Arboviruses (arthropod borne) are RNA viruses transmitted by insect vectors. Birds and mammals are the natural hosts, with the biting and sucking insects picking up and carrying the viruses. Arboviruses are often associated with a range of diseases known to produce changes in the brain or cause small hemorrhages. There are more than 520 known arboviruses of which about 100 cause disease in humans – most with mild or no apparent symptoms. Others that do cause symptoms include the following: encephalitis, yellow fever, denge fever, numerous tropical fevers (mayaro, kyasanur, bunyamwere, marituba, punta toro, candira, etc.), chikungunya (meaning ‘that which bends up’), and o’nyong-nyong (meaning ‘weakening of the joints’), which are similar to denge fever found in Africa and Asia. The most common carriers of these diseases are the Aedes aegypti variety of mosquito, ticks, sand flies. Other less common carriers are flies and mites.
In Africa, there are three viral hemorrhagic fevers that occur:
- Dengue fever, which is mosquito-borne
- Yellow fever, which is also mosquito borne
Filoviruses are filamentous viruses that are tentatively classified in a family called Filoviridae. Two have been identified so far. One is called the Marburg virus, with a mortality rate of 25%; and the other is called Ebola, with a 90% mortality rate. They are the most lethal viruses known to date. Ironically, the Ebola virus is shaped like a question mark since not much is known about this virus. The Marburg virus is rod-shaped and can roll up tightly for protection. The virus that causes Ebola attacks every single organ and tissue in the human body, except skeletal muscles and bone. Rapidly, it turns the body tissues into a predigested slime. A new type of Ebola has emerged called Ebola Côte d’Ivoire. The virus causes such severe illness and high mortality in chimpanzees that these animals are clearly not the natural hosts for the virus as some have tried to lead others into believing.
Dengue Fever is a viral disease transmitted by mosquitoes (particularly Aedes aegypti), and is the Spanish name for a similar Swahili disease called ‘Kidenga pepq.’ It was also known as ‘break-bone fever’ at the time that it reached the US in the late 1700s. Dengue fever is second only to malaria among the insect-borne diseases. Symptoms of infection include the following: a sudden high fever, nausea, vomiting, horrendous headache, pain in the muscles and joints, and a rash that appears after a twenty-four-hour pause in the fever. Victims often develop a mincing walk to lessen the excruciating pain in their joints. Convalescence is symptomatic, with treatment involving complete bedrest and an increased fluid intake.
A far more dangerous form is the dengue hemorrhagic fever. It first appeared in the 1950s in Thailand and the Philippines, and, later, in Cuba, India, and Venezuela. It is thought that these were once confined to each geographic area, but, with modern travel, the four types have evolved into one. Another Aedes mosquito (A. albopictus, or Asian Tiger) can also transport the dengue microbe. In 1985, it arrived in Houston from Japan, and is now well established in almost half the states. Although this mosquito has not been found to carry the dengue microbe thus far, another dangerous arbovirus, eastern equine encephalitis, has been found on the mosquito A. albopictus in Florida.
Another variation of the hemorrhagic viruses is the Huntavirus. The virus is carried by rodents and is spread by breathing air contaminated by urine, feces, and saliva of infected rodents. As with other hemorrhagic-type viruses, the huntavirus causes the capillaries of its victims to leak blood, resulting in eventual organ failure. Infection sometimes begins in the lungs, producing fever, muscle pain, and occasionally diarrhea and vomiting. About four to five days later, the victim may start to cough and experiences shortness of breath. Shock may follow from fluid loss in the lungs as well as a decrease in blood pressure. Death almost always is the result. Those that do recover may recover completely. If infection begins in the kidneys, it will, like the lungs, start with fever, headache, backache, and abdominal pain. Three or four days later, tiny patches appear on the whites of the eyes and on the roof of the mouth. An abdominal rash will also appear. As kidney function deteriorates, its ability to filter the blood also decreases rapidly, resulting in a buildup of toxic substances in the blood. A more severe kidney infection can also develop. Typically, there is a wide-spread reddening of the face, much like sunburn. Three to five days after infection, pinpoint bleeding appears on the roof of the mouth, and, later, on any part of the skin where pressure is applied. Blood also begins oozing from the eyes. A few days later, the blood pressure will suddenly plunge, followed by shock. About the eighth days, the blood pressure returns to normal. About the eleventh day, the production of urine begins to increase. It is about this time that bleeding may occur in the brain, resulting in death. Fatal kidney infection occurs about 5% of the time, leaving the others with permanent kidney damage. Masks should be worn and great care taken when such cleaning areas as barns, where rodents may have contaminated the dust.
A type of arbovirus called ‘nairoviruses’ was isolated in the 1960s, and was called Crimean although researchers found the same virus in Africa, and called it Congo. This hemorrhagic fever has a high mortality rate, causing a rash, bleeding gums and other membranes, sometimes internally. It was first reported in the USSR during WWII. In Africa, the virus is carried by ticks, cattle, goats, hedgehogs, and gnats. Rift Valley fever, causing problems for both humans and livestock, is found in the area south of the Sahara Desert. It is caused by an arbovirus of the Bunyaviridae family, transmitted by Aedes and other kinds of mosquitoes. It was particularly deadly after the construction of the Aswan Dam in Egypt because it created new wetlands for mosquito breeding. Repeated happenings occurred at other dam constructions sites in Mauritania, Senegal, and Madagascar. The California and St. Louis are two of the five arboviruses known in the US. Both cause encephalitis and are carried by mosquitoes. The other three cause the often fatal eastern equine encephalitis, western equine encephalitis, and Colorado tick fever, transmitted by the wood tick Dermacentor andersoni.
Togaviruses and Flaviviruses belong to the families of Togaviridae and Flaviviridae, which contain about 250 related viruses. Both are RNA viruses with an envelope and a cubical symmetry. They constitute a major portion of a group of viruses that have traditionally been called arthropod-borne viruses, referred to as arboviruses. These viruses are passed back and forth between hosts as a continual means of infection. The viruses are first injected into the tissues by bites of an infected arthropod, where they multiply in the endothelial cells lining the blood vessels. Within four to seven days, the viruses are released into the bloodstream, where they are spread to various other tissues, producing characteristic symptoms. Most do not progress beyond the mild or subclinical stage. A dozen or so such viruses are able to cause serious diseases that progress to more such serious symptoms as fever and a rash (arthralgia), hemorrhagic fevers with lesions in the blood vessels, kidneys, and liver, and encephalitis. Zika fever is the result of flavivirus, but is not as dangerous to humans as is Yellow fever, dengue, and other henorrhagic fevers. A closely related virus is the cause of Spondweni fever.
Rubella (German measles or three-day measles) is a mild disease that is of little consequence to children or adults, but can have a disastrous effect on a developing fetus. The common names for the disease often lead to confusion with regular measles. The virus that causes rubella was finally isolated in the early 1960s; and only one serotype has been found. The rubella virus is a member of the family Togaviridae, and is a ss-RNA with an envelope. It is often confused with the measles virus from the family Paramyxoviridae. The disease has the same pathogenesis as many other diseases; that is, the virus is inhaled into the respiratory tract, followed by passage through the lymphatic system into the blood. After an incubation period of about fourteen days, the signs and symptoms produced are usually so trivial as to go almost unnoticed. There may be some swollen lymph nodes, a mild fever, and a slight rash.
However, when a pregnant female is infected, the rubella virus can infect the developing fetus and cause a disease known as congenital rubella syndrome, responsible for such defects as cataracts, with complete or partial blindness, loss of hearing, heart defects, mental retardation, or generalized tissue damage. The probability that the developing baby will sustain serious damage due to congenital rubella is much greater if infection occurs during the first trimester of pregnancy. Severe damage results in about 50% of the fetuses infected during the first month, but serious effects are rare if the mother contracts the disease after the fourth month of pregnancy. It is theorized that the rubella virus has such damaging effects on the fetus because of the mild nature of the virus. More virulent viruses, if they were to infect a fetus, would cause such severe damage to result in fetal death, leading to a spontaneous abortion. Instead, the rubella virus simply slows cell growth and damages or kills a limited number of cells, but enough to cause malformation of the areas involved. Rubella babies born with the syndrome continue to shed the virus in their saliva, urine, and other body secretions for up to six years after birth.
The dangerous time of the disease is during the first trimester of a pregnancy when it can cause deformities in the developing infant. The scientist who found this link was Australian ophthalmologist Norman Gregg. He reported noticing that mothers who had ruebella had infants who developed congenital cataracts. He was roundly criticized around the world, including by an editorial in The Lancet in 1944. Later, the theory was accepted – once again proving that arrogance has no place in science. It has also been established that not only did the virus contribute to cataracts, but to a host of other defects as well including the following: heart problems, deafness, language disorders, and bone lesions.