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As of 2009, loiasis is endemic to 11 countries, all in western or central Africa, and an estimated 12–13 million people have the disease. The highest incidence is seen in Cameroon, Republic of the Congo, Democratic Republic of Congo, Central African Republic, Nigeria, Gabon, and Equatorial Guinea. The rates of "Loa loa" infection are lower but it is still present in and Angola, Benin, Chad and Uganda. The disease was once endemic to the western African countries of Ghana, Guinea, Guinea Bissau, Ivory Coast and Mali but has since disappeared.
Throughout "Loa loa"-endemic regions, infection rates vary from 9 to 70 percent of the population. Areas at high risk of severe adverse reactions to mass treatment (with Ivermectin) are at present determined by the prevalence in a population of >20% microfilaremia, which has been recently shown in eastern Cameroon (2007 study), for example, among other locales in the region.
Endemicity is closely linked to the habitats of the two known human loiasis vectors, "Chrysops dimidiata" and "C. silicea".
Cases have been reported on occasion in the United States but are restricted to travelers who have returned from endemic regions.
In the 1990s, the only method of determining "Loa loa" intensity was with microscopic examination of standardized blood smears, which is not practical in endemic regions. Because mass diagnostic methods were not available, complications started to surface once mass ivermectin treatment programs started being carried out for onchocerciasis, another filariasis. Ivermectin, a microfilaricidal drug, may be contraindicated in patients who are co-infected with loiasis and have associated high microfilarial loads. The theory is that the killing of massive numbers of microfilaria, some of which may be near the ocular and brain region, can lead to encephalopathy. Indeed, cases of this have been documented so frequently over the last decade that a term has been given for this set of complication: neurologic serious adverse events (SAEs).
Advanced diagnostic methods have been developed since the appearance the SAEs, but more specific diagnostic tests that have been or are currently being development (see: Diagnostics) must to be supported and distributed if adequate loiasis surveillance is to be achieved.
There is much overlap between the endemicity of the two distinct filariases, which complicates mass treatment programs for onchocerciasis and necessitates the development of greater diagnostics for loiasis.
In Central and West Africa, initiatives to control onchocerciasis involve mass treatment with Ivermectin. However, these regions typically have high rates of co-infection with both "L. loa" and "O. volvulus", and mass treatment with Ivermectin can have severe adverse effects (SAE). These include hemorrhage of the conjunctiva and retina, heamaturia, and other encephalopathies that are all attributed to the initial L. loa microfilarial load in the patient prior to treatment. Studies have sought to delineate the sequence of events following Ivermectin treatment that lead to neurologic SAE and sometimes death, while also trying to understand the mechanisms of adverse reactions to develop more appropriate treatments.
In a study looking at mass Ivermectin treatment in Cameroon, one of the greatest endemic regions for both onchocerciasis and loiasis, a sequence of events in the clinical manifestation of adverse effects was outlined.
It was noted that the patients used in this study had a "L. loa" microfilarial load of greater than 3,000 per ml of blood.
Within 12–24 hours post-Ivermectin treatment (D1), individuals complained of fatigue, anorexia, and headache, joint and lumbar pain—a bent forward walk was characteristic during this initial stage accompanied by fever. Stomach pain and diarrhea were also reported in several individuals.
By day 2 (D2), many patients experienced confusion, agitation, dysarthria, mutism and incontinence. Some cases of coma were reported as early as D2. The severity of adverse effects increased with higher microfilarial loads. Hemorrhaging of the eye, particularly the retinal and conjunctiva regions, is another common sign associated with SAE of Ivermectin treatment in patients with "L. loa" infections and is observed between D2 and D5 post-treatment. This can be visible for up to 5 weeks following treatment and has increased severity with higher microfilarial loads.
Haematuria and proteinuria have also been observed following Ivermectin treatment, but this is common when using Ivermectin to treat onchocerciasis. The effect is exacerbated when there are high "L. loa" microfilarial loads however, and microfilariae can be observed in the urine occasionally. Generally, patients recovered from SAE within 6–7 months post-Ivermectin treatment; however, when their complications were unmanaged and patients were left bed-ridden, death resulted due to gastrointestinal bleeding, septic shock, and large abscesses.
Mechanisms for SAE have been proposed. Though microfilarial load is a major risk factor to post-Ivermectin SAE, three main hypotheses have been proposed for the mechanisms.
The first mechanism suggests that Ivermectin causes immobility in microfilariae, which then obstructs microcirculation in cerebral regions. This is supported by the retinal hemorrhaging seen in some patients, and is possibly responsible for the neurologic SAE reported.
The second hypothesis suggests that microfilariae may try to escape drug treatment by migrating to brain capillaries and further into brain tissue; this is supported by pathology reports demonstrating a microfilarial presence in brain tissue post-Ivermectin treatment.
Lastly, the third hypothesis attributes hypersensitivity and inflammation at the cerebral level to post-Ivermectin treatment complications, and perhaps the release of bacteria from L. loa after treatment to SAE. This has been observed with the bacteria "Wolbachia" that live with "O. volvulus".
More research into the mechanisms of post-Ivermectin treatment SAE is needed to develop drugs that are appropriate for individuals suffering from multiple parasitic infections.
One drug that has been proposed for the treatment of onchocerciasis is doxycycline. This drug has been shown to be effective in killing both the adult worm of "O. volvulus" and "Wolbachia", the bacteria believed to play a major role in the onset of onchocerciasis, while having no effect on the microfilariae of "L. loa". In a study done at 5 different co-endemic regions for onchocerciasis and loiasis, doxycycline was shown to be effective in treating over 12,000 individuals infected with both parasites with minimal complications. Drawbacks to using Doxycycline include bacterial resistance and patient compliance because of a longer treatment regimen and emergence of doxycycline-resistant "Wolbachia". However, in the study over 97% of the patients complied with treatment, so it does pose as a promising treatment for onchocerciasis, while avoiding complications associated with L. loa co-infections.
Human loiasis geographical distribution is restricted to the rain forest and swamp forest areas of West Africa, being especially common in Cameroon and on the Ogooué River. Humans are the only known natural reservoir. It is estimated that over 10 million humans are infected with "Loa loa" larvae.
An area of tremendous concern regarding loiasis is its co-endemicity with onchocerciasis in certain areas of west and central Africa, as mass ivermectin treatment of onchocerciasis can lead to serious adverse events (SAEs) in patients who have high "Loa loa" microfilarial densities, or loads. This fact necessitates the development of more specific diagnostics tests for "Loa loa" so that areas and individuals at a higher risk for neurologic consequences can be identified prior to microfilaricidal treatment. Additionally, the treatment of choice for loiasis, diethylcarbamazine, can lead to serious complications in and of itself when administered in standard doses to patients with high "Loa loa" microfilarial loads.
The World Health Organization recommends mass deworming—treating entire groups of people who are at risk with a single annual dose of two medicines, namely albendazole in combination with either ivermectin or diethylcarbamazine citrate. With consistent treatment, since the disease needs a human host, the reduction of microfilariae means the disease will not be transmitted, the adult worms will die out, and the cycle will be broken. In sub-Saharan Africa, albendazole (donated by GlaxoSmithKline) is being used with ivermectin (donated by Merck & Co.) to treat the disease, whereas elsewhere in the world, albendazole is used with diethylcarbamazine. Transmission of the infection can be broken when a single dose of these combined oral medicines is consistently maintained annually for a duration of four to six years. Using a combination of treatments better reduces the number of microfilariae in blood. Avoiding mosquito bites, such as by using insecticide-treated mosquito bed nets, also reduces the transmission of lymphatic filariasis.
The Carter Center's International Task Force for Disease Eradication declared lymphatic filariasis one of six potentially eradicable diseases. According to medical experts, the worldwide effort to eliminate lymphatic filariasis is on track to potentially succeed by 2020.
For similar-looking but causally unrelated podoconiosis, international awareness of the disease will have to increase before elimination is possible. In 2011, podoconiosis was added to the World Health Organization's Neglected Tropical Diseases list, which was an important milestone in raising global awareness of the condition.
The efforts of the Global Programme to Eliminate LF are estimated to have prevented 6.6 million new filariasis cases from developing in children between 2000 and 2007, and to have stopped the progression of the disease in another 9.5 million people who had already contracted it. Dr. Mwele Malecela, who chairs the programme, said: "We are on track to accomplish our goal of elimination by 2020." In 2010, the WHO published a detailed progress report on the elimination campaign in which they assert that of the 81 countries with endemic LF, 53 have implemented mass drug administration, and 37 have completed five or more rounds in some areas, though urban areas remain problematic.
About 37 million people are infected with this parasite; about 300,000 of those had been permanently blinded. As of 2008, about 99% of onchocerciasis cases occurred in Africa. Onchocerciasis is currently endemic in 30 African countries, Yemen, and isolated regions of South America. Over 85 million people live in endemic areas, and half of these reside in Nigeria. Another 120 million people are at risk for contracting the disease. Due to the vector’s breeding habitat, the disease is more severe along the major rivers in the northern and central areas of the continent, and severity declines in villages farther from rivers. Onchocerciasis was eliminated in the northern focus in Chiapas, Mexico, and the focus in Oaxaca, Mexico, where "Onchocerca volvulus" existed, was determined, after several years of treatment with ivermectin, as free of the transmission of the parasite.
According to a 2002 WHO report, onchocerciasis has not caused a single death, but its global burden is 987,000 disability adjusted life years (DALYs). The severe pruritus alone accounts for 60% of the DALYs. Infection reduces the host’s immunity and resistance to other diseases, which results in an estimated reduction in life expectancy of 13 years.
Some types of helminthiases are classified as neglected tropical diseases. They include:
- Soil-transmitted helminthiases
- Roundworm infections such as lymphatic filariasis, dracunculiasis, and onchocerciasis
- Trematode infections, such as schistosomiasis, and food-borne trematodiases, including fascioliasis, clonorchiasis, opisthorchiasis, and paragonimiasis
- Tapeworm infections such as cysticercosis, taeniasis, and echinococcosis
Areas with the highest prevalence of helminthiasis are tropical and subtropical areas including sub-Saharan Africa, central and east Asia, and the Americas.
Diethylcarbamazine has been shown as an effective prophylaxis for "Loa loa" infection.
A study of Peace Corps volunteers in the highly Loa—endemic Gabon, for example, had the following results: 6 of 20 individuals in a placebo group contracted the disease, compared to 0 of 16 in the DEC-treated group. Seropositivity for antifilarial IgG antibody was also much higher in the placebo group. The recommended prophylactic dose is 300 mg DEC given orally once weekly. The only associated symptom in the Peace Corps study was nausea.
Researchers believe that geo-mapping of appropriate habitat and human settlement patterns may, with the use of predictor variables such as forest, land cover, rainfall, temperature, and soil type, allow for estimation of Loa loa transmission in the absence of point-of-care diagnostic tests. In addition to geo-mapping and chemoprophylaxis, the same preventative strategies used for malaria should be undertaken to avoid contraction of loiasis. Specifically, DEET-containing insect repellent, permethrin-soaked clothing, and thick, long-sleeved and long-legged clothing ought to be worn to decrease susceptibility to the bite of the mango or deer fly vector. Because the vector is day-biting, mosquito (bed) nets do not increase protection against loiasis.
Vector elimination strategies are an interesting consideration. It has been shown that the "Chrysops" vector has a limited flying range, but vector elimination efforts are not common, likely because the insects bite outdoors and have a diverse, if not long, range, living in the forest and biting in the open, as mentioned in the vector section.
No vaccine has been developed for loiasis and there is little report on this possibility.
Elephantiasis caused by lymphatic filariasis is one of the most common causes of disability in the world. A 2012 report noted that lymphatic filariasis affected 120 million people and one billion people at risk for infection. About 40 million people were disfigured or incapacitated by the disease in 2015. It is considered endemic in tropical and subtropical regions of Africa, Asia, Central and South America, and Pacific Island nations.
In areas endemic for podoconiosis, prevalence can be 5% or higher. In communities where lymphatic filariasis is endemic, as many as 10% of women can be afflicted with swollen limbs, and 50% of men can suffer from mutilating genital symptoms.
Filariasis is considered endemic in 73 countries; 37 of these are in Africa.
- In the Americas, it is present in Brazil, Costa Rica, the Dominican Republic, Guyana, Haiti, Suriname, and Trinidad and Tobago.
- In Asia, it is present in Bangladesh, Cambodia, India, Indonesia, Laos, Malaysia, Maldives, the Philippines, Sri Lanka, Thailand, Timor-Leste, and Vietnam.
- In the Middle East, it is present only in Yemen.
- In the Pacific region, it is endemic in American Samoa, the Cook Islands, Fiji, French Polynesia, Micronesia, Niue, Papua New Guinea, Samoa, Tonga, Tuvalu, and Vanuatu.
In many of these countries, considerable progress has been made towards elimination of filariasis. In July 2017, the World Health Organization (WHO) announced that the disease had been eliminated in Tonga. Elimination of the disease has also occurred in Cambodia, China, the Cook Islands, Niue, the Marshall Islands, South Korea, and Vanuatu, according to the WHO.
Prevention focuses on protecting against mosquito bites in endemic regions. Insect repellents and mosquito nets are useful to protect against mosquito bites. Public education efforts must also be made within the endemic areas of the world to successfully lower the prevalence of "W. bancrofti" infections.
Secondary bacterial infection is common among patients with filariasis. Compromised immune function due to lymphatic damage in addition to lymph node ulcerations and abscesses exposure and impaired circulation due to elephantiasis can cause secondary bacterial or fungal infection. Elephantiasis, in addition to the physical burden of a swollen limb, can be a severely dehabilitating condition given bacterial infection. Part of the WHO's "Strategy to Eliminate Lymphatic Filariasis" targets hygiene promotion programs in order to alleviate the suffering of affected individuals (see Prevention Strategies).
However, clinical manifestations of infection are variable and depend on several factors, including host immune system, infectious dose, and parasite strain differences. Most infections appear asymptomatic, yet vary from individual to individual. Individuals living in endemic areas with microfilaremia may never present with overt symptoms, whereas in other cases, only a few worms can exacerbate a severe inflammatory response.
The development of the disease in humans, however, is not well understood. Adults typically develop worse symptoms, given the long exposure time required for infection. Infection may occur during childhood, but the disease appears to take many years to manifest. The incubation period for infection ranges from 1 month to 2 years and typically microfilariae appear before overt symptoms. Lymphedema can develop within six months and development of elephantiasis has been reported within a year of infection among refugees, who are more immunologically naive. Men tend to develop worse symptoms than women.
Deworming treatments in infected children may have some nutritional benefit, as worms are often partially responsible for malnutrition. However, in areas where these infections are common, there is strong evidence that mass deworming campaigns do not have a positive effect on children's average nutritional status, levels of blood haemoglobin, cognitive abilities, performance at school or survival. To achieve health gains in the longer term, improvements in sanitation and hygiene behaviours are also required, together with deworming treatments.
Filariasis can also affect domesticated animals, such as cattle, sheep, and dogs.
Secondary bacterial infection is often observed with lymphatic filariasis. Rigorous hygiene practices, including washing with soap and water daily and disinfecting wounds can help heal infected surfaces, and slow and potentially reverse existing tissue damage. Promoting hygiene is essential for lymphatic filariasis patients given the compromised immune and damaged lymphatic systems and can help prevent suffering and disability.
The WHO is coordinating an effort to eradicate filariasis. The mainstay of this programme is the mass use of antifilarial drugs on a regular basis for at least five years.
In April 2011, Sri Lanka was certified by the WHO as having eradicated this disease.
Ivermectin kills the parasite by interfering with the nervous system and muscle function, in particular, by enhancing inhibitory neurotransmission. The drug binds to and activates glutamate-gated chloride channels. These channels, present in neurons and myocytes, are not invertebrate-specific, but are protected in vertebrates from the action of ivermectin by the blood–brain barrier. Ivermectin is thought to irreversibly activate these channel receptors in the worm, eventually causing an inhibitory postsynaptic potential. The chance of a future action potential occurring in synapses between neurons decreases and the nematodes experience flaccid paralysis followed by death.
Ivermectin is directly effective against the larval stage microfilariae of "O. volvulus"; they are paralyzed and can be killed by eosinophils and macrophages. It does not kill adult females (macrofilariae), but does cause them to cease releasing microfilariae, perhaps by paralyzing the reproductive tract. Ivermectin is very effective in reducing microfilarial load and reducing number of punctate opacities in individuals with onchocerciasis.
Snakebite was added to the list in 2017, after years of criticism of the WHO by activists for not making it a priority. The greatest burden of snakebite morbidity is in India and Southeast Asia. Globally, there are an estimated 421,000 envenomings each year (about 1 in 4 snakebites) and 20,000 deaths, but snakebites often go unreported.
Filarial diseases in humans offer prospects for elimination by means of vermicidal treatment. If the human link in the chain of infection can be broken, then notionally the disease could be wiped out in a season. In practice it is not quite so simple, and there are complications in that multiple species overlap in certain regions and double infections are common. This creates difficulties for routine mass treatment because people with onchocerciasis in particular react badly to treatment for lymphatic filariasis.
Anthelmintics such as diethylcarbamazine and albendazole have shown promise in the treatment of "Brugia timori" filariasis. Some researchers are confident that "Brugia timori" filariasis may be an eradicable disease. Related filarial nematodes have been found highly sensitive to elimination of their endosymbiotic Wolbachia bacteria, and this may be a powerful attack route against "Brugia timori" as well.
Brugia timori is a human filarial parasitic nematode (roundworm) which causes the disease "Timor filariasis." While this disease was first described in 1965, the identity of "Brugia timori" as the causative agent was not known until 1977. In that same year, "Anopheles barbirostris" was shown to be its primary vector. There is no known animal reservoir host.
Mansonelliasis is found in Latin America from the Yucatán peninsula to northern Argentina, in the Caribbean, and in Africa from Senegal to Kenya and south to Angola and Zimbabwe. "M. ozzardi" is found only in the New World, "M. steptocerca" is found only in the Congo basin, and "M. perstans" is found in both the previously described areas of Africa and Latin America. Prevalence rates vary from a few percent to as much as 90% in areas like Trinidad, Guyana and Colombia.
Infection is more common and has a higher microfilarial dose with age, though studies have found microfilarial dose not to be correlated with symptoms. In parts of rural South America, men have been found more susceptible than women, possibly due to more outdoors work by males as children, and possibly due to cooking fires serving as deterrents to vectors for women who perform more domestic duties. One study in central Africa found "M. perstans" to be a much more common cause of filariasis symptoms compared to Loa loa and Wuchereria bancrofti.
Since most Mansonelliasis is asymptomatic, it has been considered a relatively minor filarial disease, and has a very low, if any, mortality, though there is little data to base estimates on.
Prevention can be partially achieved through limiting contact with vectors through the use of DEET and other repellents, but due to the predominantly relatively mild symptoms and the infection being generally asymptomatic, little has formally been done to control the disease.
Parasitic worms and nematodes regulate many immune pathways of their host in order to increase their chances of survival. For example, molecules secreted by "Acanthocheilonema vitae" actually limit host effective immune mechanisms. These molecules are called excretory-secretory products. An effective excretory-secretory product released from "Acanthochelionema vitae" is called ES-62, which can affect multiple immune system cell types. ES-62 has anti-inflammatory effects when subjected to mice. The anti-inflammatory effect occurs because of a phosphorylcholine (PC)-containing moiety and signal transduction. More research needs to be completed; however there is some evidence that "Acanthocheilonema vitae" may have anti-inflammatory effects, and should be researched further.
Acanthocheilonemiasis is caused by the parasite, "mansonella perstans." "M. perstans" is primarily found in central Africa and in some areas of South America, therefore the most affected populations are located in these areas. Acanthocheilonemiasis affects humans in these areas in equal numbers. The prevalence of this condition does significantly increase with age. Furthermore, the parasite is most commonly found in areas of tropical forests with alternating swamps and open ground.
Approximately 114 million people in Africa are infected with "M. perstans", including 33 sub-Saharan African countries. Recent studies focused on Gabon specifically, where febrile and tropical diseases are common. Contrary to popular recent suggestions, "M. perstans" does not influence the emergence of febrile diseases, including HIV, tuberculosis, bacteremia, and malaria. In general, hemoglobin levels in individuals with malaria are severely reduced from that of a healthy individual. Reduced levels occur because the malaria parasite, "Plasmodium falciparum," utilizes human hemoglobin as its major energy source. Filariasis, in combination with severe malaria, actually shows higher hemoglobin levels than in severe malaria alone. In addition, "M. perstans" did not have adverse effects on those with HIV, as there were actually higher levels of CD4 in HIV patients co-infected with "M. perstans". Further research in this area may allude to clinical manifestations of this infectious disease, as there could be possible benefits by contracting "M. perstans".
Some of the strategies for controlling tropical diseases include:
- Draining wetlands to reduce populations of insects and other vectors, or introducing natural predators of the vectors.
- The application of insecticides and/or insect repellents) to strategic surfaces such as clothing, skin, buildings, insect habitats, and bed nets.
- The use of a mosquito net over a bed (also known as a "bed net") to reduce nighttime transmission, since certain species of tropical mosquitoes feed mainly at night.
- Use of water wells, and/or water filtration, water filters, or water treatment with water tablets to produce drinking water free of parasites.
- Sanitation to prevent transmission through human waste.
- In situations where vectors (such as mosquitoes) have become more numerous as a result of human activity, a careful investigation can provide clues: for example, open dumps can contain stagnant water that encourage disease vectors to breed. Eliminating these dumps can address the problem. An education campaign can yield significant benefits at low cost.
- Development and use of vaccines to promote disease immunity.
- Pharmacologic pre-exposure prophylaxis (to prevent disease before exposure to the environment and/or vector).
- Pharmacologic post-exposure prophylaxis (to prevent disease after exposure to the environment and/or vector).
- Pharmacologic treatment (to treat disease after infection or infestation).
- Assisting with economic development in endemic regions. For example, by providing microloans to enable investments in more efficient and productive agriculture. This in turn can help subsistence farming to become more profitable, and these profits can be used by local populations for disease prevention and treatment, with the added benefit of reducing the poverty rate.
- Hospital for Tropical Diseases
- Tropical medicine
- Infectious disease
- Neglected diseases
- List of epidemics
- Waterborne diseases
- Globalization and disease
In 1975 the Special Programme for Research and Training in Tropical Diseases (TDR) was established to focus on neglected infectious diseases which disproportionately affect poor and marginalized populations in developing regions of Africa, Asia, Central America and South America. It was established at the World Health Organization, which is the executing agency, and is co-sponsored by the United Nations Children's Fund, United Nations Development Programme, the World Bank and the World Health Organization.
TDR's vision is to foster an effective global research effort on infectious diseases of poverty in which disease endemic countries play a pivotal role. It has a dual mission of developing new tools and strategies against these diseases, and to develop the research and leadership capacity in the countries where the diseases occur. The TDR secretariat is based in Geneva, Switzerland, but the work is conducted throughout the world through many partners and funded grants.
Some examples of work include helping to develop new treatments for diseases, such as ivermectin for onchocerciasis (river blindness); showing how packaging can improve use of artemesinin-combination treatment (ACT) for malaria; demonstrating the effectiveness of bednets to prevent mosquito bites and malaria; and documenting how community-based and community-led programmes increases distribution of multiple treatments. TDR history
The current TDR disease portfolio includes the following entries:
- Chagas disease
- (also called "American trypanosomiasis") is a parasitic disease which occurs in the Americas, particularly in South America. Its pathogenic agent is a flagellate protozoan named "Trypanosoma cruzi", which is transmitted mostly by blood-sucking assassin bugs, however other methods of transmission are possible, such as ingestion of food contaminated with parasites, blood transfusion and fetal transmission. Between 16 and 18 million people are currently infected.
- Dengue
- Helminths
- African trypanosomiasis
- or sleeping sickness, is a parasitic disease, caused by protozoa called trypansomes. The two responsible for African trypanosomiasis are Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense.These parasites are transmitted by the tsetse fly
- Leishmaniasis
- caused by protozoan parasites of the genus Leishmania, and transmitted by the bite of certain species of sand fly.
- Leprosy
- (or Hansen's disease) is a chronic infectious disease caused by Mycobacterium leprae. Leprosy is primarily a granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract; skin lesions are the primary external symptom. Left untreated, leprosy can be progressive, causing permanent damage to the skin, nerves, limbs, and eyes. Contrary to popular conception, leprosy does not cause body parts to simply fall off, and it differs from tzaraath, the malady described in the Hebrew scriptures and previously translated into English as "leprosy".
- Lymphatic filariasis
- is a parasitic disease caused by thread-like parasitic filarial worms called nematodes, all transmitted by mosquitoes. Loa loa is another filarial parasite transmitted by the deer fly. 120 million people are infected worldwide. It is carried by over half the population in the most severe endemic areas. The most noticeable symptom is elephantiasis: a thickening of the skin and underlying tissues. Elephantiasis is caused by chronic infection by filarial worms in the lymph nodes. This clogs the lymph nodes and slows the draining of lymph fluid from a portion of the body.
- Malaria
- Caused by a Protozoan parasites transmitted by female "Anopheles" mosquitoes, as they are the blood-feeders. The disease is caused by species of the genus Plasmodium. Malaria infected an estimated 190-311 million people in 2008 and 708,000-1,003,000 died mostly in Sub-Sahara Africa.
- Onchocerciasis ()
- or river blindness is the world's second leading infectious cause of blindness. It is caused by "Onchocerca volvulus", a parasitic worm. It is transmitted through the bite of a black fly. The worms spread throughout the body, and when they die, they cause intense itching and a strong immune system response that can destroy nearby tissue, such as the eye. About 18 million people are currently infected with this parasite. Approximately 300,000 have been irreversibly blinded by it.
- Schistosomiasis ()
- also known as "schisto" or snail fever, is a parasitic disease caused by several species of flatworm in areas with freshwater snails, which may carry the parasite. The most common form of transmission is by wading or swimming in lakes, ponds and other bodies of water containing the snails and the parasite. More than 200 million people worldwide are infected by schistosomiasis.
- Sexually transmitted infections
- TB-HIV coinfection
- Tuberculosis
- (abbreviated as TB), is a bacterial infection of the lungs or other tissues, which is highly prevalent in the world, with mortality over 50% if untreated. It is a communicable disease, transmitted by aerosol expectorant from a cough, sneeze, speak, kiss, or spit. Over one-third of the world's population has been infected by the TB bacterium.