chinchona tree. The active principal of quinine was isolated in 1820 and for years was the only drug available. In the second half of the 20th century a number of synthetic antimalarials were developed. Parasite resistance has rendered many of these ineffective. The rediscovery of the herbal remedy qinghao su (first recorded in China in 200 BC) by Chinese scientists led to the Nobel Prize for Tu Youyou in 2015. Artemisinin was extracted from the common Sweet Wormwood weed, Artemisia annua. Artemisinin and its derivatives in combination with a number of known antimalarials now represent the standard of treatment for malaria. However, reports of P. falciparum resistant to these combinations in Cambodia are a source of great concern. There are no vaccines for malaria at present. Several candidate vaccines are undergoing clinical trials in the laboratory and in the field, and there is general optimism that an effective malaria vaccine may be available within the next few years.


Figure 2. Anopheles dirus, one of the primary vectors of malaria in SE Asia. The mosquito is pictured feeding on the author’s arm.
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Figure 3. Anopheles gambiae, the primary vector of malaria in sub-Saharan Africa, pictured feeding on the arm of the author.
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Malaria pathology is extraordinarily complex and varied. The classic symptoms are the periodic chills and fever which can begin 10 to 14 days after the bite of an infected mosquito. The 48 hour cycle of development of P. falciparum produces a rapid increase in the number of parasitized erythrocytes. In pregnant women theses parasitized erythrocytes adhere to endothelial cells and can cause blockage of placental capillaries resulting in foetal wastage, low birth weight, stillbirth or spontaneous abortion. In adults, but more frequently children, blockage of cerebral capillaries causes “cerebral malaria” with resulting seizures, coma and frequent death. Survivors of a bout of cerebral malaria may suffer permanent neurological damage. Low level persistent malarial infection can produce anaemia and predisposition to death from otherwise mild diseases such as measles.

Malaria can be controlled by attacking the mosquito vector, usually with insecticides in programs of indoor residual spraying, reducing contact with night-feeding mosquitoes with insecticide impregnated bed nets, and the use of drugs for prevention or treatment and cure. None of the control strategies can work alone and at best are only partially successful.

Bubonic plague

Bubonic plague is a bacterial infection of rodents caused by Yersinia pestis [4-6]. As a zoonosis it is found in numerous rodent species around the world and is transmitted from animal to animal by various species of fleas. In rats, the usual vector is the oriental rat flea, Xenopsylla cheopis (Figure 4). It is from the rat and its flea that human infections usually result [5].


Figure 4. Xenopsylla cheopis, the oriental rat flea, the primary vector of the plague bacterium from infected rats to humans (source: CDC, US Gov.).
[please click on the image to enlarge]

Three major epidemics of plague have been recorded. The First, the Plague of Justinian occurred in the 6th century and resulted in the death of 25 to 50 million people over two centuries in the Eastern Mediterranean area. The Second plague, 1340-1400 entered Europe through Constantinople and spread across the continent. It is estimated that between 75 and 200 million people died, between 30 and 60% of the total population of Europe. It is interesting to note that Warsaw and its environs were spared from the plague. In 1771, plague struck Moscow and over 100 000 died, 1/3 of the population of the city. This was the last major plague epidemic in Eurasia. The Third pandemic of plague originated in Eastern China in the 19th century. By 1896 it had spread into India where over 12 million perished. In 1898 the plague moved to Hawaii, then on to Australia and the USA.

There are three major manifestations of the infection in humans. The classic bubonic plague, usually results after the bite of an infected flea. The bacteria multiply and spread through the lymphatic system. Chills, malaise, high fever, seizures, and characteristic painful swelling of lymph glands causing buboes, the pathognomonic sign of bubonic plague. Septicemic plague can result from contact with infected tissues and fluids from dead animals or human victims and results in an infection of the circulatory system. Pneumonic plague occurs when the bacteria invade the respiratory system. This form is rare, but highly contagious and usually fatal.

Epidemic typhus

Epidemic typhus or louse-borne typhus is a rickettsial (bacterial) disease of humans. There is no regular animal reservoir for the typhus organism Rickettsia prowazekii, although flying squirrels in the eastern United States have been found to carry the infection. The human body louse, the insect vector, Pediculus humanus humanus (Figure 5) is present only on humans and is a common ectoparasite throughout the world.


Figure 5. Pediculus humanus humanus, the human body louse, the primary vector of the epidemic typhus rickettsiae from human to human (source: CDC, US Gov.).
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Epidemic typhus is usually associated with disruptions in human behaviour. Wars, prisons, concentration camps, famines, and home-lessness all create situations in which the louse vector can thrive. Confined living eases the movement of the wingless louse from person to person. Because the louse is normally found on clothing, while moving on and off the body to feed, the inability of the human host to regularly change and wash clothing facilitates the louse’s explosive ability to feed and multiply. Unlike most blood feeding insects, the infected louse does not inject the pathogenic organisms while feeding. Rather, the rickettsiae growing in the louse gut are defecated on the skin and scratched into the site of the bite.

Typhus has an illustrious past and has had a major effect on human development and history [4]. The Plague of Athens (430 BC) was most certainly epidemic typhus. In England (1577 to 1579), 10% of the population was killed by typhus. Napoleon’s Grand Armée, marching from Poland to Moscow in 1812 was destroyed, not by Russian arms, but by epidemic typhus. During the First World War typhus killed 3-4 million people in Russia, Poland and Romania. The Serbian army suffered over 150 000 deaths in the trenches where crowding of troops was the norm. An additional 3 000 000 typhus deaths were recorded during the Russian Civil War (1918-1922) [7, 8].

In World War II (WW II), typhus was a recurring problem in the German Army in Russia and in civilian populations in North Africa. It is estimated that among inmates of German concentration camps, typhus was the primary cause of death. Anne Frank and her sister died of typhus while in the Bergen-Belsen concentration camp.

Toward the end of WW II and afterward in refugee camps, typhus epidemics were prevented by the use of the new “wonder drug” DDT by Allied public health programs. DDT powder could be sprayed into the clothing of individuals effectively killing body lice before they could become a problem (Figure 6).


Figure 6. US Army soldier spraying DDT into clothing of refugee to kill body lice and prevent transmission of typhus (source: US Army).
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The symptoms of epidemic typhus include severe headache, sustained high fever and severe muscle pain. A rash begins to cover most of the body around five days after the fever.

Epidemic typhus infections can be effectively treated with a number of antibiotics including azithromycin, doxycycline, tetracycline and chloramphenicol. Vaccines for epidemic typhus have been developed but are not currently available. Personal hygiene, regular changing and washing of clothing, is the most effective weapon against the louse. Resistance to DDT in the body louse is now common. Other compounds, including 1% permethrin, are regularly available. Oral ivermectin appears to be effective against lice as a systemic insecticide.

These three great plagues of history are very much with us today. Malaria remains one of the greatest scourges of the human race. It kills today as it has throughout the ages, infects millions annually, and continues to be a major impediment to development in the poorer parts of the world. Bubonic plague remains a persistent epizootic in many countries including the USA with the potential for re-emergence as a human disease at any time. Epidemic typhus smoulders with the capacity to erupt given the right conditions During the 1997-98 war in Burundi, 500 000 cases of typhus were reported mostly among refugees [9].

Arbovirus infections–the new plagues

The arboviruses (AR-arthropod, BO-borne) are a large and diverse group of organisms transmitted by mosquitoes, sandflies and ticks. Over 600 arboviruses have been described and characterized to date. More than 100 of these can infect humans. Arboviruses normally infect vertebrate animals and in most cases the infections are transmitted from animal to animal. In many cases, the virus can also be transmitted through the vector to its offspring, via transovarial transmission. Humans are usually a dead-end host for the virus. However, with some of the viral species, human to human transmission is the rule.

Yellow fever

Yellow fever (YF) is a flavivirus which causes hemorrhagic fevers and high mortality. There are two cycles of YF infection. A sylvatic cycle sees the virus circulating between monkeys, primarily in Africa, but since the time of European exploration, in monkeys in South and Central America, and transmitted by forest dwelling mosquitoes. A second cycle involves urban transmission where Aedes aegypti and Ae. albopictus are the primary mosquito vectors. When individuals are infected in the forest and return to an urban setting, transmission is initiated as an urban cycle. YF has had a major effect on human development. The parasite and its Ae. aegypti mosquito vector arrived in the New World with colonists and their slaves. The first recorded epidemic was in the Yucatan, Mexico in 1648. Epidemics have been reported as far south as Uruguay and Chile and as far north as Quebec, Canada. YF was a recurring problem in the American colonies during the Revolutionary War. In 1730, YF broke out in Cadiz Spain with over 2000 cases and infections quickly spread to French and British seaports. The French attempt to build a canal through the Isthmus of Panama in the 1900s was stifled by yellow fever and malaria.

The WHO estimates that today, 900 million people live at risk to YF infection (Figure 7). In the last decade these populations have seen over 200 000 cases per year and have averaged 80 000 deaths per year. In 2013, Africa recorded 170 000 cases and over 60 000 deaths. In December 2015, major YF outbreaks were reported in Angola and the Democratic Republic of the Congo. In South America in 2016, YF has been reported in Brazil, Colombia and Peru. Clearly, yellow fever remains very much a major public health problem.


Figure 7. Countries currently endemic for yellow fever (source: WHO).
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Yellow fever in Asia. One of the mysteries of international public health concerns the absence of yellow fever in Asia. Ae. aegypti, the most efficient and aggressive of the YF vectors, is common in Asia and regularly transmits other arboviruses. There is a significant movement of Chinese businessmen and labourers to and from Africa. The Chinese government recently recorded a case of YF in an unimmunized citizen returning from Angola. Public Health authorities in China and India are well aware of the dangers posed by a YF introduction and transmission in the region.

The signs and symptoms of YF start 3-6 days after the infectious bite and include high fever, chills, headache, muscle aches, backache and vomiting. After a brief recovery, the patient may experience shock, bleeding, kidney failure and liver failure. The case fatality rate may reach 50%. There are diagnostic blood tests for YF. There is no specific treatment for the infection. Supportive therapy should be administered as necessary.

There is an effective vaccine for yellow fever. Dr. Max Theiler of the Rockefeller Foundation produced a live attenuated virus, strain 17D, in 1938. He received the Nobel Prize for his work in 1951. The 17D vaccine may give life-long protection, although revaccination is needed every 10 years. Most countries in the endemic zones require proof of immunization for admittance as do countries in Asia like China and India.

Control of the mosquito vectors coupled with immunization are the most effective tools for controlling YF. The primary vector of YF is Ae. aegypti, originating in Africa and spread across the tropical and sub tropical world, in sailing ships in the earliest days of exploration (Figure 8). This mosquito feeds almost exclusively on humans, and feeds outdoors, usually in the early evening or early morning. It is an urban, container-breeding mosquito which lays its eggs in small water-filled containers such as flower pots, bird baths, house gutters, metal cans, and discarded tires among others.


Figure 8. Aedes aegypti, the yellow fever mosquito, the primary vector of yellow fever, dengue, chikungunya and Zika infections. Note the lyre and two string pattern on the thorax of the mosquito (source: CDC, US Gov.).
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At the house by house level, keeping these containers water free and empty is the most effective way to control mosquito breeding. Ae. albopictus is a less efficient secondary vector of YF (Figure 9).


Figure 9. Aedes albopictus, the Asian tiger mosquito. This is a very invasive species severing as an important secondary vector of yellow fever, dengue, chikungunya and Zika infections. Note the single stripe on the thorax (source: Vichai Maikul, Department of Entomology/Smithsonian Institution).
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It has container breeding habits similar to Ae. aegypti but is more peri-urban in its habitat prefence. Ae. albopictus is native to Asia and was introduced into North America in 1985. Thereafter it has spread rapidly and has become established in South and Central America, Europe and Africa. For personal protection mosquito repellants containing DEET can reduce contact with the vector. Although the breeding sites of these two mosquito species are confined and well defined, they are particularly hard to control.

Dengue fever

Dengue fever, often referred to as “breakbone fever” is the most common of the arthropod-borne viruses with more than 400 million cases worldwide each year. Dengue has resurged in the 21st century and is now endemic throughout Asia including India (20 000 cases in 2016), China, Japan, Thailand, Cambodia, Indonesia and Malaysia. In spite of highly organized mosquito control programs, dengue continues to plague Singapore. Dengue is endemic in most countries of Africa where it is generally under recognized and underreported. Central and South America are experiencing a major epidemic at the present time. Brazil reported over 1.5 million infections in 2015. There have been over 1.2 million cases in the first four months of 2016. In Europe, dengue is not uncommon, but usually in travellers and tourists returning from endemic areas such as Madeira (Figure 10).

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Figure 10. Countries where dengue fever is currently endemic (source: WHO).
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The signs and symptoms of dengue are many and varied and often may be clinically indistinguishable from influenza, measles and rubella. Symptoms appear 1 to 8 days after the infectious mosquito bite and include high fever, headache, rash, retro-orbital pain, myalgia, arthralgia, and bone pain (thus the name “breakbone fever). There is no specific anti-viral treatment.

There are four serotypes of the dengue virus in circulation. Reinfection with a second serotype may lead to a very severe and often fatal manifestation called Dengue Hemorrhagic Fever (DHF). DHF was first described in the Philippines in 1953. The spread has been rapid although not yet reported from Africa. There are over 500 000 cases of DHF annually with at least 25 000 deaths. Symptoms of DHF are similar to regular dengue with the addition of hemorrhagic tendencies, thrombocytopenia, plasma leakage, weak rapid pulse, narrow pulse pressure, and cold clammy skin.

There is no vaccine for dengue at this time but several candidates are in the final stages of clinical trial and may reach the market soon. Because of the four dengue serotypes, any vaccine must be effective against all four.

Dengue is transmitted by the same mosquitoes that transmit yellow fever, Aedes aegypti and Ae. albopictus. Consequently the same vector control strategies and personal repellant strategies must be employed.


Chikungunya is an alphavirus of the family Togaviridae. The name derives from the Makonde language and means “that which bends up joints” referring to the characteristic contortion of the back and limbs of an infected individual. The disease was first described in Tanzania in 1952, and the virus isolated and characterized. Like many viruses it is maintained in a sylvan monkey to monkey cycles of transmission by forest dwelling mosquitoes. The WHO estimates that there are over 3 million cases annually with a case fatality rate of less than 1%.

The movement of the chikungunya virus around the world is sobering example of how an infectious disease can invade new territories. After its discovery during an outbreak in East Africa in 1952, the disease remained in its sylvan cycle. However, in 2005 it began to move. In 2006 it was reported in La Reunion Island in the Indian Ocean. By 2006 it was established in India and by 2008 was endemic throughout most of South East Asia. In 2007, chikungunya transmission was reported in Ravenna, Italy (probably via India) [10] and then in France (from Africa) and Croatia (again from India). Outbreaks of the diseases where first reported in Central America and the Caribbean Islands in 2013 with occasional cases in the USA. By 2014 the virus was established in South America. In India there have been over 1.5 million cases of chikungunya infection since 2005. There have been over 1.5 million cases in the Caribbean and South American since 2015 (Figure 11).


Figure 11. Areas where chikungunya fever has been introduced since the year 2000 (source: CDC, US Gov.).
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Chikungunya disease is characterized by high fever which appears 3 to 7 days after the infectious mosquito bite. Fever is accompanied by headache, myalgia, conjunctivitis, nausea and a muculopapular rash. Joint swelling, arthritis and polyarthralgia are common. Long term musculo-skeletal pain may persist for years after the initial infection. In rare cases the CNS may become involved. There is no specific anti-viral treatment. There is no vaccine available for this disease; several vaccine candidates are in clinical trials.

Chikungunya is normally transmitted by Aedes aegypti and Ae. albopictus much like dengue and yellow fever. Ae. albopictus is the more likely vector in more temperate regions. Mosquito control (difficult) and use of repellants for personal protection are advised.

West Nile fever

West Nile is an arbovirus caused by a flavivirus transmitted by mosquitoes of the Culex pipiens complex. This is a virus which normally infects birds, but can secondarily be transmitted to a number of animals. Horses are particularly sensitive to infection. The normal cycle for this virus is from bird to bird with transmission to other animals incidental and usually a dead end. The virus was first isolated and described from the West Nile region of Uganda in 1937. The virus remained unremarkable until an outbreak of the infection in Algeria in 1994. Thereafter, the virus began a rapid spread from its African base to Asia, Europe and beyond. There was a major outbreak in Romania in 1996 (Figure 12).


Figure 12. Countries where West Nile virus is endemic (source: CDC, US Gov.).
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Clearly the most dramatic event was the discovery of West Nile fever activity in New York City in 1999. By 2001 the virus could be detected in most Northeastern States and by 2011 was present in all of the continental USA, Canada and Mexico. 2012 was the worst year in the USA with over 2 000 cases and 286 deaths. The most dramatic manifestation of the early years was the massive killing of birds, particularly crows and bluejays and other members of the bird family Corvidae. As the virus became a more stable, endemic entity, the birds became resistant and flocks are now back to pre infection levels. The signs of West Nile virus infection are typical for most arboviruses: high fever, headache and stiff neck. These symptoms may be followed by confusion, tremors, convulsions, paralysis, coma and sometimes death. There are no antivirals for treatment. Vaccines have been developed for horses and are commercially available. A human vaccine has been developed, but there appears to be little interest in the vaccine industry for production.

The mosquito vectors of the West Nile virus are members of the Culex pipiens complex (Figure 13) and can be found throughout Europe, North America and Asia. Cu. pipiens quinquefasciatus is found across the circum-tropical regions of the world. A large number of other mosquito species have been found infected with the virus, but it is unclear if they are involved in transmission to humans.


Figure 13. Culex pipiens, the most common vector of West Nile virus in temperate climates (source: CDC,US Gov.).
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Cu. pipiens mosquitoes can breed in a wide variety of sites. From flower pots, wash tubs to abandoned swimming pools to cess pits and latrines, this mosquito has a high tolerance for pollution. It is primarily an indoor, night feeding species: Cu. pipiens is called the “Northern House Mosquito”.

Repellents, long sleeved shirts and mosquito nets can provide some degree of personal protection. Insecticide sprays and treatment or removal of standing water can reduce breeding.

Zika virus

In 1947, a routine surveillance for yellow fever virus in the Zika forest in Uganda detected a previously unknown flavivirus. It was isolated from a sentinel rhesus monkey [12]. Rhesus monkeys are not native to Africa but are very sensitive to infection with arboviruses. A sentinal animal is one confined in an area where it may likely be infected by forest mosquitoes. The virus was named Zika for the location of its discovery. In 1948, an Aedes africanus mosquitoes was found carrying the Zika virus in the same area. Ae. africanus is closely related to Ae. aegypti, it is commonly involved in the sylvan (forest) cycle of transmission from monkey to monkey for a number or arboviruses. In the ensuing decades, the Zika virus was occasionally found in arbovirus surveys across Africa. Sporadic human infections were reported, but symptoms were mild and unremarkable. Beginning in 1969, the Zika virus began to appear in surveys in Asia and by 1983 could be found in India, Indonesia, Malaysia and Pakistan. Serosurveys showed widespread human population exposure, but little disease: infections usually were mild or showed no symptoms. A total of 14 cases of Zika virus infection were reported across Asia during this period.

The first significant outbreak of Zika was on the Micronesian island of Yap in the Pacific north of New Guinea in 2007. There were 185 documented cases in a population of 11 250 people. A subsequent sero-survey showed that 73% of the island’s population had been infected. There were no deaths, no hospitalizations and no neurological complications from these infections. There are no monkeys on Yap so we must assume human to human transmission. The most likely vector was Aedes hensilli, a close relative of Ae. aegypti, with container breeding, human feeding, domestic dwelling habits.

In 2013, 2014 the virus jumped 5 000 miles across the Pacific Ocean to the islands of French Polynesia, Easter Island, the Cook Islands, and New Caledonia (Figure 14).


Figure 14. Countries where Zika virus is endemic or has been introduced since 2000 (source: CDC,US Gov.).
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The documented infections were generally mild although there were reports of congenital malformations, Guillain-Barré syndrome, and severe neurological and autoimmune complications. The relationships of these complications to Zika infections were confounded by a concurrent dengue outbreak on the islands. Evidence for potential sexual transmission of the virus and probable transplacental transmission also appeared.

In early 2015, the most devastating spread of the virus occurred when Brazil initially suffered an outbreak of an illness characterized by skin rash. There were over 7 000 cases in the northeastern states of the country. It was only later that the infection was shown to be caused by the Zika virus. Given that more than 80% of Zika infections can be very mild or asymptomatic, the number of infections was certainly much higher than reported. By the end of 2015, Brazilian health authorities estimated that there had been between 500 000 and 1.5 million Zika infections. Brazil has stopped counting. By the end of 2015, Zika had spread to 26 countries in the Americas and to the Cape Verde Islands off the coast of West Africa. Columbia, to the west of Brazil, reported over 20 000 cases. The Zika epidemic has continued into 2016. The concerns regarding Zika and the 2016 Brazil Olympic Games proved unfounded. No cases of Zika were reported in visitors to the games.

The primary signs and symptoms of Zika virus infection are similar to many of the flaviviruses. Most infected individuals show no symptoms, but 20% may show an exanthematous rash, fever, arthralgia, myalgia, headache and conjunctivitis. A worrisome symptom of this new epidemic is the post infection appearance of Guillain-Barré syndrome [13], a usually rare autoimmune disease in which nerve cells are damaged. The syndrome can sometimes lead to paralysis and death. More ominous is the association of Zika infection in pregnant women with congenital birth defects, miscarriage and the birth of babies with microcephaly [14]. Prior to 2015, microcephaly was relatively rare in Brazil and usually associated with a mother infected with diseases like herpes, cytomegalovirus or syphilis. Health officials estimate about 500 cases of microcephaly per year prior to Zika. To date, Brazil has recorded over 2 000 cases of microcephaly associated with Zika. The relationship between Zika and microcephaly is not clear and may require a coinfection or a nutritional component. Most of the 2 033 cases of microcephaly in Brazil have been confined to the northeastern states of the country. In nearby Colombia, on the northwest border of Brazil, there have been about 100 000 diagnosed Zika infections and only 46 cases of microcephaly.

There are no antivral drugs which can be used to treat the Zika infection. There are no vaccines for Zika, but a number of candidates are in advanced stages of evaluation.

Zika control has focused on control of the mosquito vector. As with yellow fever, dengue and chikungunya, Ae. aegypti and Ae. albopictus are the primary vectors in the Americas, Africa and Asia [15]. Other related Aedine mosquitoes of the sub-genus Stegomyia may also have the capacity to transmit the disease. As noted above, mosquito control can be relatively effective and consists primarily in removing the water filled containers in which these mosquitoes lay their eggs.


From the dawn of time, vector transmitted infectious diseases have infected humans, caused extraordinary levels of morbidity, and with regular epidemics, uncountable mortality. The great plagues of the past are still very much with us. To these ancient scourges, we have been constantly adding new ones. Now, in the 21st century, with modern medicine, vaccines, and public health awareness, we still find ourselves falling victim to new and deadly outbreaks.

The reasons for these new threats are many and varied. There are many diseases, endemic or dormant for centuries in one region of the world when given the opportunity, jump to another region where the ecology is more hospitable and the hosts non-immune or genetically predisposed to infection. There are hundreds of arboviruses described but considered of no threat [16]. There are probably thousands of arboviruses that have not yet been described. The Zika virus was considered a mild pathogen in Africa when discovered in 1947. Today, 60 years later, it is a major cause of disease in the Americas and a major threat in Asia.

Likewise, the vectors have the capacity to move and establish themselves in new regions. Aedes albopictus was introduced into the United States in 1985 and quickly spread throughout the eastern and southern states. It is considered the most efficient among the invasive mosquito species. It is second only to Ae. aegypti in its capacity to transmit yellow fever, dengue fever, chikungunya and Zika. It was solely responsible for the outbreaks of dengue in Hawaii in 2011 and 2015/16 and the transmission of chikungunya in Italy in 2007. Aedes japonicus, the Asian Bush Mosquito, is another fiercely invasive mosquito species. It is native to Japan and Korea where it is a major vector of Japanese encephalitis, a flavivirus related to the West Nile virus. It was first found in New York and New Jersey in 1998 and has spread across the whole of the eastern US to the Mississippi River and as far north as Hudson’s Bay in Canada. It was discovered in northern France in 2000 and is now found in Austria, Belgium, France, Germany, the Netherlands, Russia and Slovenia. This mosquito has been shown to be capable of transmitting chikungunya, dengue and West Nile in addition to Japanese encephalitis and should be able to transmit the Zika virus.

Infectious diseases know no borders. Universal air travel can move infected human or animal hosts from continent to continent in a matter of hours. The insect vectors travel with equal ease. Finally, major environmental and habitat changes are underway. Deforestation, urbanization, refugee migration and global climate change all contribute toward creating new habitats for pathogen and parasite alike. We are only at the beginning of an age of new infectious diseases.


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Conflict of interest: none declared

Author's affiliation:
1Captain, US Public Health Service (ret.)

Corresponding author:
Robert W. Gwadz, PhD
7108 Fairfax Rd.
Bethesda, MD
e-mail: Rwgwadz@comcast.net

To cite this article: Gwadz RW. Vector-borne plagues of the twenty-first century. World J Med Images Videos Cases 2016; 2:e44-60.

Submitted for publication: 04 November 2016
Accepted for publication: 23 November 2016
Published on: 12 December 2016

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