Wednesday, August 29, 2007

Indonesia : Researchers Confirm Bird Flu Virus Passed From Human To Human During April 2006 "Cluster" Outbreak

World Health Organisation Failed To Raise Alert Level When Eight Members Of Same Family Died From H5N1

"We Dodged A Bullet"


How close did we come to a pandemic outbreak of the bird flu virus amongst humans in 2006?

American researchers now claim we "dodged a bullet", because the H5N1 virus did pass from family member to family member during a surge of deaths in Indonesia in April, 2006 :

Ira Longini and colleagues at the Fred Hutchinson Cancer Research Centre in Seattle looked at two clusters - one in which eight family members died in Sumatra in 2006, and another in Turkey in which eight people were infected and four died.

Experts were almost certain the Sumatra case was human-to-human transmission, but were eager to see more proof.

"We find statistical evidence of human-to-human transmission in Sumatra, but not in Turkey," they wrote in a report published in the journal Emerging Infectious Diseases.

"This does not mean that no low-level human-to-human spread occurred in this outbreak, only that we lack statistical evidence of such spread."

In Sumatra, one of Indonesia's islands, a 37-year-old woman appears to have infected her 10-year-old nephew, who infected his father. DNA tests confirmed that the strain the father died of was very similar to the virus found in the boy's body.

"It went two generations and then just stopped, but it could have gotten out of control," Mr Longini said.

"The world really may have dodged a bullet with that one, and the next time, we might not be so lucky."

The researchers estimated the secondary-attack rate, which is the risk that one person will infect another, was 20 per cent. This is similar to what is seen for regular, seasonal influenza A in the United States.


The Indonesian government admitted there was probably human to human spread in the April-May, 2006, "cluster" of deaths. Here's a report on that.

Back in June, 2006, a spokesman for the World Health Organisaion referred to the Indonesian outbreak, where ultimately eight members of the same family died, as "the mother of all (bird flu) clusters".

There was a very real sense of panic, particularly in the Indonesian government and the World Health Organisation, that this was it, the beginning of a worldwide pandemic. But little of that terror filtered through to the media.

The WHO admitted, back then, it was possible that human to human transmission had occurred, but denied the virus had mutated into one that could pass more easily amongst humans, the event that all concerned fear the most.

If human to human transmission did occur during the Sumatra "cluster" of deaths, it is interesting to look back now on a decision by the World Health Organisation mid last year to not raise the pandemic 'Alert' level they use, and of which we have heard nothing about since June 2006 :

WHO won't yet raise the Global Pandemic Alert level from Phase 3 to Phase 4..

Phase 3 translates as Human Infection : Rare Human To Human Transmission

Phase 4 translates as Human Infections : Small Clusters With Limited Human To Human Transmission, but during which the spread is highly localised.

There is good reason for the World Health Organisation to be reluctant to go with Phase 4.

When they officially confirmed that seven members of the same family had died of the bird flu virus, the Indonesian currency plummeted and stocks in airliners and travel companies plunged on fears of a pandemic cutting into airline industry profits, and of a general weakening of the Indonesian tourism industry due to decreased tourists, scared off by fears of the virus.

It's an incredibly fine balancing act that the World Health Organisation must conduct in raising its bird flu-related alert and warning levels.

Ramping up from Phase Three to Phase Four can slash billions from a nation's economy virtually overnight, as stocks tumble and tourists cancel trips.

But delaying the increased level of threat and warning over human deaths could also see the virus spreading much farther than it might have if the warnings were raised earlier. The further the virus spreads through a country or region, and the more people it kills, the greater the economic damage.

It's clear now that the World Health Organisation probably should have moved the Alert level from Phase Three to Phase Four, because there were clear signs of "clusters" and limited spread of the virus from human to human.

They didn't do this, but the bird flu deaths in humans slowed. In the end the WHO made the right decision and probably saved the Indonesian economy from suffering more damage than it did.

The bullet was dodged.


There were nine officially recognised bird flu-related deaths in Indonesia in only ten days through late March and early April this year, and at least 12 in a 30 day period.

April 7 : A 29 year man who died on Thursday in Central Java was confirmed Saturday as being H5N1 positive.

April 6 : 16 year old girl dies in Jakarta, believed to have had contact with sick chicekns.

April 5 : 29 year man in Central Java dies.

April 4 : 23 year old woman dies.

March 29 : 14 year old boy in West Sumatra dies - 28 year old woman in Jakarta dies.

March 28 : 39 year old man dies in Surabaya.

March 27 : 15 year old boy in West Java dies - 22 year old woman in Sumatra dies.

March 20 : 21 year woman in East Java dies.

March 16 : 32 year old man dies in Jakarta.

March 12 : 20 year old woman dies in East Java.


May, 2006 : Five Members Of Indonesian Family Die From Bird Flu In One Week

June, 2006 : The Bird Flu "Storm" In Indonesia


June, 2006 : Bird Flu Is Now "Probably" Spreading Human To Human In Indonesia

"The Mother Of All Bird Flu Clusters"

1 comment:

Dipl.-Ing. Wilfried Soddemann said...

Another one whistleblower:

H5N1 avian flu: Spread by drinking water
Human to human and contact transmission of influenza occur - but are overvalued immense. Influenza epidemics in Germany rarely appear together with recognized clusters (9% of the cases in the season 2004/2005). Recent research must worry: So far the virus had to reach the bronchi and the lungs in order to infect humans. Now in Indonesia it infects the upper respiratory system (mucous membranes of the throat e.g. when drinking and mucous membranes of the nose and probably also the conjunctiva of the eyes as well as the eardrum e.g. at showering). In three cases (Viet Nam, Thailand) stomach and intestine by the H5N1 virus were stricken but not the bronchi and the lungs. The virus must have been thus orally taken up, e.g. when drinking contaminated water.
http://www.cidrap.umn.edu/cidrap/content/influenza/avianflu/news/jun0607indonesia.html
http://www.who.int/mediacentre/factsheets/avian_influenza/en/index.html#history
http://www.cidrap.umn.edu/cidrap/content/influenza/panflu/news/mar1307transmit.html
http://www.cdc.gov/ncidod/EID/vol12no12/06-0829.htm?s_cid=eid06_0829_x

Influenza: Initial introduction of influenza viruses to the population via abiotic water supply versus biotic human viral respirated droplet shedding

The primary, initial transmission of the human influenza epidemics by the biotic droplet infection is not proven (BRANKSTON et al. 2007) and extremely improbably as influenza epidemics

• appear only in 9% of the cases (season 2004/2005 in Germany) together with recognized clusters.
• appear virologically locally singularly (influenza-subtypes and precision typing).
• appear geographically locally singularly.
• are not proven with priority in large cities and densely populated areas.
• appear predominantly in the colder regions of Germany.
• regularly reach their maxima in certain districts/cities.
• in temperate climates strictly run parallel to the course of the sum of coldness during the winter.
• can hardly spread via saliva droplets. Saliva contains far less Influenza viruses than the - heavier - droplets from throat and nose.


The facts

Influenza epidemics in Germany rarely appear together with recognized clusters (9% of the cases in the season 2004/2005) (RKI 2006).

Influenza epidemics appear virologically locally singularly (influenza-subtypes and precision typing) (AGI 2007).

Influenza epidemics also run geographically locally singularly. They are not proven with priority in large cities and densely populated areas. They arise predominantly in the colder regions of Germany (in the east with cold continental climate in the winter, southeast, altitudes) (RKI 2007). They reach their maxima regularly in certain districts/cities (RKI 2007).

In temperate climates Influenza epidemics run strictly parallel to the course of the sum of coldness during winter.

In hot climates/tropics the flood-related influenza is typical after extreme weather and natural after a flood. Virulence of influenza virus depends on temperature and time. If young and fresh contaminated water from a local low well, a cistern, tank, rain barrel or rice field is used water temperature may be higher. In the tropics there are often outdoor cisterns, tanks, rain barrels, rice fields or local low wells for water supply. In Germany about 98% inhabitants have a central public water supply with older and better protected water. In Germany therefore coldness is decisive as to virulence of influenza viruses in drinking water.

Influenza epidemics can hardly spread by saliva droplets. Saliva contains far less influenza viruses than the substantially heavier droplets from throat and nose (ANONYMOUS 2003) (GOLDMANN 2001).

Human influenza viruses could be proven in the excretions of mammals such as pigs (faecal and oronasal), wild boar (faecal and oronasal), cattle and goats, so that the transmission path from the environment over waters and the drinking water in principle is possible (BROWN 2004) (GRAVES et al. 1975) (KADEN et al. 2001) (KAWAOKA et al. 1986) (LANDOLT et al. 2003) (MARKOWSKA DANIEL et al. 1999) (RKI 1999) (VICENTE et al. 2002) (WEBSTER 1998) (ZHOU et al. 1996) (CARPENTER 2001). With considerable certainty further animal species that are infected with influenza A will be discovered in the future (WEBSTER 1998).


Elimination and inactivating of viruses during the drinking water treatment

Drinking water is often not or only roughly filtered in Germany. The very small viruses are not definitely removed thereby. For groundwater treatment fast speed filtration plants for the elimination of iron and manganese do not possess any effect regarding the elimination of viruses (WHO 2004). Even the plants in Germany which are known to be particularly efficient regarding the flocculation and filtration can not reach the elimination and inactivating goals demanded from the WHO (WHO 2004); not even under the consideration of the common disinfection procedures, whose efficiency decreases with sinking water temperature [Chlorine and ozone treatment] and that are only of limited efficiency when microorganisms are embedded in particles or in biofilm [Chlorine, ozone treatment and UV irradiation].


"Cooling chain of the public water supply"

Coldness is by far the most important parameter for the preservation of virulent influenza viruses in water. The temperature minimum of the dam water in Germany values in January and February 3-4°C. Every year, river water has its temperature minimum also in January and February. Close to the surface ground water in Germany has its temperature minimum - similar to the soil in 100 cm depth - at the ground water surface of about 3°C in February and March. Ground water taken from wells of larger depth can also be colder than the deeper ground water due to the affection of surface water that infiltrates in the case of unsatisfactory sealing between the fountain and the surrounding rock. River water draining away and reaching wells on short ways can have the same effect. Bank filtrate from wells, which was drilled near the bank from surface water, adopts the temperature of the cold surface water. The same applies to wells, from which ground water enriched with surface water is pumped. The soil temperatures in a meter of depth correspond to the temperatures of the drinking water pipelines that are laid frost-protected in the soils. The temperature minima of the soil temperatures in a 100 cm depth value in Germany during the months February and March 3-5°C (DWD 2007). The temperatures of the drinking water pipelines and the drinking water transported in them adapt themselves to the soil temperatures. In the winter cold raw water remains cold in the drinking water treatment plants and after the treatment to drinking water in the water tanks and water pipelines until the connection to the consumers. The temperature minimum of the drinking water when connecting to the consumers follows in particular the run of the wintry cold sum in the soil and in the water pipelines. It arises in the months February/March. The cold drinking water is first mixed in the dwellings at the taps with warm water from the house installation. Thus the continuous "cooling chain of the public water supply" is described from the water winning up to the consumers with a drinking water temperature of about 4-5°C in the months February/March. Cold, young, freshly by Influenzaviruses contaminated drinking water, taken out from surface water and badly protected surface near ground water as well as out of the ground water from karst can be the abiotic vehicle, which conserves virulent Influenzaviruses in the winter at 4-5°C and transports them over the "cooling chain of the public water supply" to humans.


Transmission paths of the drinking water

Infections by drinking water will not be transmitted alone by drinking the water. Further transmission paths are the inhalation of aerosols and the contact with the drinking water. Access for humans are the conjunctiva, the nose mucous membrane, the mouth mucous membrane, the eardrum, wounds and by catheters affected other mucous membranes.


Conclusions

The primary transmission of the influenza by the biotic “warm” droplet infection from human to human is, already because of the strict dependence on environmental temperatures in temperate climates, extremely improbable. The influenza must be triggered by an abiotic vehicle, which is increasingly efficient regarding the spread of infections with increasingly cold environmental temperatures. Therefore it has to be searched for abiotic vehicles dependent on cold environmental temperatures for the transmission of the influenza in temperate climates. Drinking water is such an abiotic vehicle.

The stated references and indications show that cold drinking water can be that abiotic vehicle, by which virulent human Influenza viruses from the reservoirs reach humans and triggers predominantly the seasonal influenza epidemics.

That applies in particular also to the extremely lethal H5N1 bird flu, whose faecal transmission is indisputable.


References

AGI (2007): Arbeitsgemeinschaft Influenza http://influenza.rki.de/agi
ANONYM (2003): Understanding Sars and other Respiratory Infections May 2003.
http://www.ifh-homehygiene.org/2003/2downloadabledoc/SARS.pdf
BRANKSTON et al. (2007): Transmission of influenza A in human beings. Lancet Infect Dis. 2007 Apr;7 (4):257-65. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17376383&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
BROWN (2004): Influenza Virus Infections of Pigs, Part 1: swine, avian & human influenza viruses. http://www.pighealth.com/influenza.htm ; Part 2: Transmission between pigs and other species. Veterinary Laboratories Agency, UK.
http://www.pighealth.com/influenzaB.htm
DWD (2007): Deutscher Wetterdienst (DWD), Wetterstation Erfurt-Bindersleben, Erdbodentemperaturen aus 100 cm Tiefe
GOLDMANN (2001): Epidemiology and Prevention of Pediatric Viral Respiratory Infections in Health-Care Institutions, Children’s Hospital and Harvard Medical School, Boston, Massachusetts, USA, Emerging Infectious Diseases, Special Issue.
http://www.cdc.gov/ncidod/eid/vol7no2/goldmann.htm
GRAVES et al. (1975): Human viruses in animals in West Bengal: An ecological analysis, Human Ecology, Volume 3, Number 2 / April, 1975, 105-130.
http://www.springerlink.com/content/u5408wx5t622ll82/
KADEN et al. (2001): Gefährliche Verwandtschaft. Schwarzwild - ein natürliches Reservoir für Infektionserreger und Ansteckungsquelle für Hausschweine? Bundes-forschungsanstalt für Viruskrankheiten der Tiere: Forschungsreport 1/2001: 24-28.
http://ticker-grosstiere.animal-health-online.de/20010902-00002/
KAWAOKA et al. (1986): Intestinal replication of influenza A viruses in two mammalian species, Archives of Virology, Volume 93, Numbers 3-4 / December, 1987, 303-308.
http://www.springerlink.com/content/g352726672xj5703/
LANDOLT et al. (2003): Comparison of the Pathogenesis of Two Genetically Different H3N2 Influenza A Viruses in Pigs, J Clin Microbiol. 2003 May; 41(5): 1936–1941.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstract&artid=154671
MARKOWSKA-DANIEL et al. (1999): Seroprevalence of influenza virus among wild boars in Poland. National Veterinary Research Institute, Swine Diseases Departement, Pulawy, Poland. http://www.medwet.lublin.pl/Year%201999/vol99-05/art222-98.htm
RKI (1999): Robert Koch-Institut (RKI) Merkblatt für Ärzte Influenza – Verhütung und Bekämpfung (Stand 1999).
www.gapinfo.de/gesundheitsamt/alle/seuche/infekt/viru/grippe/mba/index.htm
RKI (2006): Infektionsepidemiologisches Jahrbuch meldepflichtiger Krankheiten für 2005, Datenstand: 1. März 2006)
RKI (2007): Robert Koch-Institut Berlin, RKI, Datenbank der nach Infektionsschutzgesetz meldepflichtigen Infektionskrankheiten in Deutschland; http://www3.rki.de/SurvStat/
VICENTE et al. (2002): Antibodies to selected viral and bacterial pathogens in European wild boars from southcentral Spain. J Wildl Dis. 38(3): 649-52.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12238391&dopt=Abstract
WEBSTER (1998): Influenza: An Emerging Disease. Emerging Infectious Diseases 4(3). http://www.cdc.gov/ncidod/eid/vol4no3/webster.htm
WHO (2004): World Health Organization (WHO), 2004, Guidelines for drinking-water quality, 3rd Ed., http://www.who.int/water_sanitation_health/dwq/gdwq3/en/print.html
ZHOU et al. (1996): Influenza infection in humans and pigs in southeastern China, Archives of Virology, Volume 141, Numbers 3-4 / March, 1996, 649-661. http://www.springerlink.com/content/p220471r1r337521/
ZIMMERMANN (2001): Krankheiten des Schweines. Veterinärmedizinische Fakultät der Universität Bern, Vorlesungsskript: 49-51.
http://www.vetmed.unibe.ch/studvet/download/year4/Erkr%20der%20Schweine_Skript_WZimmermann_234JK_WS0102_081101.pdf

Contact:
Bauassessor Dipl.-Ing. Wilfried Soddemann
eMail: soddemann-aachen@t-online.de