Clinical Features

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After an incubation period that can range from a minimum 2 days (RVF) to a maximum of 35 days (Hantaviruses), a nonspecific clinical picture of fever, myalgia, and prostration emerges. Subsequently, devolution to florid shock and multi-system organ failure may occur. A petechial rash can also be a leading clue to the presence of a VHF. Hepatic inflammation/dysfunction can be seen as well.

Important distinguishing features can be used to delineate the various hemor-rhagic fever viruses. The vascular bed is a major target for all these viruses.

Arenaviruses

After an incubation period of 3 to 16 days, an illness with an insidious onset ensures. Fever, chills, malaise, and retroocular pain herald the initial symptoms. Lassa is known to cause a purulent pharyngitis and aphthous ulcers. Conjunctivitis and exanthem of the face, upper thorax, and neck may be seen. However, hepato-splenomegaly is not observed. After a week of illness, symptom severity intensifies, culminating in hemorrhaging from the gums, nose, stomach, intestines, urinary tract, and uterus. Death ensues as the result of renal failure or hypovolemic shock. If the fever should break, recovery may follow.

Lassa Fever does not have a pronounced hemorrhagic component (17%), and neurological impairment is rare except for sensorineural deafness (the most common cause of deafness in West Africa). On the other hand, Bolivian Hemorrhagic Fever has neurological impairment as a prominent feature (headache, tremor, encephalitis).

Laboratory abnormalities include leukopenia, thrombocytopenia, and albuminuria. However, with Lassa Fever leukocytosis and liver function test (LFT) abnormalities can be present. Case fatality rates range from 10 to 30%.

Bunyaviruses

Crimean-Congo Hemorrhagic Fever. A sudden onset of fever, chills, and myalgias heralds the onset of this disease after an incubation period of 2 to 9 days. Sore throat, conjunctivitis, photophobia, and diarrhea may also be present. The patient may exhibit a labile mood. Three to six days into the illness, the hemorrhagic manifestations may erupt. A petechial rash and hemorrhage from most orifices and organ systems can ensue as disseminated intravascular coagulation (DIC) emerges. The liver may be enlarged and tender. Resolution of the rash may be a sign of recovery. Leukopenia, thrombocytopenia, abnormal LFTs, and abnormal clotting tests will be present. The case fatality rate is between 30 and 50%.

Rift Valley Fever. Most infections with this virus are mild self-limited febrile illnesses; however, 1-2% of patients develop hemorrhagic complications or fatal encephalitis.

Hantavirus

Hantavirus infection is responsible for two distinct clinical entities: Old World Hemorrhagic Fever with Renal Syndrome (HFRS) and New World Hantavirus Pulmonary Syndrome (HPS).

Hemorrhagic Fever with Renal Syndrome. HFRS occurs upon infection with the Hantaan (or related) subtype Hantavirus. The incubation of this illness can last up to 42 days, and 80% of the cases are mild to moderate; however, 20% progress to severe illness.

The illness can be broken into five phases: febrile, hypotensive, oliguric, diuretic, and convalescent. The febrile phase lasts 5 days. Fever, backache, facial flush, and con-junctival injection are present. Petechial hemorrhages and albuminuria will appear. In the 3-day hypotensive phase the temperature can return to normal; however, nausea, vomiting, and abdominal pain will be present. Capillary leakage ensues, leading to an increased hematocrit along with severe proteinuria, leukocytosis, thrombocytopenia, and diminishing renal function. The 4-day oliguric phase is heralded by extravascular fluid resorption, resulting in hypervolemia, hypertension, metabolic acidosis, and renal failure. Pulmonary edema may also develop. Renal function may normalize in the diuretic phase, with the consequent fluid and electrolyte shifts and imbalances. The convalescent phase may last for months. Case fatality is less than 5%.

Hantavirus Pulmonary Syndrome. The Sin Nombre subtype of Hantavirus is the most common cause of this clinical syndrome. It is heralded by a nonspecific viral prodrome of symptoms, after which follows a cardiopulmonary phase of dyspnea, hypoxia, and non-cardiogenic pulmonary edema. Renal involvement is minimal.

Increased levels of LDH and abnormal liver function tests may occur, as well as thrombocytopenia and leukocytosis. Clotting abnormalities are present. Metabolic acidosis occurs in severe cases. If survival is to occur, recovery usually begins a week after onset of the cardiopulmonary phase. Case fatality is 40 to 50%.

Filoviruses

Marburg and Ebola virus infections are likely the most feared of the VHFs. The high mortality (ranging to 90%) coupled with DIC make them particularly worrisome.

After an incubation period of 3 to 9 (Marburg) or 3 to 18 (Ebola) days, an abrupt onset of headache, backache, and myalgias begins. Nausea, vomiting, and profuse watery and bloody diarrhea occur about 3 days later. A maculopapular rash erupts, and by days 4-5 diffuse hemorrhage occurs. Death occurs frequently by day 8 or 9. Leukopenia, thrombocytopenia, clotting abnormalities, proteinuria, and amylasemia will occur. EKG changes may also reflect myocardial involvement. Case fatality reaches 30% with Marburg and 90% with Ebola.

Flaviviruses

Yellow Fever. Yellow fever is named for the jaundice it causes secondary to liver dysfunction/failure. The disease has a spectrum of presentation from a "viral-like illness" to fulminant liver failure and hemorrhage leading to death. Up to 50% of infected individuals may be asymptomatic. Mild cases present with fevers, headaches, con-junctival injection, facial flushing, and a relative bradycardia. Initial infection may resolve or become biphasic with the more ominous complications: bleeding, liver failure, shock, renal failure, myocardial dysfunction, coma, seizures, and death. With severe cases mortality approaches 50%.

Dengue Hemorrhagic Fever. Dengue Hemorrhagic Fever does not occur with primary infection of Dengue Fever. At least four serotypes exist, and infection with a different serotype triggers an immunologic mechanism leading to capillary leakage, bleeding diathesis, and shock. The onset of the illness is associated with high fevers, retroorbital headaches, nausea, muscle pains, sore throat, and abdominal pain. Easy bruising, petechiae, epistaxis, and gum bleeding can also occur. Most cases are moderately severe or mild, and when the fever subsides recovery ensues. However, severe cases can be associated with shock. On laboratory findings, leukopenia, thrombocytopenia, and evidence of plasma leakage by at least a 20% increase in the hematocrit. Case fatality is between 2 and 10%.

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