MVD is caused by two viruses Marburg virus (MARV) and Ravn virus (RAVV)family Filoviridae

Marburgviruses are endemic in arid woodlands of equatorial Africa. Most marburgvirus infections were repeatedly associated with people visiting natural caves or working in mines. In 2009, the successful isolation of infectious MARV and RAVV was reported from healthy Egyptian rousettes ("Rousettus aegyptiacus") caught in caves. This isolation strongly suggests that Old World fruit bats are involved in the natural maintenance of marburgviruses and that visiting bat-infested caves is a risk factor for acquiring marburgvirus infections. Further studies are necessary to establish whether Egyptian rousettes are the actual hosts of MARV and RAVV or whether they get infected via contact with another animal and therefore serve only as intermediate hosts. Another risk factor is contact with nonhuman primates, although only one outbreak of MVD (in 1967) was due to contact with infected monkeys. Finally, a major risk factor for acquiring marburgvirus infection is occupational exposure, i.e. treating patients with MVD without proper personal protective equipment.

Contrary to Ebola virus disease (EVD), which has been associated with heavy rains after long periods of dry weather, triggering factors for spillover of marburgviruses into the human population have not yet been described.

Prognosis is generally poor. If a patient survives, recovery may be prompt and complete, or protracted with sequelae, such as orchitis, hepatitis, uveitis, parotitis, desquamation or alopecia. Importantly, MARV is known to be able to persist in some survivors and to either reactivate and cause a secondary bout of MVD or to be transmitted via sperm, causing secondary cases of infection and disease.

Of the 252 people who contracted Marburg during the 2004–2005 outbreak of a particularly virulent serotype in Angola, 227 died, for a case fatality rate of 90%.

Although all age groups are susceptible to infection, children are rarely infected. In the 1998–2000 Congo epidemic, only 8% of the cases were children less than 5 years old.

Marburg virus is a hemorrhagic fever virus of the "Filoviridae" family of viruses and a member of the species "Marburg marburgvirus", genus "Marburgvirus". Marburg virus (MARV) causes Marburg virus disease in humans and nonhuman primates, a form of viral hemorrhagic fever. Considered to be extremely dangerous, the WHO rates it as a Risk Group 4 Pathogen (requiring biosafety level 4-equivalent containment). In the United States, the NIH/National Institute of Allergy and Infectious Diseases ranks it as a Category A Priority Pathogen and the Centers for Disease Control and Prevention lists it as a Category A Bioterrorism Agent. It is also listed as a biological agent for export control by the Australia Group.

The virus can be transmitted by exposure to one species of fruit bats or it can be transmitted between people via body fluids through unprotected copulation and broken skin. The disease can cause bleeding (haemorrhage), fever and other symptoms much like Ebola. Funeral rituals are a particular risk. Actual treatment of the virus after infection is not possible but early, professional treatment of symptoms like dehydration considerably increase survival chances.

In 2009, expanded clinical trials of an Ebola and Marburg vaccine began in Kampala, Uganda.

The viral strains fall into two clades — Ravn virus and Marburg virus. The Marburg strains can be divided into two — A and B. The A strains were isolated from Uganda (five from 1967), Kenya (1980) and Angola (2004–2005) while the B strains were from the Democratic Republic of the Congo epidemic (1999–2000) and a group of Ugandan isolates isolated in 2007-2009.

The mean evolutionary rate of the whole genome was 3.3 × 10 substitutions/site/year (credibility interval 2.0–4.8).The Marburg strains had a mean root time of the most recent common ancestor of 177.9 years ago (95% highest posterior density 87–284) suggesting an origin in the mid 1800s. In contrast the Ravn strains origin dated back to a mean 33.8 years ago (early 1980s). The most probable location of the Marburg virus ancestor was Uganda whereas that of the RAVV ancestor was Kenya.

Viral hemorrhagic septicemia (VHS) is a deadly infectious fish disease caused by viral hemorrhagic septicemia virus (VHSV). It afflicts fish of over 50 species of freshwater

and marine fish in several parts of the northern hemisphere.

VHS is caused by viral hemorrhagic septicemia virus (VHSV), different strains of which occur in different regions, and affect different species. There are no signs that the disease affects human health. VHS is also known as "Egtved disease," and VHSV as "Egtved virus."

Historically, VHS was associated mostly with freshwater salmonids in western Europe,

documented as a pathogenic disease among cultured salmonids since the 1950s. Today it is still a major concern for many fish farms in Europe and is therefore being watched closely by the European Community Reference Laboratory for Fish Diseases.

It was first discovered in the US in 1988 among salmon returning from the Pacific in Washington State. This North American genotype was identified as a distinct, more marine-stable strain than the European genotype. VHS has since been found afflicting marine fish in the northeastern

Pacific Ocean, the North Sea, and the Baltic Sea. Since 2005, massive die-offs have occurred among a wide variety of freshwater species in the Great Lakes region of North America.

Spring viraemia of carp, also known as Swim Bladder Inflammation, is caused by a rhabdovirus called "Rhabdovirus carpio". It is listed as a notifiable disease under the World Organisation for Animal Health.

Swine influenza is an infection caused by any one of several types of swine influenza viruses. Swine influenza virus (SIV) or swine-origin influenza virus (S-OIV) is any strain of the influenza family of viruses that is endemic in pigs. As of 2009, the known SIV strains include influenza C and the subtypes of influenza A known as H1N1, H1N2, H2N1, H3N1, H3N2, and H2N3.

The Swine flu was initially seen in humans in Mexico in 2009, where the strand of the particular virus was a marriage of 3 types of strands. Six of the genes are very similar to the H1N2 influenza virus that was found in pigs around 2000.

Swine influenza virus is common throughout pig populations worldwide. Transmission of the virus from pigs to humans is not common and does not always lead to human flu, often resulting only in the production of antibodies in the blood. If transmission does cause human flu, it is called zoonotic swine flu. People with regular exposure to pigs are at increased risk of swine flu infection.

Around the mid-20th century, identification of influenza subtypes became possible, allowing accurate diagnosis of transmission to humans. Since then, only 50 such transmissions have been confirmed. These strains of swine flu rarely pass from human to human. Symptoms of zoonotic swine flu in humans are similar to those of influenza and of influenza-like illness in general, namely chills, fever, sore throat, muscle pains, severe headache, coughing, weakness, shortness of breath, and general discomfort.

In August 2010, the World Health Organization declared the swine flu pandemic officially over.

Cases of swine flu have been reported in India, with over 31,156 positive test cases and 1,841 deaths up to March 2015.

Although there is no formal national surveillance system in the United States to determine what viruses are circulating in pigs, an informal surveillance network in the United States is part of a world surveillance network.

Thoroughly cleaning boats, trailers, nets and other equipment when traveling between different lakes and streams also

helps. The only EPA-approved disinfectant proven effective against VHS is Virkon AQUATIC (made by Dupont). Chlorine bleach kills the VHS virus, but in concentrations that are much too caustic for ordinary use. Disinfecting stations can be found at various inland lake boat launches in the Great Lakes region.

Clinical symptoms of viral infection include external hemorrhaging, pale gills, and ascites. In some cases, mortality can occur without any apparent clinical signs of the disease. The virus has been found in high concentrations in the liver and kidney, but lower numbers of virions have been isolated from the spleen. The virus has been shown to persist subclinically in fish populations up to 10 weeks following experimental infection. Currently efforts have been made to prevent infection by the virus through the development of DNA vaccines and immunostimulatory therapeutics.

The character of the neurological injury is not clear. The disease onset is associated with high intake of cyanide from a monotonous diet of bitter cassava, which is low in protein, particularly sulfur amino acids. These are essential for the detoxification in the body of cyanide to thiocyanate, which is removed in the urine. A number of studies implicate the combination of high cyanide intake from bitter cassava and low intake of sulfur amino acids as the cause. It has now been shown that the month by month incidence of konzo is significantly correlated with the percentage of children with high urinary thiocyanate content, which is a measure of their cyanide intake. The importance of an adequate supply of protein sulfur amino acids is shown from three unrelated konzo epidemics in Mozambique, Tanzania and DRC. People of the same ethnic group living only 5 km away from those with konzo had near zero konzo prevalence, because in Mozambique they lived near the sea, in Tanzania they lived near Lake Victoria and had access to fish and in DRC they lived near the forest and had access to animal protein.

The dose-response relationship between konzo incidence and cyanide intake, together with the prevention of konzo in many villages by reducing cyanide intake from cassava (see below) and the importance of sulfur amino acids in prevention of konzo, shows that konzo is very likely due to high cyanide/low sulfur amino acid intake in a diet of bitter cassava. Konzo does not occur unless these conditions are met, which occurs only in remote villages in six tropical African countries. The total number of reported cases up to 2009 was 6788, but most cases are never reported and there was an estimate of 100,000 cases in DRC alone in 2002. Konzo is spreading geographically as cassava is being grown in new areas where there is little knowledge of processing methods to remove cyanogens. Konzo epidemics occur due to war which causes disruption of life in poor villages and drought, when the plant increases the cyanogen content of roots 2-4 times and the cyanide content of cassava flour also increases greatly. Konzo is also endemic in certain areas.

Traditional methods of processing cassava to remove cyanogens consist of sun drying and heap fermentation in East Africa, which are inadequate in removal of cyanogens even in a year of normal rainfall. In Central Africa soaking (retting) of cassava roots in water for 4–5 days is adequate, but short soaking for 1–2 days leaves large amounts of cyanogens in flour and leads to konzo. In West Africa a roasted product called gari is produced by a different method than that used to produce flour, which reduces the total cyanide content to 10-20 ppm. There are no reported cases of konzo west of Cameroon. However another neurological disease called tropical ataxic neuropathy (TAN), occurs amongst older people in south-west Nigeria, Tanzania, Uganda, Kenya, West Indies and South India, and is probably due to long term intake of cyanogens from cassava at a lower level than that needed to cause konzo.

Konzo is an epidemic paralytic disease occurring in outbreaks in remote rural areas of low income African countries. The people of these regions have been associated with several weeks of almost exclusive consumption of insufficiently processed "bitter" (high cyanide) cassava ("Manihot esculenta")—a perennial crop native to Amazonia in South America, but widely cultivated in tropical regions worldwide. It is the third most important food source in the tropics after rice and maize and is the staple food of tropical Africa. Cassava yields well in poor soils, is drought-resistant, and the roots give food security during droughts and famine. Nutritionally, the starchy roots are complemented by consumption of cassava leaves, which are rich in proteins and vitamins. Konzo was first described by Giovanni Trolli in 1938 who compiled the observations from eight doctors working in the Kwango area of the Belgian Congo (now Democratic Republic of the Congo).

Crayfish plague, "Aphanomyces astaci", is a water mold that infects crayfish, most notably the European "Astacus" which dies within a few weeks of being infected. When experimentally tested, species from Australia, New Guinea and Japan were also found to be susceptible to the infection.

This disease is most common among the elderly, infants, and children. People with immune deficiency, diabetes, alcoholism, skin ulceration, fungal infections, and impaired lymphatic drainage (e.g., after mastectomy, pelvic surgery, bypass grafting) are also at increased risk.

Most cases of erysipelas are due to "Streptococcus pyogenes" (also known as beta-hemolytic group A streptococci), although non-group A streptococci can also be the causative agent. Beta-hemolytic, non-group A streptococci include "Streptococcus agalactiae", also known as group B strep or GBS. Historically, the face was most affected; today, the legs are affected most often. The rash is due to an exotoxin, not the "Streptococcus" bacteria, and is found in areas where no symptoms are present; e.g., the infection may be in the nasopharynx, but the rash is found usually on the upper dermis and superficial lymphatics.

Erysipelas infections can enter the skin through minor trauma, insect bites, dog bites, eczema, athlete's foot, surgical incisions and ulcers and often originate from streptococci bacteria in the subject's own nasal passages. Infection sets in after a small scratch or abrasion spreads, resulting in toxaemia.

Erysipelas does not affect subcutaneous tissue. It does not release pus, only serum or serous fluid. Subcutaneous edema may lead the physician to misdiagnose it as cellulitis, but the style of the rash is much more well circumscribed and sharply marginated than the rash of cellulitis.

Crayfish plague first arrived in Europe in Italy in 1859, either with imported crayfish from North America, or in ballast water. After its original introduction in Italy in 1860, it spread quickly through Europe and was discovered in Sweden in 1907, in Spain in 1972, in Norway in 1971, in Great Britain in 1981, in Turkey in 1984 and in Ireland in 1987.

In 1959, to bolster dwindling stocks of native crayfish, the signal crayfish was introduced to Sweden. The signal crayfish was known to be resistant, and it was not recognised at that time that it was a carrier of the disease. After 150 years of contact, no resistance has been discovered in native European crayfish.

This species was studied and named by the German Mycologist, Friedrich Schikora (1859–1932), from a type specimen in Germany in 1906.

The Tanganyika laughter epidemic of 1962 was an outbreak of mass hysteriaor mass psychogenic illness (MPI)rumored to have occurred in or near the village of Kashasha on the western coast of Lake Victoria in the modern nation of Tanzania (formerly Tanganyika) near the border of Uganda.

The risk of acquiring infectious diarrhea in the wilderness arises from inadvertent ingestion of pathogens. Various studies have sought to estimate diarrhea attack rates among wilderness travelers, and results have ranged widely. The variation of diarrhea rate between studies may depend on the time of year, the location of the study, the length of time the hikers were in the wilderness,

the prevention methods used, and the study methodology.

The National Outdoor Leadership School (NOLS), which emphasizes strict hand-washing techniques, water disinfection and washing of common cooking utensils in their programs, reports that gastrointestinal illnesses occurred at a rate of only 0.26 per 1000 program days. In contrast, a survey of long-distance Appalachian Trail hikers found more than half the respondents reported at least one episode of diarrhea that lasted an average of two days. (Infectious diarrhea may last longer than an average of two days; certain forms of non-infectious diarrhea, caused by diet change etc., can be of very brief duration). Analysis of this survey found occurrence of diarrhea was positively associated with the duration of exposure in the wilderness. During any given four-week period, as many as 7.2% of Americans may experience some form of infectious or non-infectious diarrhea. A number of behaviors each individually reduced the incidence of diarrhea: treating water; routinely washing hands with soap and water after defecation and urination; cleaning cooking utensils with soap and warm water; and taking multi-vitamins.

A variety of pathogens can cause infectious diarrhea, and most cases among backpackers appear to be caused by bacteria from feces. A study at Grand Teton National Park found 69% of diarrhea affected visitors had no identifiable cause, that 23% had diarrhea due to "Campylobacter" and 8% of patients with diarrhea had giardiasis. Campylobacter enteritis occurred most frequently in young adults who had hiked in wilderness areas and drunk untreated surface water in the week prior. Another study tested 35 individuals before and after a trip to the Desolation Wilderness of California. Giardia cysts were found in fecal samples from two people after the trip, but they were asymptomatic. A third person was empirically treated for symptoms of giardiasis.

Fecal-oral transmission may be the most common vector for wilderness acquired diarrhea. There are differing opinions regarding the importance of routine disinfection of water during relatively brief backcountry visits.

One study suggests that on very long trips in the wilderness, taking multivitamins may reduce the incidence of diarrhea.

Since the advent of penicillin in the 1940s, a major preoccupation in the treatment of streptococcal tonsillitis has been the prevention of rheumatic fever, and its major effects on the nervous system (Sydenham's chorea) and heart. Recent evidence would suggest that the rheumatogenic strains of group A beta hemolytic strep have become markedly less prevalent and are now only present in small pockets such as in Salt Lake City, USA. This brings into question the rationale for treating tonsillitis as a means of preventing rheumatic fever.

Complications may rarely include dehydration and kidney failure due to difficulty swallowing, blocked airways due to inflammation, and pharyngitis due to the spread of infection.

An abscess may develop lateral to the tonsil during an infection, typically several days after the onset of tonsillitis. This is termed a peritonsillar abscess (or quinsy).

Rarely, the infection may spread beyond the tonsil resulting in inflammation and infection of the internal jugular vein giving rise to a spreading septicaemia infection (Lemierre's syndrome).

In chronic/recurrent cases (generally defined as seven episodes of tonsillitis in the preceding year, five episodes in each of the preceding two years or three episodes in each of the preceding three years), or in acute cases where the palatine tonsils become so swollen that swallowing is impaired, a tonsillectomy can be performed to remove the tonsils. Patients whose tonsils have been removed are still protected from infection by the rest of their immune system.

In strep throat, very rarely diseases like rheumatic fever or glomerulonephritis can occur. These complications are extremely rare in developed nations but remain a significant problem in poorer nations. Tonsillitis associated with strep throat, if untreated, is hypothesized to lead to pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS).

The laughter epidemic began on January 30, 1962, at a mission-run boarding school for girls in Kashasha. The laughter started with three girls and spread haphazardly throughout the school, affecting 95 of the 159 pupils, aged 12–18. Symptoms lasted from a few hours to 16 days in those affected. The teaching staff were not affected but reported that students were unable to concentrate on their lessons. The school was forced to close down on March 18, 1962.

After the school was closed and the students were sent home, the epidemic spread to Nshamba, a village that was home to several of the girls. In April and May, 217 people had laughing attacks in the village, most of them being school children and young adults. The Kashasha school was reopened on May 21, only to be closed again at the end of June. In June, the laughing epidemic spread to Ramashenye girls’ middle school, near Bukoba, affecting 48 girls.

The school from which the epidemic sprang was sued; the children and parents transmitted it to the surrounding area. Other schools, Kashasha itself, and another village, comprising thousands of people, were all affected to some degree. Six to eighteen months after it started, the phenomenon died off. The following symptoms were reported on an equally massive scale as the reports of the laughter itself: pain, fainting, flatulence, respiratory problems, rashes, attacks of crying, and random screaming. In total 14 schools were shut down and 1000 people were affected.

The most common cause is viral infection and includes adenovirus, rhinovirus, influenza, coronavirus, and respiratory syncytial virus. It can also be caused by Epstein-Barr virus, herpes simplex virus, cytomegalovirus, or HIV. The second most common cause is bacterial infection of which the predominant is Group A β-hemolytic streptococcus (GABHS), which causes strep throat. Less common bacterial causes include: "Staphylococcus aureus" (including methicillin resistant Staphylococcus aureus or MRSA ),"Streptococcus pneumoniae", "Mycoplasma pneumoniae", "Chlamydia pneumoniae", "Bordetella pertussis", "Fusobacterium" sp., "Corynebacterium diphtheriae", "Treponema pallidum", and "Neisseria gonorrhoeae".

Anaerobic bacteria have been implicated in tonsillitis and a possible role in the acute inflammatory process is supported by several clinical and scientific observations.

Under normal circumstances, as viruses and bacteria enter the body through the nose and mouth, they are filtered in the tonsils. Within the tonsils, white blood cells of the immune system destroy the viruses or bacteria by producing inflammatory cytokines like phospholipase A2, which also lead to fever. The infection may also be present in the throat and surrounding areas, causing inflammation of the pharynx.

Sometimes, tonsillitis is caused by an infection of spirochaeta and treponema, in this case called Vincent's angina or Plaut-Vincent angina.

Mass psychogenic illness (MPI), also called mass sociogenic illness or just sociogenic illness, is "the rapid spread of illness signs and symptoms affecting members of a cohesive group, originating from a nervous system disturbance involving excitation, loss, or alteration of function, whereby physical complaints that are exhibited unconsciously have no corresponding organic" cause. MPI is distinct from other collective delusions, also included under the blanket terms of mass hysteria, in that MPI causes symptoms of disease, though there is no organic cause.

There is a clear preponderance of female victims. The DSM-IV-TR does not have specific diagnosis for this condition but the text describing conversion disorder states that "In 'epidemic hysteria', shared symptoms develop in a circumscribed group of people following 'exposure' to a common precipitant."

In Rasmussen’s encephalitis, there is chronic inflammation of the brain, with infiltration of T lymphocytes into the brain tissue. In most cases, this affects only one cerebral hemisphere, either the left or the right. This inflammation causes permanent damage to the cells of the brain, leading to atrophy of the hemisphere; the epilepsy that this causes may itself contribute to the brain damage. The epilepsy might derive from a disturbed GABA release, the main inhibitory neurotransmitter of the mammalian brain.

The cause of the inflammation is not known: infection by a virus has been suggested, but the evidence for this is inconclusive. In the 1990s it was suggested that auto-antibodies against the glutamate receptor GluR3 were important in causing the disease, but this is no longer thought to be the case. However, more recent studies report the presence of autoantibodies against the NMDA-type glutamate receptor subunit GluRepsilon2 (anti-NR2A antibodies) in a subset of patients with Rasmussen's encephalitis. There has also been some evidence that patients suffering from RE express auto-antibodies against alpha 7 subunit of the nicotinic acetylcholine receptor. By sequencing T cell receptors from various compartments it could be shown that RE patients present with peripheral CD8+ T-cell expansion which in some cases have been proven for years after disease onset.

Rasmussen's encephalitis has been recorded with a neurovisceral porphyria, acute intermittent porphyria and after ADEM (acute disseminated encephalomyelitis).

There is no known treatment for FTS, as the cause is not yet known. There are conflicting reports on whether the paralysis is reversible; some sources claim that moving an elephant away from the area in which it contracted the condition will allow it to recover, while others claim that damage to the trunk is irreversible.

In some extreme cases, wildlife managers have killed affected elephants for humane reasons.