EMERGING VIRUSES - Oakland University

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EMERGING VIRUSES - Oakland University

EMERGING AND RE EMERGING VIRALPATHOGENS Contd.,• NIPAH VIRUS ENCEPHALITIS• RIFT VALLEY FEVER• VIRAL HGIC FEVERS• DENGUE FEVER• WEST NILE VIRUS• ?SMALL POX• NEW SARS-CHINA,HONGKONG LTRI


ARENA VIRUSES.• ARENAVIRIDAE.• ASSOCIATED WITH RODENT TRANSMITTEDDISEASES.• COMMON IN SOME PARTS OF THE WORLD.• SPHERICAL,110-130 nm.,ENVELOPED• LIPID MEMBRANE.• CROSS SECTION:GRAINY RIBOSOMALPARTICLES(LATIN ARENA=SANDY.• GENOME:RNA ONLY,BUDDIND VIRIONS.


DISEASES CAUSED BY ARENAVIRUSES• LASSA VIRUS• JUNIN VIRUS• MACHUPO VIREUS• GUANARITO VIRUS• SABIA• LASSA FEVER• ARGENTINE HGIC F.• BOLIVIAN HGIC F.• VENEZUELAN HGIC• BRAZILIAN HGIC F. .


DISEASES CAUSED BY ARENAVIRIDAE• ZOONOTIC.• RODENTS ARE NATURALRESERVOIRS.• LCM/LASSA COMPLEX WITH OLDWORLD RATS(FAMILY MURIDAE,SUBMURINAE)• NEW WORLD GROUP,TACARIBECOMPLEX,SUB:SIGMODOTINAE.• EUROPE,ASIA,AFRICA,AMERICAS.


HUMAN INFECTIONS CAUSED BY AV• RODENTS ARE CHRONICALLY INFECTED.NOT ILL.• GENERATIONAL SPREAD TO OFFSPRINGS.• VIRUSES ARE SHED IN URINE ANDDROPPINGS.• INCIDENTAL HUMAN INFECTION FROMRODENTEXCRETA.CONTACT,AEROSOL,INGESTION.


Arenaviridae• Name derived from “arenosus” (Latin “sandy”) describingappearance of virions on examination by electron microscopy• Enveloped virus, round or pleomorphic, 50-300 nm in diameter• Single-stranded genome divided into 2 RNA segments: small(~3.4 kb) and large (~7.1 kb)• 2 genes on each segment, arranged in unique “ambisense”orientation, encoding 5 proteins• Inactivated by:– heating to 56 o F– pH8.5– UV/gamma irradiation– detergents


Arenaviridae• Arenaviruses associated with human diseaseVirus Origin of Name Year DistributionLassa Town, Nigeria 1969 West AfricaJunin Town, Argentina 1957 South AmericaMachupo River, Bolivia 1962 South AmericaGuanarito Area, Venezuela 1989 South AmericaSabia Town, Brazil 1990 South AmericaLCMV Clinical disease 1933 Worldwide


Epidemiology• Endemic in areas of West Africa, including Nigeria,Liberia, Sierra Leone, and Guinea• Estimated 300,000-500,000 infections/year, with5000 deaths• Rodent-to-human transmission (the “multimammaterat”, Mastomys species-complex)• Secondary human-to-human transmission with thepotential for nosocomial outbreaks with high casefatality


Known Distribution of MastomysMASTOMYSDISTRIBUTIONLASSA 1969


Rodent Reservoir• Mastomys speciescomplex• Taxonomy stillunclear– M. huberti: morecommon inperidomestic habitat– M. erytholeucus: morecommon in brushhabitat– Others


Transmission• Rodent-to-human:– Inhalation of aerosolized virus– Ingestion of food or materialscontaminated by infected rodent excreta– Catching and preparing Mastomys as afood source


Transmission• Human-to-human:– Direct contact with blood, tissues,secretions or excretions of infectedhumans– Needle stick or cut– Inhalation of aerosolized virus


Pathogenesis• Endothelial cell damage/capillary leak• Platelet dysfunction• Suppressed cardiac function• Cytokines and other soluble mediators ofshock and inflammation


Clinical Aspects• Incubation period of 5-21 days• Gradual onset of fever, headache, malaise and other nonspecificsigns and symptoms• Pharyngitis, myalgias, retro-sternal pain, cough andgastrointestinal symptoms typically seen• A minority present with classic symptoms of bleeding,neck/facial swelling and shock• Case fatality of hospitalized cases: 15-20%• Particularly severe in pregnant women and their offspring• Deafness a common sequela


Clinical Signs and SymptomsFeverHeadacheArthralgias/MyalgiasRetro-sternal PainWeaknessDizzinessSore throat/PharyngitisCoughVomitingAbdominal Pain/TendernessDiarrheaConjunctivitis/Sub-conjunctivalHemorrhage ChillsDeafnessLymphadenopgathyBleedingConfusionSwollen Neck or Face0 10 20 30 40 50 60 70 80 90 100Percent


Lassa Fever in Pregnancy• Increased maternal mortality in third trimester(>30%)• Increased fetal and neonatal mortality (>85%)• Increased level of viremia in pregnant women• Placental infection• Evacuation of uterus improves mother’s chanceof survival


Sensorineural Hearing Deficit inLassa Fever• Typically appears during early convalescence• Not related to severity of acute illness• Occurs in one-third of cases• May be bilateral or unilateral• May persist for life in up to one-third of thoseaffected


Lassa Fever in Children and Infants• Significant cause of pediatric hospitalizations insome areas of West Africa• Signs and symptoms most often similar to adults• “Swollen Baby Syndrome”- Edema/Anasarca- Abdominal distension- Bleeding- Poor prognosis


Differential Diagnosis ofLassa Fever• Malaria• Typhoid fever• Streptococcalpharyngitis• Leptospirosis• Bacterial sepsis• Bacterial meningitis• Arboviral infection• Anicteric hepatitis• Enterovirus infection• Bacterial or viralconjuctivitis


Diagnostics• Clinical diagnosis often difficult• ELISA (Enzyme-linked immunosorbentassays) for antigen, IgM, and IgG• As research tools:– Virus isolation– Immunohistochemistry (for post-mortemdiagnosis)– RT-PCR (Reverse transcription-polymerasechain reaction)


• Supportive measuresTreatment• Ribavirin– Most effective when started within the first 6days of illness– Major toxicity: mild hemolysis andsuppression of erythropoesis. Both reversible– Presently contraindicated in pregnancy,although may be warranted if mother’s life atrisk– Does not appear to reduce incidence orseverity of deafness


Associated with Poor Prognosisin Lassa Fever• High viremia• Serum AST level >150 IU/L• Bleeding• Encephalitis• Edema• Third trimester of pregnancy


Prevention and Control• Village-based programs for rodent controland avoidance• Hospital training programs to avoidnosocomial spread: barrier nursingmanual• Diagnostic technology transfer• Specific antiviral chemotherapy (ribavirin)


Rodent Control• Proper storage of food in rodent-proofcontainers• Cleaning around homes• Trapping and killing rodents with properand safe disposal of carcasses• Avoid rodents as a food source


Ongoing Lassa Fever Research in• Natural history of disease– Where it came from– How clinical course progresses– Whom it affects• Diagnosis: Clinical/Laboratory• Immunopathogenesis• Treatment• Rodent population dynamics• Prevention and controlGuinea, West AfricaCollaboration between CDC/SPB and the Guinean Institute for Research and Applied Biology


EBOLA HEMORRHAGIC FEVER• SEVERE OFTEN FATAL DISEASE.• HUMANS AND PRIMATES.• INITIAL RECOGNITION 1976.• EBOLA VIRUS NAMED AFTER A RIVER.• ZAIRE/DEM REPUBLIC OF CONGO.• FILOVIRDAE.• FOUR SUBTYPES:ZAIRE,SUDAN,IVORYCOAST, NON HUMAN-RESTON.


EBOLA• ORIGIN UNKNOWN.• NATURAL RESERVOIR UNKNOWN.• ZOONOTIC.• ANIMAL BORNE.• MAITAINED IN ANIMAL HOST IN AFRICA.• NON HUMAN PRIMATE STRAIN, RESTONIMPORTED TO U.S FROM PHILIPPINES.• CONFIRMED CASES INCONGO,GABON,SUDAN,IVORYCOAST,UGANDA.• SPORADIC OUTBREAKES.1976-2002.


CLINICAL EHF• ACUTE.• NO CARRIER STATE.• ?FIRST CONTACT FROM INFECTED ANIMAL.• SPREADS TO OTHERS FROM DIRECTCONTACT WITH BLOOD AND SECRETIONSOF ONFECTED PERSON.• FAMILIES AND FRIENDS;CONTNEEDLES.HEALTH CARE SETTING.• WITHOUT PROTECTIVE CLOTHING.NONDISPOSABLE NEEDLES AND SHARPS.


CLINICAL ASPECTS OF EHF• INCUBATION PERIOD:2-20 DAYS.• ABRUPT ONSET.• FEVER,HEADACHE,JOINT ANDMUSCLE ACHES,SORETHROAT,WEAKNESS,FOLL BYDIARRHEA,VOMTING AND WEAKNESS.• RASH,RED EYES,INTERNAL ANDEXTERNAL BLEEDING IN SOME.• SOME PATIENTS RECOVER.


DIAGNOSIS OF EHF• DIFFICULT.• ISOLATE SUSPECTED CASES.• CDC NOTIFICATION.• BLOOD,BODY FLUID PRECAUTIONS.• ELISA,IgM ELISA,PCR,VIRUSISOLATION.IMMUNOHISTOCHEMISTRY IN DECEASED PATIENTS.


PREVENTION OF EHF• ISOLATION PRECAUTIONS.• BARRIER NURSING.• PROTECTIVE CLOTHING.• MASKS,GLOVES,GOWNS,GOGGLES.• EQUIPMENT STERILIZATION.• NO ANTIVIRAL THERAPY AVAILABLE.


HENDRA VIRUS DISEASE AND NIPAHVIRUS ENCEPHALITIS• HENDRA VIRUS WAS FORMERLY CALLEDEQUINE MORBILIVIRUS.• PARAMYXOVIRIDAE FAMILY.• FIRST ISOLATED IN 1994 INHENDRA,AUSTRALIA.• RESPIRATORY AND NEUROLOGICALILLNESS OF HORSES AND HUMANS.• NEPAH VIRUS,1999,A RELATEDVIRUS,FROM ENCEPHALITIS AND RESPDISEASE AMONG ADULT MEN IN MALAYSIAAND SINGAPORE.


HENDRA AND NIPAH VIRUSES• NATURAL RESERVOIR:FLYINGFOXES(BAT,PLEROPUS GENUS)FPR BOTH.• DISEASE IN HORSES IN INITIALLY INAUSTRALIA DUE TO HENDRA.• HUMAN EXPOSURE DUE TO DIRECTEXPOSURE TI INFECTED TISSUES ANDSECRETIONS.• NIPAH VIRUS CAUSES MILD DISEASE INPIGS IN MALAYSIA AND SING.TRANSMITTEDTO HUMANS AND CATS AND DOGS..


HENDRA AND NIPAH• THREE HUMAN CASES OF HENDRA VIRUS.SEVERE FLU LIKE ILLNESS.• NIPAH IS ASSOCIATED WITH ENCEPHALITIS.• MENTAL CONFUSION.• PROGRESSES TO COMA WIYHIN 24-48 HRS.• SOME EARLY RESP ILLNESS.• HENDRA OCC CAUSE DELAYEDENCEPHALITIS.• NIPAH CAUSES PERSISTENT SEQUELE-CONVULSIONS AND PERSONALITYCHANGES.


HENDRA AND NIPAH• HENDRA:1/3 DELAYEDENCEPHALITIS,2/3 DIED.• NIPAH:40%MORTALITY IN PTS WITHSERIOUS CNS DISEASE.• RIBAVIRIN ACTIVE IN VITRO.NOCLINICAL TRIALS.• PREVENTION BY USINGAPPROPRIATE P.P.E. DURINGCONTACT WITH INFECTED ANIMALS.• MALAYSIA-SINGAPORE OUTBREAK,99.


OUTBREAK OF NIPAH VIRUS—MALYSIAAND SINGAPORE,1999.• 257 CASES OF ENCEPHALITIS.• LAB RESULTS FROM 65 DECEASED PTSCONFIRMED RECENT NIPAH INFECTION.• APPARENT SOURCE OF INFECTION IS EXPOSURETO PIGS.• 64% REPORTED SICK PIG HANDLING ANDTOUCHING.• NO HUMAN TO HUMAN TRANSMISSION• DEAD DOG WAS AUTOPSIED.VIRUS ISOLATION BYIMMUNOHISTOCHEMISTRY.• NO NEW CASES IN SINGAPORE AFTER STOPPINGPIG IMPORTATION FROM MALAYSIA.


VIRAL HEMORRHAGIC FEVERS• SEVERE MULTISYSTEM DISEASE.• DAMAGE TO VASCULAR SYSTEM.• IMPAIRED ABILITY TO REGULATE BODYFUNCTIONS.• HEMORRHAGE.• MILD TO SEVERE LIFE THREATENINGILLNESS.• BIOSAFETY LEVEL 4(BSL-4)PATHOGENS.• ARENA,FILO,BUNYA AND FLAVIVIRUSESARE IMPLICATED.


HEMORRHAGIC FEVER VIRUSES.• RNA VIRUSES.• ENVELOPED IN LIPID COATING.• SURVIVAL IS DEPENDENT ON AN ANIMAL ORINSECT HOST(NATURAL RESERVOIR)• GEOGRAPHICALLY RESTRITED TO AREAS WHEREHOST SPECIES LIVE.• HUMANS INFECTED WHEN CONTACT WITHINFECTED ANIMALS.NOT A NATURAL RESERVOIR.• HUMAN CASES OCCUR SPORADICALLY ANDIRREGULARLY.• NO EFFECTIVE TREATMENT.


VIRAL HEMORHAGIC FEVERS• VIRUSES ARE ZOONOTIC,• RESIDE AND TOTALLY DEPENDENT ON THEIRHOSTS.• RODENTS AND ARTHROPODS.• MULTIMMATE RAT,COTTON RAT,DEER MOUSE.• EBOLA AND MARBURG VIRUSES ARE EXAMPLES.• DISTRIBUTED ALL OVER THE GLOBE.• HPS(HANTAVIRUS PUL SYNDROME)AMERICAS.• HFRS(HGIC FEVER WITHRENALSYNDROME)EUROPE AND ASIA.• SEOUL VIRUS UNIVERSAL.


VHF EPIDEMIOLOGY• LOCAL EPIDEMICS.• IMPORTED HOST ANIMALS CANCARRY THE VIRUS.• MARBURG VIRUS IN GERMANY ANDYUGOSLAVIA.• INFECTED PTS TRAVEL AND INFECTOTHERS.EBOLA FROM GABON TOS.AFRICA.RISING THREAT.


VHF:CLINCAL ASPECTS• VIRUSES ARE TRANSMITTED FROM RODENTS TOHUMANS VIA URINE,FECES,SALIVA, AND BODYEXCRETIONS.• ALSO FROM MOSQUITO OR TICK BITES FROMARTHROPOD VECTORS.• SOMETIMES FROM SLAUGHTERING INFECTEDANIMALS.• HUMAN TO HUMAN TRANSMISSION IN CERTAINHGIC FEVERS:EBOLA,MARBURG,LASSA ANDCRIMEAN CONGO HGIC FEVER.• ALSO BODY FLUIDS AND CONTAMINATEDSYRINGES AND NEEDLES.


VHF:SYMPTOMS• VARY WITH VIRUS.• HIGH FEVER.• FATIGUE.• MYOARTHRALGIAS.• DIZZINESS.• LOSS OF STRENGTH.• EXHAUSTION.• BLEEDING FROM MULTIPLE ORGANS.• SEVERE CASES:SHOCK,CNSSX,DELIRIUM,SEIZURES AND RENAL FAILURE.


VHF:TREATMENT AND PREVENTION• SUPPORTIVE.• RIBAVIRIN LIMITED SUCCES IN LASSA.• CONVALESCENT SERUM.(ARG HGICFEVER.)• VACCINES FOR AHF AND YELLOW FEVER.• AVOID CONTACT WITH HOST SPECIES.• PREVENT HUMAN TO HUMAN TRANSFER.• RODENT AND ARTHROPOD VECTORCONTROL.


MARBURG HEMORRHAGIC FEVER• A RARE HGIC FEVER,SEVERE TYPE.• AFFECTS BOTH HUMANS AND NON HUMANPRIMATES.• GENETICALLY UNIQUE ZOONOTIC RNA VIRUS.• FILOVIRUS FAMILY.• FIRST RECOGNIZED IN 1967.• OUTBREAKS IN MARBURG AND FRANKFURTGERMANY AND IN BELGRADE.• 37 LAB,MEDICAL PERSONAL AND THEIR FAMILYMEMBERS AFTER EXPOSURE TO IMPORTEDAFRICAN GREEN MONKEYS.


MARBURG• 1965:EUROPE OUTBREAK.• 1975:TRAVLER INFECTED INZIMBABWE BECAME ILL INS.AFRICA.SPREAD TO A NURSE AND AFELLOW TRAVELER.• 1980:TWO OTHER CASES IN KENYAAND UGANDA.PT’S PHYSICIAN DIED.• 1987:ANOTHER SPORADIC CASE.• 1998:OUTBREAK IN CONGO.


MARBURG• INDIGENOUS TO AFRICA.• KENYA,UGANDA,ZIMBABWE.• ANIMAL HOST REMAINS A MYSTERY.• MAY SPREAD TO ANOTHER CLOSCONTACT.• DROPLETS,BODYFLUIDS,BLOOD,NEEDLES &SHARPS.


CLINCAL ASPECTS OF MHF• INCUBATION PERIOD:5-10 DAYS.• SUDDEN ONSET.• FEVER,HEADACHE,CHILLS,MYALGIA.• MACULOPAPULAR RASH ON DAY 5.• MOST PROMINENT ON THE TRUNK.• G.I. SX FOLLOW,JAUNDICE IN SOME.• PANCREATITIS,WTLOSS,SHOCK.HGE,LIVER AND M.O.F.


CLINICAL ASPECTS OF MHF• ELISA,IGM ELISA,PCR,VIRUS ISOLATIONFOR DX.• PROLONGED RECOVERY.• ORCHITIS,RECURRENTHEPATITIS,TRANSVERSE MYELITIS,UVEITIS.• CASE FATALITY 23-25%• RX NONE SPECIFIC.SUPPORTIVE CARE.• FRESH FROZENPLASMA.HEPARN,ELECTRLYTEREPLACEMENT.• QUARANTINE EXPOSED PTS.


RIFT VALLEY FEVER(RVF)• ACUTE FEBRILE ILLNESS.• AFFECTS DOMESTIC ANIMALS.• CATTLE,BUFFALO,SHEEP GOATS,CAMELS.• HUMANS .• MOSQUITO BORNE.• EPIDEMICS DURING HEAVY RAINFALL.• EASTERN AND SOUTHERN AFRICA.• ALSO IN SUBSAHARAN AFRICA,MADAGASCAR.• RECENTLY (2000)SAUDI ARABIA AND YEMEN.


HUMAN METAPNEUMOVIRUS(HMPV):ANEW PATHOGEN IN LRTI.TOM MADHAVAN M.D.,F.A.C.P.,LAUREATE OF AMERICANCOLLEGE OF PHYSICIANS.


HMPV• Metapneumovirus.• Previously a strict avian virus.• Responsible for 2% of all LRTI in winter.• Clinical and epidemiologic similarity toRSV.• 2% of swabs PCR + for HMPV in U.K.• LRTI in 6,symptoms of cough,wheezing,sputum production. All recovered.


HMPV (Contd.,)• CANADIAN EXPERIENCE.• 11/71 specimens were + by PCR.• 7 females.4 males.• 6 months to 89 years.• All had fever,70% cough,50% rhinitis,sorethroat and flu like symptoms.• ICH,CVD,COPD, Prematurity, all high risk.


HMPV:CLINICAL ASPECTS• All age groups.• Fever,chills,cough,dyspnea andtachycardia.• Bronchiolitis.• Pneumonia.• Otitis media.• Flu like illness.• Similar to RSV or Influenza A.

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