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In this section we are going to highlight some of the diseases that are caused by microbes, regardless of whether they are viral, bacterial, or fungal. The particular vector may or may not be mentioned. Again, this is intended as an introduction, so we will discuss only a few throughout this course.
Despite medical advances that have produced hundreds of drugs that are safe and effective against bacteria, viruses, fungi and parasites, infectious diseases are still a major cause of death, disability and social and economic upheaval for millions around the world. The report, Microbial Threats to Health: Emergence, Detection, and Response, points out that the impact of infectious diseases on the United States has only increased.
Today, the mosquito is among the most dangerous spreaders of disease on earth. From malaria and yellow fever to West Nile virus, mosquito-borne diseases strike millions. Malaria alone kills about one million children under the age of five each year.
Vector-borne diseases have posed serious threats to public health for many centuries, e.g., bubonic plague. In that case, the virus was carried by rats and transmitted by the fleas living on rats to people. Between genetic engineering and the plethora of vectors disease is here and the potential for new ones is on the rise. The following are vector-borne diseases:
In about twenty African countries, trypanosomiasis is one of the major public health problems. It is estimated that every year, some 250,000 to 300,000 people die for lack of diagnosis and treatment.
Trypanosomiasis is an infection caused by the parasite Trypanosoma cruzi, a flagellate protozoan, transmitted to humans and mammals by insects that are found living in cracks and holes of substandard housing. Those insects are known by numerous common names varying by country, including assassin bug, benchuca, vinchuca, kissing bug, chipo, barbeiro, et cetera.
Other forms of transmission are possible, though, such as ingestion of food contaminated with parasites, blood transfusion and fetal transmission. Infection is often spread to humans when an infected bug deposits feces. For untreated cases of trypanosomiasis, death is certain.
Human trypanosomiasis is a vector-borne parasitic disease. The vector is found in Africa, between the fifteenth parallels north and south. Its habitat is the vegetation along lakes, forest edges and gallery forests, extending to vast areas of scrub savanna. The tsetse fly feeds on the blood of animals and humans.
African trypanosomiasis, or sleeping sickness, is caused by Trypanosoma brucei. It is transmitted to humans through the bite of a tsetse fly. More than 66 million women, men and children in 36 countries of sub-Saharan Africa suffer from human African trypanosomiasis.
There are two forms of African sleeping sickness, caused by two different parasites:
Once inoculated by an infected fly, the trypanosomes proliferate and gradually invade all the organs of the host. Most of the parasites are effectively destroyed by the host’s natural defenses, but some trypanosomes manage to evade the immune system by modifying their surface membrane antigenic variation. (See antigenic shift and drift). The trypanosome can express thousands of variants, multiplying with each new surface change.
At first, the main clinical signs of human trypanosomiasis are high fever, weakness, headache, joint pains, and pruritus. Gradually, the immune defense mechanisms and the patient’s resistance are exhausted. As the parasite develops in the lymph and blood of the patient, the initial symptoms become more pronounced and other manifestations such as anemia, cardiovascular and endocrine disorders, abortion, and kidney disorders appear.
In advanced stages of the disease, the parasite invades the central nervous system. The patient’s behavior changes; no longer can he/she concentrate and they become indifferent to their environment. Sudden and unpredictable mood changes become increasingly frequent, giving rise to lethargy with bouts of aggressiveness. Patients are overcome by such extreme torpor that eating, speaking, walking or even opening the eyes calls for great effort. At night they suffer insomnia and during the day are exhausted by periods of sleep-like unconsciousness. Finally, patients fall into a deep coma and die.
Cryptosporidiosis is a diarrheal disease caused by microscopic parasites of the genus Cryptosporidium. Once an animal or person is infected, the parasite lives in the intestine and passes in the stool. The parasite is protected by an outer shell that allows it to survive outside the body for long periods of time and makes it very resistant to chlorine- based disinfectants. Both the disease and the parasite are commonly known as “crypto.”
During the past two decades, crypto has become recognized as one of the most common causes of waterborne disease within humans in the United States. The parasite may be found in drinking water and recreational water in every region of the United States and throughout the world.
This parasite can be spread by oral fecal transmission by people or animal infected with Cryptosporidium. Examples are: swallowing recreational water contaminated with Cryptosporidium; accidentally swallowing Cryptosporidium picked up from surfaces contaminated with feces from an infected person; eating uncooked food contaminated with Cryptosporidium.
Some people with crypto will have no symptoms at all. While the small intestine is the site most commonly affected, Cryptosporidium infections could possibly affect other areas of the digestive or the respiratory tract. Symptoms of cryptosporidiosis generally begin 2 to 10 days (average 7 days) after becoming infected with the parasite. The most common symptom of cryptosporidiosis is watery diarrhea.
Other symptoms include:
People who are most likely to become infected with Cryptosporidium include children who attend day care centers, including diaper-aged children. Others at risk are hikers and campers who drink unfiltered, untreated water. In addition, at risk persons are swimmers who swallow water while swimming in swimming pools, lakes, rivers, ponds, and streams, and people who drink from shallow, unprotected wells.
Today, approximately 300 million people worldwide are affected by malaria and between 1 and 1.5 million people die from it every year. Previously extremely widespread, the malaria is now mainly confined to Africa, Asia and Latin America. The problems of controlling malaria in these countries are aggravated by inadequate health structures and poor socioeconomic conditions. The situation has become even more complex over the last few years with the increase in resistance to the drugs normally used to combat the parasite that causes the disease.
Malaria is caused by protozoan parasites of the genus Plasmodium. Four species of Plasmodium can produce the disease in its various forms:
(P. Falciparum is the most widespread and dangerous of the four: untreated it can lead to fatal cerebral malaria.)
In endemic regions, where transmission is high, people are continuously infected so that they gradually develop immunity to the disease. Until they have acquired such immunity, children remain highly vulnerable.
The hope of global eradication of malaria was finally abandoned in 1969 when it was recognized that this was unlikely to be achieved. Malaria is currently endemic in 91 countries with small pockets of transmission occurring in a further eight countries.
Eighty per cent of the cases occur in tropical Africa, where malaria accounts for 10% to 30% of all hospital admissions and is responsible for 15% to 25% of all deaths of children under the age of five.
Malaria is present in:
Malaria is diagnosed by the clinical symptoms and microscopic examination of the blood. In certain regions, however, the parasites have developed resistance to certain antimalarial drugs, particularly chloroquine. Patients in these areas require treatment with other more expensive drugs.
Any group of infectious diseases caused by microorganisms classified between bacteria and viruses are known as rickettsias. Typhus diseases are characterized by high fever and an early onset of rash and headache. Epidemic typhus, the most serious in the group, is caused by Rickettsia prowazeki, which is transmitted in the feces of body lice. It occurs in crowded, unsanitary conditions and has historically been a major killer in wartime. It occurs more commonly in cooler climates and seasons.
They respond to antibiotic treatment with tetracycline and chloramphenicol and can be prevented by vaccination.
Endemic murine typhus is primarily a disease of rodents and is spread to humans by rat fleas. The symptoms are milder than those of epidemic typhus. Scrub typhus (Tsutsugamushi fever) is carried to humans by infected mites. It occurs primarily in East Asia and the Southeast Pacific islands.
All the viruses that cause VHF are zoonotic RNA viruses. Viral hemorrhagic fevers are simple RNA viruses with lipid envelopes. They are stable at a neutral pH and able to survive in blood for long periods, which leads to the high infection rate of patients accustomed to spending time near domestic animal slaughters. These viruses are linked to the ecology of their vector, whether rodent or arthropod, which helps in finding a diagnosis.
The specific viral hemorrhagic fever syndrome that develops in patients depends on numerous factors, such as viral virulence and strain characteristic, routes of exposure, dose, and host factors.
A high index of suspicion and detailed travel history are the most important steps in making the diagnosis of viral hemorrhagic fever. Patients often recall exposures to rodents (arenavirus, hantavirus), mosquitoes (Rift Valley fever virus, yellow and dengue fever viruses), or even slaughtered horses (Rift Valley fever virus, Crimean-Congo virus). Suspect viral hemorrhagic fever in patients with fever, diffuse mucosal and dermal bleeding, and known travel to an endemic area for the illness.
Leukopenia and thrombocytopenia are common, except in Lassa fever and hantavirus. Proteinuria and hematuria are both common, but their absence rules out hantavirus and Argentine and Bolivian hemorrhagic fevers. Definitive diagnosis requires specific viral diagnosis.
All viral hemorrhagic fevers primarily target vascular beds. Clinical manifestations are nonspecific and can include fever, rash, encephalitis, and myalgias. The incubation period for HFV’s ranges from 2-21 days. Typical signs include: high fever, headache, malaise, nausea, abdominal pain, non-bloody diarrhea, and myalgias. The early signs might include hypotension, bradycardia, tachypnea, and conjunctivitis. Neurologic, hematopoietic, hepatic, and pulmonary involvement can be found with more severe disease.
Among the arenaviruses, Lassa fever is not associated with hemorrhagic or neurologic manifestations, but deafness is common. It causes massive edema. Argentine and Bolivian hemorrhagic fevers have much more pronounced hemorrhagic and neurologic manifestations.
Rift Valley fever virus is primarily hepatatrophic; a small portion of patients demonstrates hemorrhagic signs. Rift Valley fever and flaviviruses are usually abrupt in onset, whereas Arenaviruses are more gradual. CNS (central nervous system) dysfunction might present itself as delirium, convulsions, cerebellar signs, or coma. They have a poor prognosis.
Limited clinical data are available on Marburg and Ebola hemorrhagic fevers. Of the flaviviruses, yellow fever virus is primarily hepatatrophic. Black vomit caused by hematemesis is common, and patients usually develop clinical jaundice and die from hepatorenal syndrome.
The differential diagnosis includes risk factors such as travel to Africa or Asia, handling of animal carcasses, contacts with sick people or animals, or has had arthropod bites within 21 days of exposure. Any case of HFV should immediately be reported to local and state health departments, who would notify the CDC immediately.
Treatment for a viral hemorrhagic fever is largely supportive. Air transport is contraindicated. Sedative and pain-relieving medications are helpful, but aspirin should be avoided. Avoid intravenous lines and catheters unless absolutely necessary. Secondary infections should be sought and aggressively treated.
Immunosuppressive agents such as steroids are contraindicated. The treatment for bleeding is controversial. However, it is generally accepted that mild bleeding should not be treated, whereas severe hemorrhage requires appropriate replacement therapy. Fluid infusions are typically safe for severe volume depletion except in the setting of pulmonary edema.
Specific treatment with ribavirin has been used and currently is being investigated as therapy for Lassa fever, hantavirus, Crimean-Congo, and Rift Valley fever. Treatment is most effective if begun within 7 days. Ribavirin has poor activity against the filoviruses and flaviviruses.
HVF’s reside in anthropod vectors. Yellow fever, Omsk hemorrhagic fever, and Kyassanur forest disease are NOT transmissible from person to person easily however; those in close contact with one another can get infected. It is not yet known if person to person-airborne transmission is possible. All of these viruses can lead to thrombocytopenia and filoviruses are known to be extremely virulent in nonhuman primates/and humans.
The only established and licensed virus-specific vaccine against any of the VHF viruses is the yellow fever vaccine. It is mandatory for those traveling into endemic areas of Africa and South America. Current trials are underway for further vaccines and antibody therapies.
The best known of the viral hemorrhagic fever agents is the Ebola virus. First recognized in Zaire in 1976, the virus has been linked to 3 outbreaks in Africa and is associated with a 53-92% mortality rate. A related virus was discovered in Reston, VA, in 1989 in association with an outbreak of illness among cynomolgus monkeys imported from the Philippines. No human cases occurred with this latter outbreak.
These viruses each are characterized by an acute generalized illness that includes malaise, prostration, increased vascular permeability, and abnormalities of circulatory regulation.
| Ebola | High fever, myalgias, rash, (diffuse), by day 5. Bleeding and disseminated intravascular coagulation | 2-21 |
| Marburg | High fever, myalgias, rash of face, neck, trunk and arms. Bleeding intravascular coagulation | 2-14 |
| Lassa Fever | Gradual onset of fever, nausea, abdominal pain, sore throat (severe), cough, conjunctivitis, ulceration of buccal mucosa, cervical lymphadenopathy, pharyngitis, swelling of neck and head, pleural and pericardial effusions. | 5-16 |
The Bunyaviridae family comprises more than 200 named viruses. The family is divided into 5 genera:
It is generally accepted that Bunyaviruses, with the exception of hantaviruses, are transmitted in nature by arthropods. Mosquitoes are the most frequent vectors, but occasionally sand flies and ticks are vectors.
The arenaviridae are a family of viruses whose members are generally associated with rodent-transmitted disease in humans. Each virus usually is associated with a particular rodent host species in which it is maintained.
The virus particles are spherical and have an average diameter of 110-130 nanometers. All are enveloped in a lipid (fat) membrane. Viewed in cross-section, they show grainy particles that are ribosomes acquired from their host cells. It is this characteristic that gave them their name, derived from the Latin ‘arena’ which means ‘sandy’. Their genome, or genetic material, is composed of RNA only, but their replication strategy is not completely understood.
Lassa fever is an acute, often fatal viral disease endemic to West Africa. It is characterized by high fever. Other symptoms include: headache, ulcers of the mucous membranes, disturbances of the gastrointestinal tract, muscle aches, mouth ulcers, and bleeding of the skin.
The disease was first recognized in Lassa, Nigeria, in 1969. The causative virus belongs to a group of arenaviruses and is harbored by a rat, Mastomys natalensis. The virus is spread to humans via the rat’s urine in airborne droplets or contaminated food. Infection can be transmitted to medical personnel treating patients in hospitals.
The incubation period of Lassa fever is 3 to 17 days. Following fever and general malaise, later stages of the disease may include abdominal pain, diarrhea, vomiting, and petechiae, tiny purplish spots in the skin caused by leakage of blood from the capillaries. Heart and kidney failure may also occur in advanced stages, and mortality is high, ranging from about 25% to 30%. Treatment by injection of the antiviral drug ribavirin is often successful if begun early.
Filovirus is another family of viruses that cause hemorrhagic fever. They have single-stranded RNA as their genetic material. It is interesting to note that there are four subtypes of Ebola that are known. They are: Zaire, Sudan, Ivory Coast, and Reston.
Ebola is a deadly virus that causes fearsome symptoms, the most prominent being high fever and massive internal bleeding. Ebola virus kills as many as 90% of the people it infects. It is an extremely contagious filovirus causing an acute hemorrhagic fever and is spread through contact with bodily fluids or secretions of infected persons and also by airborne particles.
Epidemics of Ebola virus have occurred mainly in African countries including Zaire (now the Democratic Republic of Congo), Gabon, Uganda, the Ivory Coast, and Sudan. Ebola virus is a hazard to laboratory workers and, for that matter, anyone who is exposed to it.
Ebola virus is transmitted by contact with blood, feces or body fluids from an infected person or by direct contact with the virus, as in a laboratory. People can be exposed to Ebola virus from direct contact with the blood or secretions of an infected person. This is why the virus has often been spread through the families and friends of infected persons: in the course of feeding, holding, or otherwise caring for them, family members and friends would come into close contact with such secretions. People can also be exposed to Ebola virus through contact with objects, such as needles, that have been contaminated with infected secretions. The incubation period —the period between contact with the virus and the appearance of symptoms — ranges from 2 to 21 days.
The initial symptoms are usually high fever, headache, muscle aches, stomach pain, and diarrhea. There may also be sore throat, hiccups, and red and itchy eyes. The symptoms that tend to follow include vomiting and rash and bleeding problems with epistaxis, hemoptysis, hematemesis, and conjunctival hemorrhages. Chest pain, shock, and death follow.
A protein on the surface of the virus has been discovered that is responsible for the severe internal bleeding. The protein attacks and destroys endothelial cells lining in the blood vessels, causing the vessels to leak and bleed.
There is no specific treatment for the disease. Death can occur within 10 days of the onset of symptoms.
The flavivirus family consists of about 70 members, 13 of which cause disease in humans. Many flaviviruses are transmitted via arthropod vectors to humans and tick-borne encephalitis and Kyansanur Forest disease are tick-borne. Most flaviviruses are group B arboviruses. Flavivirus was declared a separate family in 1984.
Another member of the flavivirus family is Hepatitis C virus (HCV). Hepatitis C is a non-arthropod-borne virus that was placed in this family due to its physical structure, properties and replication strategy. Hepatitis C was discovered in 1989 after a number of post transfusion non-A, non-B hepatitis cases were investigated. Hepatitis C is as common in developed nations as hepatitis A or B.
Although 75% of infections are sub-clinical, chronic disease progresses to cirrhosis in 20% of cases. HCV infection may induce the development of hepatocellular carcinoma in rare cases. Most infected individuals contract the disease from unscreened blood transfusions, IV drug use or sexual promiscuity. Hepatitis G virus is also a transfusion associated flavivirus. It was first reported in 1996 and currently very little is known about the virus.
1, 2, 3, 4. Dengue — fever, rash, arthralgia, myalgia. Dengue is an infectious disease carried by mosquitoes and caused by any of four related dengue viruses. It has been known about for more than 200 years. It is a mosquito-borne tropical viral disease responsible for about 50 million cases worldwide. This disease used to be called break-bone fever because it sometimes causes severe joint and muscle pain.
The virus producing dengue fever initially replicates in the skin at the site of the mosquito bite. Next the lymph nodes are affected and viremia results. Fever and rash lasting 3-9 days define the symptomology.
Dengue fever is usually self-limiting but dengue hemorrhagic fever often involves additional processes that produce extreme vascular permeability, shock and death.
5. West Nile — fever, rash, arthralgia, myalgia.
West Nile Encephalitis (WNE) is transmitted by mosquitoes. In most cases no disease results. Mild, flu-like cases may be referred to as “West Nile fever”. More severe cases of “West Nile encephalitis” or “West Nile meningitis” indicate central nervous system involvement that can lead to death.
6. St. Louis encephalitis — encephalitis
7. Japanese encephalitis — encephalitis
8. Murray Valley encephalitis; Kunjin Rocio — encephalitis
9. Yellow fever — fever, hemorrhage, and jaundice. This is a severe systemic disease. The virus replicates producing liver damage and intestinal hemorrhages. Typically, phase 1 presents with a fever, headache, nausea and vomiting, while phase 2 shows toxicity, jaundice, shock and death.
10. Kyasanur Forest disease — fever, hemorrhage, encephalitis
11. Omsk hemorrhagic fever — fever, hemorrhage
12. Tick-borne encephalitis — encephalitis
13. Hepatitis C and Hepatitis G — hepatitis
Most arbovirus infections are not treated with anti-virals. Dengue, although it is a horrible disease, usually resolves itself within a week and has a low case-fatality. Yellow fever and Japanese encephalitis that are more deadly are currently being prevented through routine vaccination in endemic areas. Unlike hepatitis, most arboviruses cause acute rather than chronic infection.
Chronic hepatitis C infection can be managed with interferon therapy. Alpha interferon must be injected three times a week at dosages of 2-3 million units in order for ATL (alanine transferase activity levels) to be reduced in chronic hepatitis patients. Although some patients go into remission due to therapy, a large proportion of patients relapse after interferon is discontinued. Ribavarin therapy may also be effective in controlling HCV before cirrhosis is induced.
The spread of mosquito-borne flaviviruses can be prevented by requiring vaccination (within 10 years) of all individuals traveling into or out of flavivirus endemic regions. Insect quarantines and strict airport controls should also be implemented to prevent the introduction of infectious arthropods into new areas.
In endemic regions, pesticides and insect repellents (DEET) should be utilized and stagnant pools of water drained to reduce the population of mosquitoes in the vicinity of towns. Since the development of pesticide resistance, it has become even more difficult to kill the mosquitoes.
Ticks persist throughout the year and live through more than a single breeding cycle of their host. Thus they are more difficult to control than mosquitoes. Little can be done to reduce the size of tick populations, and so humans protect themselves through vaccination and avoidance of milk from infected animals.
Screening the blood supply can prevent hepatitis C infection. It is anticipated that reducing the number of IV drug users and encouraging safer sex practices can also reduce the incidence of HCV.
Infectious diseases are still a major cause of death, disability, and social-economic upheaval for millions around the world. Trypanosomiasis also called Chagas Disease is one of the major public health problems in about twenty African countries.
Human trypanosomiasis is a vector-borne parasitic disease and the vector is the tsetse fly that feeds on the blood of animals and humans. More than 66 million women, men and children in 36 countries of sub-Saharan Africa suffer from human African trypanosomiasis. There are two forms of African sleeping sickness, caused by two different parasites.
Cryptosporidiosis is a diarrheal disease caused by microscopic parasites of the genus Cryptosporidium. During the past two decades, cryptosporidium has become recognized as one of the most common causes of waterborne disease within humans in the United States. The parasite may be found in drinking water and recreational water in every region of the United States and throughout the world. This parasite can be spread by oral fecal transmission by people or animal infected with Cryptosporidium.
Today, approximately 300 million people worldwide are affected by malaria and between one and 1.5 million people die from it every year. Previously extremely widespread, malaria is now mainly confined to Africa, Asia and Latin America.
Any group of infectious diseases caused by microorganisms classified between bacteria and viruses are known as rickettsias. Typhus diseases are characterized by high fever and an early onset of rash and headache. Epidemic typhus, the most serious in the group, is caused by Rickettsia prowazeki.
Viral hemorrhagic fevers (VHFs) refer to a group of illnesses that are caused by four distinct families of viruses. They are the arenaviruses, filoviruses, bunyaviruses, and flaviviruses. Each of these families has several features in common. For example, they are all RNA viruses, and all enveloped (covered in a lipid coating). Their survival is dependent on their natural reservoirs, such as animals, whereas humans are not the natural reservoir for these viruses.