viral+zoonosis1

8/8/2019 Viral+Zoonosis1

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Viral ZoonosesBy

Mohammed Abd ElFattah Mohammed

Ass.lecturer of Tropical medicine

Under supervision of

Dr./ Salah Seif ElDin

Professor of Tropical medicine


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Definition Zooneses are diseases of vertebrate animals that can be transmitted

to man: eitherdirectly orindirectly through an insect vector.

Anthroponosis (Reverse Zoonosis): is an infectious disease in which a

disease causing agent carried by humans is transferred to other animals. It

may cause the same disease or a different disease in other animals.

When an insect vector is involved, the disease is also known as an

arboviral disease.

However, not all arboviral diseases are zoonosis: where thetransmission cycle takes place exclusively between insect vector

and human e.g. dengue and urban yellow fever.

Examples of viral zoonoses that can be transmitted to man directly

include rabies, hantaviruses, lassa, ebola fevers, avian flu and

SARS.


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Rabies Virus Member of the Lyssavirus of the Rhabdoviridae.

ssRNA enveloped virus, characteristic bullet-shaped appearance

with 6-7 nm spike projections. Virion 130-240nm * 80nm

-ve stranded RNA codes for 5 proteins; G, M, N, L, S

Exceedingly wide range of hosts.

There are 6 other members of Lyssavirus : Mokola, Lagosbat,Duvenhage, (European bat lyssavirus) EBL-1, EBL-2, and

(Australian bat lyssavirus) ABLV.

Duvenhage and EBL-2 have been associated with human rabies.


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Rabies Virus

Structure of rabies virus

Rabies virus particles


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EpidemiologyRabies is a zoonosis which is prevalent in wildlife. The main

animals involved differs from continent to continent.

Europe fox, bats

Middle East wolf, dog

Asia dog

Africa dog, mongoose, antelope

N America foxes, skunks, raccoons,insectivorous bats

S America dog, vampire bats


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Pathogenesis The commonest mode of transmission in man is by the bite of a

rabid animal, usually a dog. Rabies is an acute infection of the CNS

which is almost invariably fatal.

Following inoculation, the virus replicates in the striated or connective tissue at the site of inoculation and enters the peripheral

nerves through the neuromuscular junction.

It then spreads to the CNS in the endoneurium of the Schwann cells.

Terminally, there is widespread CNS involvement but few neurons

infected with the virus show structural abnormalities. The nature of

the profound disorder is still not understood.


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Laboratory Diagnosis Histopathology -Negri bodies are pathognomonic of rabies. However,

Negri bodies are only present in 71% of cases.

Rapid virus antigen detection - in recent years, virus antigen detection

by IF had become widely used. Corneal impressions or neck skinbiopsy are taken. The Direct Fluorescent Antibody test (DFA) iscommonly used.

Virus cultivation - The most definitive means of diagnosis is by viruscultivation from saliva and infected tissue. Cell cultures may be usedor more commonly, the specimen is inoculated intracerebrally intoinfant mice. Because of the difficulties involved, this is rarely offeredby diagnostic laboratories.

Serology - circulating antibodies appear slowly in the course of infection but they are usually present by the time of onset of clinicalsymptoms.


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Negri Body in neuron cell Positive DFA test

Diagnosis ofRabies


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Management and Prevention Pre-exposure prophylaxis - Inactivated rabies vaccine may be

administered to persons at increased riskof being exposed to rabies e.g.vets, animal handlers, laboratory workers etc.

Post-exposure prophylaxis - In cases of animal bites, dogs and cats in arabies endemic area should be held for 10 days for observation. If signsdevelop, they should be killed and their tissue examined.

Wild animals are not observed but if captured, the animal should bekilled and examined. The essential components of post exposureprophylaxis are the local treatment of wounds and active and passiveimmunization.

Once rabies is established, there is nothing much that could be doneexcept intensive supportive care. To date, only 2 persons with proven

rabies have survived.


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Rabies VaccinesThe vaccines which are available for humans are present are inactivated whole

virus vaccines.

Nervous Tissue Preparation e.g. Semple Vaccine - associated with the rare

complication of demyelinating allergic encephalitis.

Duck Embryo Vaccine - this vaccine strain is grown in embryonated duck

eggs This vaccine has a lower risk of allergic encephalitis but is considerably

less immunogenic.

Human Diploid Cell Vaccine (HDCV) - this is currently the best vaccine

available with an efficacy rate of nearly 100% and rarely any severe reactions.However it is very expensive.

Other Cell culture Vaccines - because of the expense of HDCV, other cell

culture vaccines are being developed for developing countries. However

recent data suggests that a much reduced dose of HDCV given intradermally

may be just be effective.


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Control ofRabies Urban - canine rabies accounts for more than 99% of all human

rabies. Control measures against canine rabies include;

stray dog control. Vaccination of dogs

quarantine of imported animals

Wildlife - this is much more difficult to control than canine

rabies. However, there are on-going trials in Europe where baitcontaining rabies vaccine is given to foxes. Success had been

reported in Switzerland.


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Australian bat lyssavirus (ABLV) is a zoonotic virusclosely related to rabies virus.

It was first identified in a Black flying fox (Pteropusalecto) collected in Australia in 1996 during a national

surveillance program for the recently identified Hendravirus.

ABLV is the seventh member of the lyssavirus genus

(which includes rabies virus) and the only one present inAustralia.


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ABLV is distributed throughout Australia ina variety of bat species which are believedto be the primary reservoir for the virus.

Two strains of the virus exist, oneoccurring in insectivorous bats and theother in fruit bats.


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Arenaviruses Enveloped ssRNA viruses

virions 80-150nm in diameter

genome consists of 2 pieces of

ambisense ssRNA. 7-8 nm spikes protrude from the

envelope.

host cell ribosomes are usually seen

inside the outer membrane but play

no part in replication.

Members of arenaviruses include

Lassa fever, Junin and Macupo

viruses.

Lassa fever virus particles budding

from the surface of an infected cell.

(Source: CDC)


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Lassa Fever Found predominantly in West Africa, in

particular Nigeria, Sierra Leone and Liberia.

The natural reservoir is multimammate rat

(Mastomys)

Man may get infected through contact with

infected urine and faeces.

Man to man transmission can occur through

infected bodily fluids and Lassa fever had caused

well-documented nosocomial outbreaks.

Mastomys


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Clinical Manifestations Incubation period of 3-5 days.

Insidious onset of non-specific symptoms such as fever, malaise,

myalgia and a sore throat. Typical patchy or ulcerative pharyngeal lesions may be seen.

Severe cases may develop the following:

Haemorrhagic manifestations

Myocarditis

Pneumonia Encephalopathy

Shock

The reported mortality rate for hospitalized cases of Lassa fever is 25%.

It carries a higher mortality in pregnant women.


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Laboratory DiagnosisLaboratory diagnosis should only be carried out in specialized centers.

Detection of Virus Antigen - the presence of viral antigen in sera can be

detected by EIA. The presence of viral antigen precedes that of IgM.

Serology - IgM is detected by EIA. Using a combination of antigen and

IgM antibody tests, it was shown that virtually all Lassa virus

infections can be diagnosed early.

Virus Isolation - virus may be cultured from blood, urine and throat

washings. Rarely carried out because of safety concerns. RT-PCR- being used experimentally.


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Management and Prevention Good supportive care is essential.

Ribavirin - had been shown to be effective against Lassa fever with a 2to 3 fold decrease in mortality in high risk Lassa fever patients. Must

be given early in the illness. Hyperimmune serum - the effects of hyperimmune serum is still

uncertain although dramatic results have been reported in anecdotal

case reports.

Postexposure Prophylaxis - There is no established safe prophylaxis.

Various combinations of hyperimmune immunoglobulin and/or oralribavirin may be used.

There is no vaccine available, prevention of the disease depends on

rodent control.


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Junin and Macupo Viruses Junin and Macupo viruses are the causative agents of Argentine

and Bolivian Haemorrhagic fever respectively.

Calomys musculinis and Ccallosus are the rodent vectors. The clinical presentations are similar to that of Lassa fever.

Neurological signs are much more prominent than in Lassa

fever.

Unlike Lassa virus, no secondary human to human spread had

been recorded.

Hyperimmune serum and ribavirin had been shown to be

effective in treatment.


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Hantaviruses

Forms a separate genus in the

Bunyavirus family.

Unlike under bunyaviridae, itstransmission does not involve an

arthropod vector.

Enveloped ssRNA virus.

Virions 98nm in diameter with a

characteristic square grid-like

structure.

Genome consists of three RNA

segments: L, M, and S.


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History Haemorrhagic Fever with Renal Syndrome (HFRS: later

renamed hantavirus disease) first came to the attention of the

West during the Korean war when over 3000 UN troops were

affected.

It transpired that the disease was not new and had been

described by the Chinese 1000 years earlier.

In 1974, the causative was isolated from the Korean Stripped

field mice and was called Hantaan virus.

In 1995, a new disease entity called hantavirus pulmonary

syndrome was described in the four corners region of the U.S.


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Some Subtypes of hantaviruses

associated with human disease Hantaan, Porrogia and related viruses - This group is found in China,

Eastern USSR, and some parts of S. Europe. It is responsible for the severe

classical type of hantavirus disease. It is carried by stripped field mice.

(Apodemus agrarius) Seoul type - associated with moderate hantavirus disease. It is carried by

rats and have a worldwide distribution. It has been identified in China,

Japan, Western USSR, USA and S.America.

Puumala type - mainly found in Scandinavian countries, France, UK and

the Western USSR. It is carried by bank voles (Clethrionomys glareolus)and causes mild hantavirus disease (nephropathia epidemica).

Sin Nombre - found in many parts of the US, Canada and Mexico. Carried

by the Deer Mouse ( Peromyscus maniculatus) and causes hantavirus

pulmonary syndrome.


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RodentCarriers of Hantaviruses

Stripped field mouse (Apodemus agrarius)

Bank vole (Clethrionomys glareolus)

Deer Mouse (Peromyscus maniculatus) Rat (Rattus)


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Clinical Features of Hantavirus

Disease The multisystem pathology of HVD is characterized by damage to

capillaries and small vessel walls, resulting in vasodilation and

congestion with hemorrhages.

Classically, hantavirus disease consists of 5 distinct phases. Thesephases may be blurred in moderate or mild cases.

Febrile phase - abrupt onset of a severe flu-like illness with a

erythematous rash after an incubation period of 2-3 days.

Hypotensive phase - begins at day 5 of illness

Oliguric phase - begins at day 9 of illness. The patient may develop acute

renal failure and shock. Haemorrhages are usually confined to petechiae.

The majority of deaths occur during the hypotensive and oliguric phases

Diuretic phase - this occurs between days 12-14 .

Convalescent phase - this may require up to 4 months.


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Hantavirus Pulmonary Syndrome (HPS)

More than 250 cases of HPS have been reported throughout North

and South America with a mortality rate of 50%

In common with classical HVD, HPS has a similar febrile phase.

However, the damage to the capillaries occur predominantly in the

lungs rather than the kidney.

Shock and cardiac complications may lead to death.

The majority of HPS cases are caused by the Sin Nombre virus.The other cases are associated with a variety of other hantaviruses

e.g. New York and Black Creek Canal viruses.


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Diagnosis Serological diagnosis - a variety of tests including IF, HAI, SRH, ELISAs

have been developed for the diagnosis of HVD and HPS.

Direct detection of antigen - this appears to be more sensitive than

serology tests in the early diagnosis of the disease. The virus antigen can

be demonstrated in the blood or urine.

RT-PCR - found to of great use in diagnosing hantavirus pulmonary

syndrome.

Virus isolation - isolation of the virus from urine is successful early inhantavirus disease. Isolation of the virus from the blood is less consistent.

Sin Nombre virus has never been isolated from patients with HPS.

Immunohistochemistry - useful in diagnosing HPS.


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Treatment and Prevention Treatment of HVD and HPS depends mainly on supportive

measures.

Ribavirin - reported to be useful if given early in the course ofhantavirus disease. Its efficacy is uncertain in hantavirus

pulmonary syndrome.

Vaccination - an inactivated vaccine is being tried out in China.

Other candidate vaccines are being prepared. Rodent Control - control measures should be aimed at reducing

contact between humans and rodents.


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Avian influenza in birds Avian influenza is an infection caused by avian (bird)Avian influenza is an infection caused by avian (bird)

influenza (flu) viruses.influenza (flu) viruses.

These influenza viruses occur naturally among birds.These influenza viruses occur naturally among birds.

Wild birds worldwide carry the viruses in their intestines,Wild birds worldwide carry the viruses in their intestines,

but usually do not get sick from them.but usually do not get sick from them.

However, avian influenza is very contagious among birdsHowever, avian influenza is very contagious among birds

and can make some domesticated birds, includingand can make some domesticated birds, including

chickens, ducks, and turkeys, very sick and kill them.chickens, ducks, and turkeys, very sick and kill them.


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Infection with avian influenza viruses in domestic poultryInfection with avian influenza viruses in domestic poultrycauses two main forms of disease that are distinguished bycauses two main forms of disease that are distinguished by

low and high extremes of virulence.low and high extremes of virulence.

The low pathogenic form may go undetected and usuallyThe low pathogenic form may go undetected and usually

causes only mild symptoms (such as ruffled feathers and acauses only mild symptoms (such as ruffled feathers and a

drop in egg production).drop in egg production).

However, the highly pathogenic form spreads more rapidlyHowever, the highly pathogenic form spreads more rapidly

through flocks of poultry. This form may cause diseasethrough flocks of poultry. This form may cause disease

that affects multiple internal organs and has a mortalitythat affects multiple internal organs and has a mortality

rate that can reach 90rate that can reach 90--100% often within 48 hours.100% often within 48 hours.


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Human infection with avian

influenza viruses There are many different subtypes of type A influenza

viruses.

These subtypes differ because of changes in certain proteins

on the surface of the influenza A virus (hemagglutinin [HA]

and neuraminidase [NA] proteins).

There are 16 known HA subtypes and 9 known NA subtypes

of influenza A viruses.


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Many different combinations of HA and NA proteins areMany different combinations of HA and NA proteins are

possible. Each combination represents a different subtype.possible. Each combination represents a different subtype.

All known subtypes of influenza A viruses can be found inAll known subtypes of influenza A viruses can be found in

birds.birds.

Usually, avian influenza virus refers to influenza AUsually, avian influenza virus refers to influenza Aviruses found chiefly in birds, but infections with theseviruses found chiefly in birds, but infections with these

viruses can occur in humans.viruses can occur in humans.

The risk from avian influenza is generally low to mostThe risk from avian influenza is generally low to mostpeople, because the viruses do not usually infect humans.people, because the viruses do not usually infect humans.


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However, confirmed cases of human infection from severalHowever, confirmed cases of human infection from several

subtypes of avian influenza infection have been reportedsubtypes of avian influenza infection have been reported

since 1997.since 1997.

Most cases of avian influenza infection in humans haveMost cases of avian influenza infection in humans have

resulted from contact with infected poultry (e.g.,resulted from contact with infected poultry (e.g.,

domesticated chicken, ducks, and turkeys) or surfacesdomesticated chicken, ducks, and turkeys) or surfaces

contaminated with secretion/excretions from infectedcontaminated with secretion/excretions from infected

birds.birds.

The spread of avian influenza viruses from one ill personThe spread of avian influenza viruses from one ill person

to another has been reported very rarely, and has beento another has been reported very rarely, and has been

limited, inefficient andlimited, inefficient and unsustainedunsustained..


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Avian Influenza A (H5N1) Influenza A (H5N1) virus also called H5N1 virus is

an influenza A virus subtype that occurs mainly in birds, is

highly contagious among birds, and can be deadly to them.

H5N1 virus does not usually infect people, but infections

with these viruses have occurred in humans.

Most of these cases have resulted from people havingdirect or close contact with H5N1-infected poultry or

H5N1-contaminated surfaces.


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Human health risks during

the H5N1 outbreak Of the few avian influenza viruses that have crossed theOf the few avian influenza viruses that have crossed the

species barrier to infect humans, H5N1 has caused thespecies barrier to infect humans, H5N1 has caused the

largest number of detected cases of severe disease andlargest number of detected cases of severe disease and

death in humans.death in humans.

However, it is possible that those cases in the mostHowever, it is possible that those cases in the most

severely ill people are more likely to be diagnosed andseverely ill people are more likely to be diagnosed and

reported, while milder cases go unreported.reported, while milder cases go unreported.


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Of the human cases associated with the ongoing H5N1Of the human cases associated with the ongoing H5N1

outbreaks in poultry and wild birds in Asia and parts ofoutbreaks in poultry and wild birds in Asia and parts of

Europe, the Near East and Africa, more than half of thoseEurope, the Near East and Africa, more than half of those

people reported infected with the virus have died.people reported infected with the virus have died.

Most cases have occurred in previously healthy childrenMost cases have occurred in previously healthy children

and young adults and have resulted from direct or closeand young adults and have resulted from direct or closecontact with H5N1contact with H5N1--infected poultry or H5N1infected poultry or H5N1--

contaminated surfaces.contaminated surfaces.

In general, H5N1 remains a very rare disease in people.In general, H5N1 remains a very rare disease in people.The H5N1 virus does not infect humans easily, and if aThe H5N1 virus does not infect humans easily, and if a

person is infected, it is very difficult for the virus to spreadperson is infected, it is very difficult for the virus to spread

to another person.to another person.


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While there has been some human-to-human spread of

H5N1, it has been limited, inefficient and unsustained.

For example, in 2004 in Thailand, probable human-to-

human spread in a family resulting from prolonged and

very close contact between an ill child and her mother was

reported.

In June 2006, WHO reported evidence of human-to-human

spread in Indonesia. In this situation, 8 people in one

family were infected.

No further spread outside of the exposed family was

documented or suspected.


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Treatment and vaccination forTreatment and vaccination for

H5N1 virus in humansH5N1 virus in humans

The H5N1 virus is resistant to amantadine andThe H5N1 virus is resistant to amantadine and

rimantadinerimantadine, two antiviral medications commonly, two antiviral medications commonly

used for influenza.used for influenza.

Two other antiviral medications,Two other antiviral medications, oseltamiviroseltamivir andand

zanamivirzanamivir, would probably work to treat influenza, would probably work to treat influenza

caused by H5N1 virus, but additional studies stillcaused by H5N1 virus, but additional studies still

need to be done to demonstrate their effectiveness.need to be done to demonstrate their effectiveness.


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Global path of H5N1


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Cumulative Number ofConfirmed Human Cases of

Avian Influenza A/(H5N1) Reported to WHO2003 2004 2005 2006 2007 2008 2009 2010 total

cases deaths cases deaths cases deaths cases deaths cases deaths cases deaths cases deaths cases deaths cases deaths

Egypt 0 0 0 0 0 0 18 10 25 9 8 4 39 4 22 9 112 36

Total 4 4 46 32 98 43 115 79 88 59 44 33 73 32 39 20 507 302


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SARS Respiratory disease in humans which is caused by the SARS

coronavirus (SARS-CoV)

Initial symptoms are flu-like and may include:

fever

myalgia lethargy

gastrointestinal symptoms

cough

sore throat

The only symptom that is common to all patients appears to

be a fever above 38C (100.4F). Shortness of breath

may occur later.


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Coronaviruses are positive-strand, enveloped RNA viruses that are

important pathogens of mammals and birds.

This group of viruses cause enteric or respiratory tract infections

in a variety of animals including humans, livestock and pets.

In May 2003, studies from samples of wild animals sold as food in

the local market in Guangdong, China found that the SARScoronavirus could be isolated frompalm civets (Paguma sp.), but

the animals did not always show clinical signs.

Virus was also later found in raccoon dogs (Nyctereuteus sp.),ferret badgers (Melogales spp.) and domestic cats.

In 2005, two studies identified a number of SARS-like

coronaviruses in Chinese bats.


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SARS coronavirus originated in bats and spread tohumans either directly, or through animals held in

Chinese markets.

The bats did not show any visible signs of disease,but are the likely natural reservoirs ofSARS-like

coronaviruses.


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Palm civet Ferret badger

Raccoon dog Flying fox


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DIAGNOSISDIAGNOSIS


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The chest X-ray (CXR) appearance of SARS is variable. There

is no pathognomonic appearance of SARS but is commonly felt

to be abnormal with patchy infiltrates in any part of the lungs.

ELISA (enzyme-linked immunosorbent assay) detects

antibodies to SARS reliably but only 21 days after the onset of

symptoms.

Immunofluorescence assay, can detect antibodies 10 days after

the onset of the disease

Polymerase chain reaction (PCR) test that can detect geneticmaterial of the SARS virus in specimens ranging from blood,

sputum, tissue samples and stools.


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Probable case:

SARS may be suspected in a patient who has:

Any of the symptoms, including a fever of 38

C(100.4F) or higher, and

Either a history of:

1. Contact (sexual or casual) with someone

with a diagnosis of SARS within the last 10 days OR2. Travel to any of the regions identified by the

WHO as areas with recent local transmission of SARS

(affected regions as of 10 May 2003 were parts of China,

Hong Kong, Singapore and the province of Ontario, Canada).

Laboratoryconfirmed SARS:

Probable case + one of the approved tests positive

(ELISA, immunofluorescence or PCR).


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Treatment Treatment of SARS so far has been largely supportive with

antipyretics, supplemental oxygen and ventilatory support

as needed.

Suspected cases of SARS must be isolated, preferably innegative pressure rooms, with complete barrier nursing

precautions taken for any necessary contact with these

patients.

Combinations of drugs that have yielded a more positive

clinical outcome (when administered early) have included

the use ofKaletra, Ribavirin and corticosteroids.


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Vector borne infections


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Vector-Borne Infectious Diseases

Are More Complex Multiple interconnected & complex cycles

Pathogens adapted to vertebrate &

invertebrate species Vector interacts with host & agent

Environment affects vector abundance &

ability to transmit infection Multiple host species


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Commonalities ofMosquito-Borne Zoonoses

Humans rarely develop high titer ofpathogens

in blood, CSF, or tissue (i.e., do not amplify*).

Large outbreaks rare but can be explosive

Clinical cases usually severe High mortality

Finding source of infection (reservoir)

important for disease control (source reduction,depopulation)

* Excluding yellow fever virus


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Big Concepts & Definitions Unique to

Vector-Borne Diseases

Vector Does not itself cause disease. Instead, vectorstransmit infection by moving pathogen from one host to

another. Infection generally lasts vectors life & can killvector.

Bridging vector Mosquito feeds on amplifying hosts & other

species causing infections in other hosts. Bridge betweenone cycle & another.


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Bridging

Bridging mosquito species in yellow feverBridging mosquito species in yellow fever


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Viral persistence strategies

Allow re-emergence ofpathogen in next yeardespite unfavorable environmental conditions:

Reintroduction by migratory birds

Alternate arthropod vectors

Long-term survival of infected, dormantfemales

Continued feeding & transmission year-around

Chronic infection of vertebrate hosts

Transovarial transmission


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Mosquitoes, Sandflies & Human DiseaseInfectious Disease AgentsInfectious Disease Agents

Vector genera Virus Bacterial Protozoal

AnophelesOnyong-nyong

(Alphavirus)??

Plasmodium

(Malaria)

Aedes /Ochlerotatus

(Stegomyia)

Yellow fever & Dengue

(Flavivirus)

Chikungunya virus

(Alphavirus)

Francisella

tularensis*??

Culex

West Nile virus

Japanese encephalitis

virus

St. Louis encephalitis

virus

Francisella

tularensis*

??

Phelbotomus &

Lutzomyia

Sandfly Fever

(Phlebovirus)

Bartonella

(Oroya Fever)

Leishmania

(Kala Azar)

* Mechanical transfer of bacteria


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Japanese encephalitis serocomplex (14 viruses)

Viruses that cause human encephalitis

Japanese encephalitis virus

West Nile virus (Variant: Kunjin)

St. Louis encephalitis virus

Murray Valley encephalitis virus (Variant: Alfuy)

Rocio virus

Ilheus virus

Bussuquara virus (?) Viruses that do not cause human encephalitis but may cause

animal infections/illnesses

Usutu (?), Cacipacore, Koutango, Yaounde, & Stratfordviruses


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Commonality of Viruses in JESerocomplex Human infections:

Most asymptomatic

Small number of rash-fever or febrile illness cases

< 1% associated with central nervous system illness

Very low virus titer in human serum & CSF:

No human-mosquito-human transmissionNo human-to-human transmission

Surface Envelope protein similar across complex

Culex mosquitoes are vectors

Amplifying hosts: Birds JE & MVE Ardeid birds

In JE, pigs also serve as amplifying hosts

WNV & SLE Passerine birds


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West Nile virus was firstisolated in 1937 from the

blood of a febrile woman inthe West Nile province of

Uganda


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West Nile VirusWest Nile Virus

Approximate Geographic Range in 1998Approximate Geographic Range in 1998


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West Nile Virus Human Illness


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West NileWest Nile neuroinvasiveneuroinvasive

disease(WNND)disease(WNND)

Encephalitis, meningitis,Encephalitis, meningitis, myelitismyelitis

Increasedrisk with age & coIncreasedrisk with age & co--morbidmorbidconditionsconditions

Reportable conditionReportable condition


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WNF (10-30%)

West Nile fever(WNF)West Nile fever(WNF)

Noovert CNS involvementNoovert CNS involvementFever, rash, headache, myalgia, arthralgiaFever, rash, headache, myalgia, arthralgia

Not areportable conditionNot areportable condition

1010 --30% infections30% infections


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Asymptomatic WNAsymptomatic WN

infection (70infection (70--90%)90%)

AsymptomaticinfectionAsymptomaticinfection

Not reportable conditionNot reportable condition

Same virus / antibody kineticsSame virus / antibody kinetics

LifeLife--longimmunitylongimmunity

Potential problem forbloodPotential problem forblood

banking & organdonationbanking & organdonation

7070--90% infections90% infections


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ClinicalSpectrum of WNV

Illness: Revised

WN EncephalitisWN Encephalitis

WN PoliomyelitisWN PoliomyelitisInflammatory NeuropathyInflammatory NeuropathyRadiculopathy / plexopathyRadiculopathy / plexopathy

WN FeverWN FeverWN MeningitisWN Meningitis


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Weather conditions (temperature & precipitationWeather conditions (temperature & precipitation

WildWild--bird population:bird population:

Sick/dead birdsSick/dead birds test for virus (WNV, Usutu)test for virus (WNV, Usutu)

Healthy birdsHealthy birds test for antibodiestest for antibodies Sentinel chicken flocksSentinel chicken flocks test for antibodiestest for antibodies

Mosquito collectionsMosquito collections test for virustest for virus

Horses

Horses encephalitisencephalitis test for antibodiestest for antibodies

Human illnessesHuman illnesses

ViremicViremic blood donors (WNV)blood donors (WNV)

Surveillance formosquitoSurveillance formosquito--borneborne zoonoseszoonoses


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West Nile Virus - The most widespread of the JEserocomplex flaviviruses


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Disease Control

i b i l i f i


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Strategies to prevent arboviral infections Alter environment:

Reduce mosquito breeding habitats Screen windows/doors

Kill mosquitoes:

Larvicide/ Bacillus thuringienis

applications Aerial spraying (adulticide)

Tailor to habits of specific vector

Mosquito fish & copepods

Humans & personal protection: Restrict outdoor activity at dawn & dusk

Wear long-length clothing

Mosquito repellant use


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