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Diagnosis of MVD is similar to diagnosis of EVD using the [[Enzyme-Linked ImmunoSorbent Assay]] (ELISA) test.<ref>[http://www.mayoclinic.com/health/ebola-virus/DS00996/DSECTION=tests-and-diagnosis]</ref> Polymerase Chain Reaction (PCR) technique has been successfully used for detection of Marburg virus. [http://books.google.com/books?id=VS5bqBQ9RWoC&pg=PA111&dq=Haenninen+Marburg&ei=Jiz4S96dM5SCyQSaxKXXCg&hl=fi&cd=1#v=onepage&q=Haenninen%20Marburg&f=false PCR detection for Marburg virus by Hänninen 2001]
Diagnosis of MVD is similar to diagnosis of EVD using the [[Enzyme-Linked ImmunoSorbent Assay]] (ELISA) test.<ref>[http://www.mayoclinic.com/health/ebola-virus/DS00996/DSECTION=tests-and-diagnosis]</ref> Polymerase Chain Reaction (PCR) technique has been successfully used for detection of Marburg virus. [http://books.google.com/books?id=VS5bqBQ9RWoC&pg=PA111&dq=Haenninen+Marburg&ei=Jiz4S96dM5SCyQSaxKXXCg&hl=fi&cd=1#v=onepage&q=Haenninen%20Marburg&f=false PCR detection for Marburg virus by Hänninen 2001]


== Prevention ==
==Prevention==
There are currently no [[Food and Drug Administration]]-approved [[vaccine]]s for the prevention of MVD. Many candidate vaccines have been developed and tested in various animal models.<ref name=Warfield2004>{{Cite pmid|15308377}}</ref><ref name=Hevey1997>{{Cite pmid|9426460}}</ref><ref name=Swenson2005>{{Cite pmid|15811650}}</ref><ref name=Hevey2002>{{Cite pmid|11672925}}</ref><ref name=Riemenschneider2003>{{Cite pmid|12922144}}</ref><ref name=Wang2006>{{Cite pmid|16820184}}</ref><ref name=Hevey1998>{{Cite pmid|9813200}}</ref><ref name=Garbutt2004>{{Cite pmid|15113924}}</ref><ref name=Jones2005>{{Cite pmid|15937495}}</ref><ref name=Daddario-DiCaprio2006>{{Cite pmid|16973570}}</ref><ref name=Swenson2008>{{Cite pmid|18444889}}</ref> Of those, the most promising ones are [[DNA vaccination|DNA vaccines]]<ref name=Riemenschneider2003/> or based on [[Venezuelan equine encephalitis virus]] [[Replicon (genetics)|replicons]]<ref name=Hevey1998/>, [[vesicular stomatitis virus|vesicular stomatitis Indiana virus (VSIV)]]<ref name=Jones2005/><ref name=Daddario-DiCaprio2006/> or [[virus-like particle|filovirus-like particles (VLPs)]]<ref name=Swenson2008/> as all of these candidates could protect nonhuman primates from marburgvirus-induced disease. DNA vaccines have entered clinical trials.<ref name="NIAIDVaccineDevelopment">{{Cite press release|title=Ebola/Marburg Vaccine Development|publisher=National Institute of Allergy and Infectious Diseases|date=2008-09-15|url=http://www3.niaid.nih.gov/topics/ebolaMarburg/default.htm}}</ref> Marburgviruses are highly [[infection|infectious]], but not very [[Contagious disease|contagious]]. Importantly, and contrary to popular belief, marburgviruses due not get transmitted by [[aerosol]] during natural MVD outbreaks. Due to the absence of an approved vaccine, prevention of MVD therefore relies predominantly on behavior modification, proper [[personal protective equipment]], and [[sterilization]]/[[disinfection]].
Marburgviruses are biosafety level-four agent ([[BSL-4]]), and thus requires the highest level of precautions by caregivers and researchers.<ref>{{cite web
| url = http://www.phac-aspc.gc.ca/msds-ftss/msds98e-eng.php
| title = Marburg virus - Material Safety Data Sheets (MSDS)
| accessdate = 2008-10-12
| date = 1997-10-11
| publisher = Public Health Agency of Canada
}}</ref> In the presence of the virus, barrier infection control measures are necessary, including double gloves, impermeable gowns, face shields, eye protection and leg and shoe coverings.


===In endemic zones===
A few [[research]] groups are working on antiviral drugs and vaccines to treat or prevent viral disease. In 1998, a group at the [[United States Army Medical Research Institute of Infectious Diseases]] (USAMRIID) published the first peer reviewed article detailing the development of an experimental Marburg virus vaccine that completely protected animals from lethal Marburg virus infection.<ref name="Hevey1998">{{Cite doi|10.1006/viro.1998.9367}}</ref> In 2002, [[Genphar]], a company doing research for the [[United States Army]]'s[[biodefense]] program, announced that an experimental vaccine protected animals from a high dose of Marburg virus. The tests were conducted at USAMRIID. According to the company, all animals in the control group died within days whereas all animals that received the regular dosage of the vaccine were fully protected.{{Citation needed|date=April 2011}}
The natural maintenance hosts of marburgviruses remain to be identified unequivocally. However, the isolation of both MARV and RAVV from [[bats]] and the association of several MVD outbreaks with bat-infested mines or caves strongly suggests that bats are involved in marburgvirus transmission to humans. Avoidance of contact with [[bats]] and abstaining from visits to caves is highly recommended, but may not be possible for those working in mines or people dependent on bats as a food source.


===During outbreaks===
In June 2005, scientists at [[Canada]]'s [[National Microbiology Laboratory]] announced that they had also developed vaccines for both Marburg and [[Ebola]] that showed significant promise in primate testing. Studies on mice also suggested that the vaccine might be an effective treatment for the disease if it is administered shortly after a patient is infected. To make the vaccines, the scientists fused a surface protein from the viruses they hope to protect against onto an animal virus - [[vesicular stomatitis virus]] - which is thought to be of no threat to humans.<ref name="Jones2006">{{cite journal | author=Jones SM, Feldmann H, Stroher U ''et al.'' | title=Live attenuated recombinant vaccine protects nonhuman primates against Ebola and Marburg viruses | journal=Nature Med | year=2005 | volume=11 | issue=7 | pages=786–90 | pmid=15937495 | doi=10.1038/nm1258 }}</ref> In the[[rhesus macaque]] monkey model of the disease, the vaccine is effective even after infection with the virus.<ref name="Daddario-DiCaprio2006">{{cite journal|author=Daddario-DiCaprio KM, Geisbert TW, Ströher U, ''et al.'' |title=Postexposure protection against Marburg haemorrhagic fever with recombinant vesicular stomatitis virus vectors in non-human primates: an efficacy assessment |journal=Lancet |volume=367 |issue=9520 |pages=1399–404 |year=2006 |pmid=16650649 |doi=10.1016/S0140-6736(06)68546-2|url=http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(06)68546-2}}</ref>
Since marburgviruses are not spreading via aerosol, the most straightforward prevention method during MVD outbreaks is to avoid direct (skin-to-skin) contact with patients, their [[excretion]]s and [[body fluids]], or possibly [[contamination|contaminated]] materials and utensils. Patients ought to be isolated but still have the right to be visited by family members. Medical staff should be trained and apply strict barrier nursing techniques (disposable face mask, gloves, goggles, and a gown at all times). Traditional [[burial]] rituals, especially those requiring [[embalming]] of bodies, ought to be discouraged or modified, ideally with the help of local [[traditional healer]]s.<ref>{{Cite book|last=Centers for Disease Control and Prevention and World Health Organization|title=Infection Control for Viral Haemorrhagic Fevers in the African Health Care Setting|url=http://www.cdc.gov/ncidod/dvrd/spb/mnpages/vhfmanual/entire.pdf|format=PDF|accessdate=2009-05-31|year=1998|publisher=Centers for Disease Control and Prevention|location=Atlanta, Georgia, USA|ref=CITEREFCDCWHO1998}}</ref>

===In the laboratory===
Marburgviruses are [[World Health Organization]] Risk Group 4 Pathogens, requiring [[Biosafety|Biosafety Level 4-equivalent containment]]. Laboratory researchers have to be properly trained in BSL-4 practices and wear proper personal protective equipment.


== Treatment ==
== Treatment ==

Revision as of 13:13, 8 October 2011

Marburg virus disease
SpecialtyInfectious diseases Edit this on Wikidata

Marburg virus disease (MVD) is the name for the human disease caused by any of the two marburgviruses Marburg virus (MARV) and Ravn virus (RAVV). MVD is a viral hemorrhagic fever (VHF), and is clinically indistinguishable from Ebola virus disease (EVD).

Classification

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.[1]

Signs and symptoms

MVD is clinically indistinguishable from Ebola virus disease (EVD), and it can also easily be confused with many other diseases prevalent in Equatorial Africa, such as other viral hemorrhagic fevers, falciparum malaria, typhoid fever, shigellosis, rickettsial diseases, cholera, gram-negative septicemia or EHEC enteritis. 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.[2] MVD has an incubation period of 3-21 days and begins with a sudden onset of an influenza-like stage characterized by general malaise, fever with chills, arthralgia and myalgia, and chest pain. Nausea is accompanied by abdominal pain, anorexia, diarrhea, and vomiting. Respiratory tract involvement is characterized by pharyngitis with sore throat, cough, dyspnea, and hiccups. The central nervous system is affected as judged by the development of severe headaches, agitation, confusion, fatigue, depression, seizures, and sometimes coma. The circulatory system is also frequently involved, with the most prominent signs being edema and conjunctivitis. Hemorrhagic symptoms are infrequent (the reason why Ebola hemorrhagic fever (EHF) is a misnomer) and include hematemesis, hemoptysis, melena, and bleeding from mucous membranes (gastroinestinal tract, nose, vagina and gingiva). A maculopapular rash, petechiae, purpura, ecchymoses, and hematomas (especially around needle injection sites) are other 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.[2][3][4][5][6][7][8][9][10][11][12][13]

Causes

Main article: Marburgvirus

MVD is caused by two viruses classified in the genus Marburgvirus: Marburg virus (MARV) and Ravn virus (RAVV).

Genus Marburgvirus: species and its MVD-causing viruses
Species name Virus name (Abbreviation)
Marburg marburgvirus* (accepted)[14] Marburg virus (MARV; previously MBGV)
Ravn virus (RAVV; previously Marburg virus Ravn)

Table legend: "*" denotes the type species and "accepted" refers to a taxon that has been accepted by the Executive Committee of the ICTV but that has yet to be ratified.

Risk factors

In 2009, the successful isolation of infectious RAVV was reported from caught healthy Egyptian rousettes (Rousettus aegyptiacus) [15] This isolation, together with the isolation of infectious RAVV[15], strongly suggests that Old World fruit bats are involved in the natural maintenance of marburgviruses. Further studies are necessary to establish whether Egyptian rousettes are the actual hosts of RAVV and MARV or whether they get infected via contact with another animal and therefore serve only as intermediate hosts.

The disease is spread through bodily fluids, including blood, excrement, saliva, semen, and vomit.

Triggers

Virology

Main article: Marburg virus

Genome

Like all mononegaviruses, marburgvirions contain non-infetious, linear nonsegmented, single-stranded, non-infectious RNA genomes of negative polarity that possesses inverse-complementary 3' and 5' termini, do not possess a 5' cap, are not polyadenylated, and are not covalently linked to a protein.[16] Marburgvirus genomes are approximately 19 kb long and contain seven genes in the order 3'-UTR-NP-VP35-VP40-GP-VP30-VP24-L-5'-UTR.[17] The genomes of the two different marburgviruses (MARV and RAVV) differ in sequence.

Structure

Like all filoviruses, marburgvirions are filamentous particles that may appear in the shape of a shepherd's crook or in the shape of a "U" or a "6", and they may be coiled, toroid, or branched.[17] Marburgvirions are generally 80 nm in width, but vary somewhat in length. In general, the median particle length of marburgviruses ranges from 795-828 nm (in contrast to ebolavirions, whose median particle length was measured to be 974-1,086 nm ), but particles as long as 14,000 nm have been detected in tissue culture.[18]. Marburgvirions consist of seven structural proteins. At the center is the helical ribonucleocapsid, which consists of the genomic RNA wrapped around a polymer of nucleoproteins (NP). Associated with the ribonucleoprotein is the RNA-dependent RNA polymerase (L) with the polymerase cofactor (VP35) and a transcription activator (VP30). The ribonucleoprotein is embedded in a matrix, formed by the major (VP40) and minor (VP24) matrix proteins. These particles are surrounded by a lipid membrane derived from the host cell membrane. The membrane anchors a glycoprotein (GP1,2) that projects 7 to 10 nm spikes away from its surface. While nearly identical to ebolavirions in structure, marburgvirions are antigenically distinct.

Replication

The marburgvirus life cycle begins with virion attachment to specific cell-surface receptors, followed by fusion of the virion envelope with cellular membranes and the concomitant release of the virus nucleocapsid into the cytosol. The virus RdRp partially uncoats the nucleocapsid and transcribes the genes into positive-stranded mRNAs, which are then translated into structural and nonstructural proteins. Marburgvirus L binds to a single promoter located at the 3' end of the genome. Transcription either terminates after a gene or continues to the next gene downstream. This means that genes close to the 3' end of the genome are transcribed in the greatest abundance, whereas those toward the 5' end are least likely to be transcribed. The gene order is therefore a simple but effective form of transcriptional regulation. The most abundant protein produced is the nucleoprotein, whose concentration in the cell determines when L switches from gene transcription to genome replication. Replication results in full-length, positive-stranded antigenomes that are in turn transcribed into negative-stranded virus progeny genome copies. Newly synthesized structural proteins and genomes self-assemble and accumulate near the inside of the cell membrane. Virions bud off from the cell, gaining their envelopes from the cellular membrane they bud from. The mature progeny particles then infect other cells to repeat the cycle.[19]

Diagnosis

Diagnosis of MVD is similar to diagnosis of EVD using the Enzyme-Linked ImmunoSorbent Assay (ELISA) test.[20] Polymerase Chain Reaction (PCR) technique has been successfully used for detection of Marburg virus. PCR detection for Marburg virus by Hänninen 2001

Prevention

There are currently no Food and Drug Administration-approved vaccines for the prevention of MVD. Many candidate vaccines have been developed and tested in various animal models.[21][22][23][24][25][26][27][28][29][30][31] Of those, the most promising ones are DNA vaccines[25] or based on Venezuelan equine encephalitis virus replicons[27], vesicular stomatitis Indiana virus (VSIV)[29][30] or filovirus-like particles (VLPs)[31] as all of these candidates could protect nonhuman primates from marburgvirus-induced disease. DNA vaccines have entered clinical trials.[32] Marburgviruses are highly infectious, but not very contagious. Importantly, and contrary to popular belief, marburgviruses due not get transmitted by aerosol during natural MVD outbreaks. Due to the absence of an approved vaccine, prevention of MVD therefore relies predominantly on behavior modification, proper personal protective equipment, and sterilization/disinfection.

In endemic zones

The natural maintenance hosts of marburgviruses remain to be identified unequivocally. However, the isolation of both MARV and RAVV from bats and the association of several MVD outbreaks with bat-infested mines or caves strongly suggests that bats are involved in marburgvirus transmission to humans. Avoidance of contact with bats and abstaining from visits to caves is highly recommended, but may not be possible for those working in mines or people dependent on bats as a food source.

During outbreaks

Since marburgviruses are not spreading via aerosol, the most straightforward prevention method during MVD outbreaks is to avoid direct (skin-to-skin) contact with patients, their excretions and body fluids, or possibly contaminated materials and utensils. Patients ought to be isolated but still have the right to be visited by family members. Medical staff should be trained and apply strict barrier nursing techniques (disposable face mask, gloves, goggles, and a gown at all times). Traditional burial rituals, especially those requiring embalming of bodies, ought to be discouraged or modified, ideally with the help of local traditional healers.[33]

In the laboratory

Marburgviruses are World Health Organization Risk Group 4 Pathogens, requiring Biosafety Level 4-equivalent containment. Laboratory researchers have to be properly trained in BSL-4 practices and wear proper personal protective equipment.

Treatment

There is currently no Food and Drug Administration-approved marburgvirus-specific therapy for MVD. Treatment is primarily supportive in nature and includes minimizing invasive procedures, balancing fluids and electrolytes to counter dehydration, administration of anticoagulants early in infection to prevent or control disseminated intravascular coagulation, administration of procoagulants late in infection to control hemorrhaging, maintaining oxygen levels, pain management, and administration of antibiotics or antimycotics to treat secondary infections.[34][35]. Experimentally, recombinant vesicular stomatitis Indiana virus (VSIV) expressing the glycoprotein of MARV has been used successfully in nonhuman primate models as post-exposure prophylaxis.[36] Novel, very promising, experimental therapeutic regimens rely on antisense technology: phosphorodiamidate morpholino oligomers (PMOs) targeting the MARV genome could prevent disease in nonhuman primates.[37]

Prognosis

Prognosis is generally poor (average case-fatality rate of all MVD outbreaks to date = 82%). 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.[38][39][40][12]

Epidemiology

Marburg virus disease (MVD) outbreaks
Year Virus Geographic location Human cases/deaths (case-fatality rate)
1967 MARV Marburg and Frankfurt, West Germany; and Belgrade, Yugoslavia 31/7 (23%)
1975 MARV Rhodesia and Johannesburg, South Africa 3/1 (33%)
1980 MARV Kenya 1/1 (100%)
1987 RAVV Kenya 1/1 (100%)
1988 MARV Koltsovo, Soviet Union 1/1 (100%) [laboratory accident]
1990 MARV Koltsovo, Soviet Union 1/0 (0%) [laboratory accident]
1998–2000 MARV + RAVV Durba and Watsa, Democratic Republic of the Congo 154/128 (83%)
2004–2005 MARV Angola 252/227 (90%)
2007 MARV + RAVV Uganda 3/1 (33%)
2008 MARV Uganda, Netherlands 1/1 (100%)

1967 MVD outbreak

MVD was first documented in 1967, when 31 people became ill in the German towns of Marburg and Frankfurt am Main, and in Belgrade, Yugoslavia. The outbreak involved 25 primary MARV infections and seven deaths, and six nonlethal secondary cases. The outbreak was traced to infected grivets (species Chlorocebus aethiops) imported from Uganda and used in developing poliomyelitis vaccines. The monkeys were received by Behringwerke, a Marburg company founded by the first winner of the Nobel Prize in Medicine, Emil von Behring. The company, which at the time was owned by Hoechst, was originally set up to develop sera against tetanus and diphtheria. Primary infections occurred in Behringwerke laboratory staff while working with grivet tissues or tissue cultures. Secondary cases involved two doctors, a nurse, a post-mortem attendant, and the wife of a veterinarian. All secondary cases had direct contact, usually involving blood, with a primary case. Both doctors became infected through accidental skin pricks when drawing blood from patients.

1975 MVD outbreak

In 1975, an Australian hitchhiker became infected with MARV by unknown means in Rhodesia. He died in a hospital in Johannesburg, South Africa. His girlfriend and an attending nurse subsequently came down with MVD, but survived.

1980 and 1987 MVD outbreaks

A single lethal case of MARV infection occurred in 1980 in Kenya after a French man had visited Kitum Cave. In 1987, a single lethal case of RAVV infection was recorded in a Danish boy, who also had visited this cave.

1998-2000 MVD outbreak

The next major outbreak occurred among illegal gold miners in Durba and Watsa, Democratic Republic of Congo from 1998 to 2000, when co-circulating MARV and RAVV caused 154 cases of MVD and 128 deaths.[41]<

The 2005 MVD outbreak

In early 2005, the World Health Organization (WHO) began investigating an outbreak of viral hemorrhagic fever in Angola, which was centered in the northeastern Uíge Province. The disease may have surfaced as early as March 2004 in a crowded children's ward. A doctor noted that a child, who subsequently died, was displaying signs of haemorrhagic fever. By October, the death rate on the ward went from three to five children a week to three to five a day. On March 22, 2005, as the death toll neared 100, the cause of the illness was identified as the Marburg virus. By July 2005, Angola's health department reported more than 300 cases were fatal. There were cases in 7 of 18 provinces but the outbreak was mostly confined to Uige province.

The virus has also taken a toll on health care workers, including 14 nurses and two doctors.

There has been speculation that the high death rate among children in the early stages of this outbreak may simply be due to the initial appearance of the disease in the children's ward at the Uige hospital. Early death rates (prior to effective monitoring) are meaningless as only the dead are adequately counted.

Countries with direct airline links, such as Portugal, screened passengers arriving from Angola. The Angolan government asked for international assistance, pointing out that there are only approximately 1,200 doctors in the entire country, with some provinces having as few as two. Health care workers also complained about a shortage of personal protective equipment (PPE) such as gloves, gowns and masks. Médecins Sans Frontières (MSF) reported that when their team arrived at the provincial hospital at the center of the outbreak, they found it operating without water and electricity. Contact tracing is complicated by the fact that the country's roads and other infrastructure have been devastated after nearly three decades of civil war and the countryside remains littered with land mines.

One innovation in the Angola outbreak has been the use of a portable laboratory operated by a team of Canadian doctors and technicians. The lab, which can operate on a car battery, has eliminated the need to send blood samples outside the country for testing. This has reduced the turnaround time from days or weeks to about 4 hours.

Meanwhile, at Americo Boa Vida Hospital in the capital, Luanda, an international team prepared a special isolation ward to handle cases from the countryside. The ward was able to accommodate up to 40 patients, but there was some resistance to medical treatment. Because the disease almost invariably resulted in death, some people came to view hospitals and medical workers with suspicion, and there was a brief period when medical teams, suited in full protective gear, were gruesomely attacked in the countryside.[42]

A specially-equipped isolation ward at the provincial hospital in Uige was reported to be empty during much of the epidemic, even though the facility was at the center of the outbreak. WHO was forced to implement what they described as a "harm reduction strategy" which entailed distributing disinfectants to affected families who refused hospital care.

Monthly Reported Deaths
Month year Deaths reported during month
October 2004  17
November 2004   4
December 2004   7
January 2005  20
February 2005  30
March 2005  47
April 2005 123 *
May 2005  80 †
* This represents the difference between WHO reports of April 1 and April 29.
† This represents the difference between WHO reports of April 29 and May 27.
Weekly Reported Deaths
WHO report date Cumulative deaths Deaths during prior week
April 1, 2005 132 n/a
April 8, 2005 180 48
April 15, 2005 * 207 27
April 22, 2005 244 37
April 29, 2005 255 11
May 6, 2005 277 22
May 11, 2005 † 276 -1§
May 18, 2005 311 35
May 27, 2005 ‡ 335 24
June 7, 2005 ‡ 357 22
June 17, 2005 ‡ 356 -1§
July 13, 2005 312 n/a
* No WHO report was issued between the 15th and the 21st. This appears associated with the administrative reclassification of cases.
† Not an entire week. No WHO report for the 13th.
‡ Over a week.
§ No explanation provided for the decrease in cumulative deaths.
¶ Report states that a review of data has led to a downward estimation in total deaths.

Of the 252 people who contracted Marburg during the 2004–2005 outbreak in Angola, 227 died, for a case fatality rate of 90%.[43]

Although all age groups are susceptible to infection, children are more rarely infected. In the 1998-2000 Congo epidemic, only 8% of the cases were children less than 5 years old.[44]

2007 MVD outbreak

MARV infection was confirmed in a 29-year-old man in Uganda. The man became symptomatic on 4 July 2007, was admitted to hospital on 7 July and died on 14 July. The disease was confirmed by laboratory diagnosis on 30 July. The man had had prolonged close contact with a 21-year-old co-worker with a similar illness to whom he had been providing care. The 21-year-old had developed symptoms on 27 June and was hospitalized with a haemorrhagic illness. He then recovered and was discharged on 9 July. Both men were working in a mine in western Uganda.

2008 MVD outbreak

On July 10, 2008, the Netherlands National Institute for Public Health and the Environment, declared that a Dutch woman, who had visited the Python Cave during her holiday in Uganda, had been infected with the Marburg virus, and had been admitted to a hospital in the Netherlands. The woman died when under treatment in the Leiden University Medical Centre in Leiden on 11 July.[45] The Ugandan Ministry of Health closed the cave after this case.[46]

Possible cases

On February 9, 2009, it was reported that in January 2008, a US Citizen from Colorado was the 1st patient treated in the United States for Marburg. The patient had contracted the virus while overseas in Uganda and traveled back to the USA, where she was later treated successfully for the infection. [2],[3]

Society and culture

Weaponization

The former Soviet Union reportedly had a large biological weapons program involving Marburg.[47] The development was conducted in Vector Institute under the leadership of Dr. Nikolai Ustinov, who died after accidentally injecting himself with the virus. The post-mortem samples of Marburg taken from Dr. Ustinov's organs were more powerful than the original strain.[citation needed] This new strain, called "Variant U," was successfully weaponized and approved by Soviet Ministry of Defense in 1990.[48] Biodefence grants in the United States are funding research to develop a vaccine for Marburg virus.[49]

  • In the TV series Millennium, at the End of Season 2 a prion version of the Marburg virus breaks out in Seattle, killing (amongst others) Frank Black's wife, Catherine. In the Season 3 Episode Collateral Damage Peter Watt's daughter is infected with the virus by a Gulf War Veteran who claims that the Millennium Group did the same to American soldiers in the First Gulf War.
  • In the crossover event of the TV series Medical Investigation, episode 17, and Third Watch, season 6 episode 16, the Marburg virus breaks out in New York City, killing 5 from a total of 6 infected persons.
  • In the Sarah Jane Smith series of audios (Series Two) the virus is used as a weapon by a doomsday cult.
  • In the short story Hell Hath Enlarged Herself by Michael Marshall Smith, one of the original scientists is infected with Marburg in an attempt to test ImmunityWorks ver. 1.0.
  • In the non-fiction thriller, The Hot Zone, Richard Preston investigates the origins of incidents involving hemorrhagic fevers and both the Ebola and Marburg viruses.
  • In the novel Microserfs by Douglas Coupland, the Marburg virus is mentioned several times as a metaphor for the spread of information through the internet.
  • In the novel Resident Evil: Caliban Cove an insane scientist and former professor named Nicolas Griffith is referred to by Rebecca Chambers as having infected three men with the Marburg virus after they had been led to believe it was a harmless cold virus.
  • In the novel Pandora's Legion by Harold Coyle and Barrett Tillman, an Al-Qaeda cell in Pakistan injects volunteers with Marburg virus, who then board flights to major international airports in the Western world where the large flow of people would facilitate the spreading of the virus into a pandemic.

References

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  11. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 8800792, please use {{cite journal}} with |pmid=8800792 instead.
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Bibliography

  • Kuhn, Jens H. (2008). Filoviruses — A Compendium of 40 Years of Epidemiological, Clinical, and Laboratory Studies. Archives of Virology Supplement, vol. 20. Vienna, Austria: SpringerWienNewYork. ISBN 978-3211206706.
  • Ryabchikova, Elena I.; Price, Barbara B. (2004). Ebola and Marburg Viruses - A View of Infection Using Electron Microscopy. Columbus, Ohio, USA: Battelle Press. ISBN 978-1574771312.
  • Klenk, Hans-Dieter; Feldmann, Heinz (2004). EBOLA and MARBURG VIRUSES - Molecular and Cellular Biology. Wymondham, Norfolk, UK: Horizon Bioscience. ISBN 978-0954523237.
  • Klenk, Hans-Dieter (1999). Marburg and Ebola Viruses. Current Topics in Microbiology and Immunology - Ergebnisse der Mikrobiologie und Immunitätsforschung, vol. 235. Berlin, Germany: Springer-Verlag. ISBN 978-3540647294.
  • Martini, G. A.; Siegert, R. (1971). Marburg Virus Disease. Berlin, Germany: Springer-Verlag. ISBN 978-0387051994.

Further reading

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