The conjunctiva provides lining for the inside of the eyelid as well as a coating for the sclera, the white portion of the eyeball. It typically serves to provide lubrication for the eye through the production of mucus and tears. When infected with AHC, patients will experience painful, red eyes, swelling of the conjunctival tissue, and frequent mucus discharge from the eyes accompanied by excessive tearing and subconjunctival hemorrhaging. This hemorrhaging is caused by the rupture of blood vessels beneath the conjunctiva giving the eyes a bright red appearance. Some patients also experience blurry vision and fever in addition to the common symptoms and one in every ten thousand cases exhibits paralysis similar to that of polio.

Acute hemorrhagic conjunctivitis (AHC) (also spelled acute haemorrhagic conjunctivitis) is a derivative of the highly contagious conjunctivitis virus, otherwise known as pink eye. Symptoms include excessively red, swollen eyes as well as subconjuntival hemorrhaging. Currently, there is no known treatment and patients are required to merely endure the symptoms while the virus runs its five- to seven-day course. While it was first identified in Ghana, the virus has now been seen in China, India, Egypt, Cuba, Singapore, Taiwan, Japan, Pakistan, Thailand, and the United States.

Signs and symptoms of VHFs include (by definition) fever and bleeding. Manifestations of VHF often also include flushing of the face and chest, small red or purple spots (petechiae), bleeding, swelling caused by edema, low blood pressure (hypotension), and shock. Malaise, muscle pain, headache, vomiting, and diarrhea occur frequently. The severity of symptoms varies with the type of virus. The “VHF syndrome” (capillary leak, bleeding diathesis, and circulatory compromise leading to shock) appears in a majority of people with filovirus hemorrhagic fevers (e.g., Ebola and Marburg virus), Crimean–Congo hemorrhagic fever (CCHF), and the South American hemorrhagic fevers caused by arenaviruses, but only in a small minority of patients with dengue, Rift Valley fever, and Lassa fever.

"Pharyngoconjunctival fever" is a specific presentation of adenovirus infection, manifested as:

- high fever that lasts 4–5 days

- pharyngitis (sore throat)

- conjunctivitis (inflamed eyes, usually without pus formation like pink eye)

- enlargement of the lymph nodes of the neck

- headache, malaise, and weakness

- Incubation period of 5–9 days

It usually occurs in the age group 5–18. It is often found in summer camps and during the spring and fall in schools. In Japan, the illness is commonly referred to as "pool fever" as it is often spread via public swimming pools.

Apart from respiratory involvement, illnesses and presentations of adenovirus include gastroenteritis, conjunctivitis, cystitis, and rash illness. Symptoms of respiratory illness caused by adenovirus infection range from the common cold syndrome to pneumonia, croup, and bronchitis. Patients with compromised immune systems are especially susceptible to severe complications of adenovirus infection. Acute respiratory disease (ARD), first recognized among military recruits during World War II, can be caused by adenovirus infections during conditions of crowding and stress.

Initial signs of FVR include coughing, sneezing, nasal discharge, conjunctivitis, and sometimes fever (up to 106) and loss of appetite. These usually resolve within four to seven days, but secondary bacterial infections can cause the persistence of clinical signs for weeks. Frontal sinusitis and empyema can also result.

FHV-1 also has a predilection for corneal epithelium, resulting in corneal ulcers, often pinpoint or dendritic in shape. Other ocular signs of FHV-1 infection include conjunctivitis, keratitis, keratoconjunctivitis sicca (decreased tear production), and corneal sequestra. Infection of the nasolacrimal duct can result in chronic epiphora (excess tearing). Ulcerative skin disease can also result from FHV-1 infection. FHV-1 can also cause abortion in pregnant queens, usually at the sixth week of gestation, although this may be due to systemic effects of the infection rather than the virus directly.

In chronic nasal and sinus disease of cats, FHV-1 may play more of an initiating role than an ongoing cause. Infection at an early age may permanently damage nasal and sinus tissue, causing a disruption of ciliary clearance of mucus and bacteria, and predispose these cats to chronic bacterial infections.

There are a number of symptoms of the virus. In the first 1–8 days the first phase begins. The symptoms in this phase are:

- chills

- headache

- pain in the lower and upper extremities and severe prostration

- a rash on the soft palate

- swollen glands in the neck

- appearance of blood in the eyes (conjunctival suffusion)

- dehydration

- hypotension

- gastrointestinal symptoms (symptoms relating to the stomach and intestines)

- patients may also experience effects on the central nervous system

In 1–2 weeks, some people may recover, although others might not. They might experience a focal hemorrhage in mucosa of gingival, uterus, and lungs, a papulovesicular rash on the soft palate, cervical lymphadenopathy (it occurs in the neck which that enlarges the lymph glandular tissue), and occasional neurological involvement. If the patient still has OHF after 3 weeks, then a second wave of symptoms will occur. It also includes signs of encephalitis. In most cases if the sickness does not fade away after this period, the patient will die. Patients that recover from OHF may experience hearing loss, hair loss, and behavioral or psychological difficulties associated with neurological conditions.

Symptoms of HFRS usually develop within 1 to 2 weeks after exposure to infectious material, but in rare cases, they may take up to 8 weeks to develop. Initial symptoms begin suddenly and include intense headaches, back and abdominal pain, fever, chills, nausea, and blurred vision. Individuals may have flushing of the face, inflammation or redness of the eyes, or a rash. Later symptoms can include low blood pressure, acute shock, vascular leakage, and acute kidney failure, which can cause severe fluid overload.

The severity of the disease varies depending upon the virus causing the infection. Hantaan and Dobrava virus infections usually cause severe symptoms, while Seoul, Saaremaa, and Puumala virus infections are usually more moderate. Complete recovery can take weeks or months.

The course of the illness can be split into five phases:

- Febrile phase: Symptoms include redness of cheeks and nose, fever, chills, sweaty palms, diarrhea, malaise, headaches, nausea, abdominal and back pain, respiratory problems such as the ones common in the influenza virus, as well as gastro-intestinal problems. These symptoms normally occur for three to seven days and arise about two to three weeks after exposure.

- Hypotensive phase: This occurs when the blood platelet levels drop and symptoms can lead to tachycardia and hypoxemia. This phase can last for 2 days.

- Oliguric phase: This phase lasts for three to seven days and is characterised by the onset of renal failure and proteinuria.

- Diuretic phase: This is characterized by diuresis of three to six litres per day, which can last for a couple of days up to weeks.

- Convalescent phase: This is normally when recovery occurs and symptoms begin to improve.

This syndrome can also be fatal. In some cases, it has been known to cause permanent renal failure.

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.

Viral hemorrhagic fevers (VHFs) are a diverse group of animal and human illnesses in which fever and hemorrhage are caused by a viral infection. VHFs may be caused by five distinct families of RNA viruses: the families "Arenaviridae", "Filoviridae", "Bunyaviridae", "Flaviviridae", and "Rhabdoviridae". All types of VHF are characterized by fever and bleeding disorders and all can progress to high fever, shock and death in many cases. Some of the VHF agents cause relatively mild illnesses, such as the Scandinavian "nephropathia epidemica" (a Hantavirus), while others, such as Ebola virus, can cause severe, life-threatening disease.

In 80% of cases, the disease is asymptomatic, but in the remaining 20%, it takes a complicated course. The virus is estimated to be responsible for about 5,000 deaths annually. The fever accounts for up to one-third of deaths in hospitals within the affected regions and 10 to 16% of total cases.

After an incubation period of six to 21 days, an acute illness with multiorgan involvement develops. Nonspecific symptoms include fever, facial swelling, and muscle fatigue, as well as conjunctivitis and mucosal bleeding. The other symptoms arising from the affected organs are:

- Gastrointestinal tract

- Nausea

- Vomiting (bloody)

- Diarrhea (bloody)

- Stomach ache

- Constipation

- Dysphagia (difficulty swallowing)

- Hepatitis

- Cardiovascular system

- Pericarditis

- Hypertension

- Hypotension

- Tachycardia (abnormally high heart rate)

- Respiratory tract

- Cough

- Chest pain

- Dyspnoea

- Pharyngitis

- Pleuritis

- Nervous system

- Encephalitis

- Meningitis

- Unilateral or bilateral hearing deficit

- Seizures

Clinically, Lassa fever infections are difficult to distinguish from other viral hemorrhagic fevers such as Ebola and Marburg, and from more common febrile illnesses such as malaria.

The virus is excreted in urine for 3–9 weeks and in semen for three months.

Diagnosis of FVR is usually by clinical signs, especially corneal ulceration. Definitive diagnosis can be done by direct immunofluorescence or virus isolation. However, many healthy cats are subclinical carriers of feline herpes virus, so a positive test for FHV-1 does not necessarily indicate that signs of an upper respiratory tract infection are due to FVR. Early in the course of the disease, histological analysis of cells from the tonsils, nasal tissue, or nictitating membrane (third eyelid) may show inclusion bodies (a collection of viral particles) within the nucleus of infected cells.

In documented BPF cases, the symptoms include high fever (101.3 degrees F or higher), nausea, vomiting, severe abdominal pain, septic shock, and ultimately death. A history of conjunctivitis 30 days prior to the onset of fever was also present in the documented BPF cases.

The physical presentation of children infected with BPF include purpuric skin lesions affecting mainly the face and extremities, cyanosis, rapid necrosis of soft tissue, particularly the hands, feet, nose, and ears. Analysis of the fatalities due to BPF showed hemorrhage in the skin, lungs, and adrenal glands. Histopathology showed hemorrhage, intravascular microthrombi and necrosis in the upper dermis, renal glomeruli, lungs, and hepatic sinusoids.

Hantavirus hemorrhagic fever with renal syndrome (HFRS) is a group of clinically similar illnesses caused by species of hantaviruses from the family "Bunyaviridae". It is also known as Korean hemorrhagic fever, epidemic hemorrhagic fever, and nephropathis epidemica. The species that cause HFRS include Hantaan River virus, Dobrava-Belgrade, Saaremaa, Seoul, Puumala and other hantaviruses. It is found in Europe, Asia, and Africa. Of these species, Hantaan River virus and Dobrava-Belgrade virus cause the most severe form of the syndrome and have the highest morbidity rates.

Both hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS) appear to be immunopathologic, and inflammatory mediators are important in causing the clinical manifestations.

A positive BPF diagnosis includes the clinical symptoms (mainly the fever, purpuric lesions, and rapid progression of the disease), isolation of "Haemophilus Influenzae" Biogroup aegyptius from blood, and negative laboratory tests for "Neisseria meningitidis".

The negative tests for "Neisseria meningitidis" rules out the possibility of the symptoms being caused by meningitis, since the clinical presentations of the two diseases are similar.

The illness in humans is a severe form of hemorrhagic fever. Typically, after a 1–3 day incubation period following a tick bite or 5–6 days after exposure to infected blood or tissues, flu-like symptoms appear, which may resolve after one week. In up to 75% of cases, signs of bleeding can appear within 3–5 days of the onset of illness in case of bad containment of the first symptoms: mood instability, , mental confusion and throat petechiae; and soon after nosebleeds, vomiting, and black stools. The liver becomes swollen and painful. Disseminated intravascular coagulation may occur, as well as acute kidney failure, shock, and sometimes acute respiratory distress syndrome. People usually begin to recover after 9–10 days first symptoms appeared. Up to 30% of infected people die by the end of the second week of illness.

Omsk hemorrhagic fever is a viral hemorrhagic fever caused by a Flavivirus.

It is found in Siberia. It is named for an outbreak in Omsk.

The infection has a slow onset with fever, malaise, headache and muscular pains, very similar to Malaria symptoms. Petechiae (blood spots) on the upper body and bleeding from the nose and gums are observed when the disease progresses to the hemorrhagic phase, usually within seven days of onset.

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.

Lábrea fever has a sudden onset, with jaundice (yellowing of the skin), anorexia (lack of appetite), hematemesis (vomiting of blood), headache, fever and severe prostration. Death occurs by acute liver failure (ALF). In the last phase, neurological symptoms such as agitation, delirium, convulsions and hemorrhagic coma commonly appear.

Lassa fever, also known as Lassa hemorrhagic fever (LHF), is a type of viral hemorrhagic fever caused by the Lassa virus. Many of those infected by the virus do not develop symptoms. When symptoms occur they typically include fever, weakness, headaches, vomiting, and muscle pains. Less commonly there may be bleeding from the mouth or gastrointestinal tract. The risk of death once infected is about one percent and frequently occurs within two weeks of the onset of symptoms. Among those who survive about a quarter have deafness which improves over time in about half.

The disease is usually initially spread to people via contact with the urine or feces of an infected multimammate rat. Spread can then occur via direct contact between people. Diagnosis based on symptoms is difficult. Confirmation is by laboratory testing to detect the virus's RNA, antibodies for the virus, or the virus itself in cell culture. Other conditions that may present similarly include Ebola fever, malaria, typhoid fever, and yellow fever. The Lassa virus is a member of the "Arenaviridae" virus family.

There is no vaccine. Prevention requires isolating those who are infected and decreasing contact with the rats. Other efforts to control the spread of disease include having a cat to hunt vermin, and storing food in sealed containers. Treatment is directed at addressing dehydration and improving symptoms. The antiviral medication, ribavirin may be useful when given early. These measures improve outcomes.

Descriptions of the disease date from the 1950s. The virus was first described in 1969 from a case in the town of Lassa, in Borno State, Nigeria. Lassa fever is relatively common in West Africa including the countries of Nigeria, Liberia, Sierra Leone, Guinea, and Ghana. There are about 300,000 to 500,000 cases which result in 5,000 deaths a year.

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.

Venezuelan hemorrhagic fever (VHF) is a zoonotic human illness first identified in 1989. The disease is most prevalent in several rural areas of central Venezuela and is caused by the Guanarito virus (GTOV) which belongs to the Arenaviridae family. The short-tailed cane mouse ("Zygodontomys brevicauda") is the main host for GTOV which is spread mostly by inhalation of aerosolized droplets of saliva, respiratory secretions, urine, or blood from infected rodents. Person-to-person spread is possible, but uncommon.

Crimean–Congo hemorrhagic fever (CCHF) is a viral disease. Symptoms may include fever, muscle pains, headache, vomiting, diarrhea, and bleeding into the skin. Onset of symptoms is less than two weeks following exposure. Complications may include liver failure. In those who survive, recovery generally occurs around two weeks after onset.

The CCHF virus is typically spread by tick bites or contact with livestock carrying the disease. Those affected are often farmers or work in slaughterhouses. It can also spread between people via body fluids. Diagnosis is by detecting antibodies, the virus's RNA, or the virus itself. It is a type of viral hemorrhagic fever.

Prevention involves avoiding tick bites. A vaccine is not commercially available. Treatment is typically with supportive care. The medication ribavirin may also help.

It occurs in Africa, the Balkans, the Middle East, and Asia. Often it occurs in outbreaks. In 2013 Iran, Russia, Turkey, and Uzbekistan documented more than fifty cases. The risk of death among those affected is between 10 and 40%. It was first detected in the 1940s.

Argentine hemorrhagic fever (AHF) or O'Higgins disease, also known in Argentina as mal de los rastrojos, stubble disease, is a hemorrhagic fever and zoonotic infectious disease occurring in Argentina. It is caused by the "Junín virus" (an arenavirus, closely related to the "Machupo virus", causative agent of Bolivian hemorrhagic fever). Its vector is a species of rodent, the corn mouse.