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Transcript
Hantavirus Diseases
By
Christie Alston
Hemal Bhatt
http://www.umm.edu/imagepages/17201.htm
MORPHOLOGY/GENOME

SPHERICAL AND
ENVELOPED

NEGATIVE SENSE RNA
GENOME

TRISEGMENTED
LARGE – RDRP
MEDIUM – G1 AND G2
SMALL – NP

80-110NM DIAMETER
TAXONOMY

FAMILY – Bunyaviridae

GENUS – Hantavirus

MORE THAN 30 DIFFERENT HANTAVIRUS
SPECIES HAVE BEEN FOUND (20 OF WHICH
ARE KNOWN TO BE PATHOGENIC TO
HUMANS)
TAXONOMY
THREE MAIN GROUPS BASED
ON THEIR CARRIERS

SIGMODONTINAE – NEW
WORLD MICE AND RATS

MURINAE – OLD WORLD
MICE AND RATS

ARVICOLINAE – VOLES
AND LEMMINGS
DISTRIBUTION OF NEW AND OLD WORLD
HANTAVIRUSES
Hantavirus Disease

HANTAVIRUSES ARE KNOWN TO CAUSE TWO DIFFERENT
DISEASES IN HUMANS.

1. HEMORRHAGIC FEVER WITH RENAL SYNDROME (HFRS)
– SPECIES KNOWN TO CAUSE DISEASE ARE DOBRAVA,
HANTAAN, PUUMALA AND SEOUL.

2. HANTAVIRUS PULMONARY DISEASE (HPS)
– THERE ARE MANY SPECIES THAT CAUSE HPS. SIN NOMBRE
VIRUS (SNV) HAS BEEN THE CAUSE OF MOST OF THE HPS
CASES IN NORTH AMERICA.
History

1951-1954: HEMORAGIC FEVER WITH RENAL FAILURE FIRST
RECOGNIZED AS A PATHOGEN AFTER AN OUTBREAK IN HANTAAN
KOREA.

1976: DISEASE ISOLATED AND NAMED AFTER HANTAAN RIVER.

1978: IT WAS CONFIRMED THAT THE VIRUS IS CARRIED BY
RODENTS.

1981: FIRST SUCCESSFUL PROPAGATION OF VIRUS IN CELL
CULTURE.

1993: OUTBREAK OF HPS IN FOUR CORNER REGION OF
COLORADO, NEW MEXICO, ARIZONA AND UTAH.
Hantavirus Vectors
Deer Mouse
Rice Rat
http://www.uwrf.edu/~W1001260/Epidemiology.html
Cotton Rat
White Footed Mouse
http://www.uwrf.edu/~W1001260/Pathogenesis.html
Transmission of virus

HANTAVIRUSES DO NOT ADVERSELY AFFECT THEIR HOSTS.

HOSTS WILL AQUIRE A LIFE-LONG CHRONIC INFECTION.

THE INFECTIOUS VIRUS IS SHED THROUGH HOST SALIVA,
URINE AND FECAL MATTER.

HUMANS ARE INFECTED BY INHALING THE VIRUS FROM
AEROSOLS PRODUCED WHILE HOST IS EXCRETING WASTE.

AEROSOLS CAN ALSO OCCUR BY DISTURBING
CONTAMINATED NESTING MATERIALS.
Four Corners Outbreak

IN 1993 THERE WAS AN OUTBREAK OF HPS IN THE FOUR CORNER
REGION OF NEW MEXICO, COLORADO, ARIZONA AND UTAH.

HPS FIRST RECOGNIZED AS A HANTAVIRUS DISEASE.

32 OF THE 53 PEOPLE INFECTED DIED.

A WARM WINTER ALLOWED FOR AN INCREASE IN THE HOST
POPULATION.

OUTBREAK WAS CAUSED BY THE SIN NOMBRE STRAIN. 30% OF
THE MICE IN THIS AREA CARRIED THIS STRAIN.
THE DISTRIBUTION OF THE CASES OF
HPS IN U.S.A
TOTAL CASES- 396
MALE- 247
FEMALE- 149
MEAN AGE – 38YR
CASE FATALITY- 36%
CLIMATE AND HANTAVIRUS DISEASE

RESEARCH SHOWS THAT THE 1993 OUTBREAK FOLLOWED A DRAMATIC
INCREASE IN PRECIPITATION. AN EVENT RESULTING FROM THE 1992/1993
EL NINO.

SIMILAR PATTERN OF ABOVE AVERAGE RAINFALL FOLLOWED BY
DROUGHT DURING 1995/96 IN PARAGUAY LEAD TO HPS OUTBREAK.

ABOVE NORMAL PRECIPITATION LEAD TO ABUNDANCE IN FOOD
RESOURCES FOR RODENTS  LEADING TO AN INCREASE IN RODENT
POPULATION  WHEN FOOD SOURCES DEPLETED, RODENTS MOVED INTO
A LESS COMPETITIVE ENVIRONMENT INHABITTED BY HUMANS 
CAUSING THE LIKELIHOOD OF TRANSMISSION TO INCREASE.

DOES HUMAN ACTIVITIES AFFECT CLIMATE CHANGE/EL NINO EVENTS??
(STILL NOT CLEAR).
NEGATIVE CORELATION BETWEEN HPS CASES
AND TIME AFTER EL NINO EVENT
THE MAXIMUM NUMBER OF CASES
REPORTED DURING THE LATE SPRING AND
EARLY SUMMER
PRECIPITATION AND
TEMPERATURE CHANGE
MAXIMUM NUMBER OF CASES IN NEW MEXICO – SEVILLETA
NATIONAL WILDLIFE REFUGE HAD 20 FOLD INCREASE IN
RODENT POPULATION
Symptoms of HFRS







HFRS has a 2 to 3 week incubation phase, followed by the onset
of flu-like symptoms, lasting 3 to 5 days.
Hemorrhaging can occur during this time, along with a high
amount of protein in the urine.
Next comes a hypotensive phase, usually lasting hours to days.
Nausea and vomiting are common in this phase of the disease.
About 1/3 of the patients die due to shock, and vascular leakage.
The oliguric phase is next where half of the fatalities occur due to
renal failure.
The diuretic phase is next, where patients show improved renal
functions, but may still die due of pulmonary complications or
shock.
The final phase is the convalescent phase. This lasts weeks to
months before the patient is completely recovered.
HFRS has a 7% fatality rate.
Symptoms of HPS

HPS has a 14 to 17 day incubation period.
 At the onset of symptoms patients will have a headache,
fever, muscular pain and a general feeling of discomfort.
 Following this a patient will have abdominal pain, nausea
vomiting and a low platelet count.
 Most patients will seek medical attention once their
cardiopulmonary system becomes compromised.
 Usually 48 hours after cardiopulmonary involvement a
patient will have severe edema in the lungs and retro
peritoneal space.
 Death usually occurs due to shock and cardiac
complications.
 HPS has a 40% fatality rate.
HFRS TREATMENTS

CURRENTLY NO FDA APPROVED ANTIVIRAL
DRUG AVAILABLE FOR THE TREATMENT OF HFRS.

PROMPT DIAGNOSIS AND GOOD MANAGEMENT
OF ILLNESS (HFRS) IS EFFECTIVE IN IMPROVING
PATIENT’S SURVIVAL.

THERE IS NO VACCINE FOR HFRS.
HPS TREATMENTS

HPS IS MORE SERIOUS AND RAPIDLY
PROGRESSIVE ILLNESS.

RIBAVIRIN NOT EFFECTIVE

THE MOST IMPORTANT PART OF TREATMENT IS
THE AGGRESSIVE SUPPORTIVE CARE AND EARLY
DIAGNOSIS. THESE MEASURES SIGNIFICANTLY
IMPROVE THE CHANCES OF SURVIVAL.
 THERE IS NO VACCINE FOR HPS.
Prevention

AVOID CONTACT WITH RODENTS AND THEIR HABITATS.

DO NOT KEEP RODENTS AS PETS.

KEEP ALL FOOD IN SEALED CONTAINERS.

VIRIONS MAY BE STABLE FOR 2 DAYS ON A DRY SURFACE
SO DISINFECT AREAS CONTAMINATED BY RODENTS.

DISINFECT USING A 10% SOLUTION OF HOUSEHOLD
BLEACH.

ERADICATION UNLIKELY DUE TO THE LARGE PERCENTAGE
OF RODENTS WHICH CARRY THESE VIRUSES.
SOME INTERESTING ASPECTS

EACH HANTAVIRUS HAS A SINGLE NATURAL RESERVOIR
(RODENT), WHICH ARE DISTRIBUTED IN DIFFERENT
REGIONS GLOBALLY. THIS SUGGESTS THAT THESE
VIRUSES DO NOT ADAPT EASILY TO NEW HOSTS. THEY
ARE ADAPTED FOR SUCCESS WITHIN THEIR HOST, WHICH
MAY BE DUE TO THOUSANDS OF YEARS OF COEXISTENCE.

ANTIBODIES AGAINST HANTAVIRUS ARE ALSO FOUND IN
BOTH DOMESTIC AND WILD ANIMALS.

DETECTION OF HANTAVIRUS ANTIGENS IN THE LUNG
SUSPENSION OF DIFFERENT BIRD SPECIES CAPTURED
FROM EASTERN RUSSIA.

HANTAVIRUS CAN BE POTENTIALLY TRASMITTED
THROUGH BIRDS AND DOMESTICATED/WILD ANIMALS.
HOWEVER NO SPECIFIC CASES DEMONSTRATED.
Refrences








Madigan, Michael and John m. Martinko Brock Biology of Microorganisms. 11ed.
Upper Saddle River, NJ. USA. Pearson Prentice Hall. 2006
Lednicky, John Hantaviruses A Short Review, Arch Pathogen and Laboratory Medicine.
January 2003;127:30-35
Schmaljoh, Connie and Brain Hjelle, Hantaviruses: A global Disease Problem. [online]
http://www.cdc.gov/ncidod/EID/vol3no2/schmaljo.htm
www.cdc.gov/ncidod/dvrd/spb/mnpages/rodentmanual/text.pdf
Engelthaler David. Climate and Environment… CDC Journal of Infectious Diseases
Jan-March 1999. 5:1
www.cdc.gov/ncidod/diseases/hanta/hps/noframes/casemap.htm
Plyusnin A. Genetics of hantaviruses: implications of taxonomy. Arch Vir (2002)
147:665-682.
Zeier Martin. New Ecological Aspects… Virus Genes. 30:2 157-180, 2005
Questions?