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Interesting from Promed concerning Marburg:
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From: Philippe Hovette hovette.philippe@wanadoo.fr [translated by LM]

Angola: Comments on the Nature of the Marburg Hemorrhagic Fever Outbreak

As an internist and tropical medicine specialist, I am interested in the outbreak of Marburg hemorrhagic fever in Angola. I know little about diseases caused by iloviruses, and certain points intrigue me.

Firstly, this is the 1st epidemic caused by a filovirus which has developed in an urban environment, whereas previously they have been rural zoonoses. Which means of contagion allows an urban epidemic? In an urban zone rodents are the first suspects, but could fructivorous
bats, already accused in Durba and in the epidemics of Ebola hemorrhagic fever, be the origin of the spread?

Secondly, 75 percent of the deceased are children of less than 5 years of age (thus not in school and generally carried on the backs of their mothers), whereas in the 1st epidemic of Marburg hemorrhagic fever which developed in Durba in Zaire, miners and their associates were the victims. There is probably a local factor which has not been highlighted yet. Several assumptions can be considered: viral variation, a local activity responsible for the spread, or infection of children admitted to the hospitals of Uige for another infection [measles, malaria, and typhoid have all been reported from the adjacent Democratic Republic of Congo (see: WHO Bulletin of 19 Jan
2005)].

Thirdly, more surprising is the fact that mothers are little affected despite very close contact with their infants.

Finally, it seems to me that the high mortality compared to the sporadic outbreaks (25 percent) and the epidemic of Durba (82 percent) are explainable by the fact that the population initially consults traditional practitioners and "kimbandeiros," since the disease is locally ascribed to fate. They go to hospital only after failure of these treatments and often arrive moribund. The sparse resources available to the centers of provincial care are also in
question as well as contaminations by re-used needles.

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[This outbreak -- like prior outbreaks of viral hemorrhagic fevers -- began outside the urban environment but transmission was potentiated in the hospital setting. The index case may well have been an adult male whose wife was infected after caring for him, and who then infected their child(ren). An infected child was then hospitalized
in an environment where infectious disease isolation is not routinely practiced, and where supplies are limited so that needles and syringes (or other medical devices) may not be adequately sterilized between uses. Beds may have become contaminated and although washed between patients, perhaps not sufficiently to eliminate the virus.

All of the above were described as sources of transmission in prior viral hemorrhagic fever outbreaks in which the hospital served as a potentiator for transmission of the virus.

The outbreak then took hold in the pediatric ward, among patients that were already admitted for other illnesses not related to Marburg. Because these were hospitalized children, the direct contact with their families was a bit more limited than if they had stayed home. But I suspect that there was more transmission to the family members who then stayed at home and were ill (and died) at home, away from the attention of the formal health sector. That
would explain the early apparent waves in the pediatric population, but now the shifting age distribution involving the hospital staff, and probably family members of the children. I suspect the final epidemiologic reports will reflect this.

With the above theory, the index case probably had the more "traditional route" (whatever that may be) of primary infection -- exposure to bat droppings (as postulated from an isolated Ebola case related to spelunking in Kenya, and for the outbreak in miners in the Democratic Republic of Congo), or exposure to an infected primate through skinning and preparing for food (I do not know if monkeys are eaten in Angola, but I suspect they are, especially in a zone where food resources are limited).

I suspect that the observed high mortality rate may be a function of "in-hospital" mortality rate, and the true rate may be closer to that seen in the Durba outbreak. The disparity from earlier reported mortalities with Marburg may be related to either a different strain,
or more likely to level of medical care available (earlier outbreaks were in more highly developed areas). It will be interesting to see if an analysis of CFR by age group indicates a differential based on age. A true CFR would require doing a baseline serosurvey in the community to establish the denominator of infected individuals. It
is possible that there are milder cases that are not within the radarscope of the health sector. Given the high emotional state in the area, I suspect that such a serosurvey will have to wait until after things quiet down and "return to normal".
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Angola: Death Toll exceeds 200

Health officials in Angola said on Mon 11 Apr 2005 that 203 people out of 221 infected with Marburg virus had died, as local and international health workers race to stem the spread of the disease.

Most of the dead were children under 5 years of age, health workers in the northern Angolan province of Uige -- the most affected region -- said. It is the deadliest Marburg virus outbreak ever recorded.

Panic has spread through the region, with some people hiding their infected relatives and dead bodies from health workers, compounding the problem. Officials also told reporters that a local tradition of delaying the burial of loved ones risked increasing the spread of the
deadly virus. Health workers also said local residents lacked sufficient information about the disease and that hospitals failed to observe basic rules of hygiene that could help stem the epidemic.