Fear and Violence Accompany a Deadly Virus Across Angola (Marburg)

UANDA, Angola, April 8 - The death toll in Angola from an epidemic caused by an Ebola-like virus rose to 174 Friday as aid workers in one northern provincial town reported that terrified people had attacked them and that a number of health workers had fled out of fear of catching the disease.

International health officials said the epidemic, already the largest outbreak of Marburg virus ever recorded, showed no signs of abating. Seven of Angola's 18 provinces have now reported suspected cases and several neighboring countries have announced health alerts.

"It's becoming a huge problem," said Dick Thompson, a spokesman for the World Health Organization, which has dispatched surveillance teams to the country's northern provinces. "We clearly don't know the dimensions of the outbreak."

Health officials said some Angolans are hiding sick relatives out of fear that they will die if taken to the hospitals, thereby increasing the chance the disease will spread. There is no cure or vaccine for the highly contagious virus. Victims suffer a high fever, diarrhea, vomiting and severe bleeding from bodily orifices and usually die within a week.

The initial outbreak appears to have spread through a pediatric ward in Uige, a town in a farming district about 180 miles north of the capital of Luanda. More than 60 percent of the victims so far have been children.

One health official in Uige said that more than a dozen health care workers have perished from the disease, including two doctors, and that many workers are deserting the town's hospital in fear. Some townspeople are refusing to allow their sick relatives to be taken to an isolation unit set up at the hospital there by Doctors Without Borders, fearing it leads only to a graveyard.

http://www.medicalnewstoday.com/medicalnews.php?newsid=22614

Marburg team assaulted in Angola, WHO halts campaign
10 Apr 2005

Members of the World Health Organization were assaulted in Uige, Angola by residents. The residents feared the team may be spreading the Marburg virus. Uige is at the epicentre of the outbreak.

Angolan authorities say the current Marburg outbreak is the worst ever. So far over 200 cases have been officially identified, of which 184 have died.

The WHO team's job is to collect the dead bodies and teach people about the Marburg virus.

What is Marburg hemorrhagic fever?

Marburg hemorrhagic fever is a rare, severe type of hemorrhagic fever which affects both humans and non-human primates. Caused by a genetically unique zoonotic (that is, animal-borne) RNA virus of the filovirus family, its recognition led to the creation of this virus family. The four species of Ebola virus are the only other known members of the filovirus family.

Marburg virus was first recognized in 1967, when outbreaks of hemorrhagic fever occurred simultaneously in laboratories in Marburg and Frankfurt, Germany and in Belgrade, Yugoslavia (now Serbia). A total of 37 people became ill; they included laboratory workers as well as several medical personnel and family members who had cared for them. The first people infected had been exposed to African green monkeys or their tissues. In Marburg, the monkeys had been imported for research and to prepare polio vaccine.

How do humans get Marburg hemorrhagic fever?

Just how the animal host first transmits Marburg virus to humans is unknown. However, as with some other viruses which cause viral hemorrhagic fever, humans who become ill with Marburg hemorrhagic fever may spread the virus to other people. This may happen in several ways. Persons who have handled infected monkeys and have come in direct contact with their fluids or cell cultures, have become infected. Spread of the virus between humans has occurred in a setting of close contact, often in a hospital. Droplets of body fluids, or direct contact with persons, equipment, or other objects contaminated with infectious blood or tissues are all highly suspect as sources of disease.

What are the symptoms of the disease?

After an incubation period of 5-10 days, the onset of the disease is sudden and is marked by fever, chills, headache, and myalgia. Around the fifth day after the onset of symptoms, a maculopapular rash, most prominent on the trunk (chest, back, stomach), may occur. Nausea, vomiting, chest pain, a sore throat, abdominal pain, and diarrhea then may appear. Symptoms become increasingly severe and may include jaundice, inflammation of the pancreas, severe weight loss, delirium, shock, liver failure, massive hemorrhaging, and multi-organ dysfunction.

Because many of the signs and symptoms of Marburg hemorrhagic fever are similar to those of other infectious diseases, such as malaria or typhoid fever, diagnosis of the disease can be difficult, especially if only a single case is involved.

Antigen-capture enzyme-linked immunosorbent assay (ELISA) testing, IgM-capture ELISA, polymerase chain reaction (PCR), and virus isolation can be used to confirm a case of Marburg hemorrhagic fever within a few days of the onset of symptoms. The IgG-capture ELISA is appropriate for testing persons later in the course of disease or after recovery. The disease is readily diagnosed by immunohistochemistry, virus isolation, or PCR of blood or tissue specimens from deceased patients.

Are there complications after recovery?

Recovery from Marburg hemorrhagic fever may be prolonged and accompanied by orchititis, recurrent hepatitis, transverse myelitis or uvetis. Other possible complications include inflammation of the testis, spinal cord, eye, parotid gland, or by prolonged hepatitis.

Is the disease ever fatal?

Yes. The case-fatality rate for Marburg hemorrhagic fever is between 23-25%.

How is Marburg hemorrhagic fever treated?

A specific treatment for this disease is unknown. However, supportive hospital therapy should be utilized. This includes balancing the patient's fluids and electrolytes, maintaining their oxygen status and blood pressure, replacing lost blood and clotting factors and treating them for any complicating infections.

Sometimes treatment also has used transfusion of fresh-frozen plasma and other preparations to replace the blood proteins important in clotting. One controversial treatment is the use of heparin (which blocks clotting) to prevent the consumption of clotting factors. Some researchers believe the consumption of clotting factors is part of the disease process.

Who is at risk for the illness?

People who have close contact with a human or non-human primate infected with the virus are at risk. Such persons include laboratory or quarantine facility workers who handle non-human primates that have been associated with the disease. In addition, hospital staff and family members who care for patients with the disease are at risk if they do not use proper barrier nursing techniques.

Many things in your post may be wrong (refs below).

The incubation period is greater and extends to 28 days and may be ~60 days.

The case fatality rate here is much greater.

There may be airborne transmission.

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01.025.0.01.001. Marburg virus [Location of isolation: Marburg; Germany]
CHARACTERISTICS: Filoviridae; 800-100 nm elongated filamentous virion, single stranded, negative sense RNA

Virus is assigned to the genus 01.025.0.01. "Marburg–like viruses"; family 01.025. Filoviridae; order 01. Mononegavirales.

EPIDEMIOLOGY: 1967 - outbreak in Germany and Yugoslavia following exposure to African green monkeys imported from East Africa (31 cases with 7 deaths); 1975 and 1982-4 cases reported in South Africa (originated in Zimbabwe); 1980 - two cases in Kenya

Virions have a complex construction and consist of an envelope, a nucleocapsid, a polymerase complex, and a matrix. Virions are enveloped. Virions are filamentous, or pleomorphic with extensive branching, or U-shaped, 6-shaped, or circular forms occur (particularly after purification) flexible; about 80 nm in diameter; 790 nm long (after purification). The surface projections are distinctive knob-shaped peplomers evenly covering the surface. They are spaced widely apart; evenly dispersed and embedded in a lipid bilayer. The surface projections comprise surface glycoproteins (GP) and are composed of one type of protein. Surface projections are 10 nm long; spaced 10 nm apart. The nucleocapsid exhibits helical symmetry. The nucleocapsid is helical; is cross-striated; 50 nm in diameter. Axial canal is distinct; in 20 nm in diameter; basic helix is obvious; pitch of helix is 5 nm. Morphologically aberrant forms are observe (after centrifugation).

The incubation period for hemorrhagic fever Marburg virus is 2 to 21 days.

Intrahepatic Marburg

Transmission and Tissue Tropism

The mode of primary infection in any natural setting is unknown with Marburg and Ebola viruses. All secondary cases have been nosocomial or caused by intimate contact with a patient. Transmission occurs usually by contaminated blood samples. One Marburg case was acquired by sexual contact more than 60 days after the original infection. In addition, there is evidence to suggest respiratory spread of infection. Epidemiological data of the 1989 Reston outbreak suggest that droplet or vomit transmission was a major factor in virus spread within quarantine facilities. Virus is usually recovered from acute-phase sera and has also been found in throat washes, urine, soft tissue effusates, semen and anterior eye fluid, even when the specimens were obtained late in convalescence. It has also been regularly isolated from autoptic material, such as spleen, lymph nodes, liver and kidney but rarely from brain or other nervous tissues.

"The initial symptoms are a severe frontal & temporal headache, generalised aches & pains, malaise, by the second day the victim will have a fever. Later symptoms include watery diarrhoea, abdominal pain, nausea, vomiting, a dry sore throat, & anorexia. By day seven of the symptoms, the patient will have a maculopapular (small slightly raised spots) rash. At the same time the person will develop thrombocytopenia & haemorrhagic manifestations, particularly in the gastrointestinal tract, & the lungs, but it can occur from any orifice, mucous membrane or skin site. By day twelve the skin starts to peel away from the rash. Ebola causes lesions in almost every organ, although the liver & spleen are the most noticeably affected. Both are darkened & enlarged with signs of necrosis. The cause of death is normally shock, associated with fluid & blood loss into the tissues.

The haemorrhagic & connective tissue complications of the disease are not really understood, but may be related to the fact that the VP40 protein is antigenically related to human cell matrix proteins (abdominal aortic aneurism protein & MFAP-4), leading to autoimmune attack.

Why does the immune system not clear the infection?

This may be associated with the two forms of the virus glycoprotein. The glycoprotein gene has a translation stop codon in the middle of it, preventing the synthesis of the full length protein. Approximately twenty percent of the mRNA isolated from infected cells had been edited to contain an extra adenosine in a stretch of seven adenosine residues at positions 1019-1026. This causes a frame shift, allowing the synthesis of the full length protein . The larger protein (130Kd - GP) is membrane associated protein, & the truncated version (approximately 60 Kd - SGP) is secreted.

A possible role for SGP is to protect the virus from the immune system as a decoy antigen. However, SGP binds to neutrophils & interferes with their function. Moreover, GP also appears to be immunosuppressive, further interfering with the response to infection."

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