There are three main viruses that have been studied and confirmed as the agents responsible for AHC, including enterovirus 70, coxsakievirus A24 variant (CA24v) and adenovirus 11.

AHC can only exist in a human host and is transmitted through human contact with an infected individual or object, such as a towel used by an infected person. It is also easily communicable through fecal-oral pathways, thus allowing for its abundance in areas of the world with low levels of hygiene. Within one to two days of infection, symptoms will begin to become apparent.

Enterovirus 70 is a member of the genus of viruses called Enterovirus and family of the viruses Picornaviridae. Usually very small (about 30 nm in diameter), it is non-enveloped (meaning it only has a nucleic acid core and protein capsid) and has a single-stranded positive-sense RNA genome; the protein capsid the virus itself is surrounded by is icosahedral. It is known as one of the more new enteroviruses within this category. It spreads easily from one person’s eyes to another’s through contact with infected objects, like fingers, or through the eye secretion itself. Enterovirus 70 infrequently causes polio-like permanent paralysis.

The risk factors associated with BPF are not well known. However, it has been suggested that children under 5 years of age are more susceptible to BPF since they lack serum bactericidal activity against the infection. Older children and adults have much higher titers of bactericidal antibodies, which serve as a protective measure. Also children residing in warmer geographic areas have been associated with a higher risk of BPF infection.

Most household disinfectants will inactivate FHV-1. The virus can survive up to 18 hours in a damp environment, but less in a dry environment and only shortly as an aerosol.

FVR is transmitted through direct contact only. It replicates in the nasal and nasopharyngeal tissues and the tonsils. Viremia (the presence of the virus in the blood) is rare. The virus is shed in saliva and eye and nasal secretions, and can also be spread by fomites. FVR has a two- to five-day incubation period. The virus is shed for one to three weeks postinfection. Latently infected cats (carriers) will shed FHV-1 intermittently for life, with the virus persisting within the trigeminal ganglion. Stress and use of corticosteroids precipitate shedding. Most disinfectants, antiseptics and detergents are effective against the virus.

Although epidemiologic characteristics of the adenoviruses vary by type, all are transmitted by direct contact, fecal-oral transmission, and occasionally waterborne transmission. Some types are capable of establishing persistent asymptomatic infections in tonsils, adenoids, and intestines of infected hosts, and shedding can occur for months or years. Some adenoviruses (e.g., serotypes 1, 2, 5, and 6) have been shown to be endemic in parts of the world where they have been studied, and infection is usually acquired during childhood. Other types cause sporadic infection and occasional outbreaks; for example, epidemic keratoconjunctivitis is associated with adenovirus serotypes 8, 19, and 37. Epidemics of febrile disease with conjunctivitis are associated with waterborne transmission of some adenovirus types, often centering on inadequately chlorinated swimming pools and small lakes. ARD is most often associated with adenovirus types 4 and 7 in the United States. Enteric adenoviruses 40 and 41 cause gastroenteritis, usually in children. For some adenovirus serotypes, the clinical spectrum of disease associated with infection varies depending on the site of infection; for example, infection with adenovirus 7 acquired by inhalation is associated with severe lower respiratory tract disease, whereas oral transmission of the virus typically causes no or mild disease. Outbreaks of adenovirus-associated respiratory disease have been more common in the late winter, spring, and early summer; however, adenovirus infections can occur throughout the year.

"Ad14 (for adenovirus serotype 14), has caused at least 140 illnesses in New York, Oregon, Texas and Washington, according to a report from the Centers for Disease Control and Prevention. The illness made headlines in Texas in September 2007, when a so-called "boot camp flu" sickened hundreds at Lackland Air Force Base in San Antonio. A 19-year-old trainee died."

Several adenoviruses, including Ad5, Ad9, Ad31, Ad36, Ad37, and SMAM1, have at least some evidence of causation of obesity in animals, adipogenesis in cells, and/or association with human obesity. To date, the most thorough investigations have been conducted for adenovirus serotype 36 (Adv36).

Adenovirus can cause severe necrotizing pneumonia in which all or part of a lung has increased translucency radiographically, which is called Swyer-James Syndrome. Severe adenovirus pneumonia also may result in bronchiolitis obliterans, a subacute inflammatory process in which the small airways are replaced by scar tissue, resulting in a reduction in lung volume and lung compliance.

About 15–20% of hospitalized Lassa fever patients will die from the illness. The overall mortality rate is estimated to be 1%, but during epidemics, mortality can climb as high as 50%. The mortality rate is greater than 80% when it occurs in pregnant women during their third trimester; fetal death also occurs in nearly all those cases. Abortion decreases the risk of death to the mother. Some survivors experience lasting effects of the disease, and can include partial or complete deafness.

Because of treatment with ribavirin, fatality rates are continuing to decline.

The eye gnat ("Liohippelates") was thought to be the cause of the conjunctivitis epidemic which occurred in Mato Grosso do Sul in 1991. These gnats were extracted from the conjunctival secretions of the children who were infected with conjunctivitis. 19 of those children developed BPF following the conjunctivitis. Other modes of transmission include contact with the conjunctival discharges of infected people, ophthalmic instruments which have not been properly sterilized, sharing eye makeup applicators or multiple-dose eye medications.

Omsk hemorrhagic fever is caused by the Omsk hemorrhagic fever virus (OHFV), a member of the Flavivirus family. The virus was discovered by Mikhail Chumakov and his colleagues between 1945 and 1947 in Omsk, Russia. The infection is found in western Siberia, in places including Omsk, Novosibirsk, Kurgan, and Tyumen. The virus survives in water and is transferred to humans via contaminated water or an infected tick.

Investigational vaccines exist for Argentine hemorrhagic fever and RVF; however, neither is approved by FDA or commonly available in the United States.

The structure of the attachment glycoprotein has been determined by X-ray crystallography and this glycoprotein is likely to be an essential component of any successful vaccine.

Treatment is similar to hepatitis B, but due to its high lethality, more aggressive therapeutic approaches are recommended in the acute phase. In absence of a specific vaccine against delta virus, the vaccine against HBV must be given soon after birth in risk groups.

HFRS is primarily a Eurasian disease, whereas HPS appears to be confined to the Americas. The geography is directly related to the indigenous rodent hosts and the viruses that coevolved with them.

Five families of RNA viruses have been recognised as being able to cause hemorrhagic fevers.

- The family "Arenaviridae" include the viruses responsible for Lassa fever (Lassa virus), Lujo virus, Argentine (Junin virus), Bolivian (Machupo virus), Brazilian (Sabiá virus), Chapare hemorrhagic fever (Chapare virus) and Venezuelan (Guanarito virus) hemorrhagic fevers.

- The family "Bunyaviridae" include the members of the "Hantavirus" genus that cause hemorrhagic fever with renal syndrome (HFRS), the Crimean-Congo hemorrhagic fever (CCHF) virus from the "Nairovirus" genus, Garissa virus and Ilesha virus from the "Orthobunyavirus" and the Rift Valley fever (RVF) virus from the "Phlebovirus" genus.

- The family "Filoviridae" include Ebola virus and Marburg virus.

- The family "Flaviviridae" include dengue, yellow fever, and two viruses in the tick-borne encephalitis group that cause VHF: Omsk hemorrhagic fever virus and Kyasanur Forest disease virus.

- In September 2012 scientists writing in the journal PLOS Pathogens reported the isolation of a member of the "Rhabdoviridae" responsible for 2 fatal and 2 non-fatal cases of hemorrhagic fever in the Bas-Congo district of the Democratic Republic of Congo. The non-fatal cases occurred in healthcare workers involved in the treatment of the other two, suggesting the possibility of person-to-person transmission. This virus appears to be unrelated to previously known Rhabdoviruses.

The pathogen that caused the cocoliztli epidemics in Mexico of 1545 and 1576 is still unknown.

Measures to reduce contact between the vesper mouse and humans may have contributed to limiting the number of outbreaks, with no cases identified between 1973 and 1994. Although there are no cures or vaccine for the disease, a vaccine developed for the genetically related Junín virus which causes Argentine hemorrhagic fever has shown evidence of cross-reactivity to Machupo virus, and may therefore be an effective prophylactic measure for people at high risk of infection. Post infection (and providing that the person survives the infection), those that have contracted BHF are usually immune to further infection of the disease.

Preventing Omsk Hemorrhagic Fever consists primarily in avoiding being exposed to tick. Persons engaged in camping, farming, forestry, hunting (especially the Siberian muskrat) are at greater risk and should wear protective clothing or use insect repellent for protection. The same is generally recommended for persons at sheltered locations.

Rodent control in and around the home remains the primary prevention strategy, as well as eliminating contact with rodents in the workplace and campsite. Closed storage sheds and cabins are often ideal sites for rodent infestations. Airing out of such spaces prior to use is recommended. Avoid direct contact with rodent droppings and wear a mask to avoid inhalation of aerosolized rodent secretions.

Lassa virus is a member of the Arenavirida family of viruses. Specifically it is an old world arenavirus, which is enveloped, single-stranded, and bi-segmented RNA. This virus has a both a large and a small genome section, with four lineages identified to date: Josiah (Sierra Leone), GA391 (Nigeria), LP (Nigeria) and strain AV.

The VHF viruses are spread in a variety of ways. Some may be transmitted to humans through a respiratory route. According to Soviet defector Ken Alibek, Soviet scientists concluded China may have tried to weaponise a VHF virus during the late 1980's but discontinued to do so after an outbreak . The virus is considered by military medical planners to have a potential for aerosol dissemination, weaponizaton, or likelihood for confusion with similar agents that might be weaponized.

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.

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.

Lábrea fever is a coinfection or superinfection of hepatitis D or delta virus and hepatitis B (HBV). The infection by delta virus may occur in a patient who already has the HBV, or both viruses may infect at the same time a previously uninfected patient. Delta virus can only multiply in the presence of HBV, therefore vaccination against HBV prevents infection. Thus, American and Brazilian scientists have determined that the delta virusa, virus, which is a small circular RNA virus, is normally unable to cause illness by itself, due to a defect. When it is combined with HBV, Lábrea hepatitis may ensue. The main discovery of delta virus and HBV association was done by Dr. Gilberta Bensabath, a leading tropical virologist of the Instituto Evandro Chagas, of Belém, state of Pará, and her collaborators.

Infected patients show extensive destruction of liver tissue, with steatosis of a particular type (microsteatosis, characterized by small fat droplets inside the cells), and infiltration of large numbers of inflammatory cells called "morula cells", comprised mainly by macrophages containing delta virus antigens.

In the 1987 Boca do Acre study, scientists did an epidemiological survey and reported delta virus infection in 24% of asymptomatic HBV carriers, 29% of acute nonfulminant hepatitis B cases, 74% of fulminant hepatitis B cases, and 100% of chronic hepatitis B cases. The delta virus seems to be endemic in the Amazon region.

Brazilian hemorrhagic fever (BzHF) is an infectious disease caused by the Sabiá virus, an Arenavirus. The Sabiá virus is one of the arenoviruses from South America to cause hemorrhagic fever. It shares a common progenitor with the Junin virus, Machupo virus, Tacaribe virus, and Guanarito virus. It is an enveloped RNA virus and is highly infectious and lethal. Very little is known about this disease, but it is thought to be transmitted by the excreta of rodents.

There have only been three documented infections of the Sabiá virus, only one of which occurred naturally and the other two cases occurred in the clinical setting. The only naturally occurring case was in 1990, when a female agricultural engineer who was staying in the neighborhood of Jardim Sabiá near São Paulo, Brazil contracted the disease. She presented with hemorrhagic fever and died. Her autopsy showed liver necrosis. A virologist who was studying the woman's disease contracted the virus but survived. Ribavirin was not given in these first two cases. Four years later, in 1994, a researcher was exposed to the virus in a level 3 biohazard facility at Yale University when a centrifuge bottle cracked, leaked, and released aerosolized virus particle. He was successfully treated with ribavirin.

Ribavirin is thought to be effective in treating the illness, similar to other arenaviruses. Compared to the patients who did not receive ribavirin, the patient who was treated with it had a shorter and less severe clinical course. Symptomatic control such as fluids to address dehydration and bleeding may also be required.

The Sabiá virus is a Biosafety Level 4 pathogen.

This virus has also been implicated as a means for bioterrorism, as it can be spread through aerosols.

The U.S. Centers for Disease Control and Prevention (CDC) publishes a journal "Emerging Infectious Diseases" that identifies the following factors contributing to disease emergence:

- Microbial adaption; e.g. genetic drift and genetic shift in Influenza A

- Changing human susceptibility; e.g. mass immunocompromisation with HIV/AIDS

- Climate and weather; e.g. diseases with zoonotic vectors such as West Nile Disease (transmitted by mosquitoes) are moving further from the tropics as the climate warms

- Change in human demographics and trade; e.g. rapid travel enabled SARS to rapidly propagate around the globe

- Economic development; e.g. use of antibiotics to increase meat yield of farmed cows leads to antibiotic resistance

- Breakdown of public health; e.g. the current situation in Zimbabwe

- Poverty and social inequality; e.g. tuberculosis is primarily a problem in low-income areas

- War and famine

- Bioterrorism; e.g. 2001 Anthrax attacks

- Dam and irrigation system construction; e.g. malaria and other mosquito borne diseases

Methicillin-resistant Staphylococcus aureus (MRSA) evolved from Methicillin-susceptible Staphylococcus aureus (MSSA) otherwise known as common "S. aureus". Many people are natural carriers of "S. aureus", without being affected in any way. MSSA was treatable with the antibiotic methicillin until it acquired the gene for antibiotic resistance. Though genetic mapping of various strains of MRSA, scientists have found that MSSA acquired the mecA gene in the 1960s, which accounts for its pathogenicity, before this it had a predominantly commensal relationship with humans. It is theorized that when this "S. aureus" strain that had acquired the mecA gene was introduced into hospitals, it came into contact with other hospital bacteria that had already been exposed to high levels of antibiotics. When exposed to such high levels of antibiotics, the hospital bacteria suddenly found themselves in an environment that had a high level of selection for antibiotic resistance, and thus resistance to multiple antibiotics formed within these hospital populations. When "S. aureus" came into contact with these populations, the multiple genes that code for antibiotic resistance to different drugs were then acquired by MRSA, making it nearly impossible to control. It is thought that MSSA acquired the resistance gene through the horizontal gene transfer, a method in which genetic information can be passed within a generation, and spread rapidly through its own population as was illustrated in multiple studies. Horizontal gene transfer speeds the process of genetic transfer since there is no need to wait an entire generation time for gene to be passed on. Since most antibiotics do not work on MRSA, physicians have to turn to alternative methods based in Darwinian medicine. However prevention is the most preferred method of avoiding antibiotic resistance. By reducing unnecessary antibiotic use in human and animal populations, antibiotics resistance can be slowed.