Hantavirus DiseasesHantavirus Diseases

ByChristie Alston

Hemal Bhatt

http://www.umm.edu/imagepages/17201.htm

MORPHOLOGY/GENOMEMORPHOLOGY/GENOME SPHERICAL AND

ENVELOPED

NEGATIVE SENSE RNA GENOME

TRISEGMENTED LARGE – RDRP MEDIUM – G1 AND G2 SMALL – NP

80-110NM DIAMETER

TAXONOMYTAXONOMY

FAMILY – Bunyaviridae

GENUS – Hantavirus

MORE THAN 30 DIFFERENT HANTAVIRUS SPECIES HAVE BEEN FOUND (20 OF WHICH ARE KNOWN TO BE PATHOGENIC TO HUMANS)

TAXONOMYTAXONOMY

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 DISTRIBUTION OF NEW AND OLD WORLD HANTAVIRUSESHANTAVIRUSES

Hantavirus DiseaseHantavirus 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.

HistoryHistory

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.

Deer Mouse Cotton Rat

Rice Rat   White Footed Mouse

http://www.uwrf.edu/~W1001260/Epidemiology.html

HantavirusHantavirus VectorsVectors

http://www.uwrf.edu/~W1001260/Pathogenesis.html

Transmission of virusTransmission 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 OutbreakFour 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 THE DISTRIBUTION OF THE CASES OF HPS IN U.S.AHPS IN U.S.A

TOTAL CASES- 396

MALE- 247

FEMALE- 149

MEAN AGE – 38YR

CASE FATALITY- 36%

CLIMATE AND HANTAVIRUS DISEASECLIMATE 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 NEGATIVE CORELATION BETWEEN HPS CASES

AND TIME AFTER EL NINO EVENTAND TIME AFTER EL NINO EVENT

THE MAXIMUM NUMBER OF CASES THE MAXIMUM NUMBER OF CASES REPORTED DURING THE LATE SPRING AND REPORTED DURING THE LATE SPRING AND

EARLY SUMMEREARLY SUMMER

PRECIPITATION AND PRECIPITATION AND TEMPERATURE CHANGETEMPERATURE CHANGE

MAXIMUM NUMBER OF CASES IN NEW MEXICO – SEVILLETA MAXIMUM NUMBER OF CASES IN NEW MEXICO – SEVILLETA NATIONAL WILDLIFE REFUGE HAD 20 FOLD INCREASE IN NATIONAL WILDLIFE REFUGE HAD 20 FOLD INCREASE IN

RODENT POPULATIONRODENT POPULATION

Symptoms of HFRSSymptoms 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 HPSSymptoms 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 TREATMENTSHFRS 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 TREATMENTSHPS 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.

PreventionPrevention 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 ASPECTSSOME 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.

RefrencesRefrences

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?Questions?