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.Of the 252 people who contracted Marburg during the 2004–2005 outbreak of a particularly virulent serotype in Angola, 227 died, for a case fatality rate of 90%. Although all age groups are susceptible to infection, children are rarely infected. In the 1998–2000 Congo epidemic, only 8% of the cases were children less than 5 years old. Epidemiology
Below is a table of outbreaks concerning MVD from 1967 to 2021:

1967 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 an undisclosed location in 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 without adequate personal protective equipment. Secondary cases involved two physicians, a nurse, a post-mortem attendant, and the wife of a veterinarian.
Several hypotheses are given, such as it arises from sinusoidal epithelial damage, increased sinusoidal pressure due to obstruction in blood outflow from the liver, or hepatocellular necrosis.Two morphologic patterns of hepatic peliosis were described by Yanoff and Rawson. In the phlebectatic type, the blood-filled spaces are lined with endothelium and are associated with aneurysmal dilatation of the central vein; in the parenchymal type, the spaces have no endothelial lining and they usually are associated with haemorrhagic parenchymal necrosis. Some consider both patterns to be one process, initiated by focal necrosis of liver parenchyma, observed in parenchymal type, progressing into formation of fibrous wall and endothelial lining around haemorrhage of phlebectatic type. Fibrosis, cirrhosis, regenerative nodules, and tumours may also be seen. Diagnosis
The condition is typically asymptomatic and is discovered following evaluation of abnormal liver function test. However, when severe, it can manifest as jaundice, hepatomegaly, liver failure, and haemoperitoneum. Other cystic conditions of liver
Polycystic liver disease
Solitary congenital cysts
Congenital hepatic fibrosis
Hydatid cyst
Von Meyenburg complexes
Caroli disease (type V choledochal cyst)
Type IV choledochal cysts

Treatment
Treatment is usually directed towards management of the underlying cause. Withdrawal of azathioprine leads to remission in kidney transplant; bacillary peliosis responds to antibiotics. In rare circumstances partial resection of liver or transplant may be required. References


== External links ==