Marburg virus is the causative agent of Marburg haemorrhagic fever (MHF), a disease with a case fatality ratio of up to 88%. Marburg haemorrhagic fever was initially detected in 1967 after simultaneous outbreaks in Marburg, from which the disease takes its name, and Frankfurt in Germany; and in Belgrade, Serbia. Marburg and Ebola viruses are the two members of the Filoviridae family (filovirus). Though caused by different viruses, the two diseases are clinically similar. Both diseases are rare and have the capacity to cause dramatic outbreaks with high fatality rates. Marburg virus was first described in 1967. It was noticed during small outbreaks in the German cities Marburg and Frankfurt and the Yugoslav capital Belgrade in the 1960s. German workers were exposed to tissues of infected grivet monkeys (Chlorocebus aethiops) at the city's former main industrial plant, the Behringwerke, then part of Hoechst, and today of CSL Behring. During these outbreaks, 31 people became infected and seven of them died. MARV is a Select Agent. The incubation or the infection period varies from 2 to 21 days. Illness caused by Marburg virus begins abruptly, with high fever, severe headache and severe malaise. Muscle aches and pains are a common feature. Severe watery diarrhoea, abdominal pain and cramping, nausea and vomiting can begin on the third day. Diarrhoea can persist for a week. The appearance of patients at this phase has been described as showing “ghost-like” drawn features, deep-set eyes, expressionless faces, and extreme lethargy. In the 1967 European outbreak, non-itchy rash was a feature noted in most patients between 2 and 7 days after onset of symptoms. Many patients develop severe haemorrhagic manifestations between 5 and 7 days, and fatal cases usually have some form of bleeding, often from multiple areas. Fresh blood in vomitus and faeces is often accompanied by bleeding from the nose, gums, and vagina. Spontaneous bleeding at venepuncture sites (where intravenous access is obtained to give fluids or obtain blood samples) can be particularly troublesome. During the severe phase of illness, patients have sustained high fever. Involvement of the central nervous system can result in confusion, irritability, and aggression. Orchitis has been reported occasionally in the late phase of disease (15 days). In severe cases death occurs most often between 8 and 9 days after symptom onset, usually preceded by severe blood loss and shock.
There are no cases found in Brazil. Outbreaks and sporadic cases have been reported in Angola, Democratic Republic of Congo, Kenya, and South Africa (in a person who had recently travelled to Zimbabwe). The largest outbreak on record to date occurred in 2005 in Angola, and involved 374 cases, including 329 deaths. Two unrelated sporadic cases occurred during 2008 following visits to the “python cave” in the Maramagambo Forest in western Uganda; this cave is home to a large colony of Egyptian fruit bats. Both people became ill after return to their home country; one in the Netherlands and one in the USA. The most recent outbreak was in 2012 in southwestern Uganda. In Brazil, from 1993 to November 2005, there were 610 cases of HCPS, with an approximate lethality of 40 %, mostly in Minas Gerais, Paraná, São Paulo and Santa Catarina. In the Southeast, the HCPS occurs more in the months from April to July, dry season, harvest time and burning of sugar cane and production braqueária grass seeds, enjoyed food by the rodents. In the South, most cases occur in the second half, linked to working with Pinus, corn or ratada (large proliferation of rodents) , occasional event linked to the flowering of taquara8. Among the four hemorrhagic fevers that occur in Brazil are from diseases with thousands of reported cases, such as DHF / DSS, the rare diseases such as hemorrhagic fever arenaviruses. There may be subnotificção cases of hemorrhagic fever in Brazil due to the limited dissemination and knowledge of doctors about some of these diseases. All induce capillary leak and evidenciáveis bleeding disorders by raising the hematocrit and platelet count. Early clinical suspicion followed by hospitalization accelerates the installation of support measures, which is critical to the survival of patients. The four viral hemorrhagic fevers question has extensive differential diagnosis includes, usually, bacterial sepsis and leptospirosis. Specific antiviral treatment with ribavirin, is effective only in the hemorrhagic fever arenaviruses. The parenteral fluid infusion, recommended in profusion in DHF / DSS, should be cautious in HCPS. Vaccines are available for yellow fever and possibly for hemorrhagic fever arenaviruses.
There is currently no effective 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. Experimentally, recombinant vesicular stomatitis Indiana virus (VSIV) expressing the glycoprotein of MARV has been used successfully in nonhuman primate models as post-exposure prophylaxis. Experimental therapeutic regimens rely on antisense technology: phosphorodiamidate morpholino oligomers (PMOs) targeting the MARV genome could prevent disease in nonhuman primates. Leading medications from Sarepta and Tekmira both have been successfully used in European humans as well as primates.