The symptoms of leishmaniasis are skin sores which erupt weeks to months after the person is bitten by infected sand flies.

Leishmaniasis may be divided into the following types:

- Cutaneous leishmaniasis is the most common form, which causes an open sore at the bite sites, which heals in a few months to a year and half, leaving an unpleasant-looking scar. Diffuse cutaneous leishmaniasis produces widespread skin lesions which resemble leprosy, and may not heal on its own.

- Mucocutaneous leishmaniasis causes both skin and mucosal ulcers with damage primarily of the nose and mouth.

- Visceral leishmaniasis or "kala-azar" ('black fever') is the most serious form, and is potentially fatal if untreated. Other consequences, which can occur a few months to years after infection, include fever, damage to the spleen and liver, and anemia.

Leishmaniasis is considered one of the classic causes of a markedly enlarged (and therefore palpable) spleen; the organ, which is not normally felt during examination of the abdomen, may even become larger than the liver in severe cases.

Post-kala-azar dermal leishmaniasis (PKDL) is a recurrence of kala-azar that may appear on the skin of affected individuals months and up to 20 years after being partially treated, untreated or even in those considered adequately treated. In Sudan, they can be demonstrated in up to 60% of treated cases. They manifest as hypopigmented skin lesions (such as macules, papules, nodules), or facial redness. Though any organism causing kala-azar can lead to PKDL, it is commonly associated with "Leishmania donovani" which gives different disease patterns in India and Sudan. In the Indian variant, nodules enlarge with time and form plaques but rarely ulcerate, but nodules from the African variety often ulcerate as they progress. Nerve involvement is common in African variety but rare in Indian subcontinent. Histology demonstrates a mixture of chronic inflammatory cells; there can be macrophage or epitheloid granuloma. Parasite concentration is not consistent among studies, perhaps reflecting low sensitivity of diagnostic methods used in earlier entries.

Current approach to diagnosis involves 1. demonstration of parasite by microscopy, "in vitro" culture or animal inoculation; 2. immunodiagnosis of parasite antigen; 3. detection of parasite DNA in tissue. Newer PCR based tools have higher sensitivity and specificity. Emergence of PKDL has been reported in HIV affected individuals and may become a problem in future.

Sodium stibogluconate alone or in combination with rifampicin is used for the treatment of PKDL for a long course of up to 4 months. Compliance can be an issue for such a long course.

Response to infection by "Leishmania donovani" varies a great deal, not only by the strength but also by the type of the patient's immune reaction. People with a history of infection by strains of leishmania that cause visceral leishmaniasis show a continuum of immune responses from protective to non-protective. Those who acquired protective immunity (skin test positive) without ever having visceral leishmaniasis have a strong type 1 CD4+ response to leishmania antigens. Antigen specific interferon-gamma and proliferation, as well as the ability to kill intracellular leishmania, are hallmarks of protective immunity. Because visceral leishmaniasis patients lack these responses to leishmania and other antigens, they usually die of secondary infections if left untreated. In addition, increased interleukin-10 secretion is characteristic of the disease. Addition of interleukin-12, anti-interleukin-10, or anti-interleukin-4 to peripheral blood mononuclear cells from acute patients sometimes increases interferon-gamma secretion and proliferation. Acute patient peripheral blood mononuclear cells include CD8+ T regulatory cells that decrease interferon-gamma secretion and proliferation responses to leishmania and other antigens and increase interleukin-10 secretion when added to autologous peripheral blood mononuclear cells harvested after successful treatment. Thus, the CD8+ T regulatory cells reproduce the immune response characteristic of visceral leishmaniasis. CD8+ T regulatory cells are also associated with post kala azar dermal leishmaniasis. Addition of interleukin-12 or interferon-gamma does not prevent CD8+ T regulatory activity. The dominance of type 1 CD4+ T cells in skin test positive adults maybe explained by their secretion of factors that inhibit and kill CD8+ T regulatory cells. Successfully treated patients rarely develop visceral leishmaniasis a second time. Their peripheral blood mononuclear cells show a mixed T1/T2 CD4+ and CD8+ T suppressor response but do have the ability to kill intracellular leishmania.

When people develop visceral leishmaniasis, the most typical symptoms are fever and the enlargement of the spleen, with enlargement of the liver sometimes being seen as well. The blackening of the skin that gave the disease its common name in India does not appear in most strains of the disease, and the other symptoms are very easy to mistake for those of malaria. Misdiagnosis is dangerous, as without proper treatment the mortality rate for kala-azar is close to 100%. "L. donovani" itself is not usually the direct cause of death in kala-azar sufferers, however. Pneumonia, tuberculosis, and dysentery are omnipresent in the depressed regions where leishmaniasis thrives, and, as with AIDS, it is these opportunistic infections that are more likely to kill, flaring up in a host whose immune system has been weakened by the "L. donovani" infection. Progress of the disease is extremely variable, taking anywhere from one to twenty weeks, but a typical duration for the Sudanese strain of the disease is narrower, between twelve and sixteen weeks.

Even with recovery, kala-azar does not always leave its hosts unmarked. Some time after successful treatment—generally a few months with African kala-azar, or as much as several years with the Indian strain—a secondary form of the disease may set in, called post kala-azar dermal leishmaniasis, or PKDL. This condition manifests first as small, measle-like skin lesions on the face, which gradually increase in size and spread over the body. Eventually the lesions may coalesce to form disfiguring, swollen structures resembling leprosy, and occasionally causing blindness if they spread to the eyes. (This disease is not the same as cutaneous leishmaniasis, a milder disease caused by another protozoan of the Leishmania genus which also causes skin lesions.)

Mucocutaneous leishmaniasis is an especially disturbing form of cutaneous leishmaniasis, because it produces destructive and disfiguring lesions of the face. It is most often caused by "Leishmania braziliensis", but cases caused by "L. aethiopica" have also been described.

Mucocutaneous leishmaniasis is very difficult to treat. Treatment involves the use of pentavalent antimonial compounds, which are highly toxic (common side effects include thrombophlebitis, pancreatitis, cardiotoxicity and hepatotoxicity) and not very effective. For example, in one study, despite treatment with high doses of sodium stibogluconate for 28 days, only 30% of patients remained disease-free at 12 months follow-up. Even in those patients who achieve an apparent cure, as many as 19% will relapse. Several drug combinations with immunomodulators have been tested, for example, a combination of pentoxifylline (inhibitor of TNF-α) and a pentavalent antimonial at a high dose for 30 days in a small-scale (23 patients) randomised placebo-controlled study from Brazil achieved cure rates of 90% and reduced time to cure, a result that should be interpreted cautiously in light of inherent limitations of small-scale studies. In an earlier small-scale (12 patients) study, addition of imiquimod showed promising results which need yet to be confirmed in larger trials.

Leishmaniasis is a disease caused by parasites of the "Leishmania" type. It is spread by the bite of certain types of sandflies. The disease can present in three main ways: cutaneous, mucocutaneous, or visceral leishmaniasis. The cutaneous form presents with skin ulcers, while the mucocutaneous form presents with ulcers of the skin, mouth, and nose, and the visceral form starts with skin ulcers and then later presents with fever, low red blood cells, and enlarged spleen and liver.

Infections in humans are caused by more than 20 species of "Leishmania". Risk factors include poverty, malnutrition, deforestation, and urbanization. All three types can be diagnosed by seeing the parasites under the microscope. Additionally, visceral disease can be diagnosed by blood tests.

Leishmaniasis can be partly prevented by sleeping under nets treated with insecticide. Other measures include spraying insecticides to kill sandflies and treating people with the disease early to prevent further spread. The treatment needed is determined by where the disease is acquired, the species of "Leishmania", and the type of infection. Some possible medications used for visceral disease include liposomal amphotericin B, a combination of pentavalent antimonials and paromomycin, and miltefosine. For cutaneous disease, paromomycin, fluconazole, or pentamidine may be effective.

About 4 to 12 million people are currently infected in some 98 countries. About 2 million new cases and between 20 and 50 thousand deaths occur each year. About 200 million people in Asia, Africa, South and Central America, and southern Europe live in areas where the disease is common. The World Health Organization has obtained discounts on some medications to treat the disease. It is classified as a neglected tropical disease. The disease may occur in a number of other animals, including dogs and rodents.

Cutaneous

- Alopecia

- Skin lesions

- Ulcerative or exfoliative dermatitis

Visceral

- Epistaxis (nose bleeds)

- Kidney failure > increased urination and drinking

- Ocular signs

- Progressive loss of weight with decreased appetite

- Swollen lymphnodes

Visceral leishmaniasis (VL), also known as kala-azar, black fever, and Dumdum fever, is the most severe form of leishmaniasis and, without proper diagnosis and treatment, is associated with high fatality. Leishmaniasis is a disease caused by protozoan parasites of the "Leishmania" genus.

The parasite migrates to the internal organs such as the liver, spleen (hence "visceral"), and bone marrow, and, if left untreated, will almost always result in the death of the host. Signs and symptoms include fever, weight loss, fatigue, anemia, and substantial swelling of the liver and spleen. Of particular concern, according to the World Health Organization (WHO), is the emerging problem of HIV/VL co-infection.

This disease is the second-largest parasitic killer in the world (after malaria), responsible for an estimated 200,000 to 400,000 infections each year worldwide.

Canine leishmaniasis (LEESH-ma-NIGH-ah-sis) is a zoonotic disease (see human leishmaniasis) caused by "Leishmania" parasites transmitted by the bite of an infected phlebotomine sandfly. Canine leishmaniasis was first identified in Europe in 1903, and in 1940, 40% of all dogs in Rome were determined to be positive for leishmaniasis. Traditionally thought of as a disease only found near the Mediterranean basin, 2008 research claims new findings are evidence that canine leishmaniasis is currently expanding in continental climate areas of northwestern Italy, far from the recognized disease-endemic areas along the Mediterranean coasts. Cases of leishmaniasis began appearing in North America in 2000, and, as of 2008, "Leishmania"-positive foxhounds have been reported in 22 U.S. states and two Canadian provinces.

A canine vector-borne disease (CVBD) is one of "a group of globally distributed and rapidly spreading illnesses that are caused by a range of pathogens transmitted by arthropods including ticks, fleas, mosquitoes and phlebotomine sandflies." CVBDs are important in the fields of veterinary medicine, animal welfare, and public health. Some CVBDs are of zoonotic concern.

Many CVBD infect humans as well as companion animals. Some CVBD are fatal; most can only be controlled, not cured. Therefore, infection should be avoided by preventing arthropod vectors from feeding on the blood of their preferred hosts. While it is well known that arthropods transmit bacteria and protozoa during blood feeds, viruses are also becoming recognized as another group of transmitted pathogens of both animals and humans.

Some "canine vector-borne pathogens of major zoonotic concern" are distributed worldwide, while others are localized by continent. Listed by vector, some such pathogens and their associated diseases are the following:

- Phlebotomine sandflies (Psychodidae): "Leishmania amazonensis", "L. colombiensis", and "L. infantum" cause visceral leishmaniasis (see also canine leishmaniasis). "L. braziliensis" causes mucocutaneous leishmaniasis. "L. tropica" causes cutaneous leishmaniasis. "L. peruviana" and "L. major" cause localized cutaneous leishmaniasis.

- Triatomine bugs (Reduviidae): "Trypanosoma cruzi" causes trypanosomiasis (Chagas disease).

- Ticks (Ixodidae): "Babesia canis" subspecies ("Babesia canis canis", "B. canis vogeli", "B. canis rossi", and "B. canis gibsoni" cause babesiosis. "Ehrlichia canis" and "E. chaffeensis" cause monocytic ehrlichiosis. "Anaplasma phagocytophilum" causes granulocytic anaplasmosis. "Borrelia burgdorferi" causes Lyme disease. "Rickettsia rickettsii" causes Rocky Mountain spotted fever. "Rickettsia conorii" causes Mediterranean spotted fever.

- Mosquitoes (Culicidae): "Dirofilaria immitis" and "D. repens" cause dirofilariasis.

African trypanosomiasis symptoms occur in two stages. The first stage, known as the hemolymphatic phase, is characterized by fever, headaches, joint pains, and itching. Fever is intermittent, with attacks lasting from a day to a week, separated by intervals of a few days to a month or longer. Invasion of the circulatory and lymphatic systems by the parasites is associated with severe swelling of lymph nodes, often to tremendous sizes. Winterbottom's sign, the tell-tale swollen lymph nodes along the back of the neck, may appear. Occasionally, a chancre (red sore) will develop at the location of the tsetse fly bite. If left untreated, the disease overcomes the host's defenses and can cause more extensive damage, broadening symptoms to include anemia, endocrine, cardiac, and kidney dysfunctions.

The second phase of the disease, the neurological phase, begins when the parasite invades the central nervous system by passing through the blood–brain barrier. Disruption of the sleep cycle is a leading symptom of this stage and is the one that gave the disease the name 'sleeping sickness.' Infected individuals experience a disorganized and fragmented 24-hour rhythm of the sleep-wake cycle, resulting in daytime sleep episodes and nighttime periods of wakefulness.

Other neurological symptoms include confusion, tremor, general muscle weakness, hemiparesis and paralysis of a limb. Parkinson-like movements might arise due to non-specific movement disorders and speech disorders. Individuals may also exhibit psychiatric symptoms such as irritability, psychotic reactions, aggressive behaviour, or apathy which can sometimes dominate the clinical diagnosis. Without treatment, the disease is invariably fatal, with progressive mental deterioration leading to coma, systemic organ failure, and death. An untreated infection with "T. b. rhodesiense" will cause death within months whereas an untreated infection with "T. b. gambiense" will cause death after several years. Damage caused in the neurological phase is irreversible.

Neglected tropical diseases (NTDs) are a diverse group of tropical infections which are especially common in low-income populations in developing regions of Africa, Asia, and the Americas. They are caused by a variety of pathogens such as viruses, bacteria, protozoa and helminths. These diseases are contrasted with the big three diseases (HIV/AIDS, tuberculosis, and malaria), which generally receive greater treatment and research funding. In sub-Saharan Africa, the effect of these diseases as a group is comparable to malaria and tuberculosis. NTD co-infection can also make HIV/AIDS and tuberculosis more deadly.

In some cases, the treatments are relatively inexpensive. For example, the treatment for schistosomiasis is US$0.20 per child per year. Nevertheless, in 2010 it was estimated that control of neglected diseases would require funding of between US$2 billion and US$3 billion over the subsequent five to seven years. Some pharmaceutical companies have committed to donating all the drug therapies required, and mass drug administration (for example mass deworming) has been successfully accomplished in several countries. However, preventive measures are often more accessible in the developed world, but not universally available in poorer areas.

Within developed countries, neglected tropical diseases affect the very poorest in society. In the United States, there are up to 1.46 million families including 2.8 million children living on less than two dollars a day. In countries such as these, the burdens of neglected tropical diseases are often overshadowed by other public health issues. However, many of the same issues put populations at risk in developed as developing nations. For example, from poverty stem problems such as lack of adequate housing, thus exposing individuals to the vectors of these diseases.

Twenty neglected tropical diseases are prioritized by the World Health Organization (WHO), though other organizations define NTDs differently. Chromoblastomycosis and other deep mycoses, scabies and other ectoparasites and snakebite envenoming were added to the list in 2017. These diseases are common in 149 countries, affecting more than 1.4 billion people (including more than 500 million children) and costing developing economies billions of dollars every year. They resulted in 142,000 deaths in 2013—down from 204,000 deaths in 1990. Of these 20, two were targeted for eradication (dracunculiasis (guinea-worm disease) by 2015 and yaws by 2020), and four for elimination (blinding trachoma, human African trypanosomiasis, leprosy and lymphatic filariasis by 2020).

Tropical diseases are diseases that are prevalent in or unique to tropical and subtropical regions. The diseases are less prevalent in temperate climates, due in part to the occurrence of a cold season, which controls the insect population by forcing hibernation. However, many were present in northern Europe and northern America in the 17th and 18th centuries before modern understanding of disease causation. The initial impetus for tropical medicine was to protect the health of colonialists, notably in India under the British Raj. Insects such as mosquitoes and flies are by far the most common disease carrier, or vector. These insects may carry a parasite, bacterium or virus that is infectious to humans and animals. Most often disease is transmitted by an insect "bite", which causes transmission of the infectious agent through subcutaneous blood exchange. Vaccines are not available for most of the diseases listed here, and many do not have cures.

Human exploration of tropical rainforests, deforestation, rising immigration and increased international air travel and other tourism to tropical regions has led to an increased incidence of such diseases.

African trypanosomiasis, also known as sleeping sickness, is an insect-borne parasitic disease of humans and other animals. It is caused by protozoa of the species "Trypanosoma brucei". There are two types that infect humans, "Trypanosoma brucei gambiense" (TbG) and "Trypanosoma brucei rhodesiense" (TbR). TbG causes over 98% of reported cases. Both are usually transmitted by the bite of an infected tsetse fly and are most common in rural areas.

Initially, in the first stage of the disease, there are fevers, headaches, itchiness, and joint pains. This begins one to three weeks after the bite. Weeks to months later the second stage begins with confusion, poor coordination, numbness and trouble sleeping. Diagnosis is via finding the parasite in a blood smear or in the fluid of a lymph node. A lumbar puncture is often needed to tell the difference between first and second stage disease.

Prevention of severe disease involves screening the population at risk with blood tests for TbG. Treatment is easier when the disease is detected early and before neurological symptoms occur. Treatment of the first stage is with the medications pentamidine or suramin. Treatment of the second stage involves eflornithine or a combination of nifurtimox and eflornithine for TbG. While melarsoprol works for both stages, it is typically only used for TbR, due to serious side effects. Without treatment it typically results in death.

The disease occurs regularly in some regions of sub-Saharan Africa with the population at risk being about 70 million in 36 countries. An estimated 11,000 people are currently infected with 2,800 new infections in 2015. In 2015 it caused around 3,500 deaths, down from 34,000 in 1990. More than 80% of these cases are in the Democratic Republic of the Congo. Three major outbreaks have occurred in recent history: one from 1896 to 1906 primarily in Uganda and the Congo Basin and two in 1920 and 1970 in several African countries. It is classified as a neglected tropical disease. Other animals, such as cows, may carry the disease and become infected in which case it is known as animal trypanosomiasis.

There is some debate among the WHO, CDC, and infectious disease experts over which diseases are classified as neglected tropical diseases. Feasey, a researcher in neglected tropical diseases, notes 13 neglected tropical diseases: ascariasis, Buruli ulcer, Chagas disease, dracunculiasis, hookworm infection, human African trypanosomiasis, Leishmaniasis, leprosy, lymphatic filariasis, onchocerciasis, schistosomiasis, trachoma, and trichuriasis. Fenwick recognizes 12 "core" neglected tropical diseases: ascariasis, Buruli ulcer, Chagas disease, dracunculiasis, human African trypanosomiasis, Leishmaniasis, leprosy, lymphatic filariasis, onchocerciasis, schistosomiasis, trachoma, and trichuriasis.

These diseases result from four different classes of causative pathogens: (i) protozoa (for Chagas disease, human African trypanosomiasis, leishmaniases); (ii) bacteria (for Buruli ulcer, leprosy, trachoma, yaws), (iii) helminths or metazoan worms (for cysticercosis/taeniasis, dracunculiasis, echinococcosis, foodborne trematodiases, lymphatic filariasis, onchocerciasis, schistosomiasis, soil-transmitted helminthiasis); and (iv) viruses (dengue and chikungunya, rabies).

The World Health Organization recognizes the seventeen diseases below as neglected tropical diseases.

As in the majority of paracoccidioidomycosis cases, pulmonary involvement results in shortness of breath, a productive cough and hemoptysis, as well as general symptoms of weight loss, fever and fatigue. Visually, lesions (as pictured) are often present, most commonly on the face.

Paracoccidioidomycosis (PCM) (also known as "Brazilian blastomycosis," "South American blastomycosis,","Lutz-Splendore-de Almeida disease" and "paracoccidioidal granuloma") is a fungal infection caused by the fungus "Paracoccidioides brasiliensis". Sometimes called "South American blastomycosis", paracoccidioidomycosis is caused by a different fungus than that which causes blastomycosis.

Viscerotropic leishmaniasis is a systemic infection reported in soldiers fighting in Operation Desert Storm in Saudi Arabia.

A robovirus is a zoonotic virus that is transmitted by a rodent vector (i.e., "ro"dent "bo"rne).

Roboviruses mainly belong to the Arenaviridae and Hantaviridae family of viruses. Like arbovirus ("ar"thropod "bo"rne) and tibovirus ("ti"ck "bo"rne) the name refers to its method of transmission, known as its vector. This is distinguished from a clade, which groups around a common ancestor. Some scientists now refer to arbovirus and robovirus together with the term ArboRobo-virus.

An anthroponotic disease, or anthroponosis, is an infectious disease in which a disease causing agent carried by humans is transferred to other animals. It may cause the same disease or a different disease in other animals. Since humans do not generally inflict bite wounds on other animals, the method of transmissions is always a "soft" contact such as skin to skin transmission. An example is chytridiomycosis which can be spread by humans with the fungus on their skin handling frogs with bare hands.

The reverse situation, a disease transmitted from animals to humans, is known as zoonotic.

It can also be defined as a human-to-human infection with no animal vector.

Besnoitiosis is "a protozoan disease of the skin, subcutis, blood vessels, mucous membranes, and other tissues" of animals. It "is endemic in tropical and sub-tropical regions with high infection rate but low mortality"; however, it is rare in other regions.

The causative organisms of the cutaneous disease, and the affected animals include:

- "Besnoitia besnoiti" in cattle (swelling of the lymph nodes, subcutaneous swellings, diarrhea, abortion and infertility)

- "Besnoitia bennetti" in horses and donkeys (characterized by a widespread, serious dermatitis)

- "Besnoitia jellisoni" and "B. wallacei" in rodents

- "Besnoitia tarandi" in reindeer and caribou

- "Besnoitia darlingi" in lizards, opossums, and snakes

- "Besnoitia sauriana" in lizards

- Viscerotropic strains of "B.besnoiti" in African antelope

- An unidentified "Besnoitia" species in goats in Iran, New Zealand, and Kenya

Post-kala-azar dermal leishmaniasis (also known as "Post-kala-azar dermatosis") is a cutaneous condition that is characterized by depigmented macular, maculopapular and nodular eruptions found mainly on the face, arms, and upper part of the trunk. It occurs years(in the Indian variation)or a few months(in the African strain) after the successful treatment of visceral leishmaniasis

In some cases, internal and external bleeding may occur. This typically begins five to seven days after the first symptoms. All infected people show some decreased blood clotting. Bleeding from mucous membranes or from sites of needle punctures has been reported in 40–50 percent of cases. This may cause vomiting blood, coughing up of blood, or blood in stool. Bleeding into the skin may create petechiae, purpura, ecchymoses or hematomas (especially around needle injection sites). Bleeding into the whites of the eyes may also occur. Heavy bleeding is uncommon; if it occurs, it is usually located within the gastrointestinal tract.

The most detailed study on the frequency, onset, and duration of MVD clinical signs and symptoms was performed during the 1998–2000 mixed MARV/RAVV disease outbreak. A maculopapular rash, petechiae, purpura, ecchymoses, and hematomas (especially around needle injection sites) are typical hemorrhagic manifestations. However, contrary to popular belief, hemorrhage does not lead to hypovolemia and is not the cause of death (total blood loss is minimal except during labor). Instead, death occurs due to multiple organ dysfunction syndrome (MODS) due to fluid redistribution, hypotension, disseminated intravascular coagulation, and focal tissue necroses.

Clinical phases of Marburg Hemorrhagic Fever's presentation are described below. Note that phases overlap due to variability between cases.

1. Incubation: 2–21 days, averaging 5–9 days.

2. Generalization Phase: Day 1 up to Day 5 from onset of clinical symptoms. MHF presents with a high fever (~40˚C) and a sudden, severe headache, with accompanying chills, fatigue, nausea, vomiting, diarrhea, pharyngitis, maculopapular rash, abdominal pain, conjunctivitis, & malaise.

3. Early Organ Phase: Day 5 up to Day 13. Symptoms include prostration, dyspnea, edema, conjunctival injection, viral exanthema, and CNS symptoms, including encephalitis, confusion, delirium, apathy, and aggression. Hemorrhagic symptoms typically occur late and herald the end of the early organ phase, leading either to eventual recovery or worsening & death. Symptoms include bloody stools, ecchymoses, blood leakage from venipuncture sites, mucosal & visceral hemorrhaging, and possibly hematemesis.

4. Late Organ Phase: Day 13 up to Day 21+. Symptoms bifurcate into two constellations for survivors & fatal cases. Survivors will enter a convalescence phase, experiencing myalgia, fibromyalgia, hepatitis, asthenia, ocular symptoms, & psychosis. Fatal cases continue to deteriorate, experiencing continued fever, obtundation, coma, convulsions, diffuse coagulopathy, metabolic disturbances, shock and death, with death typically occurring between Days 8 and 16.

Recovery may begin between 7 and 14 days after first symptoms. Death, if it occurs, follows typically 6 to 16 days from first symptoms and is often due to low blood pressure from fluid loss. In general, bleeding often indicates a worse outcome, and blood loss may result in death. People are often in a coma near the end of life.

Those who survive often have ongoing muscular and joint pain, liver inflammation, decreased hearing, and may have continued tiredness, continued weakness, decreased appetite, and difficulty returning to pre-illness weight. Problems with vision may develop.

Additionally, survivors develop antibodies against Ebola that last at least 10 years, but it is unclear if they are immune to repeated infections.

Marburg virus disease (MVD) is the official name listed in the World Health Organization's International Statistical Classification of Diseases and Related Health Problems 10 (ICD-10) for the human disease caused by any of the two marburgviruses Marburg virus (MARV) and Ravn virus (RAVV). In the scientific literature, Marburg hemorrhagic fever (MHF) is often used as an unofficial alternative name for the same disease. Both disease names are derived from the German city Marburg, where MARV was first discovered.