Virology Compilation For Final Exam Guide

Français
Search Canada.ca 
MENU 
Canada.ca  Health  Health risks and safety  Biosafety and biosecurity
 Pathogen Safety Data Sheets
Pathogen safety data sheet: Infectious

substances – Adenovirus (serotypes 40 and 41)
PATHOGEN SAFETY DATA SHEET - INFECTIOUS

SUBSTANCES
SECTION I - INFECTIOUS AGENT
NAME: Adenovirus (Serotypes 40 & 41)
SYNONYM OR CROSS REFERENCE: Adenovirus Species F, enteric

adenovirus(1,2), fastidious adenovirus(2), ADV 40, and ADV 41.
CHARACTERISTICS: Human adenoviruses are members of the family

Adenoviridae and genus Mastadenovirus. They are nonenveloped viruses
with an icosahedral capsid, 70-90 nm in diameter and a double-stranded,
linear DNA genome(1).
SECTION II - HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Adenovirus serotypes 40 and 41 cause acute
gastroenteritis primarily in children. Symptoms may include fever, diarrhea,
vomiting, and abdominal pain, and last for approximately 10 days.
Respiratory symptoms can occur in some individuals. The disease is usually
self-limiting in immunocompetent individuals; however rare fatalities can
occur in immunocompromised individuals(1). Asymptomatic infections are
common, particularly in children(3).
EPIDEMIOLOGY: Enteric adenovirus is a common cause of acute

gastroenteritis in children worldwide(1). Enteric adenoviruses have been
identified in 9% of children with diarrhea. They are the third most common
cause of infantile gastroenteritis after rotavirus and norovirus(2). Sporadic
and endemic infections may occur year-round(1).
HOST RANGE: Humans.
INFECTIOUS DOSE: Unknown.
MODE OF TRANSMISSION: The virus is transmitted via the fecal-oral

route(1).
INCUBATION PERIOD: 3 to 10 days(1).
COMMUNICABILITY: Low communicability between close contacts in the

same household(4). Virus shedding takes place during the acute stage of the
disease, since enteric adenoviruses are rarely recovered from stool samples
more than a few weeks after recovery from gastroenteritis(1). Asymptomatic
individuals (mainly children) shed adenoviruses in their stool(3).
SECTION III - DISSEMINATION

RESERVOIR: Humans(5).
ZOONOSIS: None.
VECTORS: None.
SECTION IV - STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: None. Reports indicate that cidofovir may be
effective against adenoviruses; however, no controlled trials have been
performed so far, and the drug is not currently licensed for use(6).
SUSCEPTIBILITY TO DISINFECTANTS: Adenoviruses are resistant to lipid

disinfectants, but are inactivated by formaldehyde and chlorine(6).
Adenoviruses can be inactivated by contact with 1:5 dilution of bleach for 1-2
minutes, and by contact with alcohol-based hand gels(1).
PHYSICAL INACTIVATION: Adenoviruses are highly resistant to

inactivation(1). Adenovirus can be inactivated by heat(6): heating to 56 °C for
30 min, 60 °C for 2 min, and autoclaving will destroy infectivity(1). Adenovirus
serotype 40 is also sensitive to UV radiation(7).
SURVIVAL OUTSIDE HOST: Most serotypes are stable at 36 °C for a week, for
several weeks at room temperature, and for several months at 4 °C(1,8).
Adenoviruses are very stable in the environment and persist for 7 days to 3
months on dry inanimate surfaces(8). They can also survive for many days in
tap water, sewage effluent, and sea water(9).
SECTION V - FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms of gastrointestinal and/or
respiratory illness. Enteric adenovirus infection can be detected by electron
microscopy, agglutination tests, enzyme-linked immunosorbent assay, or by
PCR(10).
Note: All diagnostic methods are not necessarily available in all countries.
FIRST AID/TREATMENT: Illness is generally self-limiting. Treatment is

primarily oral rehydration or, in serious cases, intravenous rehydration(10).
IMMUNISATION: None.
PROPHYLAXIS: None.
SECTION VI - LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: At least 10 cases of laboratory-
acquired adenovirus infections have occurred up to 2006; however, the
serotypes involved were not reported(11).
SOURCES/SPECIMENS: Fecal samples(1,4).
PRIMARY HAZARDS: Ingestion of virus(1), accidental parenteral inoculation,

and droplet exposure of the mucous membranes of the eye, nose, or mouth.
SPECIAL HAZARDS: None.
SECTION VII - EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2(12).
CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment,

and operational practices for all work involving infectious or potentially
infectious materials, animals, and cultures.
PROTECTIVE CLOTHING: Lab coat. Gloves when direct skin contact with
infected materials or animals is unavoidable. Eye protection must be used
where there is a known or potential risk of exposure to splashes(13).
OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve

high concentrations or large volumes should be conducted in a biological
safety cabinet (BSC). The use of needles, syringes, and other sharp objects
should be strictly limited. Additional precautions should be considered with
work involving animals or large scale activities(13).
SECTION VIII - HANDLING AND STORAGE

SPILLS: Allow aerosols to settle, and while wearing protective clothing,
gently cover the spill with paper towels and apply appropriate disinfectant,
starting at the perimeter, working inwards towards the centre. Allow
sufficient contact time before clean up(13).
DISPOSAL: Decontaminate before disposal by steam sterilization,

incineration, or chemical disinfection(13).
STORAGE: In locked, leak-proof containers that are appropriately labelled

and secured(13).
SECTION IX - REGULATORY AND OTHER INFORMATION

REGULATORY INFORMATION: The import, transport, and use of pathogens
in Canada is regulated under many regulatory bodies, including the Public
Health Agency of Canada, Health Canada, Canadian Food Inspection Agency,
Environment Canada, and Transport Canada. Users are responsible for
ensuring they are compliant with all relevant acts, regulations, guidelines,
and standards.
UPDATED: November 2010
PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of

Canada.
Although the information, opinions and recommendations contained in this

Pathogen Safety Data Sheet are compiled from sources believed to be
reliable, we accept no responsibility for the accuracy, sufficiency, or
reliability or for any loss or injury resulting from the use of the information.
Newly discovered hazards are frequent and this information may not be
completely up to date.
Copyright ©
Public Health Agency of Canada, 2010
Canada
REFERENCES:
1. Robinson, C., & Echavarria, M. (2007). Adenoviruses. In P. R. Murray, E. J.
Baron, J. Jorgensen, M. Pfaller & M. L. Landry (Eds.), Manual of Clinical
Microbiology (9th ed., pp. 1589) ASM Press.
2. Gómara, M. I., Simpson, R., Perault, A. M., Redpath, C., Lorgelly, P., Joshi,
D., Mugford, M., Hughes, C. A., Dalrymple, J., Desselberger, U., & Gray, J.
(2008). Structured surveillance of infantile gastroenteritis in East Anglia,
UK: Incidence of infection with common viral gastroenteric pathogens.
Epidemiology and Infection, 136 (1), 23-33.
3. Wold, W. S. M., & Horwitz, M. S. (2007). Adenoviruses. In D. M. Knipe, &
P. M. Howley (Eds.), Fields Virology (5th ed., pp. 2395-2436). Philadelphia,
PA: Lippincott Williams & Wilkins.
4. Mistchenko, A. S., Huberman, K. H., Gomez, J. A., & Grinstein, S. (1992).
Epidemiology of enteric adenovirus infection in prospectively monitored
Argentine families. Epidemiology and Infection, 109 (3), 539-546.
5. Parija, S. C. (2009). Adenovirus. Textbook of Microbiology and Immunology
(pp. 509-512). Haryana, India: Elsevier Health Sciences.
6. Flomenberg, P. (2009). Adenovirus infections. Medicine, 37 (12), 676-678.
7. Thurston-Enriquez, J. A., Haas, C. N., Jacangelo, J., Riley, K., & Gerba, C. P.
(2003). Inactivation of feline calicivirus and adenovirus type 40 by UV
radiation. Applied and Environmental Microbiology, 69 (1), 577-582.
8. Kramer, A., Schwebke, I., & Kampf, G. (2006). How long do nosocomial
pathogens persist on inanimate surfaces? A systematic review. BMC
Infectious Diseases, 6
9. Enriquez, C. E., Hurst, C. J., & Gerba, C. P. (1995). Survival of the enteric
adenoviruses 40 and 41 in tap, sea, and waste water. Water Research, 29
(11), 2548-2553.
10. Desselberger, U., & Gray, J. (2009). Viral gastroenteritis. Medicine, 37 (11),
594-598.
11. Paragas, J., & Endy, T. P. (2006). Viral Agents of Human Disease:
Biosafety Concerns. In D. O. Fleming, & D. L. Hunt (Eds.), Biological
Safety: Principles and Practices (4th ed., pp. 179-207). Washington DC:
ASM Press.
12. Human pathogens and toxins act. S.C. 2009, c. 24, Second Session,
Fortieth Parliament, 57- 58 Elizabeth II, 2009. (2009).
13. Public Health Agency of Canada. (2004). In Best M., Graham M. L.,
Leitner R., Ouellette M. and Ugwu K. (Eds.), The Laboratory Biosafety
Guidelines (3rd ed.). Canada: Public Health Agency of Canada.
Report a problem or mistake on this page  Share this page
Date modified: 2011-04-19
Public Health Agency of Canada
Contact us
Government of Canada
All contacts
About government
Departments and agencies
Jobs Culture, history and sport
Immigration and citizenship Policing, justice and emergencies
Travel and tourism Transport and infrastructure
Business Canada and the world
Benefits Money and finance
Health Science and innovation
Taxes Indigenous peoples
Environment and natural resources Veterans and military
National security and defence Youth
Social media
Mobile applications
About Canada.ca
Terms and conditions
Privacy
Français
MENU 
Pathogen Safety Data Sheets: Infectious

Substances – Adenovirus types 1, 2, 3, 4, 5 and
7

NAME: Adenovirus (excluding serotypes 40 and 41)
SYNONYM OR CROSS REFERENCE: Acute respiratory disease (ARD),

childhood febrile illness, adenovirus species A, B, C, D, E, F, G,
pharyngoconjunctival fever.
CHARACTERISTICS: Human adenoviruses are members of the family

Adenoviridae and genus Mastadenovirus. Within the almost 100 different
serotypes of human adenovirus, 51 are known to be pathogenic in humans
1 2 . The virus is nonenveloped with an icosahedral capsid at 70-90 nm in
diameter and each contains a single linear, double-stranded DNA genome of
2
approximately 36 kb .

PATHOGENICITY/TOXICITY: Adenovirus cause generally mild respiratory
tract infections which are self-limiting and generally asymptomatic despite
3
virologic and serologic proof of infection , and only around 45% of
1
infections are manifested by disease . It is a major agent of acute
respiratory disease, mainly caused by serotypes 4 and 7, and is characterized
1
by fever, rhinitis, pharyngitis, cough, and conjunctivitis . Other common
illnesses can be observed in the respiratory tract, gastrointestinal tract, and
2
eyes (acute follicular conjunctivitis) . Common diseases caused by
various adenovirus serotypes are:
Childhood febrile illness and pharyngoconjunctival fever – 1, 2, 3, 5, 7

1
1 4
Pneumonia and other acute respiratory illnesses – 1, 2, 3, 5, 7, 14
1
Pertussis-like illness – 1, 2, 3, 5, 19, 21
1 2
Conjunctivitis – 1-4, 5, 7, 8, 19, 21
1
Keratoconjunctivitis – 3, 8, 9, 19, 37
1
Acute hemorrhagic cystitis – 11
2
Upper respiratory illness and hepatitis – 1-3, 5, 7
2
Lower respiratory illness – 3, 4, 7, 21
General infections are commonly observed in young children, particularly by

1
serotypes 1, 2, and 5 . Symptoms of infection may include fever, nasal
congestion, coryza, and pharyngitis. Other more serious illnesses such as
nephritis, neutropenia, myocarditis, hepatitis, disseminated intravascular
2 5
coagulation and meningoencephalitis can occur . Eye infections such
as acute follicular conjunctivitis, often accompanied by significant
periauricular lymphadenopathy, are often mild and complete recovery is
6
common . Neonatal disease, meningoencephalitis, myocarditis, and
2
venereal diseases are uncommon .
EPIDEMIOLOGY: Adenovirus is of worldwide prevalence, and is ubiquitous

5
throughout the year, especially during later winter and early spring .
Serotype 5 is the most common, with serotypes 1 and 2 being highly
1 2 5 7
endemic . Children are especially susceptible to infection .
Adenovirus serotypes 3, 4, 7, and 21 have been associated with outbreaks of
3 8
acute respiratory disease among military recruits . These outbreaks
8
have resulted in hospitalization and some mortality . Smaller outbreaks
of serotypes 3, 4, and 7 occur in the summertime due to contaminated
1 2
swimming pool water, which commonly resulted in conjunctivitis .
Serious adenovirus infections occur more frequently in
2 7
immunocompromised individuals .
HOST RANGE: Humans.
INFECTIOUS DOSE: Inhalation of as few as 5 adenovirus particles can cause

3
disease in susceptible individuals . The National Institutes of Health lists
the infectious dose for adenovirus serotype 7 as >150 viral units,
9
administered as nasal drops .
MODE OF TRANSMISSION: Respiratory and fecal-oral routes. Infection can

also spread through contaminated fomites, fingers, ophthalmic solutions,
2 5 1
and airborne particulates
2
INCUBATION PERIOD: Approximately 2 to 14 days .
COMMUNICABILITY: Children shed non enteric adenovirus in throat and

stool samples for 3 to 6 weeks following lower respiratory infection or
generalized illness. Chance of transmission is high in crowded and closed
settings such as day cares, boarding schools and long-term care facilities.
Transmission between family members is common. In rare cases, virus
2
shedding may last for 18 months or longer .

3 6
RESERVOIR: Humans . Experimentally, human adenovirus can infect
virtually all mammalian species, including monkeys, cotton rats, rabbits, and
6
rodents .
ZOONOSIS: None.
VECTORS: None.

DRUG SUSCEPTIBILITY: None. Many reports indicate cidofovir to be effective
against adenoviruses; however, no controlled trials have been performed so
far, and the drug is not currently licensed for use Footnote 5.
SUSCEPTIBILITY TO DISINFECTANTS: Adenoviruses are resistant to lipid

5
disinfectants, but are inactivated by formaldehyde and chlorine . They
can be inactivated by contact with 1:5 dilution of bleach for 1 minute or 2
2
minutes contact with alcohol-based hand gels .
5
PHYSICAL INACTIVATION: Adenovirus can be inactivated by heat :
heating to 56 °C for 30 min, 60 °C for 2 min, and autoclaving will destroy
2
infectivity .
SURVIVAL OUTSIDE HOST: Most serotypes are stable at 36 °C for a week, for
2 10
several weeks at room temperature, and for several months at 4 °C .
Adenoviruses are very stable in the environment and persist for 7 days to 3
10
months on dry inanimate surfaces . They can also survive for weeks in
11
tap water, sewage effluent and sea water . Adenovirus type 2 can
survive on common environmental surfaces for up to 8 weeks at room
12
temperature .

SURVEILLANCE: Monitor for symptoms. Infected cells can be observed by
microscopy, and adenoviruses can be detected using immunofluorescence,
2
enzyme-linked immunoassay, or PCR for antigen detection .
FIRST AID/TREATMENT: No formally approved effective antiviral agents

7
exist for treatment of adenoviral infections . Illness is generally self-
5
limiting and treatment is supportive . It has been suggested that
immunocompromised patients may require drug treatment with cidofovir or
7
other antiviral drugs .
IMMUNIZATION: A vaccine for adenovirus strains 4 and 7 was developed

2 8
but is no longer in production (economic reasons) .
PROPHYLAXIS: None.

LABORATORY-ACQUIRED INFECTIONS: At least 10 cases of laboratory-
acquired adenovirus infections have occurred up to 2006; however, the
serotypes involved were not reported Footnote 13.
SOURCES/SPECIMENS: Generally, fecal samples, and respiratory secretions

from an infected individual contain infectious virus. Other tissues may
2
contain virus depending on symptoms .
PRIMARY HAZARDS: Contact of mucous membranes (mouth or eyes) with

2 13 14
virus, ingestion, or inhalation of viral particles .
SECTION VII - EXPOSURE CONTROLS /

PERSONAL PROTECTION
15
RISK GROUP CLASSIFICATION: Risk Group 2 . This risk group applies
to the species as a whole, and may not apply to every serotype within the
species.

and operational practices for work involving infectious or potentially
infectious materials. These containment requirements apply to the species
as a whole, and may not apply to each serotype within the species.
16
where there is a known or potential risk of exposure to splashes .

16
work involving animals or large scale activities .

SPILLS: Allow aerosols to settle and, wearing protective clothing, gently
cover spill with paper towels and apply an appropriate disinfectant, starting
at the perimeter and working towards the centre. Allow sufficient contact
16
time before clean up .
DISPOSAL: Decontaminate all wastes that contain or have come in contact

with the infectious organism before disposing by autoclave, chemical
16
disinfection, gamma irradiation, or incineration .
STORAGE: The infectious agent should be stored in leak-proof containers

16
that are appropriately labelled .
SECTION IX - REGULATORY AND OTHER

INFORMATION
and standards.

Canada.

Copyright © Public Health Agency of Canada, 2011 Canada
REFERENCES
1 Ray, C. G. (2004). Influenza, Respiratory Syncytial Virus,
Adenovirus, and Other Respiratory Viruses. In K. J. Ryan, & C. G.
Ray (Eds.), Sherris Medical Microbiology - An Introduction to
Infectious Diseases (4th ed., pp. 495-512). USA: The McGraw-Hill
Companies, Inc.
2 Robinson, C., & Echavarria, M. (2007). Adenoviruses. In P. R.

Murray, E. J. Baron, J. Jorgensen, M. Pfaller & M. L. Landry (Eds.),
Manual of Clinical Microbiology (9th ed., pp. 1589) ASM Press.
3 Musher, D. M. (2003). How contagious are common respiratory

tract infections? New England Journal of Medicine, 348(13), 1256-
1266.
4 Centers for Disease Control and Prevention (CDC). (2010).

Outbreak of adenovirus 14 respiratory illness--Prince of Wales
Island, Alaska, 2008. MMWR.Morbidity and Mortality Weekly Report,
59(1), 6-10.
5 Flomenberg, P. (2009). Adenovirus infections. Medicine, 37(12),

676-678.
6 Wold, W. S. M., & Horwitz, M. S. (2007). Adenoviruses. In D. M.

Knipe, & P. M. Howley (Eds.), Fields Virology (5th ed., pp. 2395-
2436). Philadelphia, PA: Lippincott Williams & Wilkins.
7 Lenaerts, L., De Clercq, E., & Naesens, L. (2008). Clinical features

and treatment of adenovirus infections. Reviews in Medical
Virology, 18 , 357-374.
8 Gray, G. C., Goswami, P. R., Malasig, M. D., Hawksworth, A. W.,

Trump, D. H., Ryan, M. A., & Schnurr, D. P. (2000). Adult adenovirus
infections: Loss of orphaned vaccines precipitates military
respiratory disease epidemics. Clinical Infectious Diseases, 31 , 663-
670.
9 Collins, C. H., & Kennedy, D. A. (1999). Exposure, sources and route

of infection. Laboratory-acquired Infection: History, incidence, causes
and preventions (pp. 38-53). Oxford, UK: Butterworth-Heinemann.
10 Kramer, A., Schwebke, I., & Kampf, G. (2006). How long do

nosocomial pathogens persist on inanimate surfaces? A
systematic review. BMC Infectious Diseases, 6
11 Enriquez, C. E., Hurst, C. J., & Gerba, C. P. (1995). Survival of the

enteric adenoviruses 40 and 41 in tap, sea, and waste water. Water
Research, 29(11), 2548-2553.
12 Prince, H. N., Prince, D. L., & Prince, R. N. (1991). Principles of Viral

Control and Transmission. In S. S. Block (Ed.), Disinfection,
Sterilization, and Preservation (pp. 411-444). Malvern, PA: Lea &
Febiger.
13 Paragas, J., & Endy, T. P. (2006). Viral Agents of Human Disease:

Safety: Principles and Practices (4th ed., pp. 179-207). Washington
DC: ASM Press.
14 Collins, C. H., & Kennedy, D. A. (1999). Laboratory-acquired

infections. Laboratory-acquired Infections: History, incidence, causes
and prevention. (4th ed., pp. 12). Oxford, UK: Butterworth
Heinemann.
15 Human pathogens and toxins act. S.C. 2009, c. 24, Second Session,
Fortieth Parliament, 57-58 Elizabeth II, 2009. (2009).
16 Public Health Agency of Canada. (2004). In Best M., Graham M. L.,

Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Creutzfeldt-Jakob agent, Kuru
agent

SUBSTANCES
NAME: Creutzfeldt-Jakob agent, Kuru agent
SYNONYM OR CROSS REFERENCE: Subacute spongiform encephalopathy,

Creutzfeldt-Jakob disease (CJD), Kuru, Chronic infectious neuropathic agents
(CHINA's)
CHARACTERISTICS: Filterable, self-replicating agent, slow infectious

pathogen, prion
SECTION II - HEALTH HAZARD

PATHOGENICITY: CJD - insidious onset of confusion, progressive dementia,
myoclonic jerks with spasticity, wasting and coma; slight elevation of CSF
proteins; death usually occurs in less than 1 year; 10% cases have family
history of presenile dementia; amorphous amyloid plaques in cerebellum of
15% of cases; Kuru - CNS disease with cerebellar ataxia, incoordination,
tremors, rigidity, progressive wasting and death within 3-9 months
EPIDEMIOLOGY: CJD - Reported from 50 countries with highest incidence

found among Libyan Jews in Israel; Kuru - occured in Fore tribe of Papua
New Guinea
HOST RANGE: Humans, transmissible to chimpanzees, monkeys, guinea

pigs, mice
INFECTIOUS DOSE: Unknown
MODE OF TRANSMISSION: The mode of transmission of most cases is

unknown; iatrogenic cases of CJD reported (corneal transplant, from cortical
electrodes previously used on known patients, brain or eye surgery, human
growth hormone therapy, exposure to infected brain tissues by
pathologists), no evidence of transmission of CJD from one person to
another: Kuru-handling and eating kuru infected brain during ritualistic
cannibalism
INCUBATION PERIOD: Fifteen months to 2 years to CJD iatrogenic cases; 4

to over 20 years for Kuru
COMMUNICABILITY: CNS and other tissues are infectious throughout

symptomatic illness; lymphoid and other organs probably infectious before
signs of illness appear

RESERVOIR: Human cases constitute the only known reservoir
ZOONOSIS: No documented human infections acquired from animals

although this has been hypothesized (consumption of scrapie-infected
sheep might result in CJD; in 1996 consumption of BSE-infected beef in UK
has been associated with development of CJ-like disease)
VECTORS: None
SECTION IV - VIABILITY
DRUG SUSCEPTIBILITY: N/A
SUSCEPTIBILITY TO DISINFECTANTS: Resistance to commonly used

disinfectants is well recognized: formaldehyde, glutaraldehyde, ethanol, and
iodine. Immersion in undiluted bleach (60,000 ppm available chlorine) for 1
hour is only partially effective. Disinfection should be carried out using 1N
sodium hydroxide at room temperature for 1 hour (shorter treatments have
occasionally not inactivated the pathogen)
PHYSICAL INACTIVATION: Resistant to ultraviolet and ionizing radiation,

ultrasonication, nucleases, boiling, heat; autoclaving - 15 to 30 min at 121·C
or 132·C will not effectively inactivate pathogen, 1 hour at 132·C is
recommended)
SURVIVAL OUTSIDE HOST: Contaminated electrodes stored in ethanol-

formalin for several years were found to cause CJD in chimpanzee
SECTION V - MEDICAL
SURVEILLANCE: Monitor for clinical signs - diagnosis based on EEG,
histopathological findings, transmission to animals from biopsy specimens
FIRST AID/TREATMENT: Any skin contact with infectious materials should

be followed by washing with sodium hydroxide; no specific treatment
IMMUNIZATION: None
PROPHYLAXIS: None

LABORATORY-ACQUIRED INFECTIONS: No documented laboratory-
associated infections with spongiform encephalopathies however,
consequences of infection are grave and there are cases of infection from
contaminated EEG electrodes and corneal transplants
SOURCES/SPECIMENS: High titres in brain and CNS of persons with Kuru;

CJD brain, spleen, liver, lymph nodes, lungs, spinal cord, kidneys, cornea and
lens, blood, urine; includes formalin-fixed specimens
PRIMARY HAZARDS: Accidental parenteral inoculation; risk of infection from

aerosols, droplets, and exposure.of intact skin, gastric and mucous
membranes is not known
SPECIAL HAZARDS: Laboratory animals that have been infected and their
tissues should be considered potentially hazardous
SECTION VII - RECOMMENDED PRECAUTIONS

CONTAINMENT REQUIREMENTS: Biosafety level 3 facilities, practices and
containment equipment for activities involving these agents; also listed
under biosafety level 2 with special precautions; level of containment will
depend on the nature of the manipulations and the amount of sera,
bio/necropsy materials handled
PROTECTIVE CLOTHING: Gown and gloves when handling potentially

infectious materials; eye protection may also be indicated
OTHER PRECAUTIONS: Extreme care must be taken to avoid accidental

autoinoculation or other parenteral inoculations of infectious tissues and
fluids
SECTION VIII - HANDLING INFORMATION

SPILLS: Allow any potential aerosols to settle; wearing protective clothing,
gently cover spill with paper towel and apply 1N sodium hydroxide, starting
at perimeter and working towards the centre; allow sufficient contact time (1
hour) before clean up
DISPOSAL: Decontaminate before disposal; steam sterilization (132·C for 1

hour), disinfection with 1N sodium hydroxide for 1 hour, incineration
STORAGE: In sealed containers that are appropriately labelled
SECTION IX - MISCELLANEOUS INFORMATION

Date prepared: September 1996 Prepared by: Office of Biosafety
LCDC

Material Safety Data Sheet are compiled from sources believed to be
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 
Pathogen safety data sheets: Infectious

substances - Epstein-Barr virus
On this page
Section I: Infectious agent
Section II: Hazard identification
Section III: Dissemination
Section IV: Stability and viability
Section V: First aid and medical
Section VI: Laboratory hazards
Section VII: Exposure controls and personal protection
Section VIII: Handling and storage
Section IX: Regulatory and other information
References

Name: Epstein-Barr virus
Synonym or cross reference: Human herpesvirus 4 (HHV4); EBV, infectious

mononucleosis (IM), glandular fever, Burkitt's lymphoma (BL),
1 2
nasopharyngeal carcinoma (NPC) .
Characteristics: Epstein-Barr virus belongs to genus lymphocryptovirus of

1 2
the subfamily Gammaherpesvirinae in the Herpesviridae family . It
consists of a double-stranded 172 Kb DNA genome, enclosed within an
1 3
icosahedral capsid, surrounded by a phospholipid rich envelope .
4
Epstein-Barr virus can be cultured in lyphoblastoid cell lines . The virus
1 3 4
can infect B-cells and epithelial cells .

Pathogenicity/toxicity: Most EBV infections are acquired during childhood
1 5
and are asymptomatic . Symptoms when produced are
undistinguishable from other acute viral syndromes. Many benign and
malignant diseases, however, have been associated with Epstein- Barr virus
1 2 3
in both immunocompetent and immunocompromised patients
4 5 6 7 8 9 .
Diseases in immunocompetent hosts

Infectious Mononucleosis (IM): IM is an acute, self limiting febrile illness in
young adults, characterized by fever, sore throat, abdominal discomfort,
pharyngitis, tonsillitis, tender generalized lymphadenopathy, palatal
1
petechaie, and periorbital oedema) . Some patients also present with
maculopapular rash, splenomegaly, hepatomegaly, and jaundice. Rashes are
almost always present in patients who were given ampicillin or amoxicillin
1 5 9 . The disease generally lasts 1 to 4 weeks; however, protracted
1
illness or tiredness for up to one year can occur in some patients . Many
complications, including autoimmune hemolytic anemia, splenic rupture,
hemophagocytic lymphohistiocytosis, and neurological complications have
1 5
also been associated with infectious mononucleosis .
Burkitt's lymphoma: Burkitt's lymphoma may be endemic, sporadic or im

3
munodeficiency associated . Burkitt's lymphoma arises due to an early
4 8
infection with EBV virus resulting in infected B cells . Endemic
Burkitt's lymphoma frequently affects the facial bones, particularly the jaw,
8
maxilla, and orbit, in young children . The sporadic Burkitt's lymphoma
8
arises in the lymphoid tissues of the gut and the upper respiratory tract .
Other malignant diseases in immunocompetent hosts include various B-cell

or T-cell lymphomas, and epithelial or mesenchymal carcinomas such as
6 7 10
classical Hodgkin's lymphoma and nasopharyngeal carcinoma .
Diseases in immunocompromised hosts: In AIDS patients or other

immunosuppressed patients, many EBV-associated diseases may occur,
such as oral hairy leukoplasia, interstitial lymphocytic pneumonia, B-cell or
T-cell lymphomas and mesenchymal lymphomas (for e.g. leiomyosarcoma)
1 2 3 4 7 . In transplant patients, early and late onset
lymphoproliferative diseases are often caused by EBV.
Epidemiology: EBV infections are quite prevalent, affecting more than 90%
3
of individuals during the first two decades of life worldwide . In
developing countries, primary infections occur mainly in young children and
3 9
are often asymptomatic . In developed countries, primary EBV
infections are manifested mainly as infectious mononucleosis, and affect
3 9
adolescents and young adults . Endemic Burkitt's lymphoma occurs
frequently in young children in the equatorial regions of Africa and Papua
New Guinea and has an incidence of 50-100 cases per 1,000,000 individuals
7 . In contrast, EBV-associated sporadic lymphoma occurs in children and
young adults and has no specific geographic distribution, with an incidence
7
of 2-3 cases per 1,000,000 individuals . It accounts for 40 and 50% of
childhood non-Hodgkin's lymphomas (NHLs) and 1-2% of adult lymphomas
8
in Western Europe and the United States . Endemic Burkitt's lymphoma is
almost 100% associated with EBV, whereas, association of sporadic Burkitt's
7
lymphoma with EBV is low (15-30% of cases) . Nasopharyngeal carcinoma
(NPC) is most common in southern China, and accounts for approximately
6
20% of all adult cancers . It is extremely rare in Europe and North
6
America, with an incidence rate is <1 per 100,000 population .
Host range: Humans
Infectious dose: Not known
Mode of transmission: For infectious mononucleosis, transmission occurs

mainly via sexual contact or contact with saliva of infected persons (oral
1 2 9
route) . Possible spread via blood transfusion can also occur (not
1 9
an important route) . For Burkitt's lymphoma, EBV transmission
occurs early in life through saliva and then the lymphoma develops later
11
after malaria infection. HIV-AIDS is also a possible cofactor .
5 9
Incubation period: The incubation for IM is 30-50 days . For BL, the
12 13
incubation period is longer ranging from 4.7-9.2 years .
Communicability: The virus is contracted after repeated contact with the

4
infected person, or asymptomatic person shedding the virus . Shedding
decreases during the year following infection but persists throughout life
14 . Peaks in transmission occur between 1-6 and 14-20 years of age and
15
over 95% of adults are asymptomatic carriers of the virus .

4
Reservoir: Asymptomatic humans shedding the virus .
Zoonosis: None
Vector: None

Drug susceptibility: Nucleoside analogues such as acyclovir, ganciclovir,
and famciclovir, and pyrophosphate analogues, such as foscarnet can inhibit
1 4
viral replication .
Susceptibility to disinfectants: Most herpes viruses are susceptible to 30%

ethanol and 20% isopropanol, 2000 ppm sodium hypochlorite, 0.12 %
16
orthophenyl phenol, and 0.04% glutaraldehyde .
Physical inactivation: Herpes viruses can be inactivated by heating in

solution at 60°C to 80°C, by freeze drying, and heating at 100°C for 30
10
minutes .
Survival outside host: Unknown

4
Surveillance: Monitor for clinical symptoms . Direct detection of the viral
antigen can be done by staining for EBNA 1 using anti complement
immunofluorescence; viral RNA or DNA can be identified using in situ
hybridization, dot-blot hybridization, nucleic acid amplification testing
1
(NAAT), and southern blotting . Tests for heterophile antibodies in
mononucleosis, antibodies against viral capsid antigen (VCA), antibodies to
1 2 4
EBV nuclear antigen (EBNA) can also be used .
 Note: All diagnostic methods are not necessarily available in all

countries.
First aid/treatment: Treatment of infectious mononucleosis is mainly

4
supportive . Viral replication can be inhibited by nucleoside analogues
which can reduce or terminate viral shedding, but have no effect on the
1 4
symptoms . Airway obstruction is treated with a high dose of
1 4 9
corticosteroid and nasopharyngeal airway . Gamma interferon
treatment has been shown to be effective for patients lacking this interferon
1 . Lymphoproliferative disorders associated with EBV can be treated with
anti-CD20 monoclonal antibodies and EBV specific cytotoxic T lymphocytes
1
along with anti-viral drugs .
Immunisation: No registered vaccine is available for preventing Epstein-

Barr virus infection; however, a glycoprotein gp340 vaccine is in clinical trials
1 .
Prophylaxis: None

Laboratory-acquired infections: Low risk of laboratory acquired infection
17 . No reports of laboratory acquired infection were found in the
literature.
Source/specimens: Clinical specimens - blood, saliva and throat specimens

1 4 .
Primary hazards: Ingestion, accidental parenteral inoculation, direct

exposure of mucous membranes of the eyes, nose, or mouth, or inhalation
17
of aerosolized materials are risks associated with herpes viruses .
Special hazards: None
Section VII: Exposure controls and personal

protection
18
Risk group classification: Risk group 2 .
Containment requirements: Containment Level 2 facilities, equipment, and

operational practices for work involving infectious or potentially infectious
materials, animals, or cultures.
Protective clothing: Lab coat. Gloves when direct skin contact with infected
materials or animals is unavoidable. Eye protection must be used where
19
there is a known or potential risk of exposure to splashes .
Other precautions: All procedures that may produce aerosols, or involve

19

Spills: Allow aerosols to settle, then, wearing protective clothing, gently
cover the spill with absorbent paper towel and apply an appropriate
disinfectant, starting at the perimeter and working towards the center. Allow
sufficient contact time before starting the clean up.
Disposal: All wastes should be decontaminated before disposal either by

steam sterilization, incineration or chemical disinfection.
Storage: The infectious agent should be stored in a sealed and identified

container.

Regulatory information: The import, transport, and use of pathogens in
Canada is regulated under many regulatory bodies, including the Public
and standards.
Updated: October 2010
Prepared by: Pathogen Regulation Directorate, Public Health Agency of

Canada Although the information, opinions and recommendations
contained in this Pathogen Safety Data sheet are compiled from sources
believed to be reliable, we accept no responsibility for the accuracy,
sufficiency, or reliability or for any loss or injury resulting from the use of the
information. Newly discovered hazards are frequent and this information
may not be completely up to date.
Copyright©
Canada
References
1 Linde, A., & Falk, K. I. (2007). Epstein-Barr Virus. In P. R. Murray

(Ed.), Manual of clinical microbiology (9th ed., pp. 1564-1573).
Washington, D.C.: ASM Press.
2 Rickinson, A. B., & Kieff, E. (2007). Epstein-Barr Virus. In D. M.

Knipe, & P. M. Howley (Eds.), Fields of virology (5th ed., pp. 2655-
3 Ng, S. B., & Khoury, J. D. (2009). Epstein-Barr virus in

lymphoproliferative processes: an update for the diagnostic
pathologist. Advances in Anatomic Pathology, 16 (1), 40-55.
4 Drew, W. L. (2004). Herpesviruses. In K. J. Ryan, & C. G. Ray (Eds.),

Sherris medical microbiology: An introduction to infectious
diseases (4th ed., pp. 555-576). USA: McGraw Hill.
5 Griffiths, P. D. (2009). Herpesviruses. Medicine, 37 (12), 668-672.
6 Shah, K. M., & Young, L. S. (2009). Epstein-Barr virus and

carcinogenesis: beyond Burkitt's lymphoma. Clinical Microbiology
& Infection, 15 (11), 982-988.
7 Kutok, J. L., & Wang, F. (2006). Spectrum of Epstein-Barr virus-

associated diseases. Annual Review of Pathology, 1, 375-404.
8 Yustein, J. T., & Dang, C. V. (2007). Biology and treatment of

Burkitt's lymphoma. Current Opinion in Hematology, 14 (4), 375-
381.
9 Papesch, M., & Watkins, R. (2001). Epstein-Barr virus infectious

mononucleosis. Clinical Otolaryngology & Allied Sciences, 26 (1), 3-
8.
10 Sofer, G., Lister, D. C., & Boose, J. A. (2003). Virus inactivation in the
1990s - And into the 21st century: Part 6, inactivation methods
grouped by virus. BioPharm International, 16 (4), 42-52+68.
11 Orem, J., Mbidde, E. K., Lambert, B., de Sanjose, S., & Weiderpass,
E. (2007). Burkitt's lymphoma in Africa, a review of the
epidemiology and etiology. African Health Sciences, 7(3), 166-175.
doi:10.5555/afhs.2007.7.3.166
12 Armenian, H. K., & Lilienfeld, A. M. (1974). The distribution of

incubation periods of neoplastic diseases. American Journal of
Epidemiology, 99 (2), 92-100.
13 Beral, V., Peterman, T., Berkelman, R., & Jaffe, H. (1991). AIDS-
associated non-Hodgkin lymphoma. Lancet, 337 (8745), 805-809.
14 Luzuriaga, K., & Sullivan, J. L. (2010). Infectious mononucleosis.

The New England Journal of Medicine, 362 (21), 1993-2000.
doi:10.1056/NEJMcp1001116
15 Perera, R. A., Samaranayake, L. P., & Tsang, C. S. (2010). Shedding

dynamics of Epstein- Barr virus: A type 1 carcinogen. Archives of
Oral Biology, doi:10.1016/j.archoralbio.2010.06.009
16 Prince, H. N., & Prince, D. L. (2001). Principles of viral control and

transmission. In S. S. Block (Ed.), Disinfection, sterilization and
preservation (5th ed., pp. 543-571). Philadelphia, PA: Lippincott
Williams & Wilkins.
17 Viral agents: Human herpes virus. (1999). In J. Y. Richmond, & R.

W. Mckinney (Eds.), Biosafety in microbiological and biomedical
laboratories (BMBL) (4th ed., pp. 161). Washington, D.C.: CDC &
NIH.
18 Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of

Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II,
2009, (2009).

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Japanese encephalitis virus
MATERIAL SAFETY DATA SHEET - INFECTIOUS

SUBSTANCES
NAME: Japanese encephalitis virus
SYNONYM OR CROSS REFERENCE: JE, JEV, Japanese B encephalitis (JBE),

Arbovirus B, Mosquito-borne encephalitis virus
CHARACTERISTICS: Single stranded, positive sense RNA, enveloped, 40-50

nm diameter, Family Flaviviridae (formerly Togaviridae); prototype member
of Japanese encephalitis antigenic complex which also contains St. Louis
encephalitis virus, Murray valley virus, and West Nile virus
SECTION II - HEALTH HAZARD

PATHOGENICITY: Acute inflammatory viral diseases of short duration
involving parts of the brain, spinal cord and meninges; ranges from febrile
headache syndrome to acute encephalitis; severe infections are marked by
acute onset, headache, high fever, chills, nausea, and vomiting followed by
nuchal rigidity, photophobia and objective neurologic signs, stupor,
disorientation, coma, tremors, convulsions in children, and paralysis of the
upper extremities; infants and elderly more likely to develop severe cases;
fatality rate of 5-40%; 45-70% of severe cases develop neuropsychiatric
sequelae, parkinsonism, convulsive disorder, paralysis, mental retardation
EPIDEMIOLOGY: JE in western Pacific islands from Japan to the Philippines

and in many areas of Asia from Korea to Indonesia, China and India; cases
occur in temperature latitudes in summer and early fall, and are limited to
areas and years of high temperature and many mosquitoes
HOST RANGE: Humans, birds, pigs, cattle, horses, bats and reptiles
MODE OF TRANSMISSION: By the bite of infective mosquitoes
INCUBATION PERIOD: Usually 5-15 days
COMMUNICABILITY: Not directly transmitted from person-to-person; virus is

not usually demonstrable in the blood of human after onset of disease, but
can be isolated from the CNS fluid in 1/3 of acute cases; viremia in birds
usually lasts 2-5 days; mosquitoes are infective for life; viremia in horses
rarely present in high titer for long periods

RESERVOIR: Pigs and birds are the major amplifying hosts; humans, horses
and cattle are uncommon sources of mosquito infection; virus possibly
overwinters in birds, other animals, mosquitos;
ZOONOSIS: Yes, from infected animals via mosquito bites; causes

encephalitis in horses, spontaneous abortion and stillbirths in swine
VECTORS : Culex spp. and Aedes spp.
Most important vectors are:

-Culex tritaeniorhynchus (major epidemic vector)
-Culex vishnui complex -Culex gelidus (in the tropics)
-Culex fuscocephalus -Culex annulus
SECTION IV - VIABILITY
DRUG SUSCEPTIBILITY: Unknown
SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to disinfectants - 70%

ethanol, 2% glutaraldehyde, 3-8 % formaldehyde, 1% sodium hypochlorite,
iodine, phenol iodophors and organic solvents/detergents
PHYSICAL INACTIVATION: Inactivated by heat; 50% reduction in 10 min at

50o C, complete inactivation in 30 min at 56o C; sensitive to UV and gamma
irradiation
SURVIVAL OUTSIDE HOST: Survives for long periods in mosquito eggs

(virus can be maintained overwinter in eggs)
SECTION V - MEDICAL
SURVEILLANCE: Monitor for symptoms, serological studies (detection of
immunoglobulin M and G antibodies) or isolation of virus from blood, CSF or
other body fluid
FIRST AID/TREATMENT: No specific treatment
IMMUNIZATION: Formalin inactivated vaccine (JE-VAX) is licensed in Canada

and recommended for those of increased risk such as laboratory workers
and travellers spending more than one month in endemic/epidemic areas
during the transmission season; 3 doses of the vaccine scheduled on days 0,
7 and 30 are required for a good protection; vaccine is contraindicated for
women who are pregnant and the immunocompromised; two live vaccines
are licensed for use in China.
PROPHYLAXIS: Passively protect accidentally exposed laboratory workers by

human or animal immune serum

LABORATORY-ACQUIRED INFECTIONS: 22 cases reported up to 1980 and
no fatalities
SOURCES/SPECIMENS: Blood, cerebrospinal fluid (CFS), other tissues

(brain), infected arthropods
PRIMARY HAZARDS: Direct contact with broken skin or mucous

membranes, accidental parenteral inoculation, exposure of infectious
aerosols
SPECIAL HAZARDS: Bites or scratches from experimental animals, including

arthropods (mosquitoes)
SECTION VII - RECOMMENDED PRECAUTIONS

CONTAINMENT REQUIREMENTS: Biosafety level 3 practices, containment
equipment, and facilities are recommended for all activities involving
potentially infectious materials and infected tissue cultures, animals, or
arthropods
PROTECTIVE CLOTHING: Laboratory coat, gloves and gown (tie in back and
tight wrists) must be worn when working with infectious materials
OTHER PRECAUTIONS: Vaccination of personnel working directly and

regularly with the JE; important precautions concerning needle safety - do
not bend, break or recap needles and dispose directly into puncture-proof
container

SPILLS: Allow aerosols to settle; wearing protective clothing, the spillage
must be covered promptly with a paper towel and disinfectant poured
gently on towel, working from the outside to inwards; allow sufficient
contact time (30 min) before clean up
DISPOSAL: Decontaminate before disposal: steam sterilization, incineration,

chemical disinfection
STORAGE: In sealed containers that are appropriately labelled and locked in

a level 3 facility

Date prepared: March, 2001
Prepared by: Office of Laboratory Security, PHAC

Copyright ©
Health Canada, 2001
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Chikungunya virus

SUBSTANCES
NAME: Chikungunya virus
1-6 2 7-9
SYNONYM OR CROSS REFERENCE: CHIKV , CHIK , and
2 10
chikungunya fever .
4 10 11
CHARACTERISTICS: A member of the Togaviridae family , and
10 11
Alphavirus genus , belonging to the Semliki Forest serological
1 11
complex . CHIKV is a spherical enveloped virion that measures 60 to
1 11
70 nm in diameter , and contains a single-stranded, positive-sense
11
RNA genome .
SECTION II – HAZARD INFORMATION

PATHOGENICITY/TOXICITY: Translated from the African dialect of Swahili
1 2 12
or Makonde, chikungunya means, "that which bends up" , "what
10 13
bends" , or "to walk bent over" , and refers to the effect of the
1
incapacitating arthralgia experienced by patients with CHIKV fever .
CHIKV infection has an abrupt onset, characterised by fever, and severe
2 13 1
arthralgia , which is seen in 70% of cases . The fever rises quickly,
often reaching 39 to 40 °C and is accompanied by intermittent shaking chills
2 . The arthralgias are polyarticular, migratory and predominantly affect
2
the small joints of the hands, wrists, ankles, and feet . Cutaneous
manifestations are typical with many patients presenting a flush over the
face and trunk. This is usually followed by a maculopapular rash, involving
most commonly the trunk, and limbs, but the face, palms and soles can also
2
show lesions . Other symptoms of CHIKV include myalgia, nausea,
vomiting, headaches, nasal discharge, conjunctivitis, retrobulbar pain,
10
photophobia, and lymphadenopathy . Haemorrhagic manifestations
(petechiae, purpura, bleeding gums, nosebleeds, haematemesis, and
1 10
melena) have been documented, but only in Asia . The average
10
fatality rate is 0.4% (2.8% in children and 1.6% in elderly people) .
EPIDEMIOLOGY: CHIKV was first recognised in Tanzania (formerly

12
Tanganyika) in 1953 during an epidemic of dengue-like illness . Between
the 1960s and 1990s, the virus was isolated repeatedly from numerous
countries in Central and Southern Africa, including Sudan, Uganda,
Democratic Republic of Congo, the Central African Republic, Malawi,
3
Zimbabwe, Kenya, and South Africa . CHIKV has also been isolated in
Western African countries, including Senegal, Benin, the Republic of Guinea,
3
Côte d'Ivoire and Nigeria .
In Southeast Asia, frequent outbreaks were reported from the 1960s

through to 2003 in India, Malaysia, Indonesia, Cambodia, Vietnam,
3
Myanmar, Pakistan, and Thailand . Indeed, numerous cities, including
Bangkok and Calcutta have been identified as particularly active sites of
3
transmission and disease .
Beginning in 1986, CHIKV outbreaks resurged with major clusters

documented in Senegal (1986, 1996, and 1997), Côte d'Ivoire (1996 and1997),
Democratic Republic of Congo (1998-2000), Indonesia (2003), Kenya (2004),
Comoros (2005), the Seychelles, Mauritius, Madagascar and Réunion islands
3
(2005-2006), and India (2006 and 2007) .
Cases have also been reported in Europe (United Kingdom, Belgium,

Germany, Czech Republic, Norway, Italy, Spain and France), Hong Kong,
Canada, Taiwan, Sri Lanka and United States; however, these were directly
associated with the return of tourists from India and the affected islands of
3 13
the Indian Ocean .
At Present, CHIKV is endemic in 23 countries and phylogenetic analysis of

viral sequences has identified 3 distinct clades: West African, Central/East
3 7
African and Asian .
There are 2 epidemiological transmission cycles of CHIK fever: a sylvatic

cycle, occurring primarily in Africa mainly between wild primates and
2 3
arboreal Aedes mosquitoes , where humans are accidental hosts; and
an urban human-mosquito-human transmission cycle that typically occurs in
2
cities in Asia .
1-3 6 7 10 11 13
HOST RANGE: Humans , non-human primates,
11 13
rodents, and birds .
MODE OF TRANSMISSION: CHIKV is transmitted to humans from infected

1
non-human primates and other humans by the bite of Aedes mosquitoes
. Evidence exists that CHIKV can also be passed from an infected mother to a
2 13
developing foetus . Furthermore, inhalation of aerosolised CHIKV in
14
a laboratory setting may lead to CHIKV infection .
1 2
INCUBATION PERIOD: Usually 2 to 3 days , with a range of 1 to 10
2 10 12
days .
COMMUNICABIILTY: Person-to-person transmission is only thought to

2
occur in utero between a mother and her foetus .

RESERVOIR: Humans serve as the reservoir for CHIKV during epidemic
2 11 13
periods . Outside these periods the main reservoirs are
10 11 13 10 13 10 10 11 13
monkeys , rodents , bats , and birds .
ZOONOSIS: Yes, indirectly from mosquitoes infected by non-human

2 3
reservoir hosts (sylvatic cycle transmission) .
1-3 7 10 11 13
VECTORS: Mosquitoes . In Asia and the Indian Ocean
2 10 11
region, the main vectors are Aedes aegypti and Aedes albopictus
2 11 . A larger range of Aedes species transmit CHIKV in Africa, including
2 10 11 2 11
Aedes furcifer Aedes taylori , Aedes vittatus, Aedes fulgens ,
2 11
Aedes luteocephalus , Aedes dalzieli, Aedes vigilax, Aedes
11 2 10 2
camptorhynchites , Aedes africanus , and Aedes neoafricanus .
SECTION IV – STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: No antivirals are currently available. Under
experimental conditions, interferon-α2b, glycyrrhizin, 6-azauridine and
ribavirin have all been shown to reduce CHIKV virus yield in a concentration
4
dependent manner in vitro . Moreover there is a synergistic efficacy
4
between interferon-α and ribavirin against CHIKV in vitro .
SUSCEPTIBILITY TO DISINFECTANTS: No information specific to CHIKV;

however, most lipid enveloped viruses are sensitive to 70% (v/v) ethanol,
sodium hypochlorite, formaldehyde, glutaraldehyde, phenolics, iodophors,
15
and quaternary ammonium compounds .
PHYSICAL INACTIVATION: Inactivated by desiccation and temperatures

11
above 58°C .
SURVIVAL OUTSIDE HOST: Unknown.
SECTION V – FIRST AID / MEDICAL

2
SURVEILLANCE: Monitor for symptoms . Confirmation is via detection of
6 16 5
CHIKV in blood samples via ELISA , RT-PCR , real time RT-PCR ,
6 1 11
indirect immunofluorescence , viral culture , neutralization assays
2 17 2
, and/or haemagglutinin inhibition assays .
FIRST AID/TREATMENT: Treatments available are for symptoms only and

1 1 11
include antipyretic and anti-inflammatory drugs such as
10 10 11
diclofenac . The use of steroids and aspirin should be avoided .
2
Movement and mild exercise tend to improve stiffness in the joints .
2 10
IMMUNIZATION: A commercial vaccine does not exist , although
8
some candidate vaccines have been tested on monkeys and humans
9
(phase II) , and a phase III trial of a candidate vaccine is in preparation
11 .
PROPHYLAXIS: The only form of prophylaxis available is to minimise the risk

of being bitten by infected mosquitoes by using mosquito nets and/or
1 10
mosquito repellents .

LABORATORY-ACQUIRED INFECTIONS: Forty-one cases were reported up
14 17
until 1980 . Two more cases were reported in 1981 .
1 2
SOURCES/SPECIMENS: Blood .
14
PRIMARY HAZARDS: Inhalation of CHIKV containing aerosols .
SPECIAL HAZARDS: Exposure to infected insects whilst performing CHIKV

17
isolations in endemic areas .
SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

18
RISK GROUP CLASSIFICATION: Risk Group 3 .

infectious material.
PROTECTIVE CLOTHING: Personnel entering the laboratory should remove

street clothing and jewellery, and change into dedicated laboratory clothing
and shoes, or don full coverage protective clothing (i.e., completely covering
all street clothing). Additional protection may be worn over laboratory
clothing when infectious materials are directly handled, such as solid-front
gowns with tight fitting wrists, gloves, and respiratory protection. Eye
protection must be used where there is a known or potential risk of
19
exposure to splashes .
OTHER PRECAUTIONS: All activities with infectious material should be

conducted in a biological safety cabinet (BSC) or other appropriate primary
containment device in combination with personal protective equipment.
Centrifugation of infected materials must be carried out in closed containers
placed in sealed safety cups, or in rotors that are unloaded in a biological
19
safety cabinet . The use of needles, syringes, and other sharp objects
should be strictly limited. Open wounds, cuts, scratches, and grazes should
be covered with waterproof dressings. Additional precautions should be
considered with work involving animals or large scale activities.

SPILLS: Allow aerosols to settle and, while wearing protective clothing,
gently cover the spill with paper towels and apply suitable disinfectant,
19
sufficient contact time before clean up .
DISPOSAL: Decontaminate all materials for disposal by steam sterilisation,

19
chemical disinfection, and/or incineration .
STORAGE: In sealed, leak-proof containers that are appropriately labelled

19
and locked in a Containment Level 3 laboratory .
SECTION IX – REGULATORY AND OTHER INFORMATION

and standards.
UPDATED: August 2010.

Canada.

Copyright ©
Canada
REFERENCES:
1 Weaver, S. C. (2006). Alphavirus Infections. In R. L. Guerrant, D. H.
Walker & P. F. Weller (Eds.), Tropical Infectious Diseases: Principles,
Pathogens, and Practice. (2nd ed., pp. 831-838). Philadelphia, PA.:
Elsevier Churchill Livingston.
2 Chhabra, M., Mittal, V., Bhattacharya, D., Rana, U. V. S., & Lal, S.
(2008). Chikungunya fever: A re-emerging viral infection. Indian
Journal of Medical Microbiology, 26(1), 5-12.
3 Powers, A. M., & Logue, C. H. (2007). Changing patterns of

chikunya virus: Re-emergence of a zoonotic arbovirus. Journal of
General Virology, 88(9), 2363-2377.
4 Briolant, S., Garin, D., Scaramozzino, N., Jouan, A., & Crance, J. M.
(2004). In vitro inhibition of Chikungunya and Semliki Forest
viruses replication by antiviral compounds: Synergistic effect of
interferon-α and ribavirin combination. Antiviral Research, 61(2),
111-117.
5 Pastorino, B., Bessaud, M., Grandadam, M., Murri, S., Tolou, H. J., &
Peyrefitte, C. N. (2005). Development of a TaqMan® RT-PCR assay
without RNA extraction step for the detection and quantification
of African Chikungunya viruses. Journal of Virological Methods,
124(1-2), 65-71.
6 Litzba, N., Schuffenecker, I., Zeller, H., Drosten, C., Emmerich, P.,
Charrel, R., Kreher, P., & Niedrig, M. (2008). Evaluation of the first
commercial chikungunya virus indirect immunofluorescence test.
Journal of Virological Methods, 149(1), 175-179.
7 Powers, A. M., Brault, A. C., Tesh, R. B., & Weaver, S. C. (2000). Re-
emergence of chikungunya and o'nyong-nyong viruses: Evidence
for distinct geographical lineages and distant evolutionary
relationships. Journal of General Virology, 81(2), 471-479.
8 Levitt, N. H., Ramsburg, H. H., & Hasty, S. E. (1986). Development

of an attenuated strain of chikungunya virus for use in vaccine
production. Vaccine, 4(3), 157-162.
9 Edelman, R., Tacket, C. O., Wasserman, S. S., Bodison, S. A., Perry, J.

G., & Mangiafico, J. A. (2000). Phase II safety and immunogenicity
study of live chikungunya virus vaccine TSI-GSD-218. American
Journal of Tropical Medicine and Hygiene, 62(6), 681-685.
10 Krauss, H., Weber, A., Appel, M., Enders, B., Isenberg, H. D.,
Schiefer. H.G, Slenczka, W., Graevenitz, A. V., & Zahner, H. (2003).
Viral zoonoses. Zoonoses. Infectious Diseases Transmissible from
Animals to Humans. (3rd ed., pp. 172). Washington, D.C: ASM Press.
11 Pialoux, G., Gaüzère, B. -., Jauréguiberry, S., & Strobel, M. (2007).

Chikungunya, an epidemic arbovirosis. Lancet Infectious Diseases,
7(5), 319-327.
12 ROBINSON, M. C. (1955). An epidemic of virus disease in Southern

Province, Tanganyika Territory, in 1952-53. I. Clinical features.
Transactions of the Royal Society of Tropical Medicine and Hygiene,
49(1), 28-32.
13 Pardigon, N. (2009). The biology of chikungunya: A brief review of

what we still do not know. Pathologie Biologie, 57(2), 127-132.
14 Scherer, W. F., Eddy, G. A., & Monath, T. P. (1980). Laboratory

safety for arboviruses and certain other viruses of vertebrates.
American Journal of Tropical Medicine and Hygiene, 29(6), 1359-1381.
15 Collins, C. H., & Kennedy, D. A. (1999). Decontamination.

Laboratory-Acquired Infections: History, Incidence, Causes and
Prevention (4th ed., pp. pp. 170-176.). London, UK: Buttersworth
Heinemann.
16 Hasebe, F., Parquet, M. C., Pandey, B. D., Mathenge, E. G. M.,

Morita, K., Balasubramaniam, V., Saat, Z., Yusop, A., Sinniah, M.,
Natkunam, S., & Igarashi, A. (2002). Combined detection and
genotyping of Chikungunya virus by a specific reverse
transcription-polymerase chain reaction. Journal of Medical
Virology, 67(3), 370-374.
17 Tomori, O., Monath, T. P., & O'Connor, E. H. (1981). Arbovirus

infections among laboratory personnel in Ibadan, Nigeria.

2009, (2009).

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Colorado Tick Fever Virus

SUBSTANCES
NAME: Colorado Tick Fever Virus
SYNONYM OR CROSS REFERENCE: Colorado tick fever (CTF), mountain fever

1 2 3
and mountain tick fever , tick-borne fever , and arbovirus.
CHARACTERISTICS: Colorado tick fever virus (CTFV) is a member of the

1
genus Coltivirus and family Reoviridae . The virus is a non-enveloped
virus, 80 nm in diameter, with two outer capsid shells and a double-stranded
2
RNA genome . It is also classified as an arbovirus since it is transmitted
4
by insects .

PATHOGENICITY/TOXICITY: Colorado Tick Fever Virus (CTFV) is the
1
causative agent of CTF . CTFV causes acute febrile illness, and symptoms
can include sudden onset of fever, chills, headache, retro-orbital pain,
2 5 6
myalgia, photophobia, and nausea . Half of patients have a
biphasic fever with a period of recovery followed by a second febrile phase
5 7 7
. Most patients recover within 2 weeks . Rarely, children develop
severe complications, including meningitis, encephalitis, and hemorrhagic
3 5
disease . Persistent viremia is characteristic of the disease and virus
7
can be detected for up to 120 days in blood .
EPIDEMIOLOGY: Found in the western North America (i.e. California,

Colorado, Idaho, Montana, Nevada, New Mexico, Oregon, South Dakota,
Utah, Washington, Wyoming, Alberta and British Columbia) at elevations
2
between 4 000 and 10 000 feet . The majority of cases occur from May to
1 2
July . Approximately 200-400 cases are reported in the US each year
1 7 . The approximate male-to-female ratio is 2:1. Most cases occur in
persons 20 to 30 years old, although infection has been reported in
1 2
individuals 2 to 85 years old . Deaths from CTFV are rare .
HOST RANGE: Humans, multiple species of small mammals (e.g. squirrels,

2
chipmunks, porcupine, deer mice and bushy tailed wood rats), and ticks
5 .
MODE OF TRANSMISSION: Vector-borne (ticks). Ticks acquire the virus by

feeding on viremic hosts, and they subsequently transmit the virus in saliva
8
when they feed on a new host . Transmission from blood transfusions
2 5
has also been reported .
INCUBATION PERIOD: 0-14 days (although it typically ranges from 3-6 days)
1 2 .
COMMUNICABILITY: Not usually transmitted from person-to-person, but

2 5
transmission of CTFV through blood transfusion has been reported .

RESERVOIR: Ground squirrels, western chipmunks, wood rats, deer mice
2 5 .
3 5 6
ZOONOSIS: Yes – transmitted from animal by tick bites .
VECTORS: Ticks, primarily Dermacentor andersoni Footnote 1, Footnote 2;

however, other ticks such as D. occidentalis, D. albipictus, D. arumapertus,
Haemaphysalis leporispalustris, Otobius lagophilus, Ixodes sculptus, and I.
spinipalpus have also been found to be infected with the virus Footnote 2,
Footnote 6. An uninfected tick may become infected by feeding on an
2
infected mammalian host .

DRUG SUSCEPTIBILITY: Ribavirin has demonstrated antiviral activity against
1
CTFV in animal models, although its efficacy in humans in unknown .
3
SUSCEPTIBILITY TO DISINFECTANTS: Partially resistant to lipid solvents
. More specific information on CTFV is not available, but viruses belonging to
the family Reoviridae have been shown to be susceptible to glutaraldehyde
9
(2%) and accelerated hydrogen peroxide (AHP) (7% (v/v)) .
PHYSICAL INACTIVATION: Completely inactivated by temperature of 60 ºC

10 3
for 30 min and acidic conditions (pH 3.0) .
SURVIVAL OUTSIDE HOST: Can survive several days in a serum-saline

10
solution at 37 ºC . Also survives up to 6 weeks in refrigerated blood, and
11
16-18 months in blood clots

SURVEILLANCE: Monitor for symptoms. Virus can be isolated from blood or
detected in erythrocytes using immunofluorescence. ELISA, PCR and
5 7 8
Western blot diagnostic tests have also been developed .
1
FIRST AID/TREATMENT: CTF is usually a benign, self-limited disease . No
specific antiviral treatment is available, supportive care is the principle
2
treatment . Aspirin should be avoided as it may exacerbate the potential
for haemorrhage associated with thrombocytopenia.
IMMUNISATION: None.
PROPHYLAXIS: None.

LABORATORY-ACQUIRED INFECTIONS: 16 cases of laboratory-acquired
12
infections have been reported up to 1980 .
SOURCES/SPECIMENS: Blood, cerebrospinal fluid, and tissue from infected

2 6
humans and animals, and samples from infected ticks .
PRIMARY HAZARDS: Accidental parenteral inoculation, exposure to

infectious aerosols of virus, and bites of infected lab animals and/or
12
arthropods (ticks) .

13

infectious materials, animals, or cultures.
14

14
SECTION VIII – HANDLING AND STORAGE

14 15

14

14

and standards.
UPDATED: February, 2012

Canada.

Copyright ©
Canada
REFERENCES:
REFERENCES:
1 Klasco, R. (2002). Colorado tick fever. Medical Clinics of North
America, 86(2), 435-440.
2 Romero, J. R., & Simonsen, K. A. (2008). Powassan Encephalitis and

Colorado Tick Fever. Infectious Disease Clinics of North America,
22(3), 545-559.
3 Emmons, R. W. (1988). Ecology of Colorado tick fever. Annual

Review of Microbiology, 42, 49-64.
4 Lanciotti, R. S., & Tsai, T. F. (2007). Arboviruses. In P. R. Murray

(Ed.), Manual of Clinical Microbiology (9th ed., pp. 1486-1500).
Washington D.C.: ASM Press.
5 Kraus, H., Weber, A., Appel, M., Enders, B., Isenberg, H. D.,
Schiefer, H. G., Slenczka, W., von Graevenitz, A., & Zahner, H.
(2003). Viral Zoonoses. In H. Kraus, A. Weber, M. Appel, B. Enders,
H. D. Isenberg, H. G. Schiefer, W. Slenczka, A. von Graevenitz & H.
Zahner (Eds.), Zoonoses: Infectious Diseases Transmissible from
Animals to Humans (3rd ed., pp. 87). Washington, D.C.: ASM Press.
6 Brown, R. N., Lane, R. S., & Dennis, D. T. (2005). Geogrphic

Distributions of Tick-Borne Diseases and Their Vectors. In J. L.
Goodman, D. T. Dennis & D. E. and Sonenshine (Eds.), Tick-Borne
Diseases of Humans (pp. 363-391). Washington D.C.: ASM Press.
7 Günther, G., & Haglund, M. (2005). Tick-borne encephalopathies:

Epidemiology, diagnosis, treatment and prevention. CNS Drugs,
19(12), 1009-1032.
8 Wilson, W. R., Sande, M. A., & Drew, W. L. (2001). Current diagnosis

& treatment in infectious diseases. New York: Lange Medical
Books/McGraw-Hill. Retrieved from
http://online.statref.com/document.aspx?
FxId=66&DocID=1&grpalias=
9 Howie, R., Alfa, M. J., & Coombs, K. (2008). Survival of enveloped

and non-enveloped viruses on surfaces compared with other
micro-organisms and impact of suboptimal disinfectant exposure.
Journal of Hospital Infection, 69(4), 368-376.
10 Trent, D. W., & Scott, L. V. (1966). Colorado tick fever virus in cell
culture. II. Physical and chemical properties. Journal of
Bacteriology, 91(3), 1282-1288.
11 Pantanowitz, L., Telford III, S. R., & Cannon, M. E. (2002). Tick-borne

diseases in transfusion medicine. Transfusion Medicine, 12(2), 85-
106.


2009, (2009).

15 Burnett, L. A. C., Lunn, G., & Coico, R. (2009). Biosafety: Guidelines

for working with pathogenic and infectious microorganisms.
Current Protocols in Microbiology, (SUPPL. 13), 1A.1.1-1A.1.14.
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Coxsackievirus
SECTION I – INFECTIOUS AGENT

NAME: Coxsackievirus
SYNONYM OR CROSS REFERENCE: Picornavirus, Enterovirus, Coxsackievirus

Group A (serotypes 1-22 and 24), Coxsackievirus Group B (serotypes 1-6),
enteroviral vesicular pharyngitis (herpangina), enteroviral vesicular
stomatitis with exanthema (hand, foot and mouth disease), enteroviral
lymphonodular pharyngitis (acute lymphonodular pharyngitis), Bornholm
disease (Synonyms: epidemic myalgia, epidemic pleurodynia, Sylvest's
1 2
disease, Bamble disease and Devil's grip) .
CHARACTERISTICS: Icosahedral, non-enveloped, linear single-stranded

positive-sense RNA viruses of the Picornaviridaefamily and Enterovirus genus
1 3 .
SECTION II – HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Majority of infections are asymptomatic and self-
limiting; however, infections may lead to a variety of rare conditions, some
of which are life threatening Footnote 1Footnote 2. Clinical course can vary
1 2 4
within and between strains of Coxsackievirus .
Coxsackievirus group A associated conditions: hand-foot-and-mouth

disease, herpangina, acute lymphatic or nodular pharyngitis, aseptic
meningitis, paralysis, exanthema, hand-foot-and-mouth disease (A10, A16),
pneumonitis of infants, "common cold", hepatitis, infantile diarrhoea, acute
1 5
hemorrhagic conjunctivitis (A24) .
Coxsackievirus group B associated conditions: diabetes, pleurodynia, aseptic

meningitis, paralysis, severe systemic infection in infants,
meningoencephalitis, myocarditis, pericarditis, upper respiratory illness and
pneumonia, rash, hepatitis, and pancreatitis, Footnote 1Footnote 6-8.
Undifferentiated febrile illness and viral parkinsonism may also be
associated with Coxsackievirus group B infection; however, these are more
controversial.
Most common conditions requiring hospitalization are:

Hand-foot-and-mouth disease: characterized by fever and vesicles on the
5
mouth and extremities, sore throat, fever, and anorexia . Usually self
5
limiting and requires only symptomatic treatment .
Aseptic meningitis/meningoencephalitis: Most common clinical syndrome

1
associated with enteroviruses, resulting in medical attention . The virus
causes nonbacterial inflammation of the meninges associated with fever,
headache, photophobia, and with no apparent parenchymal involvement
1 . The infection can progress to meningoencephalitis with infection of the
parenchyma, characterized by disturbed state of consciousness, focal
1
neurologic signs, and seizures . While severe meningeal disease is
1
usually self limiting, deaths have been reported .
Myocarditis and dilated cardiomyopathy: Myocarditis is an inflammation of

the myocardium associated with damage that is unrelated to ischemic
injury, if infection/inflammation persist the syndrome may progress to
dilated cardiomyopathy (in which the heart is enlarged), potentially leading
1 7
to heart failure [very rare] .
EPIDEMIOLOGY: Coxsackieviruses are distributed worldwide and infections

2 5
predominate in summer and fall, with sporadic cases year round . All
age groups are infected but young children are more susceptible to
infection. For example, viral meningitis occurs 5-8 times more often in
2
infants than adults .
1
HOST RANGE: Human, monkey, mouse .
INFECTIOUS DOSE: Unknown; however, 15-50 TCID50 has been shown to be

infective in adult volunteers Footnote 9.
MODE OF TRANSMISSION: Infection occurs through contact with infective

secretions or excretions, and subsequent autoinoculation of mouth, nose, or
1
eyes . It is possible that ingestion of contaminated water may contribute
1
to infection . Intranasal and aerosol transmission are possible for some
1 9 10
variants through contaminated respiratory secretions . Once
inside the body, Coxsackievirusesreplicate in lymphoid tissues and then
2
disseminate in blood .
INCUBATION PERIOD: Varies from days (eg. hand-foot-and-mouth disease)

5 7 8
to years (eg. Myocarditis), depending on clinical course .
COMMUNICABILITY: Human-to-human transfer can occur readily through

1 9 10
oral, ocular, respiratory, or faecal-oral routes .
SECTION III – DISSEMINATION

1
RESERVOIR: Human .
ZOONOSIS: None.
VECTORS: None.

DRUG SUSCEPTIBILITY/RESISTANCE: No antiviral medications are currently
approved. Although Pleconaril® has been used in clinical trials to treat
severe Coxsackievirus infections, these have shown no important effects on
4 11
morbidity or mortality .
SUSCEPTIBILITY/RESISTANCE TO DISINFECTANTS: Sensitive to

formaldehyde, gluteraldehyde, strong acids, sodium hypochlorite (bleach),
1 12
and free residual chlorine . Sensitivity is dependent on sufficient
concentration, pH, and contact time and is reduced in presence of
1
extraneous organic materials . Infectious viruses are usually resistant to
many common laboratory disinfectants, including 70% ethanol, isopropanol,
1 13
dilute Lysol, and quaternary ammonium compounds . Insensitive to
1
lipid solvents, including ether and chloroform . Stable in many
1
detergents at ambient temperatures .
1
PHYSICAL INACTIVATION: Sensitive to UV mediated inactivation .
Drying conditions reduce viral titres, the degree of which is dependent on
1
the porosity of the surface and presence of extraneous organic matter .
Most are readily inactivated at 42 °C, but stability and heat resistance is
increased in the presence of sulphydral reducing agents and magnesium
1
cations .
SURVIVAL OUTSIDE HOST: Can survive for months under favourable

conditions of neutral pH, moisture, and low temperature; enhanced by
presence of organic matter Footnote 1. Survival has been documented in
seafood from Coxsackievirus-positive water supplies for up to 3 weeks at
1 14
temperatures of 1°C – 20°C .

SURVEILLANCE: Monitor for symptoms; confirm by serology, virus isolation,
or PCR from lesions or nasopharyngeal and fecal specimens Footnote
2Footnote 11. The use of viral culture is declining as not all serotypes will
grow well in culture. Molecular typing has largely replaced serotyping.
1 11
FIRST AID/TREATMENT: No specific treatment is available .
IMMUNIZATION: No general vaccine available; however, one is under

3 11
development for Coxsackievirus induced heart disease .
PROPHYLAXIS: None.
SECTION VI – LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: Responsible for 39 reported cases
15-17
up to 2006 .
SOURCES/SPECIMENS: Throat swabs, rectal swabs, stool samples, aseptic

2 16 17
meningitis cerebrospinal fluids .
PRIMARY HAZARDS: Ingestion or inhalation of aerosols, contact of mucous

1 2 9 10
membranes with infectious agents .
SECTION VII – EXPOSURE CONTROLS /

PERSONAL PROTECTION
18

19

19

19

with the infectious organism by autoclave, chemical disinfection, gamma
19
irradiation, or incineration before disposing .

19
SECTION IX – REGULATORY AND OTHER

INFORMATION
and standards.

Canada

Copyright © Public Health Agency of Canada, 2011
REFERENCES
1 Pallansch, M. A., & Roos, R. P. (2001). Enteroviruses: Polioviruses,
Coxsackieviruses, Echoviruses, and Newer Enteroviruses. In D. M.
Knipe, P. M. Howley, D. E. Griffin, M. A. Martin, R. A. Lamb, B.
Roizman & S. E. Straus (Eds.), Fields Virology (4th ed., pp. 723-775).
Philadelphia: Lippincott Williams & Wilkins.
2 Sawyer, M. H. (2002). Enterovirus infections: Diagnosis and

treatment. Seminars in Pediatric Infectious Diseases, 13(1), 40-47.
3 Henke, A., Jarasch, N., & Wutzler, P. (2003). Vaccination procedures

against Coxsackievirus-induced heart disease. Expert Review of
Vaccines, 2(6), 805-815.
4 Rotbart, H., & Webster, A. . (2001). Treatment of Potentially Life-

Threatening Enterovirus Infections with Pleconaril. Clinical
Infectious Diseases, 32(2), 228-235. Retrieved from
http://dx.doi.org/10.1086/318452
5 Frydenberg, A., & Starr, M. (2003). Hand, foot and mouth disease.
Australian Family Physician, 32(8), 594-595.
6 Jang, H., Boltz, D. A., Webster, R. G., & Smeyne, R. J. (2009). Viral
parkinsonism. Biochimica Et Biophysica Acta - Molecular Basis of
Disease, 1792(7), 714-721.
7 Esfandiarei, M., & McManus, B. M. (2008). Molecular biology and

pathogenesis of viral myocarditis
8 Tam, P. E. (2006). Coxsackievirus myocarditis: Interplay between

virus and host in the pathogenesis of heart disease. Viral
Immunology, 19(2), 133-146.
9 Couch, R. B., Cate, T. R., Gerone, P. J., Fleet, W. F., Lang, D. J.,
Griffith, W. R., & Knight, V. (1965). Production of Illness with a
Small-Particle Aerosol of Coxsackie A21*. J. Clin. Invest., 44(4), 535.
10 Couch, R. B., Douglas, R. G., JR., Lindgren, K. M., Gerone, P. J., &
Knight, V. (1970). Airborne transmission of respiratory infection
with coxsackievirus A type 21. American Journal of Epidemiology,
91(1), 78-86.
11 Wilson, W. R., Sande, M. A., Drew, W. L., STAT!Ref, & Teton Data
Systems. (2001). Current diagnosis & treatment in infectious diseases.
New York: Lange Medical Books/McGraw-Hill. Retrieved from
12 Rutala, W. A., & Weber, D. J. (1997). Uses of inorganic hypochlorite

(bleach) in health-care facilities. Clinical Microbiology Reviews, 10(4),
597-610.
13 Rutala, W. A. (1996). APIC guideline for selection and use of

disinfectants. American Journal of Infection Control, 24(4), 313-342.
14 Abad, F. X., Pintó, R. M., Gajardo, R., & Bosch, A. (1997). Viruses in
mussels: Public health implications and depuration. Journal of Food
Protection, 60(6), 677-681.

Safety: Principles and Practices (pp. 179-207). Washington, D.C.:
ASM Press.
16 Torsten, J. (1953). Laboratory infections with Coxsackie viruses.

Archives of Virology, 5(3), 250-263.
17 Shaw, E. W., Melnick, J. L., & Curnen, E. C. (1950). Infection of

laboratory workers with coxsackie viruses*. Annals of Internal
Medicine, 33(1), 32-40. doi:10.1059/0003-4819-33-1-32

2009, (2009).

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Cytomegalovirus
PATHOGEN SAFETY DATA SHEET- INFECTIOUS

SUBSTANCES
SECTION I-INFECTIOUS AGENT
NAME: Cytomegalovirus
1
SYNONYM OR CROSS REFERENCE: Human herpes virus 5 (HHV-5) , CMV
2 3 , HCMV.
CHARACTERISTICS: Member of the family Herpesviridae and subfamily

1
Betaherpesvirinae . The name cytomegalovirus is derived from the
associated enlargement of cells following infection. Complete CMV particles
have a diameter of 120-200 nm. They consist of a 235-kb double-stranded
linear DNA genome enclosed within an icosahedral capsid, surrounded by a
phospholipid rich envelope. Viral replication is slow and involves the
expression of immediate- early, early, and late genes. Replication occurs in
the nucleus of the host cell.

PATHOGENICITY/TOXICITY: CMV infection is common and usually
asymptomatic in healthy children and adults, but can cause severe disease
1
in newborns and immunocompromised children or adults . CMV is the
most common cause of congenital infection, affecting 0.2-2.4% of all infants,
and also of viral-based mental retardation and hearing deficit in children of
4
developing countries . Infections are often recurrent, caused by
reactivation of latent virus (especially in immunocompromised patients such
as bone marrow or other transplant recipients), reinfection may also occur
5 6
due to the antigenic diversity of the virus . Infection may cause a
mononucleosis-like-syndrome with prolonged fever (lasting 2-3 weeks),
malaise, atypical lymphocytosis, cervical lymphadenitis, mild hepatitis, and
1 7-9
encephalitis .
Congenital infection: Congenital infection occurs when women acquire

primary CMV infection during pregnancy. Some of these congenitally
infected infants (10-15%) develop symptoms during the newborn period.
Newborns with symptomatic disease present with a variety of congenital
defects such as low birth weight, jaundice, hepatospleenomegaly, petechiae,
thrombocytopenic purpura, myocarditis, pneumonitis, anemia, CNS
1 8 9
abnormalities, retinitis, and chorioretinitis . These infants may die
of complications within the first month of life or may survive with
neurological complications. Approximately 6-25% of infants asymptomatic at
birth develop complications such as sensory nerve hearing loss,
psychomotor mental retardation, or both later on in their lives.
Neonatal infection: Perinatally infected infants do not usually have any

apparent disease unless the infant is premature or immunocompromised
1 8 . CMV infection in premature infants can result in hepatomegaly,
thrombocytopenia, atypical lymphocytosis, or hemolytic anemia, and is
associated with high mortality and morbidity.
CMV infection in immunocompromised people: Both primary CMV infection,

or reactivation can cause serious illness in immunosuppressed patients (for
example patients with AIDS, patients with leukemia or lymphoma who are
receiving chemotherapy, and recipients of organ transplants on
1 8
immunosuppressive therapy) . The major symptoms of the disease in
organ transplant recipients include fever, myalgia, malaise, arthralgia,
leucopenia, thrombocytopenia, and hepatitis. Pneumonitis, caused by CMV
infection in bone marrow transplant recipients is associated with significant
morbidity and mortality (50-90%). CMV infection in HIV patients may spread
to visceral organs, resulting in chorioretinitis, gastrointestinal infections
(esophagitis, gastritis, and ulcerative colitis), polyradiculomyelopathy, and
neurological disorders.
EPIDEMIOLOGY: Worldwide - Cytomegalovirus (CMV) is a universally

distributed pathogen with approximately 40-100% of the world's population
3 11-12
having CMV antibody present in blood as evidence of infection ,
the highest prevalence being in countries in the developing world. In the
United States, >90% of healthy adults have become infected with CMV by the
age of 80 years. Immunocompromised patients (AIDS patients or organ
transplant recipients), premature infants, and newborns with congenital
CMV are at a high risk of developing serious, life threatening illness with
3 9 11 13
CMV infection . In the United States, approximately 30,000
children are born annually with congenital CMV infection, 20% of whom
develop permanent disabilities. Transmission of infection has been reported
1 8
to occur in day-care centers . Furthermore, the majority of these
congenital infections result from recurrent infections in pregnant women
13 .
HOST RANGE: Different strains affect humans (human cytomegalovirus) and

3
animals such as rodents and rhesus macaque .
MODE OF TRANSMISSION: Transmission can occur through direct contact

with infectious tissues, secretions or excretions (urine, saliva, breast milk,
cervical secretions, semen etc); during blood transfusion; and via organ
transplantation. Infected mothers can transmit the virus to their fetus in
utero (transplacental), to newborns at the time of delivery (intrapartum: by
contact with the virus in the birth canal), or to infants through breast
milkFootnote 1 Footnote 3 Footnote 8 Footnote 9. Sexual transmission has
also been reported to occurFootnote 1. Transmission through aerosols has
not been reportedFootnote 3.
INCUBATION PERIOD: 1-4 months post-implant in the case of organ

1
transplantation or blood transfusion , and 4-12 weeks for perinatal CMV
4
infections .
COMMUNICABILITY: CMV virus can persist in body fluids such as urine,

saliva, and seminal fluids for many years, or can remain dormant until
5 6 14
reactivation of latent infection . Transmission occurs through
direct contact with body fluids from symptomatic or asymptomatic persons
3
excreting the virus , thus infection may be transmitted between humans
15
and from adults to children through childbirth and breastfeeding .
SECTION III-DISSEMINATION
RESERVOIR: Humans, CMV strains found in many animal species are not
9 12
infectious for humans .
ZOONOSIS: No, each CMV strain causes disease in its own natural host
3
species .
VECTOR: None.
SECTION IV- STABILITY AND VIABILITY

8
DRUG SUSCEPTIBILITY: Ganciclovir inhibits viral replication in vivo .
Ganciclovir, Valganciclovir, Foscarnet, and Cidofovir have all been approved
3
for treatment of CMV in immunocompromised patients .
DRUG RESISTANCE: Both in vivo and in vitro resistant strains to antiviral

3
drugs have been reported , such as against ganciclovir, cidofovir, and
foscarnet, and strains with multiple antiviral resistant have been observed
16 .
SUSCEPTIBILITY TO DISINFECTANTS: Cytomegalovirus has been shown to

17
be susceptible to 7.5% povidone-iodine . Although not much information
is available on disinfectants specific for CMV, most herpes viruses are
susceptible to 30% ethanol and isopropanol, 1% sodium hypochlorite,
18
formaldehyde, 0.12% ortho phenylphenol, and 0.04% glutaraldehyde
19 .
PHYSICAL INACTIVATION: Inactivated by heat (56 °C for 30 min), low pH,

1
UV light, cycles of freezing/thawing .
SURVIVAL OUTSIDE HOST: Cytomegalovirus can survive on dry inanimate

surfaces (persistence varies from only a few hours up to 7 days)Footnote 2;
blanket for 2 hours; plexiglass for 4-8 hoursFootnote 20.

SURVEILLANCE: Monitor for symptoms. Diagnosis of CMV infection mainly
consists of: 1) Virus detection by demonstrating CMV cytopathic effects by
inoculating fibroblasts cells with clinical specimens, viral antigen such as
protein pp65 in peripheral blood leukocytes, or DNA in plasma or leukocytes
(using PCR)Footnote 3 Footnote 8; 2) isolation of the virus from tissues,
secretions or bloodFootnote 8; 3) serological tests to detect seroconversion
and IgM antibody to CMVFootnote 3 Footnote 8. Demonstration of
cytopathic effects is labour intensive, less sensitive, and may take 3-14 days.
Detection of CMV antigen in leukocytes is more sensitive than culture of the
blood to detect viremia.
FIRST AID/TREATMENT: Since CMV infection resolves spontaneously in

3
normal healthy patients, antiviral treatment is not usually recommended
.
Congenital infection: Because of the potential side effects associated with

anti-viral drugs, they have not been licensed for use in neonates and
infantsFootnote 1 Footnote 12; however, intravenous Ganciclovir has been
advocated for treatment of severe congenital CMV infectionFootnote 3.
Other antiviral agents which can be used for treating severe congenital
infection in neonates and infants include oral valganciclovir, intravenous
foscarnet, and intravenous cidofovirFootnote 12. Passive immunization of a
CMV infected pregnant women with CMV hyper immune globulin has also
been suggested to be effective for both the treatment and prevention of
congenital fetal infectionFootnote 21.
Infection in immunocompromised hosts (AIDS patients or organ

transplant recipients): Intravenous ganciclovir or oral valganciclovir are
the first line drugs for therapy for CMV infection in immunocompromised
3)
patients . Intravenous cidofovir and foscarnet are used as alternatives.
Once symptomatic improvement has been achieved, these drugs can also be
used for chronic maintenance therapy in patients with CMV retinitis or
neurological disease.
IMMUNISATION: No vaccine is licensed for prevention of cytomegalovirus

1 3
infection .
PROPHYLAXIS: Prophylaxis with intravenous ganciclovir is recommended

for HIV infected adults, children and adolescents who are CMV seropositive,
and have CD4+ T-cell count less than 50 cells/μl, and for organ transplant
3
recipients . Hyper immune globulin preparations with high levels of
antibody to CMV along with anti-viral agents such as ganciclovir can also be
3 8
used for prophylaxis in organ transplant recipients .
SECTION VI-LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: No infections reported.
SOURCE/SPECIMENS: Urine, blood, breast milk, tears, stool, semen,

respiratory secretions (nasopharyngeal secretions, saliva, throat washings,
1 8
and bronchoalveolar lavage fluid) and cervical secretions .
PRIMARY HAZARDS: Inhalation of concentrated aerosolized materials,

droplet exposure of mucous membranes of the eyes, nose, or mouth,
ingestion, accidental parenteral inoculation are the primary hazards
22
associated with herpes viruses including Cytomegalovirus .

23

24
infectious material .
24

24

SPILLS: Allow aerosols to settle and, while wearing protective clothing, cover
spill with absorbent paper towel. Apply an appropriate disinfectant, and,
starting from perimeter and wipe towards the center. Allow sufficient
contact time before cleaning up.

24
STORAGE: Properly labeled and sealed containers.

and standards.
UPDATED: October 2010

Canada

Copyright ©
Canada
REFERENCES:
1 Hodinka, R. L. (2007). Human Cytomegalovirus. In P. R. Murray

(Ed.), Manual of clinical microbiology (9th ed., pp. 1549-1563).
2 2. Kramer, A., Schwebke, I., & Kampf, G. (2006). How long do

3 Mocarski, E. S., Shenk, T., & Pass, R. F. (2007). Cytomegalovirus. In

D. M. Knipe, & P. M. Howley (Eds.), Fields of virology (5th ed., pp.
2701-2772). Philadelphia PA: Lipincott Williams & Wilkins.
4 Kim, C. S. (2010). Congenital and perinatal cytomegalovirus

infection. Korean Journal of Pediatrics, 53 (1), 14- 20.
5 Tegtmeier, G. E. (1986). Transfusion-transmitted cytomegalovirus

infections: significance and control. Vox Sanguinis, 51 Suppl 1 , 22-
30.
6 Cornalba, G. P., Dore, R., & Colombo, E. (1994). Abdominal

manifestations in immunocompromised patients. [Manifestazioni
addominali nei pazienti immunocompromessi] La Radiologia
Medica, 87 (5 Suppl 2), 52-61.
7 Pantoni, L., Inzitari, D., Colao, M. G., De Mayo, E., Marini, P., &
Mazzota, F. (1991). Cytomegalovirus encephalitis in a non-
immunocompromised patient: CSF diagnosis by in situ
hybridization cells. Acta Neurologica Scandinavica, 84 (1), 56-58.

Sherris medical microbiology: An introduction to infectious diseases
(4th ed., pp. 555-576). USA: McGraw Hill.
9 Ross, D. S., Dollard, S. C., Victor, M., Sumartojo, E., & Cannon, M. J.
(2006). The epidemiology and prevention of congenital
cytomegalovirus infection and disease: activities of the Centers for
Disease Control and Prevention Workgroup. Journal of Women's
Health, 15 (3), 224-229.
10 Lentz, E. B., Dock, N. L., McMahon, C. A., Fiesthumel, S. R., Arnold,

C. B., & Lamberson, H. V.,Jr. (1988). Detection of antibody to
cytomegalovirus-induced early antigens and comparison with four
serologic assays and presence of viruria in blood donors. Journal of
Clinical Microbiology, 26 (1), 133-135.
11 Freeman, R. B.,Jr. (2009). The 'indirect' effects of cytomegalovirus

infection. American Journal of Transplantation, 9 (11), 2453-2458.
12 Marshall, B. C., & Koch, W. C. (2009). Antivirals for cytomegalovirus

infection in neonates and infants: focus on pharmacokinetics,
formulations, dosing, and adverse events. Paediatric Drugs, 11 (5),
309-321.
13 Cannon, M. J. (2009). Congenital cytomegalovirus (CMV)

epidemiology and awareness. Journal of Clinical Virology, 46
(SUPPL. 4), S6-S10.
14 Biggar, R. J., Andersen, H. K., Ebbesen, P., Melbye, M., Goedert, J. J.,
Mann, D. L., & Strong, D. M. (1983). Seminal fluid excretion of
cytomegalovirus related to immunosuppression in homosexual
men. British Medical Journal (Clinical Research Ed.), 286 (6383), 2010-
2012.
15 Mosca, F., Pugni, L., Barbi, M., & Binda, S. (2001). Transmission of
cytomegalovirus. Lancet, 357 (9270), 1800. doi:10.1016/S0140-
6736(00)04914-X
16 Erice, A. (1999). Resistance of human cytomegalovirus to antiviral

drugs. Clinical Microbiology Reviews, 12 (2), 286-297.
17 Numazaki, K., & Asanuma, H. (1999). Inhibitory effect of povidone-

iodine for the antigen expression of human cytomegalovirus. In
Vivo, 13 (3), 239-241.
18 Laboratory Safety Manual (1993). (2nd ed.). Geneva: World Health

Organization.

Williams & Wilkins.
20 Faix, R. G. (1985). Survival of cytomegalovirus on environmental

surfaces. Journal of Pediatrics, 106 (4), 649-652.
21 Adler, S. P., & Nigro, G. (2009). Findings and conclusions from CMV
hyperimmune globulin treatment trials. Journal of Clinical Virology,
46 (Suppl 4), S54-7.

NIH.

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Dengue virus
SECTION I - INFECTOUS AGENT

1 2 3 4
NAME: Dengue Virus
SYNONYM OR CROSS REFERENCE: Dengue fever, break bone fever, Dengue

hemorrhagic fever (DHF) and Dengue shock syndrome (DSS), DENV, DEN
1 2
CHARACTERISTICS: Dengue Virus is an arbovirus of the Flaviviridae family

1 3
and Flavivirus genus . Dengue is an enveloped virus, 40-60 nm in size,
with an isometric nucleocapsid of 25-30 nm and an ~10.7 kb, linear, positive-
1 4
sense RNA genome . Dengue virus exists as four serotypes (Dengue
1–4) and is genetically related to other flaviviruses such as yellow fever and
1 4
tick-borne encephalitis viruses . Dengue virus may undergo 2
different cycles of transmission and amplification, sylvan and urban. In the
sylvan cycle the virus undergoes rounds of infection, amplification, and re-
5
infection between nonhuman primates and arthropod vectors . It is
believed that infected arthropod vectors then migrate from jungle
environments and initiate the urban cycle in which the cycles of infection,
amplification, and re-infection occur between humans and vector species
5 .

PATHOGENICITY/TOXICITY: Dengue virus infection can cause Dengue
fever, Dengue hemorrhagic fever (DHF), and Dengue shock syndrome (DSS)
Footnote 1. Clinical signs of Dengue fever include influenza type symptoms,
fever, rash, myalgias and arthralgias, with a febrile period lasting between 2
and 10 days Footnote 6Footnote 7. Importantly, the risk of progression to
hemorrhagic fever is higher after secondary infection with other dengue
serotypes Footnote 6, although primary DSS can occur from a single
infection especially in pediatric age groups. Epidemiological data suggest
that the serotypes differ in their ability to produce large outbreaks and
severe clinical symptoms; however, all serotypes have the potential to cause
severe disease Footnote 8. DHF and DSS are defined by four clinical
manifestations: high fever, hemorrhagic diathesis, hepatomegaly, and shock
Footnote 2. Depending on severity, relatively mild cases without shock,
grades I and II, are defined as DHF, while severe cases accompanied by
shock, grades III and IV are defined as DSS Footnote 2Footnote 9. If patients
do not receive appropriate treatment, grade IV dengue virus can cause
severe shock, in which pulse and blood pressure become undetectable,
resulting in death within 12 to 36 h Footnote 9. Mortality rates for Dengue
hemorrhagic fever can reach 20% Footnote 6.
EPIDEMIOLOGY: Cases are typical in tropical, developing countries

6
worldwide . Dengue hemorrhagic fever cases have now been confirmed
in more than 60 countries and Dengue Virus is endemic in more than 100
countries, including most of Southeast Asia, South America, Central America,
10
and the Caribbean and South Pacific region . It is estimated that 50
million infections occur each year and more than 2.5 billion people are at
9
risk of infection from dengue virus . Infection with any of the dengue
9
serotypes may be asymptomatic in the majority of cases . In Asia the risk
of developing severe disease is greater in dengue-infected children (≤15
9
years) than in adults . In contrast, in the Americas, the adult population
9
is mainly affected, with most developing mild disease symptoms .
2 11
HOST RANGE: Humans, Simians, and Mosquitoes .
50
INFECTIOUS DOSE: Human ID is <10 PFU. Fewer than 10 PFU led to
infection in 50% of volunteers treated with an attenuated dengue virus
10
vaccine candidate .
MODE OF TRANSMISSION: Dengue virus is transmitted to humans through

2
mosquito bites or through contaminated blood transfusion . Peak
mosquito biting times are 2-3 hours after dawn and several hours before
7 12
dusk .
INCUBATION PERIOD: Humans have an average incubation period of 4-7

13
days (range of 3-15 days) .
COMMUNICABILITY: Virus can be communicated from human-to-human

2
via transfusion of tainted blood . Humans are infective for mosquitoes a
few days before and after the febrile period and mosquitoes become
7 14
infective for humans 8-12 days after infection .
SECTION III – DISSEMINATION

RESERVOIR: Aedes aegypti and Aedes albopictus mosquitoes (transovarial
transmission occurs in mosquitoes and salivary glands are highly infected),
humans, and lower primates (enzootic cycles between primates and
1 7 12
mosquitoes have been found in the forests of Africa and Asia)
13 15 .
ZOONOSIS: Yes,via infected mosquitoes.
VECTOR: Dengue virus is transmitted to humans by the bite of infected

1 2
Aedes aegypti and Aedes albopictus mosquitoes . The eggs of A.
16
aegypti can survive dessication for several months .
SECTION IV: STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY/RESISTANCE: AlthoughDengue Virus is sensitive to
5
ribavirin in vitro , clinical studies with ribavirin have been disappointing.
13
Anti-Dengue Virus drugs are currently under development . Drug
resistance has not been evaluated.
SUSCEPTIBILITY/RESISTANCE TO DISINFECTANTS: Dengue Virus is

susceptible to phenol-guanidine isothiocyanate (TRIzol® LS) and chaotropic
17
salt (AVL Buffer) . Viruses are sensitive to 1% sodium hypochlorite, 2%
gluteraldehyde, 2% peracetic acid, 70 % ethanol, iodophors, phenolic
18 19
compounds, and 3-6% hydrogen peroxide .
PHYSICAL INACTIVATION: Viruses are sensitive to moist heat (121°C for at

least 15 min), dry heat (160-170°C for at least 1 hour), and low temperature
20-23
sterilization (i.e. Ethylene oxide or plasma sterilization) . The virus is
24
also inactivated at a pH of 3 .
SURVIVAL OUTSIDE HOST: The virus is stable in dried blood for up to 9

25
weeks at room temperature .

SURVEILLANCE: Monitor for symptoms. Realtime PCR assay can be used to
quantitatively measure RNA number as an indicator of viral load in infection
6 5
. Dengue induced seroconversion can be detected using ELISA .
Detection of circulating secondary antibodies directed against proteins such
as NS1, NS2, NS3 and NS5 in patient samples, indicative of prior dengue
5
exposure, can aid in evaluating risk of DHF development . RT-PCR can be
2
used for direct virus detection .
FIRST AID TREATMENT: Monitor patient's vital signs closely and transfuse
2 5
plasma fluid and/or blood in cases of severe hemorrhagic fever .
2
Solutions with dextran 70 have been used to treat hemorrhagic shock .
IMMUNIZATION: No vaccine is presently licensed for the prevention of

Dengue Virus infection; however, numerous candidates are in various stages
of pre-clinical and clinical development Footnote 10Footnote 26.
PROPHYLAXIS: None

LABORATORY ACQUIRED INFECTIONS: There have been 14 reported cases
8
of laboratory acquired infections with no deaths .
SOURCES / SPECIMENS: Infected human blood, human liver, lung, and

kidney tissue; nonhuman primate kidney cell lines, CSF, spleen and lymph
nodes Footnote 2Footnote 27Footnote 28.Aedes aegypti and Aedes
albopictus mosquitoes, and environmental samples from mosquito habitats
are also sources of infection Footnote 1Footnote 13.
PRIMARY HAZARDS: Parenteral inoculation or bites from experimentally

1 2
infected mosquito can be potentially infectious .
SPECIAL HAZARDS: None

PERSONAL PROTECTION
RISK GROUP CLASSIFICATION: Risk Group 2.

29

29

at the perimeter and working towards the center. Allow sufficient contact
29

29

29
SECTION IX – REGULATORY AND OTHER

INFORMATION
and standards.
UPDATED: December 2011

Canada
Copyright © Public Health Agency of Canada, 2011
REFERENCES
1 Paranjape, S. M., & Harris, E. (2010). Control of dengue virus
translation and replication. Current Topics in Microbiology and
Immunology, 338, 15-34.
Schiefer, H. G., Slenczka, H. G., Graevenitz, A. V., & Zahner, H.
(2003). Viral zoonoses. Zoonoses: Infectious diseases transmissible
from Animals to Humans (3rd ed., pp. 57-61). Washington, USA:
ASM press.
3 Ray, G. C. (2004). Arthropod-Borne and other zoonotic viruses. In

K. J. Ryan, & C. G. Ray (Eds.), Sherris: Medical Microbiology An
introduction to infectious diseases (4th ed., pp. 585-596). USA:
McgrawHill.
4 Dimmock, N. J., Easton, A. J., & Leppard, K. N. (2007). Appendix:

survey of virus properties. Introduction to modern virology (6th ed.,
pp. 444-453, 479). MA, USA: Blackwell Publishing.
5 Burke, D. S., & Monath, T. P. (2001). Flaviviruses. In D. M. Knipe, P.

M. Howley, D. E. Griffin, M. A. Martin, R. A. Lamb & B. Roizman
(Eds.), Fields Virology (4th ed., pp. 1043-1126). PA, USA: Lippincott
Williams and Wilkins.
6 Rico-Hesse, R. (2009). Dengue virus markers of virulence and

pathogenicity. Future Virology, 4(6), 581-589.
7 Gubler, D. J. (1998). Dengue and dengue hemorrhagic fever.

Clinical Microbiology Reviews, 11(3), 480-496.
8 Paragas, J., & Endy, P. T. (2006). Viral Agents of human disease:

Biosafety concerns. In D. O. Fleming, & D. L. Hunt (Eds.), Biological
Safety: principles and practices (4th ed., pp. 179-207). Washinton,
DC: ASM press.
9 Martina, B. E. E., Koraka, P., & Osterhaus, A. D. M. E. (2009).

Dengue virus pathogenesis: An integrated view. Clinical
Microbiology Reviews, 22(4), 564-581.
10 Blaney Jr., J. E., Durbin, A. P., Murphy, B. R., & Whitehead, S. S.

(2010). Targeted mutagenesis as a rational approach to dengue
virus vaccine development. Current Topics in Microbiology and
Immunology, 338, 145-158.
11 Carver, S., Bestall, A., Jardine, A., & Ostfeld, R. S. (2009). Influence
of hosts on the ecology of arboviral transmission: Potential
mechanisms influencing dengue, Murray Valley encephalitis, and
Ross River virus in Australia. Vector-Borne and Zoonotic Diseases,
9(1), 51-64.
12 Gurugama, P., Garg, P., Perera, J., Wijewickrama, A., & Seneviratne,
S. L. (2010). Dengue viral infections. Indian Journal of Dermatology,
55(1), 68-78. doi:10.4103/0019-5154.60357
13 Scott, T. W., & Morrison, A. C. (2010). Vector dynamics and

transmission of dengue virus: implications for dengue surveillance
and prevention strategies: vector dynamics and dengue
prevention. Current Topics in Microbiology and Immunology, 338,
115-128.
14 Esler, D. (2009). Dengue - Clinical and public health ramifications.

Australian Family Physician, 38(11), 876-879.
15 Platt, K. B., Linthicum, K. J., Myint, K. S., Innis, B. L., Lerdthusnee, K.,
& Vaughn, D. W. (1997). Impact of dengue virus infection on
feeding behavior of Aedes aegypti. The American Journal of Tropical
Medicine and Hygiene, 57(2), 119-125.
16 Hopp, M. J., & Foley, J. A. (2001). Global-Scale Relationships

between Climate and the Dengue Fever Vector, Aedes Aegypti.
Climatic Change, 48, 441-463.
17 Blow, J. A., Dohm, D. J., Negley, D. L., & Mores, C. N. (2004). Virus
inactivation by nucleic acid extraction reagents. Journal of
Virological Methods, 119(2), 195-198.
18 Collins, C. H., & Kennedy, D. A. (1999). Laboratory acquired

infections. Laboratory acquired infections: History, incidence, causes
and prevention (4th ed., pp. 1-37). Woburn, MA: BH.
19 Rutala, W. A. (1996). APIC guideline for selection and use of

disinfectants. American Journal of Infection Control, 24(4), 313-342.

for working with pathogenic and infectious microorganisms.
Current Protocols in Microbiology, (SUPPL. 13), 1A.1.1-1A.1.14.
21 Moisan, M., Barbeau, J., Crevier, M. -., Pelletier, J., Philip, N., &
Saoudi, B. (2002). Plasma sterilization. Methods and mechanisms.
Pure and Applied Chemistry, 74(3), 349-358.
22 Richmond, J. Y., & Mckinney, R. W. (1999). Fungal agents. In R. Y.

Jonathan, & M. Robert (Eds.), Biosafety in microbial and biomedical
laboratories (4th ed., pp. 118-119). Washington, USA: U.S
government printing office.
23 Wood, M. (1974). Ethylene oxide sterilization. RESP.THER., 4(1), 43-

47+75.
24 Jindadamrongwech, S., Thepparit, C., & Smith, D. R. (2004).

Identification of GRP 78 (BiP) as a liver cell expressed receptor
element for dengue virus serotype 2. Archives of Virology, 149(5),
915-927. doi:10.1007/s00705-003-0263-x
25 Prado, I., Rosario, D., Bernardo, L., Alvarez, M., Rodriguez, R.,
Vazquez, S., & Guzman, M. G. (2005). PCR detection of dengue
virus using dried whole blood spotted on filter paper. Journal of
Virological Methods, 125(1), 75-81.
doi:10.1016/j.jviromet.2005.01.001
26 Guy, B., Guirakhoo, F., Barban, V., Higgs, S., Monath, T. P., & Lang,
J. (2010). Preclinical and clinical development of YFV 17D-based
chimeric vaccines against dengue, West Nile and Japanese
encephalitis viruses. Vaccine, 28(3), 632-649.
27 Cam, B. V., Fonsmark, L., Hue, N. B., Phuong, N. T., Poulsen, A., &
Heegaard, E. D. (2001). Prospective case-control study of
encephalopathy in children with dengue hemorrhagic fever. The
28 Rico-Hesse, R. (2010). Dengue virus virulence and transmission

determinants. Current Topics in Microbiology and Immunology, 338,
45-55.

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 
Ebolaviruses: Infectious substances Pathogen

Safety Data Sheet
On this page
Section V: First aid/medical
Section VII: Exposure controls/personal protection
References
For more information on Ebolavirus, see the following:

Infection prevention and control measures for Ebola disease in acute
care settings
Infection Prevention and Control Measures for Pre-hospital Care and
Ground Transport of Patients with Suspected or Confirmed Ebola Virus
Disease
Ebola virus disease: Symptoms and treatment

Name
Ebolaviruses
Agent type
Virus
Taxonomy
Family
Filoviridae
Genus
Ebolavirus
Species
Bundibugyo ebolavirus, Reston ebolavirus, Sudan ebolavirus, Taï Forest
ebolavirus, Zaire ebolavirus, Bombali ebolavirus
Synonym or cross reference

Also known as African haemorrhagic fever, Ebola haemorrhagic fever (EHF,
Ebola HF, Ebola), Filovirus, Ebola virus (EBOV), Zaire virus (EBOV), Sudan
virus (SUDV), Ivory Coast ebolavirus (ICEBOV), Taï Forest virus (TAFV), Ebola-
Reston (REBOV, EBO-R, Reston virus, (RESTV), Bundibugyo virus (BDBV),
1 2 3 4 5
Bombali virus (BOMV) and Ebola virus disease (EVD).
Characteristics
Brief description
Ebola virus was discovered in 1976 and is a member of the Filoviridae family.
Six ebolavirus species have been identified: Zaire ebolavirus, which was first
identified in 1976 and is the most virulent; Sudan ebolavirus; Taï Forest
ebolavirus (formerly Ivory Coast ebolavirus); Reston ebolavirus, originating
from the Philippines; Bundibugyo ebolavirus, discovered in 2008; and
Bombali ebolavirus, which is the most recently discovered in 2018 and its
1 2 3 5 6 7 8
ability to cause disease is currently unknown .
Ebolaviruses are an elongated filamentous virus, which can vary between
800 - 1000 nm in length, and can reach up to 14,000 nm long (due to
2 6 9 10
concatemerization) with a uniform diameter of 80 nm. It
contains a helical nucleocapsid (with a central axis), 20 - 30 nm in diameter,
and is enveloped by a helical capsid, 40 - 50 nm in diameter, with 5 nm cross-
2 5 9 10 11
striations. The pleomorphic viral fragment may take on
several distinct shapes (e.g., in the shape of a "6", a "U", or a circle) and are
2 6
contained within a lipid membrane. Each virion contains a single-
strand of non-segmented, negative-sense viral genomic RNA of
6 12 13
approximately 19kb in length. The virion surface is coated with
13
glycoproteins of 10 nm in length, which are anchored to the membrane.
Properties
Ebolaviruses exhibit a broad cell tropism, with several cell types supporting
viral replication, including: monocytes, macrophages, dendritic cells,
14
endothelial cells, fibroblasts, hepatocytes, and adrenal cortical cells. The
viral life cycle is initiated upon virus entry in the cell by micropinocytosis
which utilizes the interaction of the GP envelope protein with cell surface
15
determinants. The viral genome is released in the host cell cytoplasm
where virus replication begins. The L protein, which contains the RNA-
dependent RNA polymerase (RdRp) domain, as well as NP, VP35, and VP30,
are required for replication. Virion assembly follows with the formation of
nucleocapsids that are released from the host cell plasma membrane via
budding. Ebolaviruses are able to evade the immune system, making them
highly infectious. VP24 and VP35 ebolavirus structural proteins play a role in
16
immune evasion by supressing the type I interferon response. sGP is
released at high levels during illness and acts as a decoy to inhibit the
protective humoral response by binding to ebolavirus-neutralizing
antibodies.

Pathogenicity and toxicity
Ebolavirus virions enter host cells through endocytosis and replication
occurs in the cytoplasm. Upon infection, the virus affects the host blood
coagulative and immune defense system and leads to severe
11 17
immunosuppression. Early signs of infection are non-specific and
flu-like, and may include sudden onset of fever, asthenia, diarrhoea,
18 19
headache, myalgia, arthralgia, vomiting, and abdominal pains.
Less common early symptoms include conjunctival injection, sore throat,
rashes, and bleeding. Shock, cerebral oedema, coagulation disorders, and
9
secondary bacterial infection may co-occur later in infection.
Haemorrhagic symptoms may begin 4 - 5 days after onset, including
hemorrhagic conjunctivitis, pharyngitis, bleeding gums, oral/lip ulceration,
20
hematemesis, melena, hematuria, epistaxis, and vaginal bleeding.
Hepatocellular damage, marrow suppression (such as thrombocytopenia
and leucopenia), serum transaminase elevation, and proteinuria may also
occur. Persons that are terminally ill typically present with obtundation,
anuria, shock, tachypnea, normothermia to hypothermia, arthralgia, and
21
ocular diseases. Haemorrhagic diathesis is often accompanied by
hepatic damage and renal failure, central nervous system involvement, and
1 2
terminal shock with multi-organ failure. Contact with the virus may
also result in symptoms such as severe acute viral illness, malaise, and
maculopapular rash. Pregnant women will usually abort their foetuses and
2 22
experience copious bleeding. Fatality rates range between 50 -
100%, with most dying of hypovolemic shock and multisystem organ failure.
23 The length of illness depends on the severity of disease, but recovery
16
typically occurs after four weeks.
Pathogenicity between the ebolaviruses does not differ greatly in that they
have all been associated with hemorrhagic fever outbreaks in humans
(excluding Reston virus) and non-human primates. Ebola virus and Sudan
virus are especially known for their virulence with up to a 90% fatality rate,
24 with reduced virulence noted in the Taï Forest virus and the more
recently discovered Bundibugyo virus, which caused a single outbreak in
7 8
Uganda. Bundibugyo virus was also responsible for an outbreak in
Isiro, Democratic Republic of Congo, in 2012. Reston virus was isolated from
cynomolgus monkeys from the Philippines in 1989 and is less pathogenic in
non-human primates. Reston virus appears to be non-pathogenic in
humans, with reported health effects limited to serological evidence of
exposure as identified in 4 animal handlers working with infected non-
25
human primates. Seven SUDV outbreaks were reported between 1976
26
and 2012, comprising 778 cases.
The largest outbreak of Ebola virus disease began in Guinea in December

19
2013. This outbreak was marked by gastrointestinal clinical
presentation, although the most common symptoms for Ebola virus disease
are fever with anorexia, asthenia, and maculopapular rash 5 to 7 days after
19
disease onset. The case fatality rate during this outbreak is estimated to
19
be around 50%.
Predisposing factors
Risk factors for Sudan virus include interaction with acutely ill patients or
27 28 29
deceased patients that were infected with ebolavirus.
Nosocomial transmission amongst patients and staff is a major source of
27 29
epidemic spread. A serosurvey of healthcare workers suggests that
seropositivity may be associated with positions that offer less occupational
30
training and access to personal protective equipment (PPE).
Comparative serological studies of gold mining communities in Western
Uganda and non-mining communities in Central Uganda identified mining,
male gender, going inside mines, cleaning corpses, and contact with
31
suspected filovirus cases as risk factors for filovirus seropositivity.
Miners have an increased risk of filovirus exposure likely to due the
increased risk of exposure to bats, a putative reservoir host.
Communicability
Communicable through contact with infected blood, body fluids or organs.
Ebolaviruses have been isolated from semen 61 to 82 days after the onset of
1 2
illness, and transmission through semen is thought to be possible.
32 33
In an outbreak, it is hypothesized that the first patient becomes infected as a

33
result of contact with an infected animal. Person-to-person
transmission occurs via close personal contact with an infected individual or
1 2
their body fluids during the late stages of infection or after death.
34 35 Principle routes of infection include injection, mucous membranes,
19
and abraded or injured skin. Nosocomial infections can occur through
direct contact with infected body fluids, for example due to the reuse of
unsterilized syringes, needles, or other medical equipment contaminated
1 2
with these fluids. Humans may be infected by handling sick or dead
non-human primates and are also at risk when handling the bodies of
2 11 36
deceased humans in preparation for funerals. The index case in
the outbreak that originated in Guinea in December 2013 is believed to have
19
resulted from consuming infected bush meat.
In laboratory settings, non-human primates exposed to aerosolized Ebola

virus from pigs have become infected; however, airborne transmission has
1 11 21 37
not been demonstrated between non-human primates.
38 Viral shedding has been observed in nasopharyngeal secretions and
39 40
rectal swabs of pigs following experimental inoculation. Intranasal
infection studies in guinea pigs suggests that transmission through direct
contact with infectious materials, including those transported in aerosols
41
over short distances, is more infectious compared to systemic infection.
Epidemiology
11
Occurs mainly in areas surrounding rain forests in equatorial Africa with
the exception of Reston virus, which is documented to have originated in the
8
Philippines. No predispositions to infection have been identified among
infected persons.
The largest recorded Ebola virus outbreak to date began in December 2013,
with initial cases reported in Guinea and then additional cases identified in
the surrounding regions (Liberia, Sierra Leone, Nigeria). A new strain of the
19 22
Ebola virus was identified as the causative agent of the outbreak
34 42 and has resulted in more than 10,000 deaths and more than 20,000
43
suspected, probable, and confirmed cases.
A Bundibugyo virus outbreak began in the Bikoro region, Equateur Province,

in the Democratic Republic of the Congo in May 2018 with confirmed cases
44 45
reaching 38 by the middle of June 2018.
Seven Sudan virus outbreaks were reported in South Sudan and Uganda
26
between 1976 and 2012, comprising 778 cases. A recent Sudan virus
46
outbreak was declared in Uganda as of 20 September 2022. According
to the Uganda Ministry of Health, as of 23 October 2022, there are 75
cumulative confirmed cases.
Host range
Natural host(s)
Humans, various monkey species, chimpanzees, gorillas, baboons, and
1 2 6 34 39 40
duikers are natural animal hosts for ebolavirus.
47 48 49 50 51 52 53 Serological evidence of immunity markers
to ebolavirus in serum collected from domesticated dogs suggests
asymptomatic infection is plausible, likely following exposure to infected
54 55
humans or animal carrion. The Ebolavirus genome was discovered
in two species of rodents and one species of shrew living in forest border
areas, raising the possibility that these animals may be intermediary hosts.
56
Other host(s)
Experimental studies of the virus have been done using mouse, pig, guinea
pig, and hamster models, suggesting wild-type ebolavirus has limited
57 58
pathogenicity in these models.
Infectious dose
Although aerosol transmission of ebolaviruses is not considered to be a
primary mode of infection, viral hemorrhagic fevers have an experimentally
determined infectious dose of 1 - 10 organisms by aerosol in non-human
59
primates. The specific infectious dose for ebolaviruses is unknown;
however, rhesus monkeys exposed by the aerosol route in an artificial
setting experience clinical disease with inhaled doses of 2.6 log10 PFUs of
60
ebolavirus particles with diameters ranging from 0.8 to 1.2 µm.
Incubation period
1 19 21 23
Range of 2-21 days, but normally 4-10 days.

Reservoir
The natural reservoir of ebolaviruses is unknown, but specific species of bat
are considered a possible natural reservoir based on the presence of serum
2 19 61 62 63 64 65
antibodies and viral RNA. Serological
evidence of infection with ebolaviruses (antibody detection to ebolaviruses,
including Ebola and/or Reston virus) has been reported in fruit bats
collected from woodland and forested areas near Ghana and Gabon, with
reduced frequency of isolation from bats collected in mainland China and
62 63 64 65
Bangladesh. Antibodies to the virus have been found in
the serum of domestic guinea pigs and wild rodents, with no relation to
56 66
human transmission.
Zoonosis/Reverse zoonosis
2 19 34 64
Zoonosis between animals and humans is suspected.
Vectors
Unknown.

Drug susceptibility
In Canada, approved vaccines or therapeutics are only available for the
prevention or post-exposure prophylaxis of the Ebola virus. The ERVEBO
67
(rVSV-ZEBOV) vaccine is the primary preventative measure, while post-
exposure measures include the monoclonal antibody (mAb)-based
therapeutics ansuvimab (Ebanga) and atoltivimab+maftivimab+odesivimab
68
(Inmazeb). The symptoms of the disease may be treated by providing
intravenous fluids and balancing electrolytes, maintaining oxygen status
and blood pressure, replacement of lost blood and clotting factors, and
69
treating other infections if they occur.
Recombinant vesicular stomatitis virus (VSV) based vaccines have

demonstrated efficacy in nonhuman primate models as both single
70
preventative vaccines and as post-exposure treatments. VSV-EBOV is an
experimental vaccine developed in Canada that contains an Ebola virus
glycoprotein instead of a VSV glycoprotein. The vaccine has undergone
clinical trials in Canada and the United States.
Candidate vaccines for Sudan virus are in development. These are several
types being trialed including a DNA vaccine, heterologous vector vaccines,
67 71 72 73 74
and replication-defective recombinant vector vaccine.
75 All vaccines encode for glycoproteins (GP) of various ebolaviruses,
primarily EBOV and SUDV.
Monoclonal antibodies have also shown great promise as an effective

treatment for Ebola virus disease. ZMapp, a cocktail of 3 highly purified
monoclonal antibodies, has shown 100% protection of nonhuman primates
76
when treatment is initiated up to 5 days post-exposure. ZMapp has not
yet been tested for safety and efficacy in a human clinical trial, although
77
trials for monoclonal antibodies are underway.
Drug resistance
There are no known antiviral treatments available for human infections.
Susceptibility to disinfectants
Ebolaviruses are susceptible to 3% acetic acid, 1% glutaraldehyde, alcohol-
based products, calcium hypochlorite (bleach powder), and dilutions of
5.25% household bleach (i.e., 0.525% to 0.0525% sodium hypochlorite for ≥
78 79 80 81
10 min). The WHO recommendations for cleaning up
spills of blood or body fluids suggest flooding the area with a 1:10 dilution of
5.25% household bleach (i.e., 1 part household bleach diluted in 9 parts
water, or 0.525% sodium hypochlorite) for 10 minutes for surfaces that can
81
tolerate stronger bleach solutions (e.g., cement, metal). For surfaces
that may corrode or discolour, careful cleaning is recommended to remove
visible stains followed by contact with a 1:100 dilution of 5.25% household
bleach (i.e., 1 part household bleach diluted in 99 parts water, or 0.0525%
sodium hypochlorite) for more than 10 minutes.
Laboratory tests have demonstrated that the use of 70% ethanol for 1
minute is effective at inactivating Mayinga and Kikwit strains of the Ebola
virus, whereas 2.5 minutes is required to inactivate the Makona variant. Use
of 0.5% and 1% sodium hypochlorite solutions (i.e., 50 mL household bleach
into 450 mL or 200mL water, respectively) for 5 minutes is effective at
82 83
inactivating all three variants. A 0.5% chlorine solution is also
recommended by the WHO to disinfect surfaces contaminated with
82
ebolavirus.
Physical inactivation
Ebolaviruses are moderately thermolabile and can be inactivated by heating
for 30 minutes to 60 minutes at 60°C, boiling for 5 minutes, or gamma
irradiation (1.2 x106 rads to 1.27 x106 rads) combined with 1%
11 78 80
glutaraldehyde. Ebola virus has also been determined to be
84
moderately sensitive to UVC radiation. Ebola virus Makona strain virions
in spike serum samples can be inactivated after incubation for 1 hour with
0.5% Tween-20 at 56°C, which is considered a more practical application in
85
the field. A high viral load in whole-blood thin-smear samples can be
86
inactivated using a 15 minute 100% methanol fixation step.
Virus inactivation is recommended for samples intended for clinical

laboratory testing. Guanidine thiocyanate-based lysis buffers commonly
used during nucleic acid extraction processes (e.g., for downstream PCR
applications) may be effective for the inactivation of enveloped RNA viruses.
87 88 89 The inactivation method should be selected based on its viral
inactivation efficacy, as well as its interference with the subsequent test
results (e.g., electrolytes, glucose, enzymes, protein, etc.). Please see the
Biosafety Guidelines for Laboratories Handling Specimens from patients
Under Investigation for Ebola Virus Disease for more information.
Survival outside host

Filoviruses have been reported capable to survive for weeks in blood and
can also survive on contaminated surfaces, particularly at low temperatures
90 91
(4°C). Under West African climate conditions of 28°C and 90%
relative humidity, ebolavirus can persist in dried human or non-human
83
primate blood for 7 to 10 days. One study could not recover any Ebola
virus from experimentally contaminated surfaces (plastic, metal or glass) at
91
room temperature. In another study, Ebolaviruses dried onto glass,
polymeric silicone rubber, or painted aluminum alloy was able to survive in
the dark for several hours under ambient conditions (between 20°C and
25°C and 30–40% relative humidity; amount of virus reduced to 37% after
15.4 hours), but was less stable than some other viral hemorrhagic fevers,
84 92
such as Lassa virus. When dried in tissue culture media onto glass
91
and stored at 4 °C, Ebola virus survived for over 50 days. Ebola virus
Makona strain suspended in organic soil has been shown to persist on steel
and plastic surfaces for up to 192 hours compared to less than 24 hours on
cotton. Ebola virus suspended in serum can persist in the environment for
82
up to 46 days. This information is based on experimental findings only
and not based on observations in nature. This information is intended to be
used to support local risk assessments in a laboratory setting.
In average West African climatic conditions of 27°C and 80% relative

humidity, Ebola virus Makona strain can remain viable on gloves (<1 hour),
cotton and goggles (<24 hours), and other PPE such as respirators, suits and
93
hoods (<72 hours).
A study on transmission of Ebola virus from fomites in an isolation ward

concludes that the risk of transmission is low when recommended infection
94
control guidelines for viral hemorrhagic fevers are followed. These
infection control protocols included decontamination of floors with 0.5%
bleach daily and decontamination of visibly contaminated surfaces with
0.05% bleach as necessary.

Surveillance
Definitive diagnosis can be reached rapidly in an appropriately equipped
laboratory using a multitude of approaches, including RT-PCR to detect viral
RNA, ELISA based techniques to detect antiviral antibodies or viral antigens,
immunoelectron microscopy to detect ebolavirus particles in tissues and
1 2
cells, and indirect immunofluorescence to detect antiviral antibodies.
20 59 It is useful to note that Marburgvirus is morphologically
indistinguishable from ebolaviruses, and laboratory surveillance of
1 2 20 95
ebolaviruses is extremely hazardous. Please see the
Biosafety Guidelines for Laboratories Handling Specimens from patients
Under Investigation for Ebola Virus Disease for more information.
Note: The specific recommendations for surveillance in the laboratory

should come from the medical surveillance program, which is based on a
local risk assessment of the pathogens and activities being undertaken, as
well as an overarching risk assessment of the biosafety program as a whole.
More information on medical surveillance is available in the Canadian
Biosafety Handbook (CBH).
First aid/treatment
Favipiravir can rescue animals following a lethal dose of Ebola virus, antiviral
activity against Ebola virus is considered relatively weak and there is no
96
efficacy data available. In Canada, post-exposure measures are
currently only available for Ebola virus, namely ansuvimab (Ebanga) and
atoltivimab+maftivimab+odesivimab (Inmazeb) which are monoclonal
67
antibody (mAb)-based therapeutics. In general, due to the lack of
effective pharmaceutical treatment available, treatment is supportive and
may include providing intravenous fluids and balancing electrolytes,
maintaining oxygen status and blood pressure, replacement of lost blood
and clotting factors, and treating other infections if they occur for
maintenance of organ function, and combating haemorrhage and shock.
34 69 97 Monoclonal antibodies are also under investigation for
96
treatment for Ebola virus disease, but have not been approved for use.
A Phase 1 clinical trial evaluating the safety and tolerability of a single
monoclonal antibody (mAb114) developed from an Ebola virus survivor is
77
underway. Convalescent blood products from survivors of Ebola virus
disease have been administered to patients in Africa, but the benefits of
96
such a treatment remain unclear.
Note: The specific recommendations for first aid/treatment in the laboratory

should come from the post-exposure response plan, which is developed as
part of the medical surveillance program. More information on the post-
exposure response plan can be found in the CBH.
Immunization
In Canada, the ERVEBO (rVSV-ZEBOV) vaccine has been approved for the
98
Ebola virus.
Other potential vaccine candidates moving towards clinical trials include

human adenovirus serotype 26 or 35 platforms with a Modified vaccinia
Ankara (MVA) boost. Vaccine efficacy has been studied in Guinea pigs
mucosally-infected with Ebola virus, as this is a more common infection
route compared to intramuscular infection in non-human primate models.
Guinea pigs infected intranasally showed 100% survival with prior
98
administration of adjuvanted Ad5-ZGP.
Note: More information on the medical surveillance program can be found

in the CBH, and by consulting the Canadian Immunization Guide.
Prophylaxis
Post-exposure measures are currently available for Ebola virus in the form
of monoclonal antibody (mAb)-based therapeutics: ansuvimab (Ebanga) and
67
atoltivimab+maftivimab+odesivimab (Inmazeb) . Management of the
ebolaviruses is also based on isolation and barrier-nursing with
9
symptomatic and supportive treatments. The vaccine rVSV-ZEBOV has
been used as post-exposure prophylaxis in humans; however, findings
suggest that immunity is insufficiently rapid to reliably prevent Ebola virus
98
disease in human beings when administered following exposure.
Français
MENU 

Substances – Echovirus

NAME: Echovirus
1
SYNONYM OR CROSS REFERENCE: Human enterovirus B , enteric
cytopathogenic human orphan (ECHO) virus, Boston exanthem disease
CHARACTERISTICS: Echoviruses are members of the genus Enterovirus and

family Picornaviridae. Parechoviruses were previously classified as members
of the genus Enterovirus, but have recently been separated into their own
2
genus based on their unique biological properties . Echoviruses are small
non-enveloped viruses with a single-stranded positive-sense RNA genome.
Echoviruses are 30 nm in diameter. There are 28 serotypes of Human
1
echoviruses, which are all classified in the species human enterovirus B .

PATHOGENICITY/TOXICITY: The majority of infections are asymptomatic.
The most common symptomatic manifestation of infection is an acute
1
nonspecific febrile illness with or without exanthem . Echoviruses are
frequently associated with aseptic meningitis. Symptoms include acute
onset of fever, headache, photophobia, nausea and vomiting. Fever may
subside for several days and then recur. Generally, symptoms resolve in
about 1 week. Severe illness and death are uncommon and most patients
3 4
completely recover . Other clinical syndromes have been less
commonly associated with echovirus infections, including paralysis,
encephalitis, respiratory disease, diarrhea, hepatic disturbance, exanthems
1
and enanthems, conjunctivitis, asthenia, pericarditis, and myocarditis
4-7 . Epidemics in neonatal intensive care units have very high morbidity
8
and mortality rates .
EPIDEMIOLOGY: Worldwide distribution. In temperate climates, incidence

peaks during the summer and fall months; in the tropics, transmission
3
occurs year-round . Enteroviruses, including echoviruses, predominantly
affect children. Other risk factors include lower socioeconomic status, large
household size, crowded living conditions, living in urban areas, and areas
3 4
with poorer sanitation .
9
HOST RANGE: Humans .
INFECTIOUS DOSE: The dose required to infect 50% of volunteers in one

10
study was calculated to be 919 pfu for Echovirus 12 .
MODE OF TRANSMISSION: Transmitted by fecal-oral (most significant),

1 3
respiratory, transplacental, perinatal, and self-inoculation routes .
3
Fomites may also transmit viruses .
9
INCUBATION PERIOD: Variable, typically 2 – 10 days .
3
COMMUNICABILITY: Can be transmitted from person-to-person . Viral
agents can be excreted for 3-4 weeks from the pharynx, and 5-6 weeks in
5
stool .

4 9
RESERVOIR: Humans
9
ZOONOSIS: No evidence of spread from animal to humans .
VECTORS: Insects (flies or cockroaches) are a possible mechanical vector,

4 9
although this has not yet been conclusively determined .

DRUG SUSCEPTIBILITY/RESISTANCE: No antiviral medications are currently
approved for the treatment of enterovirus infections. Pleconaril has shown
11
antiviral activity against echoviruses in vitro .
SUSCEPTIBILITY/RESISTANCE TO DISINFECTANTS: Echoviruses are

susceptible to 0.3% formaldehyde and 0.3 – 0.5 ppm free chlorine. They are
resistant to 70% alcohol, substituted phenolic, ether, and various detergents
9 .
PHYSICAL INACTIVATION: Can be inactivated by heat (>56 °C), ultraviolet

1 3
light, and drying .
SURVIVAL OUTSIDE HOST: Can survive 7 days on dry inanimate surfaces

12 . Echoviruses can survive for weeks in water, body liquids, and sewage
1 .

SURVEILLANCE: Traditionally diagnosed by the isolation of viral particles
from clinical specimens; however, PCR-based tests are becoming more
13
common . The use of viral culture is declining as not all serotypes grow
well in culture.
FIRST AID/TREATMENT: Most cases are self-limiting and recover with

3
supportive care. No antiviral therapy is available .
IMMUNIZATION: None
PROPHYLAXIS: None

LABORATORY-ACQUIRED INFECTIONS: At least three cases of laboratory-
14
acquired infections have been reported .
SOURCES/SPECIMENS: Cerebrospinal fluid, blood, tissues, stool, and rectal

1 13
and throat swabs .
4
PRIMARY HAZARDS: Parenteral inoculation, oral ingestion , and aerosols
1 .

PERSONAL PROTECTION

15

15

15

15

15
SECTION IX - REGULATORY AND OTHER

INFORMATION
and standards.

Canada.

REFERENCES
1 Romero, J. R. (2007). Enteroviruses and Parechoviruses. In P. R.
Murray (Ed.), Manual of Clinical Microbiology (9th ed., pp. 1392-
1404). Washington D.C.: ASM Press.
2 Joki-Korpela, P., & Hyypia, T. (2001). Parechoviruses, a novel group

of human picornaviruses. Annals of Medicine, 33(7), 466-471.
3 Khetsuriani, N., & Parashar, U. D. (2007). Enteric Viral Infections. In

D. C. Dale (Ed.), Infectious Diseases: The Clinician's Guide to
Diagnosis, Treatment and Prevention (17th ed., ). New York: WebMD
Corporation. Retrieved from
4 Pallansch, M., & Roos, R. (2007). Enteroviruses: Polioviruses,

Philadelphia PA: Lippincott Williams & Wilkins.
5 Busowski, M. T. (2009). Echoviruses.
6 Lukashev, A. N., Lashkevich, V. A., Koroleva, G. A., & Karganova, G.

G. (2002). Phylogenetic and serological characterization of
echovirus 11 and echovirus 19 strains causing uveitis. Archives of
Virology, 147(1), 131-142.
7 Grimwood, K., Huang, Q. S., Sadleir, L. G., Nix, W. A., Kilpatrick, D.

R., Oberste, M. S., & Pallansch, M. A. (2003). Acute flaccid paralysis
from echovirus type 33 infection. Journal of Clinical Microbiology,
41(5), 2230.

Nonpolio enterovirus and human parechovirus surveillance ---
United States, 2006-2008. MMWR.Morbidity and Mortality Weekly
Report, 59(48), 1577-1580.
9 Ray, G. C. (2004). Enteroviruses. In K. J. Ryan, & G. C. Ray (Eds.),

Sherris Medical Microbiology: An Introduction to Infectious Disease
(4th ed., pp. 531-539). New York: McGraw Hill.
10 Schiff, G. M., Stefanovic, G. M., & Young, E. C. (1984). Studies of

echovirus-12 in volunteers: Determination of minimal infectious
dose and the effect of previous infection on infectious dose.
Journal of Infectious Diseases, 150(6), 858-866.
11 Pevear, D. C., Tull, T. M., Seipel, M. E., & Groarke, J. M. (1999).

Activity of pleconaril against enteroviruses. Antimicrobial Agents
and Chemotherapy, 43(9), 2109-2115.

13 Muir, P. (2009). Enteroviruses. Medicine, 37(12), 691-694.
14 Pike, R. M. (1976). Laboratory associated infections: summary and

analysis of 3921 cases. Health Laboratory Science, 13(2), 105-114.

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Enterovirus 70

SUBSTANCES
NAME: Enterovirus 70
SYNONYM OR CROSS REFERENCE: EV70; acute hemorrhagic conjunctivitis;

1 3
AHC virus; Apollo 11 disease; EO-70 .
CHARACTERISTICS: Enterovirus 70 is a small (~ 30 nm in diameter), non-

enveloped virus with a single-stranded positive-sense RNA genome (~7.4 kb)
enclosed within an icosahedral capsid. It belongs to the species human
1 3
enterovirus D in the genus Enterovirus and family Picornaviridae . It
1
replicates optimally at 36°C .

PATHOGENICITY/TOXICITY: Enterovirus 70 causes acute hemorrhagic
3
conjunctivitis . The symptoms of the disease include eye pain,
photophobia, swelling of eye lid and varying redness of the conjunctiva
3 4
(from subconjunctival petechiae to hemorrhages) . Disease resolves
in less than 10 days. Transient corneal involvement may occur in some cases
3 . Acute hemorrhagic conjunctivitis can also cause non-ophthalmic
symptoms, such as neurologic dysfunction, respiratory and gastrointestinal
4
disturbances . Furthermore, permanent polio-like paralysis has been
4
reported in individuals infected with enterovirus 70 .
EPIDEMIOLOGY: The first pandemic of acute hemorrhagic conjunctivitis,

4
affecting hundreds of millions of people, occurred in 1969 in Africa .
Since then the virus has been associated with large outbreaks, mainly in
3
tropical areas .
1
MODE OF TRANSMISSION: Direct or indirect contact (introduction of the

virus into the eye through infected hands and fomites) with eye secretions
1 4 5 .
4
INCUBATION PERIOD: 24 to 48 hours .
3
COMMUNICABILITY: Highly contagious .

1
RESERVOIR: Humans .
ZOONOSIS: None.
VECTORS: None.

DRUG SUSCEPTIBILITY: Pleconaril has shown antiviral activity against
6
several enterovirus strains in vitro .
SUSCEPTIBILITY TO DISINFECTANTS: Enterovirus 70 is susceptible to a

solution of 500 p.p.m. sodium hypochlorite with a contact time of 2 minutes.
Enterovirus 70 is resistant to phenyl mercuric borate and isopropyl alcohol
7 .
PHYSICAL INACTIVATION: Enteroviruses can be inactivated by extreme

1 3
heat (>56°C), ultraviolet light, and drying .
SURVIVAL OUTSIDE HOST: Enterovirus 70 can survive at least 24 hours on

5
inanimate surfaces under high humidity conditions . Enteroviruses are
also stable in liquid environments and can survive for many weeks in water,
1
body fluids, and sewage .

SURVEILLANCE: Diagnosis is based on detection of EV 70 virus in clinical
specimens with molecular biology methods such as RT-PCR, real-time RT-
PCR, and Nucleic Acid Sequence Based Amplification (NASBA). Isolation of
EV70 virus from patients with acute hemorrhagic conjunctivitis is very
2 4
difficult .
FIRST AID/TREATMENT: Most cases are self-limiting and recover with

3
supportive care. No antiviral therapy is available .
IMMUNIZATION: None.
PROPHYLAXIS: None.

LABORATORY-ACQUIRED INFECTIONS: Laboratory acquired infections
have been reported from 2 laboratories, where virological studies were
2
being conducted on EV70 .
2 4
SOURCES/SPECIMENS: Conjunctival swabs and tears .
2
PRIMARY HAZARDS: Contact of infectious agent with eye membrane .

8
RISK GROUP CLASSIFICATION: Risk group 2 .

9
infectious materials, animals, or cultures .
9

9

cover the spill with absorbent paper towels and apply an appropriate
disinfectant, starting at the perimeter and working towards the center. Allow
sufficient contact time before clean up.

irradiation, or incineration before disposing.

that are appropriately labelled.

and standards.

Canada.

Copyright ©
Canada
REFERENCES:
1 Romero, J. R. (2007). Enteroviruses and Parechoviruses. In P. R.
2 Sasagawa, A., Kono, R., & Konno, K. (1976). Laboratory acquired

infection of the eye with AHC virus. Japanese Journal of Medical
Science and Biology, 29(2), 95-97.
3 Khetsuriani, N., & Parashar, U. D. (2007). Enteric Viral Infections. In

D. C. Dale (Ed.), Infectious Diseases: The Clinician's Guide to
Diagnosis, Treatment and Prevention (17th ed., ). New York: WebMD
Corporation. Retrieved from
4 Pallansch, M., & Roos, R. (2007). Enteroviruses: Polioviruses,

Philadelphia PA: Lippincott Williams & Wilkins.
5 Sattar, S. A., Dimock, K. D., Ansari, S. A., & Springthorpe, V. S.

(1988). Spread of acute hemorrhagic conjunctivitis due to
enterovirus-70: Effect of air temperature and relative humidity on
virus survival on fomites. Journal of Medical Virology, 25(3), 289-296.
6 Pevear, D. C., Tull, T. M., Seipel, M. E., & Groarke, J. M. (1999).

Activity of pleconaril against enteroviruses. Antimicrobial Agents
and Chemotherapy, 43(9), 2109-2115.
7 Nagington, J., Sutehall, G. M., & Whipp, P. (1983). Tonometer

disinfection and viruses. British Journal of Ophthalmology, 67(10),
674-676.

2009, (2009).

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Hantavirus spp.

SUBSTANCES
NAME: Hantavirus spp.
SYNONYM OR CROSS REFERENCE: Old world Hantavirus, New world Hanta

virus, Hemorrhagic fever with renal syndrome (HFRS), hantavirus pulmonary
syndrome (HPS), Korean hemorrhagic fever (KHF), epidemic hemorrhagic
1 2
fever, hemorrhagic nephrosonephritis .
CHARACTERISTICS: Hantaviruses belong to the family Buynaviridae. They

are enveloped viruses about 100 nm in diameter with a tripartite single-
stranded negative sense RNA genome, enclosed within a spherical capsid
2 3 . Hantaviruses can be divided into three groups, according to the
taxonomic assignment of their principle hosts: 1) Muridae (old world rats
and mice); 2) Arvicolinae (voles and lemmings); 3) Sigmodontinae (New
3
world rats and mice) . There are several species of Hantavirus which are
pathogenic to humans, including Puumala, Dobrava-Belgrade, Hantaan,
Seoul, Andes, Bayou, Black Creek Canal, Laguna Negra, New York, and Sin
3
Nombre virus .

PATHOGENICITY/TOXICITY:
Hemorrhagic fever with renal syndrome (HFRS): HFRS can manifest as mild,
4
moderate or severe disease, depending upon the causative virus . The
clinical course can be divided into five phases: prodrome (or febrile),
3 4
hypotensive, oliguric, diuretic, and convalescent . The prodrome
begins with high fever, chills, headache, blurred vision, malaise, and
anorexia, followed by abdominal or lumbar pain, gastrointestinal symptoms,
facial flushing, petechiae, and an erythematous rash. This phase typically
3
lasts 3 to 7 days . The hypotensive phase lasts several hours to many
days. It is characterized by the sudden onset of hypotension which may
progress to shock and hemorrhagic manifestations. The oliguric phase
typically lasts 3 to 7 days, and, in this time, the blood pressure may return to
normal or become high, urinary output falls dramatically, and severe
3
haemorrhage may occur . Spontaneous diuresis indicates the beginning
5
of recovery. The case fatality rate is 5 to 15% .
Hantavirus pulmonary syndrome (HPS): There are four clinical phases:

prodrome, cardiopulmonary, diuresis, and convalescence. The prodrome
phase is characterized by fever, myalgia and malaise, and other symptoms,
including headache, dizziness, abdominal pain, and gastrointestinal
symptoms, typically lasting 3-6 days. This is followed by the rapidly
progressive cardiopulmonary phase, characterized by non-cardiogenic
pulmonary edema, hypoxemia, cough, pleural effusion, gastrointestinal
symptoms, tachypnea, tachycardia, myocardial depression, and cardiogenic
shock. Hypotension and oligouria may occur. The diuresis phase involves
2 -
rapid clearance of pulmonary edema and resolution of fever and shock
4 4
. The case fatality is around 30% .
EPIDEMIOLOGY: Hantaviruses occur worldwide, with the distribution of

3 5
specific viruses limited to the habitat of their rodent hosts . For
example, Hantaan virus, which causes a severe form of HFRS, is endemic in
Russia and China, and Andes virus is responsible for HPS in the New World
1 - 3 . Approximately 150,000 to 200,000 cases of HFRS occur each year
3 4
world wide, most of which occur in China . Depending upon the
4
virus, the case fatality can range from <1% to12% . HPS is more common
in the New World, with approximately 200 cases per year, and the average
4
case fatality rate 30% . Incidence rates in different countries, however,
fluctuate with the population of rodent hosts. Infections occur
predominantly in rural areas, although some viruses (e.g., Seoul virus) occur
in urban areas. The majority of Hantavirus infections occur in males and in
4
individuals between the ages of 20-40 . Trappers, hunters, forestry
workers, farmers, and military personnel have a higher risk of contracting
2 4
the disease .
HOST RANGE: Humans, and several species of rodents (voles, mice, rats)
3 6 .
MODE OF TRANSMISSION: Transmission occurs mainly by inhalation of

aerosolized droplets of urine, saliva, or respiratory secretions from infected
rodents or of aerosolized particles of feces, dust, or other organic matter
1 3
carrying the infectious virus . They may also be transmitted by
rodent bites (however, few patients contracting hantaviruses report rodent
bites prior to symptom development), ingestion of contaminated food or
water, and direct contact of cutaneous injuries or mucous membranes with
1 - 3
the infectious virus .
INCUBATION PERIOD: 2 to 4 weeks (range from few days to 2 months) for

3 4
HFRS; and 14-17 days for HPS .
COMMUNICABILITY: Person-to-person transmission is very rare, but has

been observed for Andes virus during an outbreak in Southern Argentina
1 7 .

RESERVOIR: Small rodents (mice, rats and voles) serve as the reservoirs of
1 - 3
Hantaviruses .
1 3
ZOONOSIS: Yes, transmitted from rodents to humans . Puumala
virus – bank vole (Myodes glareolus, formerly Clethrionomys glareolus) in
northern and central Europe; Hantaan virus – striped field mouse
(Apodemus agrarius) in east Asia; Dobrava virus – yellow-necked mouse (A.
flavicollis) and striped field mouse (A. agrarius) in southern Europe; Seoul
virus - Norway rat (Rattus norvegicus) worldwide; Sin nombre virus – deer
mouse (Peromyscus maniculatus) in North America; Laguna Negra virus –
small vesper mouse (Calomys laucha) in Argentina; Andes virus – long-tailed
pygmy rice rat (Oligoryzomys longicaudatus) in South America; Bayou virus
– marsh rice rat (Oryzomys palustris) Louisiana; and Black Creek Canal virus
1
– hispid cotton rat (Sigmodon hispidus) in Florida .
VECTORS: None known.

DRUG SUSCEPTIBILITY: Susceptible to latoferrin (in vitro) and ribavirin (in
vitro and in vivo) in cases of HFRS; however, the efficacy of these drugs on
1 3 6 8
cases of HPS have not been shown .
SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to 1% solution of sodium

hypochlorite, 1-5% Clidox® (chlorine dioxide), 1-5% Dettol®
(parachlorometaxylenol), 1-5% Halamid-d® (sodium-p-toluene-
sulfonchloramide), 1-5% peracetic acid, or Virkon® with a 10 minute contact
time. Also susceptible to absolute methanol with a 10 minute contact time
9
and 70% ethanol with a 30 minute contact time .
PHYSICAL INACTIVATION: Inactivated by heat (15 min at 56ºC for viruses in

cell culture medium, and 2 hours at 56oC for dried viruses) 10 .
SURVIVAL OUTSIDE HOST: Can survive for long periods in the environment:
12-15 days in contaminated beddings, 5-11 days at room temperature in cell
culture supernatants, and 18 – 96 days at 4ºC in cell culture supernatants
10 11 .

SURVEILLANCE: Monitor for symptoms. Diagnosis is based mainly on
serological tests to detect Hantavirus specific IgM, IgG, and neutralizing
antibodies against the N protein or glycoproteins. Many different serological
methods can be used, including immunofluorescence assay,
1 - 3
haemagglutination-inhibition assay, and complement fixation tests
6 . RT-PCR assays (for the S and M genomic regions of Hanta virus) can
also be used to detect Hanataviral RNA in clinical samples such as blood,
3
serum, or tissues from both HPS and HFRS patients .
FIRST AID/TREATMENT: Treatment with antiviral ribavirin improves the

1 3
outcome of HFRS, but has not been investigated for HPS . Treatment
is supportive. Furthermore, extracorporeal CO2 elimination system should
be considered for HPS patients to prevent life threatening pulmonary edema
1 3
and cardiogenic shock .
IMMUNIZATION: None.
PROPHYLAXIS: None.

LABORATORY-ACQUIRED INFECTIONS: Yes, 226 cases (no deaths) have
7
been reported for Hantaan virus .
SOURCES/SPECIMENS: Blood, urine, cerebrospinal fluid, and respiratory

3 12
secretions, as well as rodent urine .
PRIMARY HAZARDS: Ingestion, contact of mucous membranes or broken

skin with infectious materials, inhalation, animal bites, and accidental
1 3 13
parenteral inoculation .
SPECIAL HAZARDS: Working with laboratory animals (exposure to animal

1 12
excreta, fresh necroscropy material, and animal bedding) .

14
RISK GROUP CLASSIFICATION: Risk Group 3 . The risk group
associated with Hantavirus reflects the genus as a whole, but does not
necessarily reflect the risk group classification of every species within the
genus.
CONTAINMENT REQUIREMENTS: Containment level 3 facilities, equipment

and operational practices for all work involving infectious or potentially
infectious materials, animals, or cultures. These containment requirements
apply to the genus as a whole, and may not apply to each species within the
genus.

15

placed in sealed safety cups, or in rotors that are loaded or unloaded in a
biological safety cabinet. The use of needles, syringes, and other sharp
objects should be strictly limited. Open wounds, cuts, scratches, and grazes
should be covered with waterproof dressings. Additional precautions should
15
be considered with work involving animals or large scale activities .

SPILLS: Allow aerosols to settle, and wearing protective clothing, gently
cover the spill with absorbent paper towel and apply appropriate
disinfectant starting at the perimeter and working towards the center. Allow
15
sufficient contact time before starting the clean up .
DISPOSAL: All wastes should be decontaminated before disposal either by

15
steam sterilization, incineration or chemical disinfection .

15

and standards.

Canada.

Copyright ©
Canada
REFERENCES:
1 Krauss, H., Schiefer, H. G., Weber, A., Slenczka, W., Appel, M., von
Graevenitz, A., Enders, B., Zahner, H., & Isenberg, H. D. (2003). Viral
Zoonoses. Zoonoses: Infectious Disease Transmissible from Animals
to Humans (3rd ed., pp. 77-81). Washington D.C.: ASM Press.
2 Simpson, S. Q., Spikes, L., Patel, S., & Faruqi, I. (2010). Hantavirus
Pulmonary Syndrome. Infectious Disease Clinics of North America,
24(1), 159-173.
3 Fulhorst, C. F., & Bowen, M. D. (2007). Hantaviruses. In P. R.

4 Bi, Z., Formenty, P. B., & Roth, C. E. (2008). Hantavirus infection: a

review and global update. Journal of Infection in Developing
Countries, 2(1), 3-23.
5 Schmaljohn, C. S., & Nichol, S. T. (2007). Bunyaviridae. In D. M.

Roizman & S. E. Straus (Eds.), Fields Virology (5th ed., pp. 1739-
1789). Philadelphia PA: Lippincott Williams & Wilkins.
6 Krüger, D. H., Ulrich, R., & Lundkvist, A. (2001). Hantavirus

infections and their prevention. Microbes and Infection, 3(13), 1129-
1144.

Safety: Principles and Practices (pp. 179-207). Washington, D.C.:
ASM Press.
8 Murphy, M. E., Kariwa, H., Mizutani, T., Yoshimatsu, K., Arikawa, J.,
& Takashima, I. (2000). In vitro antiviral activity of lactoferrin and
ribavirin upon hantavirus. Archives of Virology, 145(8), 1571-1582.
9 Maes, P., Li, S., Verbeeck, J., Keyaerts, E., Clement, J., & Van Ranst,
M. (2007). Evaluation of the efficacy of disinfectants against
Puumala hantavirus by real-time RT-PCR. Journal of Virological
Methods, 141(1), 111-115.
10 Kallio, E. R., Klingström, J., Gustafsson, E., Manni, T., Vaheri, A.,
Henttonen, H., Vapalahti, O., & Lundkvist, Å. (2006). Prolonged
survival of Puumala hantavirus outside the host: Evidence for
indirect transmission via the environment. Journal of General
Virology, 87(8), 2127-2134.
11 Hardestam, J., Simon, M., Hedlund, K. O., Vaheri, A., Klingström, J.,
& Lundkvist, Å. (2007). Ex vivo stability of the rodent-borne
Hantaan virus in comparison to that of arthropod-borne members
of the Bunyaviridae family. Applied and Environmental Microbiology,
73(8), 2547-2551.
12 Viral agents (other than arboviruses): Hantavirus. (1999). In J. Y.

Richmond, & R. W. and Mckinney (Eds.), Biosafety in microbiological
and biomedical laboratories (4th ed., pp. 153-154). Washington,
D.C.: CDC & NIH.


Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Hepatitis A virus (HAV)

SUBSTANCES
NAME: Hepatitis A virus (HAV).
SYNONYM OR CROSS REFERENCE: HAV, type A hepatitis, infectious

1
hepatitis, epidemic hepatitis, epidemic jaundice, and catarrhal jaundice
2 3 4 5 6 7 8 9 10 11 .
CHARACTERISTICS: HAV is a member of the Picornaviridae family and

1 2 3 11
Hepatovirus genus . It is an icosahedral, non-enveloped,
positive-sense RNA virus and is 27 to 32 nm in diameter. Seven HAV
genotypes have been identified (I-VII), 4 of which are of human origin (I, II,
3
III, and VII) .

PATHOGENICITY/TOXICITY: HAV only causes acute hepatitis and is not
1 3
associated with chronic liver disease . Most individuals infected with
HAV develop non-specific constitutional signs and symptoms followed by
gastrointestinal symptoms. Symptoms include fever, malaise, anorexia,
2 3 4 11
nausea, abdominal discomfort, dark urine, and jaundice . The
3
disease course typically lasts less than 2 months . In rare cases, HAV can
cause severe cases of fulminant hepatitis with fatal outcomes in otherwise
2 3
healthy adults .
EPIDEMIOLOGY: The World Health Organization estimates an annual total

of 1.5 million case of hepatitis A worldwide, but seroprevalence data suggest
4
that tens of millions of HAV infections occur each year . Central and South
America, Africa, India, the Middle East, and Asia have the highest
seroprevalence rates, whereas North America, Japan, and Western Europe
2 4
have among the lowest . The incidence level is highly related to the
prevailing level of hygiene and sanitation, with the disease being most
4
prevalent in less developed parts of the world .
1 2 3 4 7 8 10 11 12
HOST RANGE: Humans . Chimpanzees
and other non-human primates such as marmosets, tamarins, owl monkeys,
1 3 9 11 12
and Saimiri monkeys are also susceptible to HAV .
MODE OF TRANSMISSION: HAV transmission usually occurs via the faecal-

1 2 4
oral route . The most common reported source of HAV infection is
household or other close contact with an infected person. Other potential
sources of infection include men having sex with men, travel to countries
where HAV is endemic, and from contaminated drugs and needles following
3
illicit drug use . Consumption of contaminated food and water are
infrequent modes of transmission, and transmission by transfusion of blood
3
or blood products is even rarer .
2
INCUBATION PERIOD: Average of 28 to 30 days (range of 15 to 50 days)
3 11 .
COMMUNICABILITY: Maximum infectivity occurs in the latter half of

1 4 11
incubation and continues a few days after the onset of jaundice .
11
Chronic shedding of HAV in faeces does not occur .

1 2 3 11
RESERVOIR: Humans.
ZOONOSIS: None.
VECTORS: None.

DRUG SUSCEPTIBILITY: Triazolo[4,3-b]pyridazine derivatives show antiviral
5
activity against HAV but are not yet used clinically.
SUSCEPTIBILITY TO DISINFECTANTS: HAV is inactivated by 1 % sodium

hypochlorite, formulations of quaternary ammonium compounds and HCl
7 3 4 6
, and 2 % glutaraldehyde .
PHYSICAL INACTIVATION: Inactivation of HAV can be achieved by heating

3 4
to greater than 85°C for 1 minute .
SURVIVAL OUTSIDE HOST: HAV is exceptionally stable at ambient

temperature and at low pH, thus allowing it to survive in the environment
1 9
and to be transmitted via contaminated foods and drinking water .

SURVEILLANCE: A number of techniques have been employed to detect
HAV, including RT- PCR, radioimmunoassay, ELISA, immunoblotting, and dot-
1 2 7 8 10 12
blot gold filtration .
FIRST AID/TREATMENT: No specific treatment for HAV infection has been

2 4
shown to be effective . Bed rest and balanced nutrition are
2
recommended, as is the avoidance of alcohol or other hepatotoxins .
IMMUNIZATION: Several inactivated HAV vaccines have been shown to be

2 4 16
effective (highly immunogenic and safe) .
PROPHYLAXIS: Individuals who are known to have been exposed to HAV

should be administered HAV immune globulin (0.02ml/kg body weight)
1 2 4
within two weeks of the initial exposure . Inactivated HAV
vaccines are highly effective in pre-exposure prophylaxis for laboratory
1
workers and travellers to HAV endemic areas . There is also some
4
evidence for effective post-exposure prophylaxis with HAV vaccine .

LABORATORY-ACQUIRED INFECTIONS: Unknown.
SOURCES/SPECIMENS: Faeces of infected humans and non-human primates

1 2 3 4 9 11 . Other sources/specimens include blood, liver tissue,
1 7 8
and bile .
PRIMARY HAZARDS: Ingestion of biological samples (faeces, blood) infected

with HAV, or indirectly from contact with contaminated environmental
2 6
surfaces .

13

infectious materials, animals, cultures.
14

14
should be strictly limited . Additional precautions should be considered
14
with work involving animals or large scale activities .

cover spill with paper towels and apply suitable disinfectants starting at the
perimeter and working towards the centre. Allow sufficient contact time
14 15
before clean up (30 min) .
DISPOSAL: Decontaminate all materials for disposal by steam sterilization,

14
14
STORAGE: In sealed containers that are appropriately labelled .

and standards.
UPDATED: September 2010.

Canada.

Copyright ©
Canada
REFERENCES:
1 Martin, A., & Lemon, S. M. (2006). Hepatitis A virus: From discovery

to vaccines. Hepatology, 43 (2 SUPPL. 1), S164-S172.
2 Kemmer, N. M., & Miskovsky, E. P. (2000). Hepatitis A. Infectious

Disease Clinics of North America, 14 (3), 605-615.
3 Nainan, O. V., Xia, G., Vaughan, G., & Margolis, H. S. (2006).

Diagnosis of hepatitis A virus infection: A molecular approach.
Clinical Microbiology Reviews, 19 (1), 63-79.
4 Wasley, A., Fiore, A., & Bell, B. P. (2006). Hepatitis A in the era of
vaccination. Epidemiologic Reviews, 28 (1), 101-111.
5 Shamroukh, A. H., & Ali, M. A. (2008). Anti-HAV activity of some

newly synthesised triazolo[4,3- b]pyridazines. Arch. Pharm. Chem.
Life Sci. 341(4):223-230., 4 (223), 230.
6 Mbithi, J. N., Springthorpe, V. S., & Sattar, S. A. (1990). Chemical

disinfection of hepatitis A virus on environmental surfaces. Applied
and Environmental Microbiology, 56 (11), 3601- 3604.
7 Wang, C. -., Tschen, S. -., Heinricy, U., Weber, M., & Flehmig, B.
(1996). Immune response to hepatitis A virus capsid proteins after
infection. Journal of Clinical Microbiology, 34 (3), 707-713.
8 Shao, Z. -., Xu, D. -., Yan, Y. -., Li, J. -., Zhang, J. -., Zhang, Z. -., & Pan,
B. -. (2003). Detection of anti-HAV antibody with dot immunogold
filtration assay. World Journal of Gastroenterology, 9 (7), 1508-1511.
9 McCaustland, K. A., Bond, W. W., Bradley, D. W., Ebert, J. W., &

Maynard, J. E. (1982). Survival of hepatitis A virus in feces after
drying and storage for 1 month. . J. Clin. Microbiol., 16 (5), 957-958.
10 Delem, A. D. (1992). Comparison of modified HAVAB and ELISA for

determination of vaccine-induced Anti-HAV response. Biologicals,
20 (4), 289-291.
11 Heymann, D. L. (2004). An Official Report of the American Public

Health Association. In D. L. Heymann (Ed.), Control of
Communicable Diseases Manual. (18th ed., pp. 35-37). Washington,
D.C.: American Public Health Association.
12 Purcell, R. H., Wong, D. C., & Moritsugu, Y. (1976). A microtiter solid

phase radioimmunoassay for hepatitis a antigen and antibody.
Journal of Immunology, 116 (2), 349-356.


for working with pathogenic and infectious
microorganisms. Current Protocols in Microbiology, (SUPPL. 13),
1A.1.1-1A.1.14.
16 Public Health Agency of Canada. (2018). Canadian Immunization

Guide - Part 4: Active Vaccines. Available at
https://www.canada.ca/en/public-
health/services/publications/healthy-living/canadian-
immunization-guide-part-4-active-vaccines.html?
page=18#approve
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Hepatitis B virus (HBV)

SUBSTANCES
NAME: Hepatitis B virus (HBV).
1 - 11 1
SYNONYM OR CROSS REFERENCE: HBV , hepatitis B , HBV
1 - 3 11 4 12 13
infection , type B hepatitis , serum hepatitis,
4
homologous serum jaundice, Australia antigen hepatitis, and HB .
1 11
CHARACTERISTICS: HBV is a member of the Hepadnaviridae family ,
has a circular DNA genome that is partially double stranded and partly
1 2 4
single stranded, and is 42 nm in diameter . HBV is comprised of a
number of clinically important viral proteins, including the envelope protein,
hepatitis B surface antigen (HBsAg), hepatitis B core antigen (HBcAg), and a
3
soluble nucleocapsid protein, the hepatitis B e antigen (HBeAg) .
2 - 4 10 14 15
Eight genotypes of HBV have been identified (A to H) ,
2 14
that show differential geographical distributions and clinical
14 2
outcomes . For example, genotypes B and C are prevalent in Asia
14 , while A and D are more common in Europe, the Middle East, and India
2 14
, and A and C are the most common in North America .

PATHOGENICITY/TOXICITY: Acute hepatitis B infection: Persons with acute
hepatitis B infection may be asymptomatic or present with a clinical picture
2
varying from mild to severe hepatitis . Persons with symptomatic acute
HBV infections can show signs and symptoms that include nausea,
abdominal pain, vomiting, fever, jaundice, dark urine, changes in stool
colour, and hepatomegaly or splenomegaly as well as signs of liver
1 2 11
dysfunction . The outcome of acute HBV infection is usually
good with complete recovery from any liver damage and seroconversion to
2
anti-HBs, which represents a long-term protection from HBV infection .
Chronic hepatitis B infection: Defined as the persistence of HBsAg for more

1 2 6 11
than 6 months . Persons with chronic HBV infection may be
asymptomatic or may suffer from symptoms such as fatigue, anorexia,
nausea, abdominal discomfort and liver dysfunction. They are at
substantially increased risk for developing chronic liver diseases, including
11
cirrhosis of the liver and primary hepatocellular carcinoma .
2 4 5
EPIDEMIOLOGY: HBV infection is a worldwide health problem . It
is estimated that more than two billion people worldwide have been
infected with HBV, 240 million have chronic HBV infection and 600,000 die
1
each year from HBV-related liver diseases or hepatocellular carcinoma
4 . HBV infection is most prevalent in Asia, Africa, Southern Europe and
Latin America where the prevalence of HBsAg carriers in the general
2
population ranges from 2-20 % . In these areas, HBV infection mainly
occurs in childhood and early infancy. North America, Northern Europe, and
the Oceanic region are low prevalence areas, where HBV infection typically
occurs in adolescence and early adulthood.
1 - 7 9 11
HOST RANGE: Humans are the only known natural host
13 4 9 11
. Chimpanzees are susceptible as an experimental animal
12 16 .
MODE OF TRANSMISSION: HBV is transmitted by percutaneous or mucosal

1 3 4 11
exposure to infected blood or other body fluid . HBV
transmission has been observed with numerous forms of human contact
such as perinatal/mother to child, household (non sexual), sexual, needle
1 4 11
sharing, and occupational/health-care-related .
4
INCUBATION PERIOD: Usually 45–180 days (average 60–90 days) .
HBsAg can appear in as little as 2 weeks, or as long as 6–9 months after
exposure. The variation depends on the amount of virus in the inoculum,
mode of transmission, and host factors.
COMMUNICABILITY: All persons who are HBsAg positive are potentially

infectious, and blood can be infectious for several weeks before the onset of
4
clinical symptoms .

1
RESERVOIR: Humans .
ZOONOSIS: None.
VECTORS: None.

DRUG SUSCEPTIBILITY: Sensitive to antivirals such as interferon-α,
pegylated interferon α-2a, lamivudine, adefovir, entecavir, telbivudine, and
3
tenofovir .
SUSCEPTIBILITY TO DISINFECTANTS: Treatment of HBV diluted in

phosphate buffered saline with 1% non-ionic detergent (Triton X-100) plus
7
0.3% tri-n-butyl-phosphate leads to HBV inactivation . HBV is also
inactivated by formaldehyde, glutaraldehyde, sodium hypochlorite (5,000
ppm available chlorine), quaternary ammonium compounds, and alcohols
8
(70-80%) .
PHYSICAL INACTIVATION: Moist heat at 98°C for 1 minute will partially

13
inactivate HBV in a 1:10 serum dilution . Incubation at 60°C for 10 hours
7
(pasteurisation) will also inactivate HVB .
SURVIVAL OUTSIDE HOST: HBV can survive and remain infectious on

17
environmental surfaces for at least 7 days .

SURVEILLANCE: Monitor for symptoms. Demonstration in sera of specific
HB antigens and/or antibodies (HBsAg, anti-HBs, HBeAg, anti-HBe, and anti-
HBc) using enzyme immunoassay techniques (e.g. ELISA) confirm diagnosis
15 12 2 6
. Other tests include radioimmunoassay , PCR , real-time
6
PCR, and non-PCR based DNA assays .
FIRST AID/TREATMENT: Following exposure to HBV the affected area

should be washed immediately with soap and water. Mucous membranes
10
and conjunctivae should be irrigated thoroughly with water . If the
material involved is known to contain HBV or be positive for HBsAg then
hepatitis B immunoglobulin (HBIG) should be given, ideally within 48 hours
18
of exposure .
Seven drugs are licensed in the United States for treatment of HBV infection:
interferon-α, pegylated interferon α-2a, lamivudine, adefovir, entecavir,
3
telbivudine, and tenofovir .
4
IMMUNISATION: Effective HB vaccines are available . Vaccination
10
against HBV should now be the norm in laboratory personnel .
PROPHYLAXIS: Previously unimmunised adults exposed to HBsAg positive

blood should receive HBIG as soon as possible as well as immunization with
4 10
HB vaccine unless natural immunity can be confirmed .

LABORATORY-ACQUIRED INFECTIONS: The rates of HBV infection have
been reported to be several times greater in laboratory staff than the
general population and is one of the most frequently reported laboratory
10
acquired infection .
1 - 12
SOURCES/SPECIMENS: Blood , cerebrospinal fluid, saliva, semen,
4 12
synovial fluid , breast milk, bile, faeces, nasopharyngeal washings,
12
sweat , peritoneal, pleural, pericardial, amniotic, and unfixed tissues
4
and organs .
PRIMARY HAZARDS: Percutaneous (e.g. needlestick) or mucous membrane

4
exposures to blood that might contain HBsAg .
SPECIAL HAZARDS: There is a potential for infection via aerosols and HBV
10
contaminated surfaces .

19

infectious material, animals, or cultures.
20

20

20

20

20
that are appropriately labeled .

and standards.
UPDATED: 2021
PREPARED BY: Centre for Biosecurity , Public Health Agency of Canada.

Copyright ©
Canada
REFERENCES:
1 Shepard, C. W., Simard, E. P., Finelli, L., Fiore, A. E., & Bell, B. P.
(2006). Hepatitis B virus infection: Epidemiology and vaccination.
Epidemiologic Reviews, 28(1), 112-125.
2 Chang, M. H. (2007). Hepatitis B virus infection. Semin. Fetal

Neonatal Med. 12(3):160-167., 12(3), 160.
3 Dienstag, J. L. (2008). Hepatitis B virus infection. N. Engl. J. Med.,

359(14), 1486-1500.
4 Spradling, P. R. (2016). Hepatitis, Viral. In D. L. Heymann (Ed.),

Control of Communicable Diseases Manual. (20th ed., pp. 257-264).
American Public Health Association.
5 Chu, C. -., Keeffe, E. B., Han, S. -., Perrillo, R. P., Min, A. D., Soldevila-
Pico, C., Carey, W., Brown Jr., R. S., Luketic, V. A., Terrault, N., & Lok,
A. S. F. (2003). Hepatitis B virus genotypes in the United States:
Results of a nationwide study. Gastroenterology, 125(2), 444-451.
6 Servoss, J. C., & Friedman, L. S. (2006). Serologic and molecular

diagnosis of hepatitis B virus. Infectious Disease Clinics of North
America, 20(1), 47-61.
7 Hilfenhaus, J., Gröner, A., Nowak, T., & Weimer, T. (1997). Analysis
of human plasma products: Polymerase chain reaction does not
discriminate between live and inactivated viruses. Transfusion,
37(9), 935-940.
8 Sattar, S. A., Tetro, J., Springthorpe, V. S., & Giulivi, A. (2001).

Preventing the spread of hepatitis B and C viruses: Where are
germicides relevant? American Journal of Infection Control, 29(3),
187-197.
9 Bond, W. W., Favero, M. S., Petersen, N. J., Gravelle, C. R., Ebert, J.

W., & Maynard, J. E. (1981). Survival of hepatitis B virus after drying
and storage for one week. Lancet, 1(8219), 550-551.

11 Mahoney, F. J. (1999). Update on diagnosis, management, and

prevention of hepatitis B virus infection. Clinical Microbiology
Reviews, 12(2), 351-366.
12 Bond, W. W., Petersen, N. J., & Favero, M. S. (1977). Viral hepatitis

B: aspects of environmental control. Health Laboratory Science,
14(4), 235-252.
13 Krugman, S., Overby, L. R., & Mushahwar, I. K. (1979). Viral

hepatitis, type B. Studies on natural history and prevention re-
examined. New England Journal of Medicine, 300(3), 101-106.
14 Chu, C. -., Keeffe, E. B., Han, S. -., Perrillo, R. P., Min, A. D., Soldevila-
Pico, C., Carey, W., Brown Jr., R. S., Luketic, V. A., Terrault, N., & Lok,
A. S. F. (2003). Hepatitis B virus genotypes in the United States:
Results of a nationwide study. Gastroenterology, 125(2), 444-451.
15 Servoss, J. C., & Friedman, L. S. (2006). Serologic and molecular

diagnosis of hepatitis B virus. Infectious Disease Clinics of North
America, 20(1), 47-61.
16 Sattar, S. A., Tetro, J., Springthorpe, V. S., & Giulivi, A. (2001).

Preventing the spread of hepatitis B and C viruses: Where are
germicides relevant? American Journal of Infection Control, 29(3),
187-197.
17 Bond, W. W., Favero, M. S., Petersen, N. J., Gravelle, C. R., Ebert, J.

W., & Maynard, J. E. (1981). Survival of hepatitis B virus after drying
and storage for one week. Lancet, 1(8219), 550-551.

Guide Seventh Edition - 2006 - Part 4: Active Immunizing Agents.
Retrieved 11/24, 2010, from http://www.phac-
aspc.gc.ca/publicat/cig-gci/p04-rabi-rage-eng.php#approve

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Human immunodeficiency virus
(HIV)

Substances
Section I - Infectious Agent
NAME: Human immunodeficiency virus (HIV).
SYNONYM OR CROSS REFERENCE: HIV, acquired immune deficiency

1 - 20
syndrome, AIDS . Was previously known as lymphadenopathy-
associated virus, human T-lymphotropic virus type III (HTLV-III),
1- 20
immunodeficiency-associated virus, and AIDS-associated retrovirus .
CHARACTERISTICS: HIV is a member of the Retroviridae family, genus

14 16
Lentivirus . HIV is an icosahedral, enveloped virus, of approximately
100 to 110 nm in diameter, and has a single-stranded, linear, positive-sense
14 16 11
RNA genome . HIV has two recognised strains: HIV-1 and HIV-2
16 17 . Upon entry into the host cell, retroviral RNA is converted to DNA
by a virally encoded reverse transcriptase enzyme, the DNA transcript is
14
integrated into the host's chromosomal DNA .
Section II - HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: AIDS is characterised by symptoms and
infections caused by the breakdown of the immune system (by destruction
10 12
or functional impairment of CD4 receptors) due to HIV infection .
HIV can infect many cell types, mainly lymphocytes, but also macrophages,
and microglia in the brain, and other neurological cells, resulting in
profound asthenia, dementia and damage to the peripheral nervous system
12 . Due to immunodeficiency, patients succumb to various fungi,
10
parasites, bacteria, and/or viruses and are prone to certain tumours
12 . Globally, Mycobacterium tuberculosis is the most common cause of
death of HIV-infected individuals. The clinical features of HIV infection vary
6
depending on the stage of the disease . Acute infection is accompanied
by non-specific "flu-like" and "mononucleosis-like" symptoms such as
myalgia, arthralgia, diarrhoea, nausea, vomiting, headache,
6 16 21
hepatosplenomegaly, weight loss, and neurological symptoms .
Early-stage disease refers to the period of clinical latency between the time
of the primary infection and the development of symptoms indicative of
advanced immunodeficiency. Typically, when the patient's CD4+ T-cell count
falls below 500 cells/µL, syndromes indicative of depressed cell mediated
immunity can appear. Examples include orophayngeal and recurrent
vulvovaginal candidiasis, bacillary angiomatosis, recurrent or
multidermatomal herpes zoster, listeriosis, infections due to Rhodococcus
equi, pelvic inflammatory disease, oral hairy leukoplakia associated with
Epstein-Barr virus, cervical dysplasia, long lasting diarrhoea, idiopathic
21
thrombocytopenic purpura, and peripheral neuropathy . Late-stage
disease refers to the period when the patient's CD4+ T-cell count falls below
10 21
200 cells/µL . The loss of the integrity of cell-mediated immune
responses allows ubiquitous environmental organisms with limited virulence
6
to become life threatening pathogens . Examples of conditions (as set
out by the US Centers for Disease Control and Prevention) include
candidiasis of bronchi, trachea, lungs or oesophagus, invasive cervical
cancer, coccidioidomycosis, cryptococcosis, cryptosporidiosis,
cytomegalovirus disease (other than liver, spleen, or nodes),
cytomegalovirus retinitis (with loss of vision), HIV-related encephalopathy,
herpes simplex, histoplasmosis, isosporiasis, Kaposi's sarcoma, Burkitt's
lymphoma, immunoblastic lymphoma, primary lymphoma of the brain,
Mycobacterium avium complex, Mycobacterium tuberculosis, Pneumocystis
jirovecii pneumonia, recurrent pneumonia, progressive multifocal
leukoencephalopathy, recurrent salmonella septicaemia, toxoplasmosis of
21
the brain, and wasting syndrome due to HIV .
EPIDEMIOLOGY: HIV is a major global problem with approximately 25

million HIV-related deaths and another 40.3 (36 to 45.3) million infected
17
individuals worldwide . AIDS was first described in 1981. The new
retrovirus (HIV-1) was found in tissues from AIDS patients in 1983 and the
3
causative relationship between HIV and AIDS was established in 1984
12 . HIV-2 was discovered in 1986 and is the least pathogenic form of HIV,
4
displaying low rates of transmission and rarely causing AIDS . The
majority of people with HIV live in the developing world (approximately 95%
of the individuals infected worldwide). Sub-Saharan Africa is by far the
10
worst-affected area in the world . This region has slightly more than 10%
of the world's population but is home to more than 60% of the total
10
population living with HIV/AIDS .
Globally, infants who acquire the disease from their mothers constitute
10
about 11% of all HIV infections . Ten percent of infections worldwide are
associated with injection drug use; 5 to 10% are transmitted by sex between
10
men; and 5 to 10% occur in health care settings . The predominant
means of infection is sex between men and women, which accounts for
nearly two thirds of new infections, and 85% of existing infections worldwide
10 17 . About 50% of all new HIV infections worldwide occur in individuals
10
younger than 25 years old .
3- 6 8 10- 13 15- 17 20- 23
MODES OF TRANSMISSION: HIV is transmitted either by exposure of the

virus to oral, rectal, or vaginal mucosa during sexual activity; by
intravascular inoculation through transfusion of contaminated blood
products; by using contaminated equipment during injection drug use; or
6 16
from mother to infant during pregnancy, delivery or breastfeeding .
There are no obvious differences in disease manifestations in individuals
6
infected by mucosal versus blood-borne routes . Sexual transmission
6 16
accounts for more than 90% of HIV infections worldwide .
INCUBATION PERIOD: Variable. Commonly the time from infection to the

development of detectable antibodies is generally 1 to 3 months; however,
the time from HIV infection to diagnosis of AIDS had an observed range of
11
less than 1 year to 15 years or longer .
COMMUNICABILITY: The highest levels of per-act risk for HIV transmission

from person-to-person are: blood transfusion from an infected donor,
needle sharing by infected injection-drug users, receptive anal intercourse,
6 11 12 20
and percutaneous needle injuries . Insertive anal
intercourse, penile-vaginal exposures, and oral sex represent substantially
6 11 20
less per-act risk . HIV can also be passed from mother to child in
6 11
utero (vertical) as well as during childbirth, and from breast milk .
HIV has also been documented to have been transmitted by bite injuries
22 .The period of communicability begins early after HIV infection and is
11
thought to last throughout the life of the infected individual .
Infectiousness is related to viral load.
Section III - DISSEMINATION

6 8 10- 12 16 17 22
RESERVOIR: Humans .
ZOONOSIS: None, although current evidence suggests that HIV-1 and HIV-2
entered into the human population through multiple zoonotic infections
17
from simian immunodeficiency virus-infected non-human primates .
VECTORS: No laboratory or epidemiological evidence suggests that biting

11 16
insects have transmitted HIV infection .
Section IV – STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: Antiretroviral agents from 5 drug classes are
currently available to treat HIV infection, namely: the nucleoside reverse
transcriptase inhibitors (NRTIs), nucleotide reverse transcriptase inhibitors
(NtRTIs), non-nucleoside reverse transcriptase inhibitors (NNRTIs),
10 15
proteinase inhibitors (PIs), and fusion inhibitors .
SUSCEPTIBILITY TO DISINFECTANTS: HIV is susceptible to fresh 2%

glutaraldehyde, 2% Jodopax (detergent and iodine), hypochlorite, iodine,
7 9
phenolics, and to a lesser extent 70% ethanol, NaOH and isopropanol
18 .
PHYSICAL INACTIVATION: HIV is inactivated by ultraviolet (UV) light;

however, the level of the inactivation is heavily influenced by the proximity
of the UV source to the sample and the concentration of protein in the
sample environment. HIV is easily inactivated in a cell free medium;
however, in cell associated samples and blood samples complete
7
inactivation requires much longer exposures to the UV source . HIV is
18
also inactivated at pH higher or lower than the optimal level of 7.1 .A
temperature of 60°C for 30 minutes will likely inactivate HIV; however,
higher temperatures and incubations may be required depending on the
18
initial titre of the virus .
SURVIVAL OUTSIDE HOST: HIV can remain viable in blood in syringes at

room temperature for 42 days, and in blood and cerebrospinal fluid from
1 2
autopsies for up to 11 days . Although drying in the environment is
known to cause a rapid reduction in HIV concentration, under experimental
conditions, Cell-free HIV dried onto a glass coverslip in 10% serum can
19
survive for longer than 7 days, depending on the initial titre .
Section V - FIRST AID / MEDICAL

SURVEILLANCE: HIV is diagnosed by tests that assess whether an
individual's immune system has produced an HIV-specific immune response
16 . Common tests include the indirect binding assay, antibody capture
assay, the double antigen sandwich, ELISA, immunofluorescence, Western
16
blotting, line immunoassays, and PCR, as well as viral isolation .
FIRST AID/TREATMENT: AIDS must be managed as a chronic disease.

Antiretroviral treatment is complex, involving a combination of drugs and
11
resistance will appear rapidly if only a single drug is used . The 5
available classes of antiretroviral drugs, NRTIs, NtRTIs, NNRTIs, PIs and
fusion inhibitors, can be combined to provide highly active antiretroviral
therapy (HAART). For many (but not all) patients, HAART converts an
inexorably fatal disease into a chronic disease with a fairly good prognosis
8 13 .
IMMUNIZATION: None.
PROPHYLAXIS: HIV postexposure prophylaxis regimens are based on the

nature of the exposure. The majority of HIV exposures will warrant a two
drug regimen, using 2 NRTIs or 1 NRTI and 1 NtRTI. Combinations include:
zidovudine (ZDV) and lamivudine (3CT) or emtricitabine (FTC); stavudine
15
(d4T) and 3TC or FTC; and tenofovir (TDF) and 3TC or FTC .
The addition of a third or fourth drug should be considered for exposures

that pose an increased risk of transmission. The preferred drugs in this case
15 16
are proteinase inhibitors such as lopinavir/ritonavir (LPV/RTV) .
Section VI - LABORATORY HAZARD

LABORATORY-ACQUIRED INFECTIONS: Although there have been many
reported cases of HIV infection through occupational transmission, the
numbers of laboratory acquired infections are low. As of 2001, there have
been a total of 57 cases of documented occupationally acquired HIV among
24
U.S. health care workers .
SOURCES/SPECIMENS: Blood, semen, vaginal secretions, cerebrospinal

fluid, synovial fluid, peritoneal fluid, pleural fluid, pericardial fluid, amniotic
fluid, other specimens containing visible blood, breast milk, unscreened or
11 15
inadequately treated blood products, and infected human tissues
16 .
Faeces, nasal secretions, sputum, sweat, vomitus, saliva, tears, and urine, are
11 15
not considered potentially infectious unless they are visibly bloody .
PRIMARY HAZARDS: Needlestick, contaminated sharp objects, and/or direct

contact of non-intact skin or mucous membranes with HIV-infected
15 16
specimens/tissues .
SPECIAL HAZARDS: Extreme care must be taken to avoid spilling and/or

splashing infected materials. HIV should be presumed to be in/on all
25
equipment and devices coming in direct contact with infected materials .
Section VII - EXPOSURE CONTROLS / PERSONAL PROTECTION

26
CONTAINMENT REQUIREMENTS: Please refer to the Biosafety Directive for

Human Immunodeficiency Virus (HIV) and Human T-cell Lymphotropic Virus
Type 1 (HTLV-1).
PROTECTIVE CLOTHING: Solid-front gowns with tight-fitting wrists, gloves,

and respiratory protection should be worn over laboratory clothing when
25
infectious materials are directly handled .

safety cabinet. The use of needles, syringes, and other sharp objects should
be strictly limited. Open wounds, cuts, scratches, and grazes should be
covered with waterproof dressings. Additional precautions should be
25
considered with work involving animals or large scale activities .
Section VIII - HANDLING AND STORAGE

gently cover the spill with paper towels and apply 1% sodium hypochlorite
25

25
STORAGE: Infectious material should be stored in sealed, leak-proof

25
containers that are appropriately labelled .
Section IX - REGULATORY AND OTHER INFORMATION

and standards.
PREPARED BY: Centre for Biosecurity, Public Health Agency of Canada.

Copyright©
Canada
REFERENCES:
1 Abdala, N., Reyes, R., Carney, J. M., & Heimer, R. (2000). Survival of
HIV-1 in syringes: Effects of temperature during storage.
Substance use and Misuse, 35(10), 1369-1383.
2 Ball, J., Desselberger, U., & Whitwell, H. (1991). Long-lasting

viability of HIV after patient's death [30]. Lancet, 338(8758), 63.
3 Barre Sinoussi, F., Chermann, J. C., & Rey, F. (1983). Isolation of a T-

lymphotropic retrovirus from a patient at risk for acquired
immune deficiency syndrome (AIDS). Science, 220(4599), 868-871.
4 Clavel, F., Guétard, D., Brun-Vézinet, F., Chamaret, S., Rey, M.,
Santos-Ferreira, M. O., Laurent, A. G., Dauguet, C., Katlama, C.,
Rouzioux, C., Klatzmann, D., Champalimaud, J. L., & Montagnier, L.
(1986). Isolation of a new human retrovirus from West African
patients with AIDS. Science, 233(4761), 343-346.
5 Coffin, J., Haase, A., Levy, J. A., Montagnier, L., Oroszlan, S., Teich,
N., Temin, H., Toyoshima, K., Varmus, H., & Vogt, P. (1986). What to
call the AIDS virus? Nature, 321(6065), 10.
6 Cohen, O. J., & Fauci, A. S. (2001). Pathogenesis and Medical

Aspects of HIV-1 infection. In D. M. Knipe, & P. M. Howley (Eds.),
Fields Virology (pp. 2043-2094). Philadelphia, PA.: Lippencott-Raven.
7 Druce, J. D., Jardine, D., Locarnini, S. A., & Birch, C. J. (1995).

Susceptibility of HIV to inactivation by disinfectants and ultraviolet
light. Journal of Hospital Infection, 30(3), 167-180.
8 Greene, W. C. (2007). A history of AIDS: Looking back to see ahead.

European Journal of Immunology, 37(SUPPL. 1), S94-S102.
9 Hansen, P. J. (1989). Chemical inactivation of HIV on surfaces. BMJ

(Clinical Research Ed.), 299(6693), 260.
10 Harris, A., & Bolus, N. E. (2008). HIV/AIDS: an update. Radiologic

Technology, 79(3), 243-252; quiz 253-255.

12 Kallings, L. O. (2008). The first postmodern pandemic: 25 Years of

HIV/AIDS. Journal of Internal Medicine, 263(3), 218-243.
13 Kempen, J. H. (2008). Medical management of human

immunodeficiency virus infection. Indian Journal of Ophthalmology,
56(5), 385-390.
14 Knipe, D. M., & Howley, P. M. (Eds.). (2001). Fields Virology (4th ed.).
Philidelphia: Lippincot Williams & Wilkins.
15 Panlilio, A. L., Cardo, D. M., Grohskopf, L. A., Heneine, W., & Ross,
C. S. (2005). Updated U.S. Public Health Service guidelines for the
management of occupational exposures to HIV and
recommendations for postexposure prophylaxis.
MMWR.Recommendations and Reports: Morbidity and Mortality
Weekly Report.Recommendations and Reports / Centers for Disease
Control, 54(RR-9), 1-17.
16 Schupbach, J. (2003). Human Immunodeficiency virus. In P. R.

Murray, E. J. Baron, J. H. Jorgensen, M. A. Pfaller & R. H. Yolken
(Eds.), Manual of Clinical mircrobiology (8th ed., pp. 1253-1281).
Washinton, DC: ASM press.
17 Takebe, Y., Uenishi, R., & Li, X. (2008). Global Molecular

Epidemiology of HIV: Understanding the Genesis of AIDS Pandemic
18 Tjotta, E., Hungnes, O., & Grinde, B. (1991). Survival of HIV-1

activity after disinfection, temperature and pH changes, or drying.
Journal of Medical Virology, 35(4), 223-227.
19 Van Bueren, J., Simpson, R. A., Jacobs, P., & Cookson, B. D. (1994).
Survival of human immunodeficiency virus in suspension and
dried onto surfaces. Journal of Clinical Microbiology, 32(2), 571-574.
20 Varghese, B., Maher, J. E., Peterman, T. A., Branson, B. M., &

Steketee, R. W. (2002). Reducing the risk of sexual HIV
transmission: Quantifying the per-act risk for HIV on the basis of
choice of partner, sex act, and condom use. Sexually Transmitted
Diseases, 29(1), 38-43.
21 1993 revised classification system for HIV infection and expanded

surveillance case definition for AIDS among adolescents and
adults. (1992). MMWR.Recommendations and Reports: Morbidity and
Mortality Weekly Report.Recommendations and Reports / Centers for
Disease Control, 41(RR-17), 1-19.
22 Vidmar, L., Poljak, M., Tomazic, J., Seme, K., & Klavs, I. (1996).
Transmission of HIV-1 by human bite [2]. Lancet, 347(9017), 1762-
1763.
23 Collins, C. H., & Kennedy, D. A. (Eds.). (1983). Laboratory-acquired

Infections (4th ed.). Oxford: Butterworth-Heinermann.
24 Do, A. N., Ciesielski, C. A., Metler, R. P., Hammett, T. A., Li, J., &
Fleming, P. L. (2003). Occupationally acquired human
immunodeficiency virus (HIV) infection: national case surveillance
data during 20 years of the HIV epidemic in the United States.
Infection Control and Hospital Epidemiology: The Official Journal of
the Society of Hospital Epidemiologists of America, 24(2), 86-96.
doi:10.1086/502178


2009, (2009).
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Measles virus

SUBSTANCES
NAME: Measles virus
SYNONYM OR CROSS REFERENCE: MV, measles, morbilli, rubeola,

pneumonia, measles inclusion body encephalitis, encephalomyelitis, atypical
measles, subacute sclerosing panencephalitis, red measles, 5 or 10-day
1 3
measles, hard measles .
CHARACTERISTICS: Measles virus is a negative-sense, single stranded RNA

1
virus, which belongs to morbillivirus genus in the Paramyxoviridae family .
It cnsists of a helical nucleocapsid, 100-300 nm in diameter, surrounded by
an envelope. The envelope is lined by matrix proteins and carries
transmenbrane hemaglutinin and fusion glycoproteins which are the
virulence factors.

PATHOGENICITY/TOXICITY: The Measles virus may cause measles, a
systemic infection starting in the respiratory epithelium of the nasopharynx
3 4 . Measles may lead to severe complication and can cause death.
After an incubation period of 8-12 days, fever (approximately 38.3°C) and
3
malaise develop over 24 hours . These symptoms are followed by cough,
coryza (inflammation of the nasal mucous membranes) and conjunctivis.
After 2-3 days of cough, coryza and conjunctivitis, Koplik spots (white and
granular lesions in the lateral buccal mucosa) appear. On the forth day, a
macropapular rash appears on the head and neck, behind the ears. The rash
then spreads to the rest of the body and persists for 3-5 days before fading
2 5
. Other symptoms include anorexia and dyspnea . Subjective
3
improvement can begin 2-4 days after the rash first appears . Infants,
pregnant women, immunocompromised and malnourished patients are at a
greater risk of developing complications, and experience more severe illness
3 4 . Historically, males have had a higher mortality rate than females,
but this difference has tended to decrease with modernization of healthcare
in western countries. Common complications include bacterial
superinfection, which results in otitis media (middle ear infection),
bronchitis, croup and pneumonia (3.5-50% cases), lymphadenopathy,
3
diarrhea and encephalitis (1 in 1,000 cases) . Pneumonia is the main
cause of mortality. Encephalitis may result in coma and brain damage (25%)
or death (15%). Rarer complication includes thrombocytopenic purpura,
myocarditis, subacute sclerosing panencephalitis, abdominal pain and acute
appendicitis. During pregnancy, measles results in increased risk of
spontaneous abortion and preterm birth. In industrialized countries, the
4
fatality rate is 1-2 per 1,000 cases , while is it 15-25% in developing
2
countries . People vaccinated with killed vaccine (used between 1963 and
1968 and abandoned because protection was too short) or who receive
immunoglobulin as a prophylactic measure 6 days after infection may
4
develop atypical measles . They may experience higher fever, prominent
rash (often with petechia) on the extremities, and are at a greater risk of
developing pneumonia.
EPIDEMIOLOGY: Before vaccine introduction in 1963 in United States, 130

million cases and 7-8 million deaths were estimated to be due to measles
4 6
and 95-98% of children were infected . Endemic in metropolitan
centers, measles became epidemic every 2-3 years primarily in late winter
and early spring and spread by waves to smaller cities and rural area, where
1 7
it was more severe . Mortality declined in the first half of twentieth
century due to life quality improvement. In the 1960's, vaccine introduction
allowed substantial reduction of both incidence and mortality due to
measles. Resurgence of disease in 1989-1991 was due to low vaccination
4
coverage amongst certain populations in industrialized countries .
Measles is considered eliminated in the Americas and Europe, however
occasional outbreaks occur due to imported cases and unvaccinated
6
populations . Measles is still a common disease in developing countries
1 .
HOST RANGE: Humans are the primary host, but non-human primates can
6 8
also be a host, and measles is a threat to their conservation .
9
INFECTIOUS DOSE: 0.2 units by intranasal spray .
MODE OF TRANSMISSION: Measles can be spread by respiratory droplets

and by direct contact with secretions from nose and throat of an infected
7 8
person . Direct contact is the primary mode of transmission, and
airborne droplet and indirect contact are less common modes of
transmission.
3
INCUBATION PERIOD: 8-12 days .
3
COMMUNICABILITY: Measles is a highly communicable disease .
Patients are infectious from the onset of prodomal symptoms until 2-4 days
after rash development, but communicability is higher before rash
appearance.

4 6
RESERVOIR: The only known reservoir is human . Even if non-human
primates can be infected, the overall population is estimated to be too low
10
to maintain transmission .
11
ZOONOSIS: None known , but humans may communicate the disease
to non-human primates.
VECTORS: None.

DRUG SUSCEPTIBILITY: Measles virus has been reported to be susceptible
to Ribavirin, but it is not currently approved for therapeutic use against
12
measles .
SUSCEPTIBILITY TO DISINFECTANTS: MV is susceptible to povidone iodine,

formaldehyde, 1% sodium hypochlorite, 70% ethanol, glutaraldehyde,
13 15
phenolic disinfectants, peracetic acid, hydrogen peroxide , .
PHYSICAL INACTIVATION: Heat (30 min at 56°C), UV light, acidic pH, and
7 10 16
trypsin , .
SURVIVAL OUTSIDE HOST: Agent may survive less than 2 hours on surfaces
7
or objects . Respiratory droplets can remain infective for at least 1 hour
17
in a close space .

SURVEILLANCE: Monitor for symptoms, microbiological and serological
3
testing for measles virus or anti-measles antibodies .
FIRST AID/TREATMENT: There is currently no treatment for measles other

than supportive care. In cases of malnourishment or vitamin A deficiency,
12
vitamin A may be prescribed to help avoid complications .
IMMUNIZATION: There is a trivalent vaccine using live-attenuated virus of

measles, mumps and rubella (MMR), but this vaccine requires constant cold
3
for storage and transport, which is a problem in developing countries
10 21 . The first dose is given in the first year, and the second at the
6 21
beginning of schooling (4-6 years of age) to allow full coverage . In
Canada, vaccination is also recommended for all people born after 1957,
because first generation killed vaccine was poorly immunogenic. Before
1957, most people had contracted measles and are considered immune.
3 21
Pregnant women should not take MMR .
PROPHYLAXIS: Immunization with live virus vaccine can be given up to 72

hours post-exposure to prevent measles in unvaccinated persons. Passive
immunization with measles immunoglobulin (0.25 mL/kg, for a maximum of
15 mL) between 72 hours and 6 days following exposure or in persons for
which measles vaccine is contraindicated can be given to prevent or
3
decrease the severity of measles .
SECTION VI - LABORATORY HAZARD

LABORATORY-ACQUIRED INFECTIONS: One case of a laboratory acquired
11
infection up to 1974 .
SOURCES/SPECIMENS: MV may be isolated from urine, conjunctiva,

18
nasopharynx, and blood .
PRIMARY HAZARDS: Splashing, accidental parenteral inoculation and

droplet exposure of mucous membrane may cause a laboratory-acquired
13 21
infection .

19

20

20

time before clean up.



and standards.
UPDATED: September 2011

Canada.

Copyright ©
Canada
REFERENCES:
1 Griffin, D. E. (2007). Measles virus. In D. M. Knipe, P. M. Howley, D.
E. Griffin, R. A. Lamb, M. A. Martin, B. Roizman & S. E. Straus (Eds.),
Fields Virology (pp. 1551-1585). Philadelphia: Wolters Kluwer Health
and lippincott Williams & Wilkins.
2 Ray, C. G. (2004). Mumps virus, Measles, Rubella, and other

Childhood Exanthems. In K. J. Ryan, & C. G. Ray (Eds.), Sherris
Medical Microbiology (4th ed., pp. 513-539). United State of
America: McGraw-Hill.
3 Signore, C. (2001). Rubeola. Primary Care Update for Ob/Gyns, 8(4),

138-140. doi:DOI: 10.1016/S1068-607X(01)00073-7
4 Perry, R. T., & Halsey, N. A. (2004). The clinical significance of

measles: a review. The Journal of Infectious Diseases, 189 Suppl 1,
S4-16. doi:10.1086/377712
5 Shimatsu, Y., & Fujimori, K. (1999). Pulmonary complications in

adult measles. Kansenshogaku Zasshi.the Journal of the Japanese
Association for Infectious Diseases, 73(7), 640-645.
6 Moss, W. J. (2009). Measles control and the prospect of

eradication. Current Topics in Microbiology and Immunology, 330,
173-189.
7 Centers for Disease Control and Prevention. (2009). In Atkinson

W., Wolfe S., Hamborsky J. and McIntyre L. (Eds.), Epidemiology and
Prevention of Vaccine-Preventable Diseases (11th ed.). Washington
D.C.: Public Health Foundation.
8 Jones-Engel, L., Engel, G. A., Schillaci, M. A., Lee, B., Heidrich, J.,
Chalise, M., & Kyes, R. C. (2006). Considering human-primate
transmission of measles virus through the prism of risk analysis.
American Journal of Primatology, 68(9), 868-879.
doi:10.1002/ajp.20294
9 Knudsen, R. C. (2001). Risk assessment for working with infectious

agents in the biological laboratory. Applied Biosafety, 6, 19-26.
10 Moss, W. J., & Griffin, D. E. (2006). Global measles elimination.

Nature Reviews.Microbiology, 4(12), 900-908.
doi:10.1038/nrmicro1550
11 Sewell, D. L. (1995). Laboratory-associated infections and

biosafety. Clinical Microbiology Reviews, 8(3), 389.
12 Plemper, R. K., & Snyder, J. P. (2009). Measles control--can measles

virus inhibitors make a difference? Current Opinion in
Investigational Drugs (London, England: 2000), 10(8), 811-820.

14 Cardoso, A. I., Beauverger, P., Gerlier, D., Wild, T. F., & Rabourdin-
Combe, C. (1995). Formaldehyde inactivation of measles virus
abolishes CD46-dependent presentation of nucleoprotein to
murine class I-restricted CTLs but not to class II-restricted helper T
cells. Virology, 212(1), 255-258. doi:10.1006/viro.1995.1479
15 Kawana, R., Kitamura, T., Nakagomi, O., Matsumoto, I., Arita, M.,
Yoshihara, N., Yanagi, K., Yamada, A., Morita, O., Yoshida, Y.,
Furuya, Y., & Chiba, S. (1997). Inactivation of human viruses by
povidone-iodine in comparison with other antiseptics.
Dermatology (Basel, Switzerland), 195 Suppl 2, 29-35.
16 Tu, R. (2005). UV-inactivated measles virus stimulates human mice

naive lymphocytes to proliferate in vitro. Journal of Medical
Virology, 46(2), 133-137.
17 Bloch, A. B., Orenstein, W. A., Ewing, W. M., Spain, W. H., Mallison,

G. F., Herrmann, K. L., & Hinman, A. R. (1985). Measles outbreak in
a pediatric practice: airborne transmission in an office setting.
Pediatrics, 75(4), 676.
18 Murray, P. R., Baron, E. J., Jorgensen, J. H., Landry, M. L., Pfaller, M.

A., & Yolken, R. H. (Eds.). (2003). Manual of Clinical Microbiology (8th
ed.). Herdon, VA, United States of America: American Society for
Microbiology.

2009, (2009).


page=18#approve
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 
Pathogen Safety Data Sheet: Infectious

substances - Middle east respiratory syndrome
(MERS)-related Coronavirus
On this page
More information
Section I - Infectious agent
Characteristics
Section II - Hazard identification
Host range
Section III - Dissemination
Section IV - Stability and viability
Section V - First aid/medical
Section VI - Laboratory hazards
Section VII - Exposure controls/personal protection
Section VIII - Handling and storage
Section IX - Regulatory and other information
References
More information
For more information on MERS-CoV, see the following:
Biosafety advisories/notifications/directives: MERS-CoV Biosafety

Advisory July 7, 2015
Infection Control Guideline Series: Infection Prevention and Control
Guidance for Middle East Respiratory Syndrome Coronavirus (MERS-
CoV) in Acute Care Settings
Travel Health and Safety: Middle East Respiratory Syndrome
Coronavirus (MERS-CoV) in Middle East
Government of Canada Diseases and Conditions facts: Middle East
respiratory syndrome (MERS)
Other: Summary of Assessment of Public Health Risk to Canada
Associated with Middle East Respiratory Syndrome Coronavirus (MERS-
CoV), July 13, 2017

Name: Middle East respiratory syndrome (MERS)-related coronavirus
Agent type: Virus
Taxonomy
Family: Coronaviridae
Genus: Betacoronavirus
Species: Middle East respiratory syndrome-related coronavirus
Synonym or cross reference: Formerly Human coronavirus Erasmus

1 2
medical centre (HCoV-EMC/2012) . Also known as MERS-CoV, MERS,
2 3
and novel coronavirus (nCoV) .
Characteristics
Brief Description: MERS-CoV is the sixth coronavirus identified with the
ability to infect humans. First isolated in 2012, the virus was recognized as
the first human coronavirus in lineage C of the Betacoronavirus genus. The
closest genetic relatives to MERS-CoV are coronaviruses HKU4 and HKU5,
which were isolated from Tylomycteris pachypus and Pipistrellus abramus bats
1 . MERS-CoV is an enveloped, positive-sense, single-stranded RNA virus
that encodes 5 unique accessory proteins, including 4A and 4b, which
modulate interferon production. In contrast to Severe Acute Respiratory
Syndrome-related coronavirus (SARS-CoV), which uses angiotensin-
converting enzyme 2 (ACE2) as its receptor, MERS-CoV mediates cell entry
using the host receptor dipeptidyl peptidase 4 (DPP4). Whereas SARS-CoV
underwent extensive mutation to adapt to the human ACE2 protein, there is
no evidence to suggest that MERS-CoV has adapted to human DPP4. The
DPP4 receptor is expressed in respiratory tract cells but, due to the low
abundance in the upper respiratory tract, human-to-human transmission of
the virus may be limited. Consequently, MERS-CoV is not considered to be as
2
infectious in humans relative to SARS-CoV .
Properties: The evolutionary rate for the coding region of the MERS-CoV
viral genome is estimated to be 1.12 X 10-3 substitutions per site per year;
however, there is limited evidence of adaptation to human transmission in
4
MERS-CoV lineages .

Pathogenicity and toxicity: Clinical symptoms of MERS-CoV infection in
humans range from asymptomatic or mild respiratory illness in the upper
respiratory tract to severe acute pneumonia. A rapid progression to acute
lung injury and acute respiratory distress syndrome, followed by septic
shock, multi-organ failure and death has been reported. Patients experience
flu-like symptoms such as fever, sore throat, non-productive cough, chills,
chest pain, headache, muscle pain, and difficulty breathing. Gastrointestinal
symptoms, including abdominal pain, vomiting, and diarrhea, may also
2 5
occur . Other extrapulmonary manifestations may present, such as
acute kidney injury, liver enzyme malfunctions, or reduced lymphocyte
6
and/or platelet count .
Since MERS-CoV infection was first reported to the World Health

Organization in September 2012, there have been more than 2000 cases,
7
with a case fatality rate (CFR) of approximately 35% . Numbers continue
to increase. The CFR is known to increase with age.
Camels can develop mild rhinitis from natural MERS-CoV infection, but in
5
most cases, they remain asymptomatic . Camels experimentally
inoculated with a human isolate of MERS-CoV have also displayed
8
rhinorrhea, but no other clinical signs were apparent .
Experimentally infected rhesus macaques may develop pneumonia, but

9 10
most often experience self-limiting mild clinical disease . In contrast,
experimentally inoculated marmosets (Callithrix jacchus) can develop severe
interstitial pneumonia, some of which also experience frothy hemorrhagic
discharge from the mouth. Systemic dissemination of MERS-CoV was
suggested in these animal models based on the detection of viral RNA in the
blood. In marmosets, viral loads in the lungs were up to 1000 times higher
than those in rhesus macaques and the duration of illness was longer. In
certain marmosets, euthanization was necessary due to disease severity
11 .
Predisposing factors:
Gender:
Males account for almost 2/3 of all MERS cases seen to date, but case fatality
12
rates (CFR) between males and females are comparable . Increased
2
cases in males may be attributed to higher exposure rates .
Age:
Both primary and secondary hospital-acquired cases have occurred in older
individuals, with the average MERS patient around 50 years old. Primary
cases account for more than half of all MERS-CoV infections. The elderly
have an increased likelihood of dying following infection; the CFR is higher in
2
the elderly and lower in those 20 years and younger . In contrast,
13
secondary-acquired infections are more gender- and age-balanced .
Underlying comorbidities:
Individuals with diabetes, chronic renal and cardiac disease, obesity,
hypertension, asthma, and chronic obstructive pulmonary disease are at
higher risk of infection. Approximately 75% of all MERS-CoV cases have
2 5
occurred in patients with comorbidities .
Communicability: MERS-CoV human-to-human transmission is not

sustained; however, the virus can be shed during coughing and from
excretions from the lower respiratory tract and has been shown to spread
3 14 15
between humans in health care facilities . Spreading of the
virus between patients and health care workers in nosocomial settings, or
between family members, is likely to occur via large droplet aerosols and
direct contact, but airborne or fomite transmission is also possible since the
16
virus can persist on inanimate surfaces . MERS-CoV viral RNA can also
persist in nasal discharge, blood, urine, vomit or saliva, feces, and urine,
suggesting that direct intimate or casual contact may lead to transmission of
5 14
the virus .
Direct casual contact with a sick camel may lead to human transmission by
the respiratory route, but transmission is considered inefficient.
Consumption of contaminated camel milk, meat, or urine (a traditional
custom in the Arabian Peninsula and East Africa) may lead to infection but is
2 13 17
unlikely .
Camel-to-camel spread is believed to contribute to maintenance of MERS-

5
CoV infection in these animals . Infected calves can excrete MERS-CoV in
their feces and saliva which can lead to surface contamination and spread to
13
other camels through direct or indirect contact . Based on
experimentally infected alpacas, spreading of MERS-CoV in animals is
thought to occur mainly through intimate contact as opposed to aerosol
18
transmission .
Epidemiology: MERS-CoV is a novel coronavirus believed to have originated

in bats, and then spread to camels, which represent the primary source of
2
infection for humans . The index case occurred on June 13, 2012 in
Jeddah, Saudi Arabia, in a 60 year old man with a 7 day history of fever,
1 2
cough, expectoration, and shortness of breath . A second case of
MERS-CoV was reported 3 months later on September 22, 2012 in London,
United Kingdom, in a 49 year old man who had travelled to Saudi Arabia and
19
Qatar, where he had direct contact with camels and sheep .
Retrospective studies confirmed that MERS-CoV was also responsible for an
outbreak of respiratory disease in Zarqa, Jordan in April, 2012. Since then,
the virus caused a 2015 outbreak in South Korea, involving 186 cases, as well
as several outbreaks throughout the years in the Arabian Peninsula and
Middle East, where the disease is considered endemic. Most cases (~75%)
occur in Saudi Arabia, with other occurrences being traced to patients
2 20
travelling from the Middle East . Nosocomial outbreaks of MERS-
CoV have been reported in Saudi Arabian health care facilities. In these
15
settings, the risk for person-to-person transmission is elevated .
7
A total of 27 countries have reported cases of MERS-CoV . Secondary
cases of MERS-CoV predominated during the early stages of the outbreak,
but have been significantly reduced due to improved infection-control
2
practices . The disease is considered seasonal due to an increase in the
number of cases observed in April/May/June, coinciding with the weaning of
camel calves in the spring; however, cases are reported throughout the year
5 13 .
MERS-CoV is maintained in camels, which typically remain asymptomatic.

Humans can become infected through direct exposure to camels but the
2
virus is transmitted inefficiently among humans ; however, only a small
proportion of primary cases report having had direct contact with camels or
13
camel products . Approximately 45,000 people in Saudi Arabia are
believed to be infected by MERS-CoV without clinical illness and may play a
17
role in the spread of disease to other humans . Adult dromedary camels
have increased seropositivity compared to juvenile camels, likely due to
21
higher exposure .
Host range
Natural host(s): Dromedary camels may experience mild respiratory
symptoms from MERS-CoV infection but they are typically asymptomatic
despite exhibiting a high titer of neutralizing antibodies to the virus.
Serological evidence suggests that over 90% of adult dromedaries are
22
infected with MERS-CoV and have been infected for at least 30 years .
23
Camels are considered intermediate hosts for MERS-CoV . Goats have
also been suggested as potential intermediate hosts given that cell lines
derived from these animals can effectively replicate the virus. Goats are
more likely to use DPP4 as a receptor for MERS-CoV entry compared to mice,
16
cats, dogs, hamsters and ferrets . Natural susceptibility to MERS-CoV
infection has also been observed in alpacas, although the animals were
24
asymptomatic .
25 26 27
Other host(s): Mice transduced with human DPP4 , rabbits ,
16 28
rhesus macaques, African bats , and marmosets are susceptible to
2
MERS-CoV experimental infection . Intranasal inoculation of MERS-CoV in
29
llamas and pigs resulted in mucus secretion from the nose .
Infectious dose: Unknown. MERS-CoV has an estimated ID50 of <1 TCID50

30
and a LD50 of 10 TCID50 .
Incubation period: The incubation period ranges from 1 to 14 days, with a

2 3 15
median of 5 to 7 days . Patients with MERS-CoV pneumonia
31 32
experience viral shedding for 2 to 4 weeks .
In experimentally infected dromedary camels, shedding of infectious virus

from nasal swab specimens was detected through 7 days post-infection
(dpi) and RNA was detected through 35 dpi, but the infectious period is
believed to be short. In experimentally infected alpacas, shedding was
18
detectable up to 10 dpi . Shedding is believed to occur predominantly in
8
juvenile camels .

Reservoir: MERS-CoV is believed to have originated in African bats, and then
subsequently infected dromedary camels, both of which display little to no
16
overt symptoms of infection . Camels in Africa and the Arabian
2 22
Peninsula have displayed seropositive rates as high as 80 to 90%
33 .
34
Zoonosis/Reverse zoonosis: Yes, from dromedary camels to humans .
Bats are considered an unlikely source of zoonosis due to their limited
2
exposure to humans .
Vectors: None.

Drug susceptibility: There are no existing drugs that specifically target
MERS-CoV; however, in vitro and in vivo combination interferon-α2b and
ribavirin have reduced inflammation and disease during MERS-CoV infection
35
in rhesus macaques . Lopinavir/ritonavir treatment has shown anti-
MERS activity and a combination of interferon-β1b and mycophenolate
36
mofetil has demonstrated synergistic effects in vitro ; however, these
37
drugs have proven ineffective in randomized controlled trials .
Resveratrol may also inhibit MERS-CoV infection in humans, but this
38
compound has only been tested in vitro .
Drug resistance: Unknown.
Susceptibility to disinfectants: MERS-CoV is moderately susceptible to 70%

alcohol, but bleach (1:100 dilution of 5% sodium hypochlorite) is effective
31
against the virus .
Given the comparable genetic characteristics between SARS-CoV and MERS-

CoV, MERS-CoV may also be susceptible to the following disinfection
measures known to inactivate SARS-CoV: 5 minute contact with household
39
bleach , ice-cold acetone (90 seconds), ice-cold acetone/methanol
mixture (40:60, 10 minutes), 70% ethanol (10 minutes), 100% ethanol (5
minutes), paraformaldehyde (2 minutes), and glutaraldehyde (2 minutes)
40 . Commonly used brands of hand disinfectants also inactivate SARS-CoV
40
(30 seconds) . Disinfection methodologies should be validated to ensure
efficacy for MERS-CoV.
Physical inactivation: A 30 minute heat treatment at 63°C removed all

infectious virus from dromedary camel milk samples containing MERS-CoV
41 . 65°C for 15 minutes or 56°C for 30 minutes completely inactivates the
42
virus .
Survival outside host: MERS-CoV can persist in the environment for 24 to

48 hours under temperature and relative humidity (RH) conditions ranging
from 20-30°C and 30-80%, respectively. Viability of aerosolized MERS-CoV at
20°C and 40% RH decreases slightly by 7%, but has been shown to drop by
14 31
89% at 70% RH . The virus is stable in camel breast milk for up to 72
hours at 4°C, but viral titers rapidly lose infectivity when stored at 22°C for 48
41
hours .
Human coronavirus (HCoV) 229E, one of the 6 coronaviruses known to infect

humans, has been shown to persist on high-touch environmental surfaces
(polyvinylchloride, laminate, wood, stainless steel) in a university classroom
despite daily cleaning with a commercial cleaning solution containing
alcohol ethoxylates and sodium xylene sulfonate. Swab specimens collected
from these surfaces remained infectious for at least 7 days at ambient
43
temperature (24°C) and RH conditions (~50%) . Aerosolized HCoV 229E
can better survive at 50% RH than at 30% RH at 20°C. In general,
coronaviruses survive well in suspension. Up to 80% of HCoV 229E can
44
survive in PBS over 3 days .
As a human coronavirus with comparable genetic characteristics, MERS-CoV

may also survive outside the host under similar conditions; however,
compared to other human coronaviruses, MERS-CoV may survive on dry
surfaces for longer time periods. The virus can also survive as an aerosol
45
with a reduction of 7% over 10 minutes at 40% RH .

Surveillance: There are no specific symptoms that can accurately confirm a
MERS-CoV infection; however, MERS-CoV viral RNA can be detected in
respiratory tract specimens during the acute phase of illness using qRT-PCR.
MERS-CoV can be identified using ELISA to detect virus-specific antibodies in
serum samples collected 2 to 3 weeks after disease onset. This method
requires two different specific genomic segments for diagnosis. MERS-CoV
can also be identified using a positive immunofluorescence and/or
2
microneutralization test .

First aid/treatment: Supportive care is used for MERS-CoV patients since

46
there are no specific therapies that currently exist ; however, if
administered early on during infection, interferon-α2b, interferon-α2 and
2
ribivarin may reduce viral load titer in patient lungs and lessen damage .
Passive immunotherapy with convalescent patient plasma or MERS-CoV
specific antibodies has also been suggested as a possible therapeutic option
based on its ability to reduce the odds of mortality by 75% when
administered to patients suffering from severe acute respiratory infections
47 . Certain antiviral drugs are under review for possible clinical use,
including Lopinavir, chloroquine, chlorpromazine, mycophenolic acid, and
2
nitazoxanide .
No treatment for infected animals has been reported.

should come from the post-exposure response plan, which should be
developed as part of the medical surveillance program. More information on
the post-exposure response plan can be found in the CBH.
Immunization: There are no MERS-CoV vaccines currently approved for

46
human use ; however, inactivated, live attenuated virus, viral vector,
protein subunit, and DNA vaccines are all in various stages of preclinical
2 48
development . One DNA vaccine based on the full length viral Spike
20
(S) protein of the virus has reached Phase I clinical trials .

in the CBH, and by consulting the Canadian Immunization Guide.
Prophylaxis: The use of monoclonal antibodies (LCA60) isolated from

memory B cells of patients infected with MERS-CoV may prove effective as
49
both a pre- and post-exposure prophylaxis . A neutralizing human
antibody (m336) may also help prevent MERS-CoV infection when given
50
before exposure . These treatments are not yet approved for clinical use
46 .
Note: More information on prophylaxis as part of the medical surveillance

program can be found in the CBH.

Laboratory-acquired infections: There are no known cases of MERS-CoV
51
laboratory-acquired infections .
Please consult the Canadian Biosafety Standard (CBS) and Handbook (CBH)
for additional details on requirements and guidelines for reporting exposure
incidents.
Sources/specimens: MERS-CoV RNA has been detected in the human

respiratory tract (tracheal aspirates and sputum), nasal discharge, serum,
5 52
blood, urine, vomit, saliva, feces, and urine .
In infected animals, the virus has been recovered from nasal swabs,
oropharyngeal swabs, blood samples, raw camel milk and bronchoalveolar
2 9 53
lavage .
Primary hazards: The primary route of exposure to MERS-CoV is not well-

defined but inhalation of airborne or aerosolized infectious material, either
from infected humans or animals, is believed to be the main source of
16
infection . Exposure to infectious material on fomites has also been
13 45
considered likely .
Camels can become naturally infected through direct contact with large
8
droplets or fomite transmission . Camels are believed to have originally
become infected by bats, and have had the virus circulating between them
54
for over 20 years .
Special hazards: None.
Section VII - Exposure controls/personal

protection
Risk group classification: MERS-CoV is considered to be a Risk Group 3
Human Pathogen and Risk Group 3 Animal Pathogen.
MERS-CoV is also classified as an Emerging Animal Disease (EAD), requiring

CFIA oversight.
Containment requirements: The applicable CL3 or CL3-Ag requirements

outlined in the CBS and in the MERS-CoV Biosafety Advisory for all in vitro
propagative and in vivo activities. Non-propagative diagnostic or clinical
activities can be conducted at CL2 with additional biosafety requirements, as
specified in the MERS-CoV Biosafety Advisory.
Protective clothing: The applicable CL3 requirements for personal

protective equipment and clothing outlined in the CBS and MERS-CoV
Biosafety Advisory should be followed.
Based on a local risk assessment, appropriate hand, foot, head, body,

eye/face, and respiratory protection should be identified, and the PPE
requirements for the containment zone should be documented in Standard
Operating Procedures.
Other precautions: All activities involving open vessels of infectious

material or toxins to be performed in a certified BSC or other appropriate
primary containment device.

Spills: Allow aerosols to settle. Wearing protective clothing, gently cover the
spill with absorbent paper towel and apply suitable disinfectant, starting at
the perimeter and working towards the centre. Allow sufficient contact time
55
before clean up .
Disposal: All materials/substances that have come in contact with the

infectious agent should be completely decontaminated before they are
removed from the containment zone. This can be achieved by using a
decontamination method that has been demonstrated to be effective
against the infectious material, such as chemical disinfectants, autoclaving,
irradiation, incineration, an effluent treatment system, or gaseous
55
decontamination .
Storage: The applicable CL3 or CL3-Ag requirements for storage outlined in

the CBSshould be followed. Containers of infectious material or toxins
stored outside the containment zone should be labelled, leakproof, impact
resistant, and kept in locked storage equipment and within an area with
56
limited access .

and standards.
Work with MERS-CoV requires a Human Pathogens and Toxins Licence,

issued by the Public Health Agency of Canada. Import of MERS-CoV requires
a Health of Animals Act import permit, issued by the Canadian Food
Inspection Agency.
Updated: 2018
Prepared by: Centre for Biosecurity, Public Health Agency of Canada.
Although the information, opinions, and recommendations contained in this

Copyright©
Canada
References
1 Zaki, A.M., Van Boheemen, S., Bestebroer, T.M., Osterhaus,

A.D.M.E., and Fouchier, R.A.M. (2012) Isolation of a novel
Français
MENU 
Monkeypox virus: Infectious substances

Pathogen Safety Data Sheet
 For more information on Monkeypox virus, see the following:
Travel Health and Safety
Infection Control Guideline Series
Biosafety advisories/notifications/directives
Government of Canada Diseases and Conditions facts

Name
Monkeypox virus
Agent type
Virus
Taxonomy
Family
Poxviridae
Sub-family
Chordopoxvirinae
Genus
Orthopoxvirus
Species
Monkeypox virus

1 2 3 4
MPXV, human monkeypox
Characteristics
Brief description
Virus belongs to family Poxviridae, sub-family Chordopoxvirinae and genus
1 3 4
Orthopoxvirus . MPXV is a 200 to 250 nm brick- shaped enveloped
virus with characteristic surface tubules and a dumbbell-shaped core
3
component . The MPXV genome consists of linear double-stranded DNA.
Monkeypox virus is antigenically related to the variola and vaccinia viruses
5 .

Mpox (monkeypox) is characterised by the onset of non-specific symptoms
which can include fever, headache, backache, lymphadenopathy and fatigue
1 3 6
during a prodromal period of 2 to 3 days . This is followed by a 2
to 4 week period in which a rash develops and progresses from macules, to
papules, to vesicles, and then to pustules, followed by umbilication, scabbing
3 4 7
and desquamation . The rash usually occurs in a centrifugal
3
distribution, often spreading to the palms and soles of the feet . Lesions
can also develop on mucous membranes, conjunctivae, in the mouth, on the
4
tongue, and on the genitalia . The clinical presentation of mpox is similar
to that of smallpox except for the pronounced lymphadenopathy associated
5 8
with mpox and generally milder symptoms . Lymphadenopathy is
4 8 9
thus considered a key distinguishing feature of mpox . The case
fatality rate is approximately 1 to 10% in Africa, with higher death rates
3 7
among young children . In children unvaccinated against smallpox,
8 9
the case-fatality rate ranges from 1% to 14% .
Communicability
MPXV is transferred from infected animals through a bite or through direct
1 4 6
contact with the infected animal's blood, body fluids, or lesions
7 . It can also be transferred from human-to-human via the respiratory
tract, by direct contact with body fluids of an infected person, or with virus-
4 6 9 16
contaminated objects . The rate of person-to person
transmission is increasing, with a secondary attack rate of approximately
3 9
10% .
MPXV is capable of person-to-person transmission; a chain of up to six

3
sequential human-to-human transmission events has been documented
4 13 .
Epidemiology
Mpox affects all age groups; however, children under 16 years of age have
8
constituted the greatest proportion of cases . The virus occurs naturally
3
in West and Central Africa in the vicinity of tropical jungles . MPXV
isolates originating from West Africa appear to be less virulent and/or
transmissible to humans and non-human primates than those from the
Congo Basin in Central Africa. Furthermore, the cessation of smallpox
vaccination appears to have increased the susceptibility of humans to severe
mpox.
In 1970, the first human case of mpox was identified in a 9 month old child
in the Democratic Republic of the Congo (formerly Zaire) in a region where
5 7 10
smallpox was eradicated in 1968 . In the following year, six
additional cases of human monkeypox infection were reported in Liberia,
11
Sierra Leone and Nigeria . From 1970 to 1979, 47 human cases of mpox
3 4
were identified, 38 of which were from Zaire . In the Democratic
Republic of the Congo, a total of 338 cases were reported between 1981 and
1986, and more than 400 cases were reported between February 1996 and
12 13
October 1997 .
In 2003, the first cases of human mpox in the western hemisphere were
reported after an outbreak was reported in Midwestern United States
(Illinois, Indiana, Kansas, Missouri, Ohio and Wisconsin) due to the
1 3 6
importation of MPXV-infected West African rodents from Ghana
7 14 .
Host range
Natural host(s)
Humans, squirrels, non-human primates, black-tailed prairie dogs, African
1 2 3 4 5 6 7 10
brush-tailed porcupines, rats, and shrews
12 13 14 15 .
Infectious dose
Unknown.
Incubation period
3 7
Approximately 7 to 17 days .

Reservoir
Not fully understood but arboreal squirrels (Funisciurus spp., and to a lesser
3 5
degree, Heliosciurus spp.) are believed to be a reservoir for MPXV
12 15 .
1 3 4 5 6 7 8 10 12 13 14 15 17
Yes .
Vectors
3
Unknown .

Drug susceptibility
Cidofovir is considered as a potential therapeutic agent for MPXV infections,
as it has been shown to have activity against many DNA viruses in vitro,
18
including MPXV .
Orthopoxviruses are susceptible to 0.5% sodium hypochlorite, chloroxylenol-
based household disinfectants, glutaraldehyde, formaldehyde, and
19 20
paraformaldehyde .
19
Orthopoxviruses are inactivated by heat (autoclaving and incineration)
20 .

16
Orthopoxviruses are stable at ambient temperatures when dried .

Surveillance
Monitor for symptoms (unexplained fever, rash or prominent
lymphadenopathy) and confirm by laboratory diagnosis using virus
isolation, PCR-based assays, haemagglutination inhibition assays, electron
3 4 5
microscopy, ELISA, Western blotting, or immunohistochemistry
6 7 9 15 17 .
The specific recommendations for surveillance in the laboratory should
come from the medical surveillance program, which is based on a local risk
assessment of the pathogens and activities being undertaken, as well as an
overarching risk assessment of the biosafety program as a whole. More
information on medical surveillance is available in the Canadian Biosafety
Handbook.
First aid/treatment
There are no licensed antiviral drugs available to treat MPXV infection;
4
instead, treatment is supportive .

exposure response plan can be found in the Canadian Biosafety Handbook.
Immunization
Vaccination with vaccinia virus (smallpox vaccine) is approximately 85%
3 16
effective against mpox .

in the Canadian Biosafety Handbook, and by consulting the Canadian
Immunization Guide.
Prophylaxis
Vaccination with the smallpox vaccine, within 4 days and up to 14 days after
4 16
initial contact with a confirmed mpox case .

program can be found in the Canadian Biosafety Handbook.

Laboratory-acquired infections
16
None reported to date .
Note: Please consult the Canadian Biosafety Standard and Canadian

Biosafety Handbook for additional details on requirements for reporting
exposure incidents. A Canadian biosafety guideline describing notification
and reporting procedures is also available.
Sources/specimens
Lesion fluids or crusts, respiratory secretions, and tissues of infected hosts
4 15 16 .
Primary hazards
Ingestion, parenteral inoculation, droplet or aerosol exposure of mucous
9
membranes or broken skin, or contact with infectious fluids or tissues
16 .
Special hazards
Bite of infected non-human primates or rodents, or objects contaminated
1
with the virus (e.g. bedding, clothing) . In pregnant women, human
23
mpox may cause fetal complications .
Section VII: Exposure controls/personal

protection
Risk group classification
Monkeypox virus is a Risk Group 3 Human Pathogen, a Risk Group 3 Animal
21
Pathogen, and a Security Sensitive Biological Agent (SSBA) .
Containment requirements
Containment Level 3 facilities, equipment, and operational practices outlined
in the Canadian Biosafety Standard and in the Biosafety Advisory for
Monkeypox virus (MPXV) for work involving infectious or potentially infectious
Note that there are additional security requirements, such as obtaining a

Human Pathogens and Toxins Act Security Clearance, for work involving
SSBAs.
Protective clothing
Personnel entering the laboratory should remove street clothing and
jewellery, and change into dedicated laboratory clothing and shoes, or don
full coverage protective clothing (i.e., completely covering all street
clothing). Additional protection may be worn over laboratory clothing when
infectious materials are directly handled, such as solid-front gowns with
tight fitting wrists, gloves, and respiratory protection. Eye protection must
be used where there is a known or potential risk of exposure to splashes
22 .
The applicable Containment Level 3 requirements for personal protective

equipment and clothing outlined in the Canadian Biosafety Standard to be
followed. At minimum, use of full body coverage dedicated protective
clothing, dedicated protective footwear and/or additional protective
footwear, gloves when handling infectious materials or animals, face
protection when there is a known or potential risk of exposure to splashes
or flying objects, respirators when there is a risk of exposure to infectious
aerosols, and an additional layer of protective clothing prior to work with
infectious materials or animals.
Note: A local risk assessment will identify the appropriate hand, foot, head,
body, eye/face, and respiratory protection, and the personal protective
equipment requirements for the containment zone must be documented.
Other precautions
All activities involving open vessels of pathogens are to be performed in a
certified biological safety cabinet (BSC) or other appropriate primary
22
Additional information
For clinical diagnostic laboratories handling patient specimens that may
contain MPXV, the following resources may be consulted:
Local Risk Assessment Biosafety Guideline

Human Diagnostic Activities Biosafety Guideline

Spills
Allow aerosols to settle. Wearing protective clothing, gently cover the spill
with absorbent paper towel and apply suitable disinfectant, starting at the
before clean up (Canadian Biosafety Handbook).
Disposal
Decontaminate all materials for disposal by steam sterilization, chemical
22
disinfection, and/or incineration. .
All materials/substances that have come in contact with the infectious agent
must be completely decontaminated before they are removed from the
containment zone. This can be achieved by using decontamination
technologies and processes that have been demonstrated to be effective
decontamination (Canadian Biosafety Handbook).
Storage
In sealed containers that are appropriately labelled and locked in a
22
Containment Level 3 facility . The applicable Containment Level 3
requirements for storage outlined in the Canadian Biosafety Standard are to
be followed. Containers of security sensitive biological agents (SSBA) stored
outside the containment zone must be labelled, leakproof, impact resistant,
and kept in locked storage equipment that is fixed in place (i.e., non-
movable) and within an area with limited access (Canadian Biosafety
Handbook).
Inventory of security sensitive biological agents (SSBA) in long-term storage

to be maintained and to include:
specific identification of the pathogens, toxins, and other regulated

infectious material; and
a means to allow for the detection of a missing or stolen sample in a
timely manner

Canadian regulatory context
Controlled activities with MPXV require a Human Pathogens and Toxins
Licence issued by the Public Health Agency of Canada. MPVX is a non-
indigenous animal pathogen in Canada; therefore, importation of MPVX
requires an import permit, issued by the Canadian Food Inspection Agency.
The following is a non-exhaustive list of applicable designations, regulations,

or legislations:
Quarantine Act
Transportation of Dangerous Goods Regulations
Human Pathogen and Toxins Act and Human Pathogens and Toxins
Regulations
Non-Indigenous Animal Pathogen or OIE-listed disease (please contact
the Canadian Food Inspection Agency)
MPXV is a Security Sensitive Biological Agent (SSBA). There are additional

security requirements, such as obtaining a Human Pathogens and Toxins Act
Security Clearance, for work involving SSBAs.
The import, transport, and use of pathogens in Canada is regulated under

many regulatory bodies, including the Public Health Agency of Canada,
Health Canada, Canadian Food Inspection Agency, Environment Canada, and
Transport Canada. Users are responsible for ensuring they are compliant
with all relevant acts, regulations, guidelines, and standards.
Updated
February, 2023
Prepared by
Centre for Biosecurity, Public Health Agency of Canada.
Disclaimer
The scientific information, opinions, and recommendations contained in this
Pathogen Safety Data Sheet have been developed based on or compiled
from trusted sources available at the time of publication. Newly discovered
hazards are frequent and this information may not be completely up to
date. The Government of Canada accepts no responsibility for the accuracy,
information.
Persons in Canada are responsible for complying with the relevant laws,
including regulations, guidelines and standards applicable to the import,
transport, and use of pathogens in Canada set by relevant regulatory
authorities, including the Public Health Agency of Canada, Health Canada,
Canadian Food Inspection Agency, Environment and Climate Change
Canada, and Transport Canada. The risk classification and related regulatory
requirements referenced in this Pathogen Safety Data Sheet, such as those
found in the Canadian Biosafety Standard, may be incomplete and are
specific to the Canadian context. Other jurisdictions will have their own
requirements.
Copyright © Public Health Agency of Canada, 2023, Canada
References:
1 Reynolds, M. G., W. B. Davidson, A. T. Curns, C. S. Conover, G.
Huhn, J. P. Davis, M. Wegner, D. R. Croft, A. Newman, N. N. Obiesie,
G. R. Hansen, P. L. Hays, P. Pontones, B. Beard, R. Teclaw, J. F.
Howell, Z. Braden, R. C. Holman, K. L. Karem, and I. K. Damon.
2007. Spectrum of infection and risk factors for human
monkeypox, United States, 2003. Emerg. Infect. Dis. 13:1332-1339.
2 Rimoin, A. W., N. Kisalu, B. Kebela-Ilunga, T. Mukaba, L. L. Wright,

P. Formenty, N. D. Wolfe, R. L. Shongo, F. Tshioko, E. Okitolonda, J.
-. Muyembe, R. W. Ryder, and H. Meyer. 2007. Endemic human
monkeypox, Democratic Republic of Congo, 2001-2004. Emerg.
Infect. Dis. 13:934-937.
3 Parker, S., A. Nuara, R. M. L. Buller, and D. A. Schultz. 2007. Human

monkeypox: An emerging zoonotic disease. Future Microbiol. 2:17-
34.
4 Nalca, A., A. W. Rimoin, S. Bavari, and C. A. Whitehouse. 2005.

Reemergence of monkeypox: Prevalence, diagnostics, and
countermeasures. Clin. Infect. Dis. 41:1765-1771.
5 Acha, P. N., and B. Szyfres. 2005. Zoonoses & communicable

diseases common to man & animals, third edition: A review by
Peter Kerr. Aust. Mammal. 27:107.
6 Croft, D. R., M. J. Sotir, C. J. Williams, J. J. Kazmierczak, M. V.

Wegner, D. Rausch, M. B. Graham, S. L. Foldy, M. Wolters, I. K.
Damon, K. L. Karem, and J. P. Davis. 2007. Occupational risks
during a monkeypox outbreak, Wisconsin, 2003. Emerg. Infect.
Dis. 13:1150-1157.
7 Multistate outbreak of monkeypox - Illinois, Indiana, and

Wisconsin, 2003. 2003. Morbidity and Mortality Weekly Report,
52:537-540.
8 Heymann, D. L. 2008. Control of Communicable Diseases Manual

(19th Edition ed.). Washington, D.C.: American Public Health
Association.
9 Weber, D. J., and W. A. Rutala 2001. Risks and prevention of

nosocomial transmission of rare zoonotic diseases. Clin. Infect.
Dis. 32:446-456.
10 Ladnyj, I. D., P. Ziegler, and E. Kima. 1972. A human infection

caused by monkeypox virus in Basankusu Territory, Democratic
Republic of the Congo. Bull. World Health Organ. 46:593-597.
11 Foster, S. O., E. W. Brink, D. L. Hutchins, J. M. Pifer, B. Lourie, C. R.

Moser, E. C. Cummings, O. E. Kuteyi, R. E. Eke, J. B. Titus, E. A.
Smith, J. W. Hicks, and W. H. Foege. 1972. Human monkeypox. Bull.
World Health Organ. 46:569-576.
12 Pattyn, S. R. 2000. Monkeypoxvirus infections. OIE Rev. Sci. Tech.

12:92-97.
13 Hutin, Y. J., R. J. Williams, P. Malfait, R. Pebody, V. N. Loparev, S. L.

Ropp, M. Rodriguez, J. C. Knight, F. K. Tshioko, A. S. Khan, M. V.
Szczeniowski, and J. J. Esposito. 2001. Outbreak of human
monkeypox, Democratic Republic of Congo, 1996 to 1997.
Emerging Infect. Dis. 7:434-438.
14 Update: Multistate outbreak of monkeypox - Illinois, Indiana,

Kansas, Missouri, Ohio, and Wisconsin, 2003. 2003. Morbidity and
Mortality Weekly Report, 52:642-646.
15 Mukinda, V. B. K., G. Mwema, M. Kilundu, D. L. Heymann, A. S.

Khan, J. J. Esposito, H. Koen, M. Delfi, J. J. Muyembe-Tamfum, T. F.
Kweteminga, A. Moudi, L. Mangindula, V. N. Loparev, J. M. Parsons,
D. L. Jue, T. W. Crews, and J. C. Knight. 1997. Re-emergence of
human monkeypox in Zaire in 1996. Lancet. 349:1449-1450.
16 Centers for Disease Control and Prevention. 2007. In Richmond J.

Y., McKinney R. W. (Eds.), Biosafety in Microbiological and
Biomedical Laboratories (BMBL) (5th Edition ed.). Washingtion
D.C.: Centers for Disease Control and Prevention.
17 Dubois, M. E., and M. K. Slifka. 2008. Retrospective analysis of

monkeypox infection. Emerg. Infect. Dis. 14:592-599.
18 De Clercq, E. 2002. Cidofovir in the treatment of poxvirus

infections. Antiviral Res. 55:1-13.
Français
MENU 
Severe acute respiratory syndrome

coronavirus-2 (SARS-CoV-2): Infectious
substances Pathogen Safety Data Sheet
 For more information on SARS-CoV-2, see the following:
Biosafety Advisory
Travel Health and Safety
Government of Canada Diseases and Conditions facts

Name
Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2)
Agent type
Virus
Taxonomy
Family
Coronaviridae
Genus
Betacoronavirus
Species
Severe acute respiratory syndrome coronavirus
Subspecies/strain/clonal isolate
2

Formerly known as 2019 novel coronavirus (2019-nCoV); also referred to as
the virus responsible for COVID-19 or the COVID-19 virus
Characteristics
Brief description
1
SARS-CoV-2 is an enveloped, positive-sense, single-stranded RNA virus .
2
Virions range in size from 60 to 140 nm . Coronavirus virions have
distinctive club-shaped spikes on their surface, which give the virions the
3
appearance of a solar corona, hence the viral family name .
The SARS-CoV-2 genome varies in size from 29.8 kB to 29.9 kB and has 12
open reading frames, which encode 27 proteins including four structural
proteins: the surface/spike (S) protein for binding to the ACE2 receptor on
the host cell, the envelope (E) protein, the membrane (M) glycoprotein, and
4
the nucleocapsid (N) phosphoprotein . Two SARS-CoV-2 proteases are
5
critical for virus replication .

COVID-19, the disease caused by SARS-CoV-2, may range in severity from
6
asymptomatic to fatal . It is estimated that approximately one quarter to
7 8
one third of SARS-CoV-2 infections are asymptomatic . Children and
adolescents younger than 19 years of age are often asymptomatic, and
when symptomatic, usually have fewer and milder symptoms compared to
9
adults >25 years old . Although the risk of severe COVID-19 disease and
death increases with age, asymptomatic infection is common in the elderly
10 11 .
Common COVID-19 symptoms include chills, fever, new or worsening cough,

fatigue, myalgia, headache, and gastrointestinal symptoms (e.g., nausea,
12
vomiting and diarrhea) . Less frequent symptoms include shortness of
breath/difficulty breathing, sore throat, and loss of smell and/or taste. Some
individuals may experience rare symptoms such as skin and/or eye
manifestations. SARS-CoV-2 may also impact organ systems besides the
respiratory system to cause a multitude of extrapulmonary symptoms that
13 14
may result in fatal extrapulmonary complications . These non-
respiratory systems include the cardiovascular, renal, gastrointestinal,
hepatobiliary, endocrine, nervous, integumentary, and hematological and
immune systems.
SARS-CoV-2 infection, in certain cases, can also cause multisystem

inflammatory syndrome in children (MIS-C), a rare, sometimes fatal, post-
infectious condition with features of toxic shock syndrome and Kawasaki
15
disease . A similar syndrome, multisystem inflammatory syndrome in
16
adults (MIS-A), has also been described . Both syndromes typically occur
15 16
two to six weeks following the onset of typical COVID-19 symptoms
.
Another type of syndrome that may develop after the acute phase of illness
is 'long COVID', also known as 'post-COVID-19 condition' and 'post-acute
17 18
COVID-19 syndrome' . This syndrome usually occurs 3 months after
17
the onset of COVID-19, with symptoms lasting for at least 2 months .
Common symptoms include, but are not limited to, fatigue, shortness of
breath, and cognitive dysfunction, which can impact everyday functioning.
COVID-19 mortality rates vary widely by country for reasons including

differences in population demographics, health care capacity, and the
effectiveness of the public health interventions implemented to reduce
19
SARS-CoV-2 transmission . Global SARS-CoV-2 mortality analyses,
including case fatality rates, which vary nationally from 0.1 to 19.6%, are
available on the Johns Hopkins University and Medicine Coronavirus
Resource Centre's Mortality Analyses web page.
SARS-CoV-2 can infect a range of animal species with disease severity

ranging from asymptomatic to fatal. Outbreaks in farmed mink, an
economically important animal, have occurred in Canada, the US and in
20 21
multiple European countries . Disease severity ranges from
asymptomatic to fatal in infected mink. Clinical disease in infected dogs,
domestic cats, and big cats in zoos also ranges from asymptomatic to
22 23
symptomatic with respiratory and/or digestive symptoms .
Furthermore, mild respiratory symptoms have been reported in infected zoo
24
gorillas . In addition, infected pet ferrets have been reported to be either
25
asymptomatic, or to have mild or severe gastrointestinal symptoms
26 27 .
Predisposing factors
10 28 29
Advanced age is a risk factor for severe disease . The risk of
severe illness increases for people in their 50s and older, with those 85 years
29
of age and older at the greatest risk of severe illness . Medical
conditions that can also increase the risk of severe disease include asthma
(moderate to severe) and/or other chronic lung diseases, cancer, cystic
fibrosis, diabetes, Down syndrome, epilepsy, cardiovascular disease, kidney
disease, liver disease, dementia or other neurological disease, obesity,
pregnancy, sickle cell disease, stroke or cerebrovascular disease,
thalassemia, a history of smoking, substance use disorders, and being
12
immunosuppressed/immunodeficient .
In mink, pregnancy, advanced age, and breed may increase the risk of
30 31 32
severe disease .
Communicability
SARS-CoV-2 is a respiratory virus that is transmitted by respiratory droplets
33
and aerosols . Infectious virus can be transmitted by inhaling respiratory
droplets and/or aerosols; aerosols may remain suspended in the air for
minutes to hours. Alternatively, respiratory droplets and/or aerosols may be
deposited directly onto exposed mucous membranes in the mouth, nose or
eyes by direct splashes or sprays such as those produced by coughing.
Finally, respiratory droplets and/or aerosols may be deposited onto
inanimate objects, which act as fomites. However, the risk of SARS-CoV-2
34
transmission by fomites is considered to be low .
Furthermore, infectious virus has been detected in urine and feces,

35 36
suggesting that these can transmit infection . In addition,
epidemiological studies have concluded that SARS-CoV-2 may be
transmitted via contaminated sewage, and by contaminated bioaerosols
37 38 39
produced by plumbing connecting apartments .
Vertical transmission from mother to fetus/infant is considered possible

40
although most cases of neonatal infection appear to occur post-partum .
SARS-CoV-2 infection may be transmitted by pre-symptomatic and

asymptomatic individuals, although the extent to which such individuals
41
transmit compared to symptomatic individuals is unknown .
Furthermore, animal-to-animal transmission has been documented under

experimental conditions for some species such as ferrets, hamsters, cats
42 43
and bats . Furthermore, white-tailed deer appear to transmit to
44
each other in the wild .
Epidemiology
In early January 2020, Chinese authorities announced that they had
identified a novel coronavirus as the cause of unexplained cases of viral
45
pneumonia first reported in December 2019 in Wuhan, China . Chinese
authorities subsequently reported human-to-human transmission of this
virus in Wuhan (in the province of Hubei), outside of Wuhan, and in some
46
clusters outside of Hubei . On January 30, 2020, the International Health
Regulations (2005) Emergency Committee agreed that the outbreak met the
criteria for a Public Health Emergency of International Concern given that
the virus had spread to 18 other countries in which human-to-human
transmission was occurring in some. On March 11, 2020, the World Health
45
Organization (WHO) declared the SARS-CoV-2 outbreak a pandemic .
SARS-CoV-2 would eventually spread to most countries, with catastrophic
public health and economic consequences. Global statistics for confirmed
SARS-CoV-2 infections and deaths are available on the WHO Coronavirus
(COVID-19) Dashboard.
Host range
Natural host(s)
47
Humans are the primary SARS-CoV-2 host .
Other host(s)
Naturally-occurring infections have been reported in multiple feline species,
pet dogs and ferrets, mink (farmed and wild), otters, beavers, white-tailed
44 48 49 50 51 52
deer, hyenas, coatimundi, and gorillas .
Various mammalian species have been experimentally infected with SARS-

CoV-2. Susceptible species, which support varying degrees of viral
replication and experience varying degrees of disease severity, include non-
human primates, small animal species often used in experimental studies of
respiratory viruses (e.g., ferrets and hamsters), companion animals (e.g.,
42
cats), and various wild animal species (e.g., bank voles and fruit bats)
43 53 .
Infectious dose
54
The human infectious dose of SARS-CoV-2 is unknown . Based on non-
human primate research, the best estimate of the human infectious dose via
the inhalation route is 36-179 viral particles (plaque forming units).
Incubation period
The estimated incubation period ranges from 2-14 days, with a median of 5-
12
6 days from exposure to symptom onset . However, in some individuals,
55
especially the elderly, the incubation period may be longer .
Nonetheless, the majority of individuals who do become symptomatic will
12
do so by 11.5 days post-infection .

Reservoir
The original animal reservoir(s) that may have been responsible for
56
transmitting SARS-CoV-2 to humans is unknown .
Zoonotic transmission from farmed mink to humans has been reported in
57 58
the Netherlands and Denmark .
Reverse zoonotic transmission has occurred in multiple feline species, pet

dogs and ferrets, mink (farmed and wild), otters, beavers, white-tailed deer,
hyenas, coatimundi, and gorillas, following known or suspected contact with
44 48 49 50 51 52
infected humans .
Vectors
None confirmed to date.

Drug susceptibility
Multiple antivirals and anti-SARS-CoV-2 spike protein monoclonal antibodies
have been authorized for the treatment of COVID-19. Health Canada has
summarized complete list of authorized drugs and vaccines for COVID-19 in
Canada.
Drug resistance
SARS-CoV-2 has continued to evolve since its identification in January 2020,
acquiring mutations that have at least somewhat reduced the effectiveness
of vaccines and therapeutic monoclonal antibodies created against early
59 60
viral spike protein sequences . Viral variants with mutations that
reduce vaccine and/or drug effectiveness are referred to as 'Variants of
Concern'.
SARS-CoV-2 is susceptible to disinfectants having proven activity against
61
enveloped viruses . These disinfectants include sodium hypochlorite, i.e.,
bleach (1 000 parts per million [0.1%] for general surface disinfection, and 10
000 parts per million [1%] for disinfection of sample spills), 70% ethanol,
7.5% povidone-iodine, 0.05% chloroxylenol, 0.05% chlorhexidine, and 0.1%
benzalkonium chloride.
Furthermore, methanol (100% and ice-cold) and paraformaldehyde (4%) can

62
inactivate virus in infected cells .
Health Canada has published a list of hard-surface disinfectants with

evidence for use against COVID-19.
SARS-CoV-2 can be inactivated by heating for 15 to 30 minutes at 56°C, 10 to
63
15 minutes at 60oC to 65°C, and 2 minutes at 98°C . Furthermore, SARS-
CoV-2 loses infectivity within 1 day at pH extremes of pH 2–3 and pH 11–12
64 . SARS-CoV-2 can also be inactivated by exposure to simulated sunlight
representing natural sunlight (ultraviolet [UV] range of 280–400 nm), UVB
radiation (280–315 nm), UVC radiation of different wavelengths (i.e., 254 nm
or 200–280 nm), gamma radiation (1 Mrad), a deep ultraviolet light-emitting
diode (DUV-LED; 280 ± 5 nm), cold atmospheric plasma with argon feed gas,
65 66 67 68 69 70 71 72
and gaseous ozone .

Studies have shown that SARS-CoV-2 can survive for extended periods at
room temperature on different types of surfaces including vinyl, steel, glass,
paper and polymer banknotes (up to 28 days); cotton cloth (up to 14 days);
polymer surfaces (up to 13 days); plastic, face masks and latex gloves (up to
73 74
7 days); and cardboard and wood (up to 2 days) . The available data
74
suggest that SARS-CoV-2 is the most resistant human coronavirus .
Under experimental conditions, SARS-COV-2 was also shown to survive in

some biological fluids (i.e., nasal mucus, sputum, saliva, tears, blood, or
semen), from one to three days at 25°C/70% relative humidity (RH), for
seven days at 21°C/60% RH, and for 21 days at 5°C/75% RH, but was
75
unstable in human feces, fecal suspension, and breastmilk .
76
When aerosolized, SARS-CoV-2 can be viable for at least three hours .

Surveillance
Although viral sequencing is the most definitive method for diagnosing
SARS-CoV-2 infection, the cost and technical requirements of this technique
77
limit its feasibility . As such, the gold standard for detecting SARS-CoV-2
is the reverse transcription–polymerase chain reaction (RT-PCR) assay, which
detects viral ribonucleic acid. The RT-LAMP (RT-loop mediated isothermal
amplification) assay may also be used to detect viral nucleic acid. The
detection of viral antigens in clinical samples can also be used for diagnosis.
Virus may also be detected in tissue samples by in situ hybridization or
immunohistochemistry.

Biosafety Handbook (Canadian Biosafety Handbook).
First aid/treatment
COVID-19 treatment guidelines are evolving. Treatment may include the
antiviral remdesivir, oxygen therapy, airway management, steroids, and the
management of septic shock, depending on disease severity, in addition to
78
the management of co-infections . More information can be found on
the WHO living guidance for the clinical management of COVID-19 and the
WHO living guideline for COVID-19 therapeutics.
SARS-CoV-2-infected pets usually have mild respiratory and/or digestive

79
symptoms, which resolve with supportive care . In the case of infected
farmed mink, mass culling may be performed depending on the national or
regional capacity to contain the outbreak and manage risks using less
80
severe approaches .

exposure response plan can be found in the Canadian Biosafety Handbook.
Immunization
Multiple COVID-19 vaccines have been approved for the active immunization
of the general population, as summarized on the COVID-19 vaccine tracker.
Veterinarian vaccines, including Carnivac-Cov and FurcoVac, have been

81 82 83 84
authorized for use in various countries .

in the Canadian Biosafety Handbook, and by consulting the Canadian
Immunization Guide.
Prophylaxis
Pre-exposure prophylaxis consisting of a monoclonal antibody cocktail
specific for the SARS-CoV-2 spike protein has been authorized in some
jurisdictions for moderately to severely immunocompromised individuals
who may not respond adequately to SARS-CoV-2 vaccines, and for
85 86
individuals for whom such vaccines are contraindicated .
There are currently no post-exposure prophylaxis measures.

program can be found in the Canadian Biosafety Handbook.

Laboratory-acquired infections
At this time, there are no reported cases of laboratory-acquired SARS-CoV-2
infections.
Note: Please consult the Canadian Biosafety Standard and Canadian

Biosafety Handbook for additional details on requirements for reporting
exposure incidents. A Canadian Biosafety Guideline describing notification
and reporting procedures is also available.
Sources/specimens
Diagnostic samples typically include respiratory samples such as
nasopharyngeal, oropharyngeal, or nasal swabs, bronchoalveolar lavage
fluid, saliva, or sputum; however, stool, urine, serum, blood and tissue
77
samples may also be used .
Primary hazards
Inhalation of infectious material or exposure of mucous membranes to
33
infectious material
Special hazards
It has been suggested that SARS-CoV-2 could survive in the liquid nitrogen
and/or in the nitrogen vapours routinely used to cryopreserve biological
samples, possibly resulting in sample cross-contamination, and/or in the
87 88
infection of laboratory workers .
Since the SARS-CoV-2 genome, which consists of positive-stranded RNA, is

considered infectious, activities with intact genomic RNA pose a risk of
89
infection, despite the absence of infectious virions .
Section VII: Exposure controls/personal

protection
Risk group classification
SARS-CoV-2 is a Risk Group 3 human pathogen and Risk Group 2 animal
pathogen. Single-stranded RNA is a Risk Group 2 biological agent for
humans and a Risk Group 1 biological agent for animals.
Containment requirements
Containment Level 3 facilities, equipment, and operational practices outlined
in the Canadian Biosafety Standard and in the Biosafety advisory: SARS-CoV-
2 (Severe acute respiratory syndrome coronavirus 2) for all in vivo and in
vitro activities. Non-propagative diagnostic or clinical activities can be
conducted at containment level 2 with additional requirements, as specified
in the Biosafety advisory: SARS-CoV-2 (Severe acute respiratory syndrome
coronavirus 2).

Spills
Allow aerosols to settle. Wearing protective clothing, gently cover the spill
with absorbent paper towel and apply suitable disinfectant, starting at the
before clean up (Canadian Biosafety Handbook).
Disposal
All materials/substances that have come in contact with the infectious agent
must be completely decontaminated before they are removed from the
containment zone. This can be achieved by using a decontamination method
that has been demonstrated to be effective against the infectious material,
such as chemical disinfectants, autoclaving, irradiation, incineration, an
effluent treatment system, or gaseous decontamination (Canadian Biosafety
Handbook).
Storage
The applicable Containment Level 3 requirements for storage outlined in the
Canadian Biosafety Standard to be followed. Containers of infectious
material or toxins stored outside the containment zone should be labelled,
leakproof, impact resistant, and kept either in locked storage equipment or
within an area with limited access.

Canadian regulatory context
Controlled activities with SARS-CoV-2 require a Human Pathogens and
Toxins Licence issued by the Public Health Agency of Canada. SARS-CoV-2 is
not a reportable/notifiable animal disease. However, individuals are asked to
immediately notify the CFIA if SARS-CoV-2 is detected in an animal. The
following is a non-exhaustive list of applicable designations, regulation, or
legislation:
Human Pathogen and Toxins Act and Human Pathogens and Toxins
Regulations
Health of Animals Act and Health of Animals Regulations
Quarantine Act
Transportation of Dangerous Goods Regulations
Updated
December, 2021
Prepared by
Centre for Biosecurity, Public Health Agency of Canada.
Disclaimer
The scientific information, opinions, and recommendations contained in this
Pathogen Safety Data Sheet have been developed based on or compiled
from trusted sources available at the time of publication. Newly discovered
date. The Government of Canada accepts no responsibility for the accuracy,
information.
Persons in Canada are responsible for complying with the relevant laws,
Français
MENU 

Substances – Eastern equine encephalitis
(EEEV), Western equine encephalitis (WEEV)

SUBSTANCES
NAME: Eastern equine encephalitis (EEEV), Western equine encephalitis
(WEEV)
SYNONYM OR CROSS REFERENCE: Alphaviruses, sleeping sickness,

1-3
encephalitis, EEE, WEE, equine or western equine encephalomyelitis .
CHARACTERISTICS: EEEV and WEEV belong to the genus Alphavirus within

1
the family Togaviradae . They are 65-70 nm in diameter, small, spherical,
and enveloped viruses with an icosahedral symmetry and triangulation
1 4
number of 4 . Their genome is comprised of a single stranded
1
positive sense ssRNA of 11.5 kb . They replicate in the cytoplasm, with
4
budding from the plasma membrane .

PATHOGENICITY/TOXICITY: Eastern equine encephalitis (EEE) is the most
5
severe of the arboviral encephalitides and has a mortality of 50 to 75 % .
Symptoms of the disease include fever, headache, vomiting, respiratory
symptoms, leucocytosis, dizziness, decreasing level of consciousness,
3 5
tremors, seizures, and focal neurological signs . Death can occur
5
within 3 to 5 days of infection . Those who survive suffer from
neurological sequel, including convulsions, paralysis, and mental retardation
5 . Brain edema, ischemia, and hypoperfusion are present in early stages
3
of the disease . WEEV causes asymptomatic or mild infections in humans,
with non-specific symptoms such as sudden onset of fever, headache,
3
nausea, vomiting, anorexia, and malaise . Some patients may also
present with altered mental status and weakness, with signs of meningeal
3
irritation . In rare cases, WEEV infection may cause encephalitis or
encephalomyelitis, resulting in neck stiffness, confusion, visual disturbances,
2 3
photophobia, tonic-clonic seizures, somnolence, coma, and death .
Fifteen to fifty percent of the encephalitis survivors, especially young
children, suffer from permanent neurological damage (mental retardation,
2 3
emotional instability, and spastic paresis) . Western equine
3
encephalitis virus has mortality range of 3-7 % .
EPIDEMIOLOGY: EEEV is widely distributed throughout North, Central, and

South America; the Caribbean; coastal region of eastern Canada; Poland;
2 5
former USSR; Thailand; Philippines; andthe former Czechoslovakia .
In the United States, human infections due to EEEV are usually sporadic, with
small outbreaks occurring each summer, mostly along the Atlantic and Gulf
5
coasts . Furthermore, the Centers for Disease Control and Prevention
reported that 220 confirmed human cases of EEE occurred in the U.S.
3
between the years 1964 to 2004 . In Canada, infections due EEEV occur
mainly in spring and are associated with birds migrating from southern
2
United States to northern Canada . WEEV virus is widely distributed along
2
North and South America, but is absent from Central America . The
Centers for Disease Control and Prevention reported that 639 confirmed
3
human cases of WEE occurred in the U.S. between the years 1964 to 2004
. Children greater than 14 years of age have a higher chance of acquiring
3
WEEV infection .
HOST RANGE: Humans, reptiles, bats, pheasants, wild birds, mosquitoes,

2 3
horses, dogs, and rodents .
MODE OF TRANSMISSION: The primary EEEV and WEEV transmission cycle

occurs between birds and mosquitoes (Culiseta melanura for EEEV and
2 3
Culex tarsalis for WEEV) . Both viruses are transmitted naturally to
humans from bites of arthropods (such as Aedes , Coquillettidia , and Culex
spps. for EEEV; and Ochlerotatus melanimon , and Aedes dorsalis for WEEV)
2 3
which feed on both birds and humans .
INCUBATION PERIOD: The incubation period exceeds 1 week for EEEV

3 5 3
(range of 4-10 days) . The incubation period for WEEV is 2-7 days .
COMMUNICABILITY: Person-to-person transmission has not been reported

for EEEV or WEEV viruses. Direct bird-to-human infection can occur although
humans and horses are not amplifying hosts as virus titers in their bodies
2
are insufficient to infect mosquitoes . Eggs of mosquitoes can be infected
6
by the female .

RESERVOIR: Wild birds are the main reservoir for transmission of both EEEV
2
and WEEV virus . Humans, horses, and other animals (domestic fowl, feral
2
pigs, cattle and rodents) are not significant reservoir hosts . Amphibians
and reptiles are a possible reservoir for the virus to overwinter. Mosquitoes
6
and infected eggs are also a reservoir for the viruses .
2
ZOONOSIS: Yes . The virus can be transmitted from birds to humans via
2
mosquitoes .
VECTOR: Both viruses can be transmitted from pheasants to humans by

7
insect vectors, usually, mosquitoes . Aedes sollicitans, Aedes vexans,
Coquillettidia , and Culex spps are vectors responsible for transmission of
2
EEEV from birds to humans 3). Ochlerotatus melanimon (California), Aedes
dorsalis (Utah and New Mexico), and Aedes campestris (New Mexico) are
3
responsible for transmission of WEEV to humans .

DRUG SUSCEPTIBILITY/RESISTANCE: None.
SUSCEPTIBILITY TO DISINFECTANTS: EEEV can be inactivated by exposure

8
to 50% ethanol at concentration for 60 minutes . Most enveloped viruses
are also susceptible to 1% sodium hypochlorite, 2% glutaraldehyde,
9 10
quaternary ammonium compounds, and phenolics .
PHYSICAL INACTIVATION: Microbial inactivation is possible using moist

11 12
and dry heat . EEEV can be inactivated by UV rays .
SURVIVAL OUTSIDE HOST: Unknown.
SECTION V- FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. Both EEEV and WEEV infection can
be diagnosed using serological assays such as ELISA to detect IgM
2 3
antibodies in serum and CSF . The viruses can be isolated from
3
clinical specimens on Vero cells (African Green Monkey kidney cells) .
Molecular biology methods such as reverse transcription-polymerase chain
reaction (RT-PCR) and real-time RT-PCR can also be used to detect
2 3
WEEV/EEEV-specific RNA in clinical specimens . Virus can also be
2
detected in clinical specimens or tissues with direct IFA .
FIRST AID TREATMENT: Currently no treatment is available for EEEV or

2 5
WEEV infections . Symptomatic treatment is given to maintain vital
2
functions of the body . Passive and active physiotherapy is used during
2
the recovery phase .
13
IMMUNIZATION: None currently available .
PROPHYLAXIS: None.

LABORATORY ACQUIRED INFECTIONS: Four laboratory-acquired cases of
14
EEEV and sixteen cases of WEEV (with 4 deaths) have been reported
15 .
SOURCES / SPECIMENS: Infected wild birds; infected mosquitoes; infected

pheasants; clinical samples such as blood, CSF, central nervous systems,
2 3 14
other tissues .
PRIMARY HAZARDS: Accidental parenteral inoculation, contact of the virus

with broken skin or mucous membranes, and bites from infected laboratory
arthropods or rodents are the primary hazards associated while working
14
with these viruses . Exposure to infectious aerosols may also be a
14
potential hazard .
15
SPECIAL HAZARDS: Infection of newly hatched chickens is hazardous .

16


17

17

SPILLS: Allow aerosols to settle, then, wearing protective clothing, gently
disinfectant starting at the perimeter and working towards the center. Allow
17
sufficient contact time before starting the clean up .
DISPOSAL: All wastes should be decontaminated before disposal either by

17
steam sterilization, incineration or chemical disinfection .
STORAGE: The infectious agent should be stored in a sealed and identified

17
container .

and standards.

Canada

REFERENCES:
1 Jose, J., Snyder, J. E., & Kuhn, R. (2009). A structural and functional
perspective of alphavirus replication and assembly. Future
Microbiology, 4 (7), 837-856.
Schiefer, H. G., Slenczka, W., Graevenitz, A. V., & Zahner, H. (2003).
Viral Zoonoses: Zoonoses caused by Alphaviruses. Zoonoses:
Infectious diseases tranmissible from animals to humans (3rd ed., pp.
6-24). Washington, D.C.: ASM press.
3 Zacks, M. A., & Paessler, S. (2010). Encephalitic alphaviruses.

Veterinary Microbiology, 140 (3-4), 281-286.
4 Dimmock, N. J., Easton, A. J., & Leppard, K. N. (2007). Appendixes:

survey of virus properties. Introduction to modern virology (6th ed.,
pp. 444-479). Malden, MA: Blackwell publishing.
5 Petersen, L. R., & Gubler, D. J. (2003). Infection: Viruses:

Alphaviruses. In D. A. Warrel, T. M. Cox, J. D. Firth & E. J. Benz
(Eds.), Oxford Text Book of Medicine (4th ed., pp. 377- 379). Oxford,
New York: Oxford University Press. Retrieved from
online.statref.com/Document/Document.aspx?
FxId=94&DocId=1&SessionId=121DA8BAMRVOHFWX
6 Pfeffer, M., & Dobler, G. (2010). Emergence of zoonotic

arboviruses by animal trade and migration. Parasites & Vectors, 3
(1), 35. doi:10.1186/1756-3305-3-35
7 Kalluri, S., Gilruth, P., Rogers, D., & Szczur, M. (2007). Surveillance
of arthropod vector- borne infectious diseases using remote
sensing techniques: A review. PLoS Pathogens, 3(10), 1361-1371.
8 Ali, Y., Dolan, M. J., Fendler, E. J., & Larson, E. L. (2001). Alcohols. In
S. S. Block (Ed.), Disinfection, Sterlization, and Preservation (5th ed.,
pp. 229-240, 253). Philadephia, PA: Lippincott Williams & Wilkins.

Williams & Wilkins.
10 Collins, C.H., and Kennedy, D.A. (1999). Decontamination. .

Laboratory-Acquired Infections: History, Incidence, Causes and
Prevention. (4th ed., pp. 160-186, 170-176). London, UK.:
Buttersworth.
11 Joslyn, L. J. (2001). Sterilization by Heat. In S. S. Block (Ed.),

Disinfection, Sterilization, and Preservation (5th ed., pp. 695).
Philadelphia: Lippincott Williams & Wilkins.
12 Aguilar, P. V., Paessler, S., Carrara, A. S., Baron, S., Poast, J., Wang,
E., Moncayo, A. C., Anishchenko, M., Watts, D., Tesh, R. B., &
Weaver, S. C. (2005). Variation in interferon sensitivity and
induction among strains of eastern equine encephalitis virus.
Journal of Virology, 79 (17), 11300-11310.
doi:10.1128/JVI.79.17.11300-11310.2005
13 Steele, K. E., & Twenhafel, N. A. (2010). REVIEW PAPER: pathology

of animal models of alphavirus encephalitis. Veterinary Pathology,
47 (5), 790-805. doi:10.1177/0300985810372508
14 Agents Summary: Arboviruses and related zoonotic viruses.

(1999). In J. Y. Richmond, & R. W. Mckinney (Eds.), Biosafety in
microbiological and biomedical laboratories (4th ed., pp. 183-199).
Washington: CDC & NIH.
15 Fleming, D., & Hunt, D. (2006). Biological safety: principles and

practices (4th ed.). Washington: ASM press.

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Hepatitis C virus
Pathogen Safety Data Sheet - Infectious

Substances
Name: Hepatitis C virus (HCV).
1-13 3 12
Synonym or Cross Reference: HCV , non-A non-B hepatitis
14 , parenterally transmitted non-A non-B hepatitis, non-B transfusion-
2
associated hepatitis, post-transfusion non-A non-B hepatitis , and HCV
1-4 6 7 10 11
infection .
3 5
Characteristics: HCV belongs to the Flaviviridae family and
Hepacavirus genus, and is a small (50nm), single-stranded, enveloped RNA
2 3 14
virus . HCV was originally characterised in 1989 , and has 6 major
5
genotypes and over 100 subtypes . The main genotypes of HCV in North
1
America are types 1, 2, and 3 .
Section II - Hazard Identification

Pathogenicity/Toxicity: Acute HCV infection: Asymptomatic in most patients
1 3 5
(60-75%) . The syndrome of acute hepatitis is often preceded or
1 3
accompanied by symptoms of fatigue, myalgia, low-grade fever ,
3
right upper quadrant pain, nausea, vomiting , jaundice, mild
1
hepatosplenomegaly, maculopapular rash, and arthralgia . These
1
symptoms may last for 2 to 12 weeks .
Chronic HCV infection: While a minority of those infected will spontaneously

clear an acute infection with HCV, in most cases (50-85%), the infection will
1
become chronic . Some patients with chronic HCV infection experience:
malaise, nausea, abdominal pain and pruritis. Fluctuating alanine
transferase levels are characteristic. The late sequelae of chronic HCV
infection include serious health consequences such as chronic hepatitis,
5
cirrhosis, and hepatocellular carcinoma . If cirrhosis develops, patients
may experience jaundice, splenomegaly, ascites, oesophageal varices, and
hepatic encephalopathy. Extrahepatic manifestations are uncommon but
may include mixed essential cryoglobulinaemia, membranous or
membranoproliferative glomerulonephritis, non-Hodgkin's lymphoma,
Sjorgren's syndrome, lichen planus, and porphyria cutanea tarda.
2
Epidemiology: HCV infection is seen worldwide , with the World Health
2-5
Organization (WHO) estimating a prevalence of 2.2% to 3% , or
5
approximately 170 million people . The WHO African region and WHO
Eastern Mediterranean region have the highest prevalence of HCV infection
4 .
1-5 7 10-12 15
Host Range: Humans . Chimpanzees have been used as
2 5 9 10 13
experimental hosts .
Infectious Dose: Unknown.
Mode of Transmission: In North America HCV is mainly transmitted

parenterally by infected needles, particularly those used by intravenous
1 3 12
drug users . Other parenteral routes exist such as blood
transfusion, organ transplantation, contaminated medical equipment, and
3
from tattoo and body piercing equipment . However, for the last decade
or so the risk of HCV infection through blood transfusion in Canada, and
16
North America as well, is negligible . Less common routes of HCV
transmission are via sexual contact, from sharing razors and/or
toothbrushes, and from mother to child during pregnancy and childbirth.
1 3
Incubation Period: Ranges from 2 to 12 weeks .
Communicability: Can be transmitted from person-to-person. Transmission

rate between mother and developing child is influenced by maternal levels
of viraemia (greater than 106 copies per ml blood), and also co-infection of
2 3 5
the mother with HIV .

2 3 5
Reservoir: Humans .
Zoonosis: None.
Vextors: None.
Section IV - Stability and Viability

Drug Susceptibility: Sensitive to interferon-α (IFN), pegylated interferon,
1
and ribavirin . New antiviral treatments that work by targeting hepatitis
17
C protease and polymerase are currently in clinical trials .
Drug Resistance: Resistance has been observed to be emerging against IFN

18
and the current methods of therapy , and the outcome of treatment is
19
highly dependent on viral genotype .
Susceptibility to Disinfectants: HCV RNA is readily degraded by 2%

6
glutaraldehyde when added to biological samples at 37°C , and soaking
medical equipment (such as gastroendoscopes) in 3% glutaraldehyde is
7
effective at limiting HCV transmission . Phenolic compounds (0.4 to 3%)
are effective at inhibiting HCV binding and infectivity in VERO cell cultures
8 . Furthermore, treatment of HCV diluted in phosphate buffered saline
with 1% non-ionic detergent (Triton X-100) plus 0.3% tri-n-butyl-phosphate
13
leads to inactivation .
Physical Inactivation: HCV is inactivated when incubated at 60°C for 10

13
hours (pasteurisation) .
Survival Outside Host: HCV is relatively unstable; however, in plasma it can

survive drying and environmental exposure to room temperature for at least
9
16 hours .
Section V - First Aid / Medical

Surveillance: Monitor for symptoms. The initial test for HCV infection is an
1 2 12 1-3 12 13
enzyme immunoassay for HCV antibodies . PCR
methods are also used to detect HCV RNA. Other tests include the branched
2 3
DNA assay and transcription mediated amplification .
First Aid/Treatment: Treatment success rates with antiviral therapy have

1
improved significantly over the last 10 years . Mono-therapy with
pegylated interferon (addition of polyethylene glycol to interferon-α) and
combined therapy of pegylated interferon with ribavirin, or standard
1
interferon with ribavirin, are common methods of treating HCV infection
10 .
1 8 11
Immunization: None ; however, several vaccines that prevent
initial infection or viral persistence, or that clear viraemia in individuals with
10 20
chronic HCV infections, are in development .
Prophylaxis: Postexposure prophylaxis with immune globulin or antiviral

11
agents is not recommended .
Section VI - Laboratory Hazards

Laboratory-Acquired Infections: Unknown, although seroprevalence
studies have reported antibody to HCV rates of 1% among hospital based
(including laboratory workers and healthcare providers) in Western
12
countries .
1 3 9 12 13 1 3
Sources/Specimens: Blood , blood products
12 , and bodily fluids, tissues, or equipment contaminated with HCV
1 7 9
infected blood .
3 12
Primary Hazards: Needlestick injury , or cuts with sharp
12
instruments .
Special Hazards: None.
Section VII - Exposure Controls / Personal Protection

21
Risk Group Classification: Risk Group 2 .
Containment Requirements: Containment Level 2 facilities, equipment,

Protective Clothing: Lab coat. Gloves when direct skin contact with infected
22
Other Precautions: All procedures that may produce aerosols, or involve

22
Section VIII - Handling and Storage

Spills: Allow aerosols to settle and, wearing protective clothing, gently cover
spill with paper towels and apply an appropriate disinfectant, starting at the
before clean up.
Disposal: Decontaminate all materials for disposal by steam sterilisation,

chemical disinfection, and/or incineration.
Storage: In sealed containers that are appropriately labelled.
Section IX - Regulatory and Other Information

Regulatory Information: The import, transport, and use of pathogens in
and standards.
Updated: November 2010.
Prepared by: Pathogen Regulation Directorate, Public Health Agency of

Canada.

Copyright ©
Canada
References
1 Wong, T., & Lee, S. S. (2006). Hepatitis C: A review for primary care
physicians. Canadian Medical Association Journal, 174(5), 649-659.

3 Maheshwari A, Ray, S., & Thuluvath, P. J. (2008). Acute hepatitis C.

Lancet 372(9635):321-332. Lancet, 372(9635), 321-332.
4 Hutin, Y., Kitler, M. E., Dore, G. J., Perz, J. F., Armstrong, G. L.,
Dusheiko, G., Ishibashi, H., Grob, P., Kew, M., Marcellin, P., Seeff, L.
B., Beutels, P., Nelson, C., Stein, C., Zurn, P., Clifford, G., Vranckx, R.,
Alberti, A., Hallaj, Z. S., Hadler, S., & Lavanchy, D. (2004). Global
Burden of Disease (GBD) for Hepatitis C. Journal of Clinical
Pharmacology, 44(1), 20-29.
5 Global surveillance and control of hepatitis C: Report of a WHO

consultation organized in collaboration with the Viral Hepatitis
Prevention Board, Antwerp, Belgium. (1999). J. Viral Hepat. 6(1):35-
47., 6(1), 35-47.
6 Charrel, R. N., De Chesse, R., Decaudin, A., De Micco, P., & De

Lamballerie, X. (2001). Evaluation of disinfectant efficacy against
hepatitis C virus using a RT-PCR-based method. Journal of Hospital
Infection, 49(2), 129-134.
7 Poles, M. A., Fuerst, M., McGowan, I., Elliott, J., Rezaei, A., Mark, D.,
Taing, P., & Anton, P. A. (2001). Effectiveness of manual cleaning
and disinfection of gastroendoscopes with 3% glutaraldehyde for
decreasing the risk of transmission of hepatitis C virus. American
Journal of Gastroenterology, 96(6), 1803-1806.
8 Agolini, G., Russo, A., & Clementi, M. (1999). Effect of phenolic and
chlorine disinfectants on hepatitis C virus binding and infectivity.
American Journal of Infection Control, 27(3), 236-239.
9 Kamili, S., Krawczynski, K., McCaustland, K., Li, X., & Alter, M. J.
(2007). Infectivity of hepatitis C virus in plasma after drying and
storing at room temperature. Infection Control and Hospital
Epidemiology, 28(5), 519-524.
10 Strickland, G. T., El-Kamary, S. S., Klenerman, P., & Nicosia, A.

(2008). Hepatitis C vaccine: supply and demand. The Lancet
Infectious Diseases, 8(6), 379-386.
11 Recommendations for follow-up of health-care workers after

occupational exposure to hepatitis C virus. (1997). MMWR.Morbidity
and Mortality Weekly Report, 46(26), 603-606.
12 Alter, M. J. (1994). Occupational exposure to hepatitis C virus: a

dilemma. Infection Control and Hospital Epidemiology : The Official
Journal of the Society of Hospital Epidemiologists of America, 15(12),
742-744.
37(9), 935-940.
14 Choo, Q. -., Kuo, G., Weiner, A. J., Overby, L. R., Bradley, D. W., &
Houghton, M. (1989). Isolation of a cDNA clone derived from a
blood-borne non-A, non-B viral hepatitis genome. Science,
244(4902), 359-362.
37(9), 935-940.
16 O'Brien, S. F., Yi, Q. L., Fan, W., Scalia, V., Kleinman, S. H., &
Vamvakas, E. C. (2007). Current incidence and estimated residual
risk of transfusion-transmitted infections in donations made to
Canadian Blood Services. Transfusion, 47(2), 316-325.
doi:10.1111/j.1537-2995.2007.01108.x
17 Pawlotsky, J. M. (2009). Review: Therapeutic implications of

hepatitis C virus resistance to antiviral drugs. Therapeutic Advances
in Gastroenterology, 2(4), 205-219.
18 Pawlotsky, J. M. (2000). Hepatitis C Virus Resistance to Antiviral

Therapy. Hepatology, 32(5), 889-896.
19 Sáez-López, A., & Agüero-Balbín, J. (2006). Hepatitis C and C virus

antiviral resistance. Enferm Infecc Microbiol Clin, 24, 576-584.
20 Yu, C. I., & Chiang, B. L. (2010). A new insight into hepatitis C

vaccine development. Journal of Biomedicine & Biotechnology, 2010,
548280. doi:10.1155/2010/548280

2009, (2009).

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Hepatitis D virus

SUBSTANCES
NAME: Hepatitis D Virus
1
SYNONYM OR CROSS REFERENCE: HDV, Delta Hepatitis
CHARACTERISTICS: Hepatitis D virus is currently unclassified and has been

1
assigned to its own separate genus: Deltavirus . The HDV virion is 36 to 43
nm in diameter. It contains a circular or linear RNA genome surrounded by a
nucleocapsid protein called HDV antigen which is in turn surrounded by an
2
envelope consisting of Hepatitis B surface antigen (HBsAg) . HDV
requires hepatitis B virus (HBV) as a helper virus and as such can only infect
1 3
individuals who have also been infected with HBV .
SECTION II- HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: There are two major types of infection, HDV
and HBV coinfection and HDV superinfection in individuals with chronic
hepatitis B. Coinfection results in clinical hepatitis which is indistinguishable
4
from acute hepatitis B . Initial symptoms may include fatigue, lethargy,
1 2
abdominal discomfort, anorexia, and nausea . This leads to jaundice
and the persistence of fatigue and nausea. The disease is self-limiting and
2 5
complete viral clearance occurs in more than 90% of cases . HDV
superinfection generally causes severe acute hepatitis and leads to chronic
1
hepatitis D infection in 90% of cases . Individuals with chronic hepatitis D
can develop cirrhosis (60-70%) or fulminant hepatitis. Fulminant hepatitis is
characterized by severe hepatitis and encephalopathy and has a mortality
2
rate of almost 80%. The overall mortality rate for HDV is between 2-20% .
EPIDEMIOLOGY: HDV infections occur worldwide, and 15-20 million people

5
are thought to be coinfected or superinfected with HDV . The virus is
highly endemic in Mediterranean countries, the Middle East, Central Africa
5
and northern parts of South America . In North America, injection drug
2 3
users have the highest risk of contracting HDV .
HOST RANGE: Humans and, experimentally, chimpanzees and woodchucks

1 .
MODE OF TRANSMISSION: Transmitted through blood or blood products,

parenteral inoculation (i.e. by injection drug use), or sexual contact.
3
Individuals must also be infected with HBV .
INCUBATION PERIOD: HDV superinfection: 2-8 weeks; HBV and HDV co-
3
infection: 45- 160 days .
COMMUNICABILITY: Low communicability; can pass from person-to-person

through direct contact (e.g . blood-transfusions, contaminated needles, and
3
sexual contact) .

1
RESERVOIR: Humans .
ZOONOSIS: None.
VECTOR: None.

1
DRUG SUSCEPTIBILITY: Susceptible to alfa interferon (IFN-α) .
SUSCEPTIBILITY TO DISINFECTANTS: Unknown; however, other hepatitis

viruses are susceptible to 1-2% glutaraldehyde, 6-10% hydrogen peroxide, 8-
12% formaldehyde, iodophores (40-50 mg/L free iodine), chlorine
compounds (500-5000 mg/L free chlorine), and 0.5-3% phenolic compounds
6 .
PHYSICAL INACTIVATION: Unknown; however, other hepatitis viruses can

be inactivated by moist heat (121*C for 15 min) and dry heat (170*C for 1h
6
or 160*C for 2h) .
SURVIVAL OUTSIDE HOST: Can survive in blood and blood products under
1
the conditions used for the storage of such products .

SURVEILLANCE: Monitor for symptoms. Diagnosis is based on serological
2 4
testing for the presence of IgM or IgG antibodies to the delta antigen
1
. PCR can also be used to detect viral DNA in clinical samples .
FIRST AID/TREATMENT: Long-term treatment with high doses of IFN-α

1 4
shows some improvement in clinical outcome . Hepatitis D is highly
difficult to treat because of the severity of resulting illness and the
1
distinctiveness of this virus .
IMMUNIZATION: There is a vaccine for HBV which will prevent infection

3
with HBV and HDV in HBV seronegative individuals .
PROPHYLAXIS: Personnel exposed to HDV can be given the vaccine for

hepatitis B virus and/or hepatitis B immunoglobulin to prevent coinfection
6
of HBV and HDV .

LABORATORY ACQUIRED INFECTIONS: No cases of laboratory-acquired
HDV infection have been reported.
2
SOURCES / SPECIMENS: Blood and blood products .
PRIMARY HAZARD: Parenteral inoculation, droplet exposure of mucous

1 7
membranes, and contact exposure of broken skin .
SPECIAL HAZARD: Individuals infected with HBV are at risk for infection with
7
HDV .

8

9

9

cover the spill with paper towels and apply appropriate disinfectant starting
at the perimeter and working towards the center. Allow sufficient contact
9
DISPOSAL: Decontamination using steam sterilization, chemical disinfection,

9
or incineration must be performed before disposal of infectious waste .
STORAGE: All infectious materials should be stored in sealed containers

9
bearing the appropriate labeling .

and standards.

Canada

Copyright ©
2010 Canada
Reference:
1 Taylor, J. M., Farci, P., & Purcell, R. H. (2007). Hepatitis D (delta)
Virus. In D. M. Knipe, & P. M. Howley (Eds.), Fields Virology (5th ed.,
pp. 3031-3046). Philadelphia: Lippincott Williams and Wilkins.
2 Horvat, R. T., & Tegtmeier, G. E. (2007). Hepatitis B and D Viruses.

In P. R. Murray (Ed.), Manual of Clinical Microbiology (9th ed., ).
Washington D.C.: ASM Press.
3 American Academy of Pediatrics.Committee on Infectious

Diseases, STAT!Ref, & Teton Data Systems. (2009). Red book (28th
ed.). Elk Grove Village, IL: American Academy of Pediatrics.
Retrieved from
4 Drew, W. L. (2004). Hepatitis Viruses. In K. J. Ryan, & C. G. Ray

(Eds.), Sherris Medical Microbiology: An Introduction to Infectious
Diseases (4th ed., pp. 541-554). New York: McGraw Hill.
5 Wedemeyer, H., & Manns, M. P. (2010). Epidemiology,

pathogenesis and management of hepatitis D: Update and
challenges ahead. Nature Reviews Gastroenterology and Hepatology,
7 (1), 31-40.
6 Favero, M. S., & Bond, W. W. (1995). Transmission and Control of

Laboratory-Acquired Hepatitis Infection. In D. O. Fleming, J. H.
Richardson, J. J. Tulis & D. Vesley (Eds.), Laboratory Safety: Principles
and Practices (2nd ed., pp. 19-32). Washington, D.C.: ASM Press.
7 Viral agents (other than arboviruses): (1999). In J. Y. Richmond, &

R. W. and Mckinney (Eds.), Biosafety in Microbiological and
Biomedical Laboratories (4th ed., pp. 157-158). Washington, D.C.:
CDC & NIH.

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Hepatitis E virus

SUBSTANCES
NAME: Hepatitis E virus
SYNONYM OR CROSS REFERENCE: HEV, enterically transmitted or enteric

1 2 3
non-A non-B hepatitis (ENANB), epidemic non-A non-B hepatitis
4 , faecal-oral non-A non-B hepatitis, and A-like non-A non-B hepatitis.
CHARACTERISTICS: Hepatitis E virus (HEV) is classified as the only member of

2 4
the genus Hepevirus in the family Hepeviridae . It is identified as a
3
non-enveloped, icosahedral shaped sphere , approximately 27-34 nm in
diameter, and consisting of a single-stranded, positive sense RNA molecule
1 2 4 5
about 7.5 kilobases (kb) in length . The surface of the particle
consists of indentations and spikes, resulting in an appearance similar to
3
that of calciviruses and it is often found in faeces of infected individuals .

PATHOGENICITY/TOXICITY: The disease caused by HEV is generally self-
limiting with symptoms typical of acute viral hepatitis including, jaundice,
malaise, anorexia, abdominal pain, nausea, fever, diarrhea, discoloured stool
1 2 3 5
and/or urine, and hepatomegaly . Anicteric hepatitis and
cholestasis are also observed in some cases. Mortality rate due to infection
2
by hepatitis E have been reported to be as high as 1 % ; however, the
mortality rate may reach up to 20 % in pregnant women with each passing
trimester, making HEV infection the most severe hepatitis in pregnancy of all
recognized hepatitis viruses. Analysis of serum specimens collected from
volunteer blood donors shows that the prevalence of HEV varies from
region-to-region but is higher in endemic countries/regions as compared to
5
developed countries . Hepatitis caused by HEV is clinically
6
indistinguishable from hepatitis A disease .
EPIDEMIOLOGY: Phylogenetic studies indicate at least four distinct

5 7
genotypes of HEV (1 – 4) based on geographical origin . Genotypes 1
and 2 are considered more pathogenic, restricted to humans, and are
responsible for the large majority of cases and outbreaks in endemic
regions. Genotypes 3 and 4 are somewhat less pathogenic, infect humans,
pigs, and other animal species, and are generally responsible for sporadic
HEV infection cases within endemic and non-endemic regions. Outbreaks
and sporadic cases of HEV have occurred over a large geographic area, most
notable in regions with poor sanitation. There have been some cases of
food-borne HEV infections, but the majority of confirmed cases have been
associated with the consumption of water contaminated with feces. The
attack rate of HEV is highest in young adults between ages of 15-40. Males
are more likely to develop clinical hepatitis when infected with HEV as
compared to females. In developed countries, HEV infection is generally
reported from people who travel to HEV endemic or epidemic areas;
however, some cases of locally-acquired (autochthonous) HEV infection have
been observed in non-endemic countries including USA, Australia, France,
Greece, New Zealand, Italy, and UK. Documented epidemic outbreaks have
occurred in Algeria, Ivory Coast, Ghana, Chad, Ethiopia, Somalia, Namibia,
India, former Soviet Union, Nepal, Pakistan, Burma, Myanmar, China,
8
Vietnam, Indonesia, and Mexico .
1
HOST RANGE: Humans and animals, including swine . Several animal
species have been experimentally infected with strains of HEV, including
nonhuman primates such as African green monkeys, chimpanzees,
cynomolgus macaques, owl monkeys, rhesus monkeys, tamarins, noninbred
white mice and Wistar rats.
MODE OF TRANSMISSION: Four modes of transmission of HEV infection

have been reported: faecal-oral transmission, food-borne transmission,
5 7
blood-borne transmission, and vertical transmission . The most
common mode of transmission of HEV, also responsible for the majority of
the HEV infection outbreaks, is through the faecal-oral route, usually by
ingestion of contaminated water. Potential exists for food-borne
transmission and some cases have been observed where consumption of
raw or uncooked meat from wild boar and deer has led to HEV infection.
Blood-borne transmission is rare but has been documented in some cases
involving blood transfusions. Some cases of vertical (perinatal) transmission
from mother-to- child have been documented, particularly in India, but this
is considered to be of minor importance as a mode of transmission for HEV
and more investigation is required. Person-to- person transmission and
secondary household cases are uncommon, particularly in epidemic (poor
hygienic) conditions. In non-endemic regions, where autochthonous cases
have been observed, zoonotic transmission has been considered as the
7
likely mode of transmission, but more investigation is required .
INCUBATION PERIOD: Incubation period for HEV infection in humans

1 8
ranges from 15-60 days with a mean 40 days .
COMMUNICABILITY: Unknown. Person-to-person transmission has been

5
documented but appears to be uncommon . HEV has been detected in
the stools of infected patients after the onset of illness (jaundice) for up to
9
14 days . Maximal HEV shedding occurs during the incubation period and
during early acute stage of the disease.

RESERVOIR: Humans and animals, including monkeys, swine, rats, boars,
deer, cows, sheep, goats, camels, horses, dogs, cats, and mongoose(5,10).
All have been shown to be susceptible to infection with HEV and may act as
reservoirs for the infectious agent; however, the source(s) of HEV for some
of these wild animals has yet to be determined.
ZOONOSIS: Hepatitis E is now considered a zoonotic disease where

10
domestic pigs and wild boars are the main reservoirs . Zoonotic
transmission from deer has also been documented. Transmission may also
occur from other animals, including chickens, cats, and rats, but further
investigation is yet required.
VECTORS: None.

DRUG SUSCEPTIBILITY: Unknown.
SUSCEPTIBILITY TO DISINFECTANTS: HEV is susceptible to iodinated

disinfectants (0.075g/L or 1 % iodine)(10). It may also be sensitive to
hypochlorites (1 % sodium hypochlorite), formaldehyde (18.5 g/L; 5 %
11
formalin in water), and glutaraldehyde .
PHYSICAL INACTIVATION: HEV is more heat labile than Hepatitis A virus

(HAV) and most strains can be inactivated at temperature ≥60 °C for 15
12
minutes or more . The heat sensitivity of HEV, however, depends on the
13
heating conditions . Hepatitis E in PBS is inactivated quickly at 60 C, but
in an albumin solution is inactivated more slowly. When HEV is added to
freeze-dried fibrinogen containing stabilizers and subjected to dry heat, it is
inactivated to below detection limit within 24 hours at 80 C, but is inactivated
more slowly at 60 C. It is also susceptible to low storage temperatures
1
(between -70 °C and +8 °C) .
SURVIVAL OUTSIDE HOST: Unknown. Since HEV survives the conditions

within the intestinal tract, it is considered relatively stable in acidic and mild
4
alkaline conditions . Since HEV mainly spreads through the faecal-oral
1
route, it must be relatively stable under environmental conditions ,
possibly similar to HAV (i.e. in water and sewage for long periods).

SURVEILLANCE: Monitor for symptoms of disease. Confirm using
serological or nucleic acid tests, and by exclusion of hepatitis A and B viruses
5 . Serological tests involve enzyme-linked immunosorbent assays (i.e.
ELISA) for the detection of antibodies to HEV (IgM, IgA, and IgG), and nucleic
acid tests involve reverse transcription-polymerase chain reaction (RT-PCR)
assays for the detection of HEV RNA in serum, bile, and/or faecal samples.
4
FIRST AID/TREATMENT: Rest. No specific treatment currently available .
IMMUNIZATION: None.
PROPHYLAXIS: None.

LABORATORY-ACQUIRED INFECTIONS: No cases of laboratory-acquired
have been reported to date.
SOURCES/SPECIMENS: The main sources are of HEV are feces and sera of
1
infected human, nonhuman primates, pigs, and some other animals .
PRIMARY HAZARDS: Ingestion of feces or stool samples and other

contaminated materials. Importance of aerosol exposure has not been
demonstrated.

14

15

safety cabinet (BSC). The use of needles, syringes, and sharp objects should
15
be strictly limited . Additional precautions should be considered with
15

cover spill with paper towels and apply suitable disinfectant, starting at the
15
DISPOSAL: Decontaminate, either by steam sterilization, incineration, or

15
chemical disinfection, before disposal .
STORAGE: The infectious agent should be stored frozen in sealed containers

15
that are appropriately labelled, preferably at -70 °C or lower .

and standards.
UPDATED: August 2010

Canada.

Copyright ©
Public Health Agency of Canada, 2010 Canada
References:
1 Smith, J. L. (2001). A review of hepatitis E virus. Journal of Food
Protection, 64 (4), 572-586.
2 Chandra, V., Taneja, S., Kalia, M., & Jameel, S. (2008). Molecular
biology and pathogenesis of hepatitis E virus. Journal of
Biosciences, 33 (4), 451-464.
3 Krawczynski, K., Aggarwal, R., & Kamili, S. (2000). Hepatitis

E. Infectious Disease Clinics of North America, 14 (3), 669-687.
4 Emerson, S. U., & Purcell, R. H. (2007). Hepatitis E Virus. In D. M.

Knipe, P. M. Howley, D. E. Griffin, R. A. Lamb, M. A. Martin & B. a. S.
Roizman S.E. (Eds.), Fields Virology (5th ed., pp. 3047-3058).
Philadelphia, USA: Lippincott Williams & Wilkins.
5 Mushahwar, I. K. (2008). Hepatitis E virus: molecular virology,

clinical features, diagnosis, transmission, epidemiology, and
prevention. Journal of Medical Virology, 80 (4), 646-658.
doi:10.1002/jmv.21116
6 Goens, S. D., & Perdue, M. L. (2004). Hepatitis E viruses in humans

and animals. Animal Health Research Reviews / Conference of
Research Workers in Animal Diseases, 5 (2), 145- 156.
7 Aggarwal, R., & Naik, S. (2009). Epidemiology of hepatitis E: current

status. Journal of Gastroenterology and Hepatology, 24 (9), 1484-
1493. doi:10.1111/j.1440- 1746.2009.05933.x
8 anda, S. K., Thakral, D., & Rehman, S. (2007). Hepatitis E

virus. Reviews in Medical Virology, 17 (3), 151-180.
doi:10.1002/rmv.522
9 Clayson, E. T., Myint, K. S., Snitbhan, R., Vaughn, D. W., Innis, B. L.,
Chan, L., Cheung, P., & Shrestha, M. P. (1995). Viremia, fecal
shedding, and IgM and IgG responses in patients with hepatitis
E. The Journal of Infectious Diseases, 172 (4), 927-933.
10 Meng, X. J. (2010). Hepatitis E virus: animal reservoirs and zoonotic

risk. Veterinary Microbiology, 140 (3-4), 256-265.
doi:10.1016/j.vetmic.2009.03.017
11 Disinfection and Sterilization. (1993). Laboratory Biosafety

Manual (2nd ed., pp. 60-70). Geneva: WHO.
12 Emerson, S. U., Arankalle, V. A., & Purcell, R. H. (2005). Thermal

stability of hepatitis E virus. The Journal of Infectious Diseases,
192 (5), 930-933. doi:10.1086/432488
13 Yunoki, M., Yamamoto, S., Tanaka, H., Nishigaki, H., Tanaka, Y.,
Nishida, A., Adan-Kubo, J., Tsujikawa, M., Hattori, S., Urayama, T.,
Yoshikawa, M., Yamamoto, I., Hagiwara, K., & Ikuta, K. (2008).
Extent of hepatitis E virus elimination is affected by stabilizers
present in plasma products and pore size of nanofilters. Vox
Sanguinis, 95 (2), 94-100.

2009, (2009).

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Herpes simplex virus

Substances
NAME: Herpes simplex virus
SYNONYM OR CROSS REFERENCE: HSV-1, HSV-2, HHV-1, HHV-2, Human

1 , 2
herpes virus 1, Human herpes virus 2, cold sores, fever blisters .
CHARACTERISTICS: HSV virus, types 1 and 2, belong to the sub family

2
Alphaherpesviridae in the family Herpesviridae, genus Simplexvirus . They
are 120-300 nm in diameter and consist of a linear, double stranded DNA
genome (152 Kb for HSV-1 and 155 Kb for HSV-2) enclosed within an
icosahedral capsid, surrounded by a phospholipid rich envelope. The lipid
envelope is derived from the nuclear envelope of the infected cell.
Section II - Hazard Identification

PATHOGENICITY/TOXICITY: Although both HSV-1 and HSV-2 may infect any
area, HSV-1 is associated mainly with "above the waist" infections involving
the mouth, pharynx, face, eye, and central nervous system (CNS), whereas,
HSV-2 is associated mainly with "below the waist" infections of the genital
1 , 3
region .
Herpes labialis/cold sores: Caused mainly by HSV-1, there have been reported
1 , 2 , 4
cases caused by HSV-2 . Primary infections with HSV-1 are
1 ,
acquired usually in childhood and may be asymptomatic or subclinical
2 , 4 . Symptomatic primary infections present mainly as
gingivostomatitis, with fever, sore throat, fetor oris, anorexia, cervical
adenopathy, and mucosal edema and vesicular and ulcerative painful
1 , 2 , 4
lesions involving the buccal mucosa, tongue, gums, and pharynx
, 5 1 , 2
. Ulcers heal without scarring within 2-3 weeks . Recurrent
2
infections have generally milder symptoms and clinical course .
Recurrent lesions due to HSV-1 occur mainly on a specific area of the lip
(vermillion border of the lip), and are called "cold sores" or "fever blisters"
1 , 4 4
. The lesions heal in approximately 8-10 days .
Herpetic whitlow: Characterized by formation of painful vesicular lesions on

1
the nail or finger area .
Infections of the eye: Characteristic dendritic ulceration occurs on conjunctiva,

1
and cornea . HSV infection may cause other ocular diseases, including
blepharitis/dermatitis, conjunctivitis, dendritic epithelial keratitis, and
6
corneal ulceration .
Encephalitis: Serious infections of the CNS, affecting both children and

7
adolescents . It may occur due to primary or latent infection with HSV-1
1 , 7
virus . HSV encephalitis affects one temporal lobe, leading to focal
neurologic signs and edema. The disease can be fatal (mortality rate of
1 , 7
70%), if left untreated .
1
Genital herpes: It is a sexually transmitted disease . Genital herpes is
caused mainly by HSV-2, although HSV-1 has become as common as HSV-2
in primary genital infections in developed countries. Primary genital herpes
is characterized by formation of multiple, bilateral, painful, and extensive
genital ulcers, which heal without scarring within 12 days. Patients also
present with tender enlarged lymph nodes, fever, malaise, and myalgia.
Rarely, the disease may also cause aseptic meningitis with neck rigidity and
severe headache. Recurrent genital herpes disease is of shorter duration, is
milder and does not have systemic symptoms. The main manifestation of
the disease is prodromal paresthesias in the perineum, genitalia or buttocks,
followed by formation of grouped lesions on the external genital area. The
lesions heal without scarring in 2-5 days.
Neonatal Herpes: Neonatal herpes is an extremely severe disease with a very

high mortality rate. Neurological complications may occur in infants who
1
survive the infection . Clinical manifestations of the disease are variable
and can be classified into three groups: disseminated disease, involving
multiple visceral organs, such as lung, liver, adrenal glands, skin, eye, and
the brain (25%); CNS disease with listlessness and seizures (~ 30% of total
cases; including 60 to 75% of those cases displaying disseminated disease);
1 4
and disease limited to the skin, eyes, and/or mouth (SEM) (45%) .
EPIDEMIOLOGY: Worldwide. HSV infections occur worldwide without any

2
specific seasonal distribution . The prevalence of HSV-1 infection is
3
greater than HSV-2 infection in most geographic areas . HSV-1 causes
mainly oral infections in children and has a seroprevalence in adults of 70%
8
in developed countries and 100% in developing countries . Orolabial
herpes has an infection rate of approximately 33% in developing countries
3
and 20% in developed countries . Genital herpes, caused mainly by HSV-2,
8
is the main cause of genital ulcers worldwide . Neonatal herpes is an
uncommon but serious complication of genital herpes with occurrence rates
ranging from 1/3,000 to 1/20,000 live births, resulting in an estimated
incidence of 1,500 new cases of neonatal HSV infection annually in the
3 , 4 , 8
United States . Corneal diseases due to HSV infection are an
important cause of blindness, and account for an estimated 500,000 cases
6
annually in the United States . Herpes simplex encephalitis (HSE), caused
by HSV infection, is one of the most severe CNS infections, accounting for
approximately 10–20% of all encephalitic viral infections of the CNS, in the
7
United States .
1
HOST RANGE: Humans , but non-human primates in captivity can be
accidentally infected. Rabbits and rodents can be infected experimentally.
MODE OF TRANSMISSION: Direct contact with infected secretions or

mucous membranes/skin with lesions from an asymptomatic or
symptomatic patients shedding the virus, is the main mode of transmission
2 , 3 , 7
of HSV . Transmission of HSV-1 can also occur by respiratory
7 1 , 2
droplets . Genital herpes is transmitted sexually . Neonatal herpes
can be acquired at different times: intrauterine (in utero) in 5% of the cases,
peripartum (perinatal) in 85% of the cases, and postpartum (postnatal) in
1 , 4
10% of the cases .
INCUBATION PERIOD: Incubation period generally ranges from 1-26 days

2 . Incubation period for orolabial HSV infection is 2 to 12 days, with an
4 1
average of 4 days . Genital herpes is acquired within 5 days . Oral and
genital lesions appear approximately 19 and 24 days following
5
transplantation organ of an infected organ .
COMMUNICABILITY: HSV viruses are passed through close personal

9
contact and mainly oral-genital or genital-genital contact . Vertical
transmission can also occur in symptomatic and asymptomatic women.
Transfer may be in utero, intrapartum, or postnatal.

1 , 2
RESERVOIR: Humans
ZOONOSIS: None.
VECTOR: None.

DRUG SUSCEPTIBILITY: Antiviral drugs like acyclovir, foscarnet valacyclovir,
1
famciclovir, and penciclovir can inhibit viral replication . Foscarnet is used
1 , 2
for acyclovir-resistant HSV cases .
DRUG RESISTANCE: Acyclovir resistant strains have been isolated from

immunocompromised patients, particularly AIDS patients with
1 , 10
persistent/recurrent lesions .
SUSCEPTIBILITY TO DISINFECTANTS: HSV virus is easily inactivated by lipid

2
solvents . It can be inactivated by 0.5% Lysol in 5 min; by Listerine (1:1
mixtures) in 5 min; by 2,000 ppm (2,000 ul/liter) of bleach in 10 min; by
11
rubbing alcohol (1:1 mixtures) . HSV is also susceptible to quaternary
12
ammonium compounds . Most herpes viruses are also susceptible to
30% ethanol and isopropanol, 0.12% orthophenyl phenol, and 0.04%
13
glutaraldehyde .
PHYSICAL INACTIVATION: HSV virus is easily inactivated by exposure to PH

<4, temperatures >56°C for 30 min, pasteurization (60°C for 10 h), and
2 , 11
microwave heating for 4 min . HSV-2 is more thermolabile than HSV-
11
1 .
SURVIVAL OUTSIDE HOST: HSV virus survives for short periods of time
3
outside the host . It can survive on dry inanimate surfaces (survival
ranges from few hours to 8 weeks). They survive longer at lower humidity
14 .

SURVEILLANCE: Monitor for symptoms, including lesions in or around the
3
oral cavity . Viral culture or PCR is used to detect presence of viral
infection. Culture in cells can show multinucleated giant cells, desquamated
epithelial cells with intranuclear inclusions. Direct examination of virus in
clinical samples can also be done using fluorescent antibody (DFA) test to
detect viral antigens present within a tissue or smear specimen, Tzanck test,
2 , 3
Enzyme immunoassay (EIA) . PCR can be used to detect viral DNA in
cerebrospinal fluid in the case of encephalitis or in blood in cases of
1- 4 , 15
neonatal HSV infection .
FIRST AID/TREATMENT:
Genital herpes: Treated with antiviral drugs such as acyclovir, valacyclovir,

2
famciclovir, and penciclovir . Valacyclovir, famciclovir are approved for
1
chronic suppression of genital herpes .
Herpes labialis: Primary infection in children is treated with oral acyclovir. N-

docosanol, a non prescription topical medication, or topical acyclovir
2
reduces time to healing and duration of pain by approximately half a day
, 4 4
. Oral acyclovir and valacyclovir can be used for recurrent infections .
HSE: Treated with Acyclovir.
Neonatal HSV infection: Treated with intravenous acyclovir for 21 days for
4
disseminated infection or CNS infection, and 14 days for SEM infection .
Eye infections associated with HSV infection can be treated either with
topical trifluridine, idoxuridine, and vidarabine; or with oral acyclovir,
valacyclovir, famciclovirFootnote 2,Footnote 6.
IMMUNIZATION: None
PROPHYLAXIS: Acyclovir can be used as a prophylactic drug to prevent

reactivation of herpes labialis after exposure to ultraviolet radiation, facial
4
surgery, or exposure to sun and wind during skiing . Prophylaxis with
oral acyclovir is recommended to suppress genital HSV recurrences near the
4
end of pregnancy . Suppressive therapy with Valcyclovir may be used to
prevent frequent recurrences of genital herpes.

1
SOURCE/SPECIMENS: Virus is shed from saliva, cervix, and urethra .
PRIMARY HAZARDS: Direct contact with clinical material or viral isolates,

inhalation of concentrated aerosolized materials, droplet exposure of
mucous membranes of the eyes, nose, or mouth, ingestion, accidental
parenteral inoculation are the primary hazards associated with herpes
16
viruses including HSV 1 and 2 .

17

18

18

19

19


and standards.

Canada

Pathogen Safety Data sheet are compiled from sources believed to be
Copyright ©
Canada
References:
Sherris medical microbiology: An introduction to infectious diseases
(4th ed., pp. 555-576). USA: McGraw Hill.
2 Jerome, K. R., & Morrow, R. A. (2007). Herpes simplex viruses and

Herpes B virus. In P. R. Murray (Ed.), Manual of clinical microbiology
(9th ed., pp. 1523-1536). Washington, D.C.: ASM Press.
3 Chayavichitsilp, P., Buckwalter, J. V., Krakowski, A. C., & Friedlander,

S. F. (2009). Herpes simplex. Pediatrics in Review, 30(4), 119-129.
4 Kimberlin, D. W. (2005). Herpes simplex virus infections in

neonates and early childhood. Seminars in Pediatric Infectious
Diseases, 16(4), 271-281.
5 Miller, G. G., & Dummer, J. S. (2007). Herpes simplex and varicella

zoster viruses: forgotten but not gone. American Journal of
Transplantation, 7(4), 741-747.
6 Green, L. K., & Pavan-Langston, D. (2006). Herpes simplex ocular

inflammatory disease. International Ophthalmology Clinics, 46(2),
27-37.
7 Whitley, R. J. (2006). Herpes simplex encephalitis: adolescents and

adults. Antiviral Research, 71(2-3), 141-148.
8 Gupta, R., Warren, T., & Wald, A. (2007). Genital herpes. Lancet,
370(9605), 2127-2137.
9 Roizman, B., Knipe, D. M., & Whitley, R. J. (2007). Herpes Simplex

Viruses. In D. M. Knipe, & P. M. Howley (Eds.), Fields Virology (5th
ed., pp. 2501-2601). Philidelphia: Lippincott Williams & Wilkins.
10 Levin, M. J., Bacon, T. H., & Leary, J. J. (2004). Resistance of herpes

simplex virus infections to nucleoside analogues in HIV-infected
patients. Clinical Infectious Diseases, 39(Suppl 5), S248-57.
11 Croughan, W. S., & Behbehani, A. M. (1988). Comparative study of

inactivation of herpes simplex virus types 1 and 2 by commonly
used antiseptic agents. Journal of Clinical Microbiology, 26(2), 213-
215.
12 Wood, A., & Payne, D. (1998). The action of three

antiseptics/disinfectants against enveloped and non-enveloped
viruses. Journal of Hospital Infection, 38(4), 283-295. doi:DOI:
10.1016/S0195-6701(98)90077-9

Williams & Wilkins.

15 Strick, L. B., & Wald, A. (2006). Diagnostics for herpes simplex

virus: is PCR the new gold standard? Molecular Diagnosis &
Therapy, 10(1), 17-28.

NIH.

2009, (2009).


Leitner R., Ouellette M. and Ugwu K. (Eds.), The Laboratory
Biosafety Guidelines (3rd ed.). Canada:
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Human Coronavirus

SUBSTANCES
NAME: Human Coronavirus (excluding SARS-CoV, MERS-CoV and SARS-CoV-
2)
SYNONYM OR CROSS REFERENCE: HCoV-229E, HCoV-OC43, HCoV-NL63,

HCoV-HKU1, common cold, viral respiratory disease, viral gastroenteritis.
CHARACTERISTICS: Enveloped viruses 120- 160 nm in diameter, with a

positive stranded, capped and polyadenylated RNA genome that is 27-32 kb
1 3
in size - .There are many coronaviruses which affect animals;
however, currently, only five strains of coronavirus are known to infect
humans, classified based on antigenic cross-reactivity: HCoV-229E, HCoV-
1 4
OC43, HCoV-NL63, and HCoV-HKU1 - . HCoV-229E and HCoV-NL63 are
more related to each other than to the other coronavirus, as they share 65%
5
of their sequence identity .

PATHOGENICITY/TOXICITY: HCoV-229E and HCoV-OC43 cause the common
cold, a self-limiting upper respiratory tract infection. Infection can lead to a
number of illnesses such as bronchitis, gastroenteritis, progressive
demyelinating encephalitis, diarrhea, peritonitis, nasal obstruction,
1 5
rhinorrhea, sneezing, sore throat and cough , . They can cause more
severe lower respiratory tract infection, including pneumonia in infants,
1 3
elderly and immunocompromised individuals - . HCoV-229E is a
common agent if coryza, whereas HCoV-OC43 is generally characterized by
3
sore throats . HCoV-NL63 causes laryngotracheitis (croup) and nonfatal
upper and lower respiratory tract infections in children, elderly, and
1 3
immunocompromised individuals , . HCoV-HKU1 causes mild upper
respiratory diseases, the common cold, bronchiolitis, and pneumonia, with
symptoms such as rhinorrhoea, fever, cough, febrile seizure, and wheezing
3 6
, . More severe illness may occur in children, adults with underlying
disease, the elderly, and may be associated with gastrointestinal illness ( 1
).
EPIDEMIOLOGY: Coronaviruses have a worldwide distribution, causing 10-

15% of common cold cases. Infections show a seasonal pattern with most
7 8
cases occurring in the winter months , .
HOST RANGE: Humans.
MODE OF TRANSMISSION: Infection can be transmitted through inhalation

of respiratory droplet aerosols; virus can also be spread via the fecal-oral
1 2
route, and through fomites , .
4 8
INCUBATION PERIOD: 2-4 days , .
COMMUNICABILITY: Human-to-human transmission is possible during the

presence infectious droplets, which can cause infection via inhalation, or
8
through contaminated surfaces .

4
RESERVOIR: Humans .
ZOONOSIS: None.
VECTORS: None.

DRUG SUSCEPTIBILITY: Currently, there are no specific antiviral drugs for
4
coronavirus available .
SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to 0.1% sodium

hypochlorite, 0.1% organochlorine, 10% iodophore, 70% ethanol and 2%
glutaraldehyde. Resistant to 0.04% quaternary ammonium compound and
9
phenolics .
PHYSICAL INACTIVATION: Inactivation by UV light can be done by exposure

to 1200 µJ/cm2 for 30 minutes 10 , 11 .
SURVIVAL OUTSIDE HOST: Survives up to six days in aqueous mediums and

12
up to 3 hours on dry inanimate surfaces .

SURVEILLANCE: Coronavirus infections are not usually diagnosed due to the
mild, self-limited nature of the disease. Research laboratories have used
isolation methods, electron microscopy, serology and PCR-based assays to
4
diagnosis coronavirus infections for surveillance studies .
FIRST AID/TREATMENT: No specific treatment available, treatment should

4 7
be supportive , .
IMMUNIZATION: None.
PROPHYLAXIS: None.

LABORATORY-ACQUIRED INFECTIONS: No infections have been reported
to date. However, this may be an under-estimate of the number of
incidences as symptoms are nonspecific and self-limiting.
SOURCES/SPECIMENS: Specimens from the upper or lower respiratory tract,

2
stools .
2
PRIMARY HAZARDS: Aerosols, contact with stools .

13
RISK GROUP CLASSIFICATION: Risk group 2 . This risk group applies to
the species as a whole, and may not apply to every strain within the species.

14
infectious materials, animals, or cultures . These containment
requirements apply to the species as a whole, and may not apply to each
strain within the species.
14

14

14

14
disinfection, gamma irradiation, or incineration. .

14

and standards.
UPDATED: November, 2010

Canada.

Copyright ©
Canada
REFERENCES:
Wevers, B. A., & van der Hoek, L. (2009). Recently Discovered
1
Human Coronaviruses. Clinics in Laboratory Medicine, 29(4), 715-
724.
Mahony, J. B. (2007). Coronaviruses. In P. R. Murray (Ed.), Manual

2
of Clinical Microbiology (9th ed., pp. 1414-1423). Washington D.C.:
ASM Press.
Pyrc, K., Berkhout, B., & van der Hoek, L. (2007). Antiviral strategies
3
against human coronaviruses. Infectious Disorders Drug Targets,
7(1), 59-66.
Lai, M. M. C., Perlman, S., & Anderson, L. J. (2007). Coronaviridae.

4
In D. M. Knipe, P. M. Howley, D. E. Griffin, M. A. Martin, R. A. Lamb,
B. Roizman & S. E. Straus (Eds.), Fields Virology (5th ed., pp. 1305-
1336). Philadelphia PA: Lippincott Williams & Wilkins.
Dijkman, R., & van der Hoek, L. (2009). Human coronaviruses 229E
5
and NL63: close yet still so far. Journal of the Formosan Medical
Association = Taiwan Yi Zhi, 108(4), 270-279. doi:10.1016/S0929-
6646(09)60066-8
Perlman, S., & Netland, J. (2009). Coronaviruses post-SARS: update

6
on replication and pathogenesis. Nature Reviews.Microbiology, 7(6),
439-450. doi:10.1038/nrmicro2147
Van Der Hoek, L. (2007). Human coronaviruses: What do they

7
cause? Antiviral Therapy, 12(4 B), 651-658.
Wat, D. (2004). The common cold: A review of the literature.

8
European Journal of Internal Medicine, 15(2), 79-88.
Sattar, S. A., Springthorpe, V. S., Karim, Y., & Loro, P. (1989).

9
Chemical disinfeciton of non-porous inanimate surface
experimentally contaminated with four human pathogenic
viruses. Epidemiology and Infection, 102(3), 493-505.
Johnston, S. L., Papi, A., Bates, P. J., Mastronarde, J. G., Monick, M.

10
M., & Hunninghake, G. W. (1998). Low grade rhinovirus infection
induces a prolonged release of IL-8 in pulmonary epithelium.
Journal of Immunology (Baltimore, Md.: 1950), 160(12), 6172-6181.
Chilvers, M. A., McKean, M., Rutman, A., Myint, B. S., Silverman, M.,
11
& O'Callaghan, C. (2001). The effects of coronavirus on human
nasal ciliated respiratory epithelium. The European Respiratory
Journal : Official Journal of the European Society for Clinical
Respiratory Physiology, 18(6), 965-970.
Sizun, J., Yu, M. W. N., & Talbot, P. J. (2000). Survival of human

12
coronaviruses 229E and OC43 in suspension and after drying on
surfaces: A possible source of hospital-acquired infections. Journal
of Hospital Infection, 46(1), 55-60.
Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of

13
2009, (2009).
Public Health Agency of Canada. (2004). In Best M., Graham M. L.,

14
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Human papillomavirus

SUBSTANCES
NAME: Human papillomavirus
SYNONYM OR CROSS REFERENCE: HPV, cervical cancer, cervical and uterine

carcinoma, cervical dysplasia, genital warts (condyloma acuminatum,
venereal warts, anal and anogenital warts), the common wart ( verruca
vulgaris), papilloma venereum, the common types are 6, 11, 16, 18, 31, 45,
and 58.
CHARACTERISTICS: Part of the Papillomaviridae family, HPV is a closed

circular double-stranded DNA virus located in a non-enveloped, icosahedral
1 2
capsid that is 55 nm in diameter . Over 100 types of HPV have been
identified, 80 types have been sequenced, and it is believed that over 200
3
types exist based on partially sequenced fragments . It is a very common
sexually transmitted disease, with over 50 different types causing anogenital
4 5
infections . Of those, 25 are proven or likely human carcinogens .

PATHOGENICITY/TOXICITY: HPV viruses infect the basal epithelial cells of
cutaneous and mucosal keratinized epithelia. Cutaneous infections affect
most commonly the hands and feet, while mucosal infections target the
lining of the mouth (small nodules can develop into cancerous cells), throat,
respiratory tract, and anogenital epithelium(1). When mucosal infections do
not clear spontaneously on their own, they can progress into cervical
intraepithelial neoplasm, which can lead to cervical cancer(6). IARC has
identified 25 proven or likely high-risk types, including HPV 16, 18, 31, 33, 35,
39, 45, 58, which can lead to head, neck, and mucosal anogenital cancers(5).
All cervical cancers and 4% of all cancers are the result of HPV
infections(6,7). Low-risk genotypes, such as 6 and 11, can cause benign or
low-grade cervical tissue damage and warts (including common, genital,
and anogenital) in regions of the cervix, vagina, vulva, anus, penis, or
scrotum(8); however, 90% of infection with both high risk and low risk types
clear spontaneously within 2 years and most are asymptomatic.
EPIDEMIOLOGY: HPV infections are common worldwide, with higher

prevalence in certain population and regions, such as sub-Saharan Africa,
8
south-central and south-east Asia, Latin America, and the Caribbean . It is
one of the most common sexually transmitted diseases in North America,
with prevalence as high as 25 million cases, and 1 - 5.5 million new cases
1 9 10
occurring per year in the United States . Infection with genital
6
warts is especially prevalent in the 18 - 3 0 age group .
HOST RANGE: Observed in humans only, papillomaviruses are completely

6
species- specific .
MODE OF TRANSMISSION: Infectious cells can be transmitted through

direct virus- cell contact, such as skin-skin contact, sexual activity, and
prolonged exposure to contaminated clothing as the virus may be carried
1
on fomites . Transmission can also occur from mother-to-newborn
11
through vertical transmission, albeit rarely .
INCUBATION PERIOD: Unclear as it can vary from one month to several

years, but it is usually 3 weeks to 8 months, and most warts develop 2 - 3
months after infection(9); however, most cases of infections will never show
any symptoms(8).
COMMUNICABILITY: Visible presence of genital warts can increase chances

of infection dramatically, as 65% of people who have come in contact with
9
the warts will develop them as well .

6
RESERVOIR: Humans .
ZOONOSIS: None.
VECTORS: None.

DRUG SUSCEPTIBILITY: HPV is not susceptible to antiviral drugs. Topical
treatment using trichloacetic acid, ammonium trichloro (dioxoethylene-
O,O') tellurate (AS101), and podophyllin on external vulval and perianal
12
warts has been found to be effective with low reoccurrence rate . The
immunostimulant imiquimod is also an effective local treatment of genital
warts.
DRUG RESISTANCE: HPV is resistant to most antiviral agents as there is no

12
complete cure to date, and chances of reoccurrence are high .
SUSCEPTIBILITY TO DISINFECTANTS: Exposure to 90% ethanol for at least 1

minute, 2% glutaraldehyde, 30% Savlon, and/or 1% sodium hypochlorite can
10 13
disinfect the pathogen .
PHYSICAL INACTIVATION: Varies with different strains; sensitive to UV-

irradiation, heating to 100 °C is sufficient for ina ctivation(10).
SURVIVAL OUTSIDE HOST: HPV is resistant to heat and drying, and is able
to survive on inanimate objects such as clothing and laboratory equipment
that have come in contact with infected patients, although the precise
1 11
survival time is unknown .

SURVEILLANCE: Mild changes in the epithelium caused by HPV infections
8
can be detected by virological and cytological techniques . Abnormal
growth of squamous intraepithelial lesions (SIL) can be identified using
cytological examinations of cervical or anal smears (Pap test), and
histological examination of cervical or anal biopsies can be used to detect
intraepithelial neoplasia (CIN or AIN). Persistent infection can result in the
virus integrating into human DNA, causing cancer precursors, which can
lead to anogenital and head-and-neck cancers if untreated. Detection of
14
HPV DNA can also be used to detect infection in women and men .
FIRST AID/TREATMENT: No first aid treatment is available. Liquid nitrogen

can be used for treatment against warts.
IMMUNISATION: The quadrivalent HPV vaccine Gardasil (types 6, 11, 16, 18)
and the divalent vaccine Cervarix (16 and 18) have been found to be very
effective in decreasing prevalence of types 6, 11, 16, and 18 genital lesions in
boys between 9-15 years of age and women between 18-26 years of age.
Gardasil is also effective in males between 18- 26 years of age, and can also
9 15
be used by females . The vaccine contains papillomavirus-like
particles (empty shells of viral structural proteins) that produce a
neutralizing antibody response, which is believed to prevent papillomavirus
16
from infecting host cells . It also displays efficacy against condyloma
and penile intraepithelial neoplasia. Gardasil and Cervarix are the only two
24
HPV vaccines approved for use in Canada.
PROPHYLAXIS: Promising virus-like particle (VLP) vaccines, which are

protein shells of HPV without infective DNA, can induce high titers of type-
specific antibody. Prophylactic VLP seeks to elicit neutralizing antibody, and
would be ideally targeted to adolescent women prior to sexual intercourse
17 . Gardasil and Cervarix prevent infection of the four most common
forms of HPV, including types 16 and 18 which can cause cervical cancers
18 . Spreading awareness and knowledge of the risks posed by HPV can
19
increase self protection and lower prevalence of infection . Screening
for and removal of cervical high grade lesions is a very effective way to
prevent invasive cancer in women.

LABORATORY -ACQUIRED INFECTIONS : None reported to date.
SOURCES/SPECIMENS: Warts on perianal or common skin infected outer

9 20
skin tissues, and melanoma biopsy tissues .
PRIMARY HAZARDS: Accidental skin contact with infected wart tissue may
lead to development of common wart (verruca vulgaris), due to benign
21
cutaneous HPV types . Accidental transmission of genital HPVs from
clinical specimens has not been reported and it should be considered very
unlikely.
SECOND VII - EXPOSURE CONTROLS / PERSONAL PROTECTION

22

23

23

SPILLS: Allow aerosols to settle. While wearing protective clothing, cover
spill with absorbent paper towel. Apply appropriate disinfectant, and
starting from perimeter and wipe towards the center. Allow sufficient
contact time before cleaning up.

23
STORAGE: Properly labelled and sealed containers.

and standards.

Canada Although the information, opinions and recommendations
contained in this Pathogen Safety Data Sheet are compiled from sources
believed to be reliable, we accept no responsibility for the accuracy,
information. Newly discovered hazards are frequent and this information
may not be completely up to date.
Copyright©
Canada
1 Burd, E. M. (2003). Human papillomavirus and cervical cancer.

2 Gallangher, M. J., Giannoudis, A., Herrington, C. S., & Hiscott, P.

(2001). Human papillomavirus in pterygium. 85, 782-784.
3 Anhang, R., Goodman, A., & Goldie, S. J. (2004). HPV

communication: review of existing research and
recommendations for patient education. CA: A Cancer Journal for
Clinicians, 54 (5), 248-259.
4 de Villiers, E. M., Fauquet, C., Broker, T. R., Bernard, H. U., & zur
Hausen, H. (2004). Classification of papillomaviruses. Virology, 324
(1), 17-27. doi:10.1016/j.virol.2004.03.033
5 Bouvard, V., Baan, R., Straif, K., Grosse, Y., Secretan, B., El
Ghissassi, F., Benbrahim-Tallaa, L., Guha, N., Freeman, C., Galichet,
L., Cogliano, V., & WHO International Agency for Research on
Cancer Monograph Working Group. (2009). A review of human
carcinogens--Part B: biological agents. The Lancet Oncology, 10
(4), 321-322.
6 Stanley, M. (2010). Pathology and epidemiology of HPV infection in

females. 117, 5-10
7 Walboomers, J. M., Jacobs, M. V., Manos, M. M., Bosch, F. X.,

Kummer, J. A., Shah, K. V., Snijders, P. J., Peto, J., Meijer, C. J., &
Munoz, N. (1999). Human papillomavirus is a necessary cause of
invasive cervical cancer worldwide. The Journal of Pathology, 189
(1), 12-19. doi:2-F
8 Cutts, F. T., Franceschi, S., Goldie, S., Castellsague, X., de Sanjose,

S., Garnett, G., Edmund, W. J., Claeys, P., Goldenthal, K. L., Harper,
D. M., & Markowitz, L. (2007). Human papillomavirus and HPV
vaccines: a review. 85 (9), 719-726.
9 Giuliano, A. R., Anic, G., & Nyitray, A. G. (2010). Epidemiology and

pathology of HPV disease in males. 117, 15-19.
10 Ferenczy, A., Bergeron, C., & Richart, R. M. (1989). Human

papillomavirus DNA in fomites on objects used for the
management of patients with genital human papillomavirus
infections. Obstetrics and Gynecology, 74 (6), 950-954.
11 Hsueh, P. R. (2009). Human papillomavirus, genital warts, and

vaccines. Journal of Microbiology, Immunology, and Infection =
Wei Mian Yu Gan Ran Za Zhi, 42 (2), 101-106.
12 Friedman, M., Bayer, I., Letko, I., Duvdevani, R., Zavaro-Levy, O.,
Ron, B., Albeck, M., & Sredni, B. (2009). Topical treatment for
human papillomavirus-associated genital warts in humans with
the novel tellurium immunomodulator AS101: assessment of its
safety and efficacy. The British Journal of Dermatology, 160 (2),
403-408. doi:10.1111/j.1365-2133.2008.08853.x
13 Laboratory Safety Manual (1993). (2nd ed.). Geneva: World Health

Organization.
14 Bauer, H. M., Ting, Y., Greer, C. E., Chambers, J. C., Tashiro, C. J.,
Chimera, J., Reingold, A., & Manos, M. M. (1991). Genital Human
Papillomavirus Infection in Female University Students as
Determined by a PCR-Based Method. 265, 472-477.
15 Solomon, D., Castle, P., Hildesheim, A., Katki, H. A., Schiffman, M.,
& Wacholder, S. (2009). HPV vaccination in women aged 24-45
years. Lancet, 374 (9697), 1239; author reply 1239-40.
doi:10.1016/S0140-6736(09)61782-7
16 Steinbrook, R. (2006). The potential of human papillomavirus

vaccines. The New England Journal of Medicine, 354 (11), 1109-
1112. doi:10.1056/NEJMp058305
17 Schiffman, M., & Castle, P. E. (2003). Human Papillomavirus -

Epidemiology and Public Health. 127, 930-935.
18 Hales, D., & Lauzon, L. (Eds.). (2010). An Invitation to Health (2nd

ed.) Cengage Learning Inc.
19 Klug, S. J., Hukelmann, M., & Blettner, M. (2008). Knowledge about

infection with human papillomavirus: a systematic review.
Preventive Medicine, 46 (2), 87-98.
doi:10.1016/j.ypmed.2007.09.003
20 Dreau, D., Culberson, C., Wyatt, S., & Holder, W. D.,Jr. (2000).
Human papilloma virus in melanoma biopsy specimens and its
relation to melanoma progression. Annals of Surgery, 231 (5), 664-
671.
21 Noyes, W. F. (1968). Verrucae: virus structure, localization of

antigens, and comparison with the Shope papilloma. Cancer
Research, 28 (7), 1321-1324.

2009, (2009).
23 Public Health Angency of Canada. (2004). In Best., Graham M. L

Leiter R., Ouellette M. and Ugwu K. (Eds.) Laboratory Biosafety
Guidelines (3rd ed.). Canada: Public Health Angency of Canada

page=18#approve
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Human Parainfluenza virus

SUBSTANCES
NAME: Human Parainfluenza virus
1
SYNONYM OR CROSS REFERENCE: Human parainfluenza virus (hPIV)
2
CHARACTERISTICS: Human parainfluenza viruses (hPIV1-4) were originally

classified as members of the genus Paramyxovirus within the family
1 2
Paramyxoviridae ; however, according to new findings hPIVs are now
divided into two genera: Respirovirus (hPIV 1 and 3) and Rubulavirus (hPIV 2
3
and 4), under the subfamily Paramyxovirinae . Virus particles are
1 3
enveloped, pleomorphic, and about 150 to 300 nm in diameter . The
lipid envelop is derived from the cell membrane of the infected cell and
contains specific glycoprotein spikes which include the haemagglutinin-
neuraminidase and the "fusion" proteins. The nucleocaspid core is
herringbone-like in shape, and is filamentous since it is studded with the
"phosphoprotein" and the "large" protein. The viral genome consists of a
linear, non-segmented, negative-sense RNA molecule, usually containing
about 15,000 nucleotides.

PATHOGENICITY/TOXICITY: hPIVs generally cause upper and lower
1 3
respiratory infections . hPIVs are the second most common cause of
lower respiratory disease in young children after respiratory syncytial virus.
hPIVs primarily attack the cell within the respiratory epithelium. Infected
cells are distinguishable from normal cells due to their change in
morphology, including focal rounding and increase in size of the cytoplasm
and nucleus. In some cases, formation of multinucleated giant cells is also
observed. Common symptoms of illness caused by hPIVs include rhinorrhea,
cough, croup (acute laryngotracheobronchitis), bronchiolitis, and
pneumonia. In some cases high body temperatures of up to ~40 °C are also
1
observed . Croup in children is mainly caused by hPIV1; however, hPIV2
3
has also been shown to cause croup . Bronchiolitis and pneumonia are
caused by all four types of hPIVs, but more cases have been associated with
hPIV 1 and 3; however, more cases among hospitalized children are caused
by hPIV3. Immunocompromised children and adults may develop more
severe symptoms, which may prove fatal. hPIVs have also been linked to
acute and chronic neurological diseases, including febrile seizures,
encephalitis, ventriculitis, and cluster headaches. Other conditions such as
development of apnea and bradycardia due to hPIV infection have also been
reported in rare cases in infants. Viremia is most prominent in infected
children and the immunocompromised where it has been shown to extend
to a few months in some rare cases. Primary infections tend to be mild or
asymptomatic and repeated infections are often needed before any
protection develops. Immunity, however, is not long-lasting, as evident from
susceptibility to subsequent infections during adulthood.
EPIDEMIOLOGY: hPIVs are common community-acquired respiratory

pathogens responsible for upper and lower respiratory infections
throughout the world without any ethnic, socioeconomic, gender, age, or
geographic boundaries; however, morbidity and mortality rates are higher
3
in developing countries as compared to developed countries . The
majority of infections and deaths are observed among young infants,
immunocompromised, and elderly individuals. Malnutrition, overcrowding,
vitamin A deficiency, lack of breast feeding, and environmental
contaminants are factors that can predispose to these infections. It has been
estimated that 12% of the 500,000 to 800,000 lower respiratory infection
(LRI) cases reported annually in USA are caused by hPIV1-3. It has also been
estimated that, worldwide, 10% of the total LRIs in preschool children are
caused by hPIVs and 25 to 30% of these result in death. Nosocomial
infections are also common, especially among young infants; with hPIV3
4
being the most frequently transmitted among the four hPIVs . Although
the four serogroups of hPIV1-4 have different seasonal peaks, infections
3
caused by these viruses tend to be diagnosed throughout the year .
hPIV1 causes biennial epidemics which peak during the fall season. During
these epidemics the majority of infections (50%) occur in children aged 7 to
36 months and peaking during the second and third year of life. hPIV2 also
causes biennial infections, either with hPIV1 or during alternate years from
hPIV1, or annual epidemics, which peak during fall to early winter. The
majority of infections (60%) caused by hPIV2 occur in children younger than
5 years of age and peak between the first two years of life. Outbreaks
caused by hPIV3 tend to occur yearly and peak during early spring to
summer (for North America and Europe). The majority of these infections
(40%) occur in children during the first year of life. Little is known about the
epidemiology of hPIV4 due to the small number of studies conducted.
Generally, it has been noted that the rate of infection is relatively the same
in age groups from young infants to adults. An outbreak of hPIV4 within a
developmental disabilities unit involving 38 institutionalized children and 3
5
staff members has also been described .
1 2
HOST RANGE: Humans . hPIVs have also been shown to infect many
3
other animals under natural and experimental conditions . Infection has
been induced in hamsters, guinea pigs, adult ferrets, non-human primates
(chimpanzees, macaques, and squirrel, owl, patas, and rhesus monkeys);
however, these infections are almost always asymptomatic.
INFECTIOUS DOSE: Unknown; however, evidence exists that the infectious

2
dose for hPIV1 is small (80 TCID50 of hPIV1) . The National Institutes of
6
Health lists the infection dose for parainfluenza 1 to be ≥ 1.5 viral units,
administered through nasal drops .
MODE OF TRANSMISSION: hPIVs can be transferred through direct person-

2
to-person contact (with infected secretions) and via respiratory droplets .
Some sources, however, suggest that person-to-person transfer through
contact is less likely since hPIVs do not survive well outside the host, and
3
instead transfer through contaminated surfaces is more likely .
INCUBATION PERIOD: Incubation period for infection by hPIVs is about 2 to

1
4 days .
COMMUNICABILITY: hPIVs are transmitted between humans through

2
direct person-to- person contact . They are also transmitted by large-
droplet spread. The exact period of communicability is not known; however,
hPIV3 (the most infective hPIV) is known to shed from the oropharynx for
about 3 to 10 days during initial infection. Shedding rates are lower for
subsequent infections. In rare cases, hPIV3 has been observed to shed for
periods as long as 3 to 4 weeks.

2
RESERVOIR: Infected humans .
7
ZOONOSIS: None .
VECTORS: None

DRUG SUSCEPTIBILITY: No antiviral drugs with proven clinical efficacy
3
against hPIVs are currently available . It has been suggested that hPIVs
may be susceptible to ribavirin, some interferons, and some protein
1
inhibitors; however, further testing is required to evaluate their efficacy .
SUSCEPTIBILITY TO DISINFECTANTS: hPIVs may be sensitive to

hypochlorites (1% sodium hypochlorite), formaldehyde (18.5 g/L; 5%
8
formalin in water), 2% glutaraldehyde, and iodophores (1% iodine) .
Common detergents, disinfectants, or antiseptic agents are usually efficient
3
enough to remove hPIVs from contaminated surfaces .
PHYSICAL INACTIVATION: hPIVs are sensitive to temperatures of >37 °C,

when significant decrease in viral survival is observed, and are almost
3
completely inactivated at 50 °C for about 15 minutes . They are most
stable at 4 °C or under freezing conditions. Viral infectivity is also rapidly lost
at pH 3.0 to 3.4, under low humidity, and upon virus desiccation. They are
also inactivated by ether.
SURVIVAL OUTSIDE HOST: Existing evidence shows that hPIV1-3 can survive
for up to 10 hours on nonporous surfaces and 4 hours on porous surfaces
3 . Survival rate on human skin has been shown to be lower, as hPIV3 loses
more than 90% infectivity within the first 10 minutes when placed on fingers.
Viral infectivity can be maintained for extended periods of time, up to 26
years for hPIV1, if frozen with the addition of various reagents such as 0.5%
bovine serum albumin, skim milk, 5% dimethyl sulfoxide, or 2% chicken
serum.

SURVEILLANCE: Monitor for symptoms of disease. Isolation of viruses using
tissue culture is considered the gold standard among detection techniques
3
for hPIVs . hPIVs demonstrate the best growth in primary monkey kidney
(PMK) cell-lines. Secondary cell lines such as LLC-MK2 are also used.
Detection of hPIVs in tissue cultures is performed through
immunofluorescence (IF) assays, currently the most rapid test to detect
hPIVs in tissue cultures. Other tests used for hPIV diagnosis include
serological and nucleic acid tests. Serological tests, such as enzyme- linked
immunosorbent assays (ELISA), are used to detect antibodies to hPIV. A
major problem among these tests is with heterologous cross-reactivity, due
to closely related hPIV serogroups, which makes it difficult to differentiate
between different serogroups of hPIV during acute infection. Nucleic acid
tests (RT-PCR) are generally more sensitive and are used to detect hPIV RNA.
1
FIRST AID/TREATMENT: Treatment is mainly for symptoms .
3
Immunotherapy may be considered for patients with severe disease .
IMMUNISATION: None available to date; however, several different

9
attempts are being made to prepare a viable vaccine . Currently, two
vaccines under investigation include intranasally administered bovine PIV3
(bPIV3) vaccine and cold-adapted PIV3 vaccine; however, further testing and
2
clinical trials are required . hPIV3 is being targeted since it is considered
to be the most virulent form of hPIV.
PROPHYLAXIS: None available to date.

infections have been reported to date.
SOURCES/SPECIMENS: Nasopharyngeal samples and secretions (throat

swabs, nasopharyngeal swabs, nasal washes, and nasal aspirations) are the
1
primary source of hPIVs . hPIVs have also been isolated from
cerebrospinal fluid in some rare cases of meningitis.
PRIMARY HAZARDS: Contact with environmentally contaminated surfaces

3 , direct person- to-person contact with infected secretions, and
2
inhalation of infected respiratory droplets .

10
RISK GROUP CLASSIFICATION: Risk Group 2

and operational practices for work involving infected or potentially infected
11

11

SPILLS: Allow aerosols to settle. While wearing protective clothing, gently
disinfectant, starting at perimeter and working towards the centre. Allow
11

11
STORAGE: The infectious agent should be stored in appropriately labeled

11
sealed containers at -70 or -20 °C in a non-frost-free freezer .

and standards.

Canada.

Copyright ©
Canada
REFERENCES:
1 Vainionpaa, R., & Hyypia, T. (1994). Biology of parainfluenza

viruses. Clinical Microbiology Reviews, 7 (2), 265-275.
2 Chanock, R. M., Murphy, B. R., & Collins, P. L. (2001). Parainfluenza

Viruses. In D. M. Knipe, P. M. Howley, D. E. Griffin, R. A. Lamb, M. A.
Martin, B. Roizman & S. E. Straus (Eds.), Fields Virology (4th ed., pp.
1341-1372). Philadelphia, USA: Lippincott Williams & Wilkins.
3 Henrickson, K. J. (2003). Parainfluenza viruses. Clinical Microbiology

Reviews, 16 (2), 242-264.
4 Mufson, M. A., Mocega, H. E., & Krause, H. E. (1973). Acquisition of

parainfluenza 3 virus infection by hospitalized children. I.
Frequencies, rates, and temporal data. The Journal of Infectious
Diseases, 128 (2), 141-147.
5 Lau, S. K., To, W. K., Tse, P. W., Chan, A. K., Woo, P. C., Tsoi, H. W.,
Leung, A. F., Li, K. S., Chan, P. K., Lim, W. W., Yung, R. W., Chan, K.
H., & Yuen, K. Y. (2005). Human parainfluenza virus 4 outbreak and
the role of diagnostic tests. Journal of Clinical Microbiology, 43 (9),
4515-4521. doi:10.1128/JCM.43.9.4515-4521.2005
6 Collins, C. H., & Kennedy, D. A. (1999). Exposure, sources and route

of infection. Laboratory-acquired Infection: History, incidence, causes
and preventions (pp. 38-53). Oxford, UK: Butterworth-Heinemann.
Schiefer, H. D., Slenczka, W., Graevenitz, A., & Zahner, H. (2003).
Viral Zoonoses. Zoonoses: Infectious Disease Transmissible from
Animals to Humans (3rd ed., pp. 123). Washington, USA: ASM Press.
8 Disinfection and Sterilization. (1993). Laboratory Biosafety Manual

(2nd ed., pp. 60-70). Geneva: WHO.
9 Sato, M., & Wright, P. F. (2008). Current status of vaccines for

parainfluenza virus infections. The Pediatric Infectious Disease
Journal, 27 (10 Suppl), S123-5. doi:10.1097/INF.0b013e318168b76f

2009, (2009).

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Human rotavirus

SUBSTANCES
NAME: Human rotavirus
SYNONYM OR CROSS REFERENCE: HRV, Human reovirus-like agent,

1
infantile gastroenteritis virus , sporadic viral gastroenteritis, severe viral
gastroenteritis of infants and children, non-bacterial gastroenteritis of
infancy, and rotaviral enteritis.
CHARACTERISTICS: Human rotavirus is classified as a member of genus

2 3
Rotavirus within the family Reoviridae . Rotavirus is non-enveloped,
with a diameter of about 70 nm, and has a wheel-like appearance. It has an
icosahedral shaped, three-layered caspid shell. The viral genome consists of
11 segments of double-stranded RNA (dsRNA). Rotavirus can be classified
into seven major serogroups (A - G). Groups A, B, and C infect both humans
and animals, while the rest have only been found in animals to date. Group
A has been established as the most common rotavirus responsible for
causing human illness.

PATHOGENICITY/TOXICITY: HRV predominantly attacks enterocytes, which
2 3 4
are mature villous epithelial cells in the small intestine . The
disease caused by HRV is self-limiting in general, lasting for about 4-7 days,
with symptoms similar to those caused by other gastrointestinal agents,
although the symptoms of HRV infections are usually more severe. These
include fever, vomiting, and non-bloody diarrhoea (often watery and
explosive). This usually leads to mild to severe dehydration (usually isotonic
in nature); electrolyte imbalance; and in prolonged cases, to secondary
disaccharidase deficiency. Subsequent gastroenteritis infections tend to be
less severe compared to previous infections. A temporal association of
rotavirus infection with a variety of disease conditions has been described,
including upper and lower respiratory infection, intussusception, and others
3 . An etiologic association of rotavirus infection with necrotizing
enterocolitis, hemorrhagic gastroenteritis, and pneumatosis intestinalis in
2
infancy has been suggested . Detection of rotavirus RNA in cerebrospinal
fluid of patients with gastroenteritis suggests that neurological disorders
such as convulsions may be associated with HRV infection, but this has not
5
been confirmed .
EPIDEMIOLOGY: HRV is the major cause of severe diarrhoea

(gastroenteritis) in children throughout the world, more so in developing
countries, with about 95% of children contracting the infection by 5 years of
6
age . Death rate due to rotavirus infection is estimated at about 600,000
child deaths per year worldwide, with yearly death tolls highest in India,
Nigeria, China, Pakistan, Congo, Ethiopia, and Bangladesh. Prevalence of
disease ranges from ~30% during off season to ~70% during seasonal peaks.
Disease outbreaks demonstrate a seasonal pattern in temperate climates,
where the disease is more pronounced during drier and cooler months. In
the USA and Europe, annual epidemics begin during the months of
November/December and January respectively in the Southwest and
progress to Northeast by April/May and March, respectively. No specific
seasonal trend is observed in tropical climates. HRV infection is generally
more severe and clinically significant in children aged 3-35 months, with the
first infection being the most severe. Adults tend to be asymptomatic and/or
may demonstrate subclinical infection. Immunocompromised individuals
2
are susceptible to developing more severe disease manifestations .
Chances of spread of infection within families, day care centres, and
3
hospitals are high . Nosocomial infections are also common and are a
2 7
major cause of diarrhoea in newborns and infants . Several
outbreaks have been observed in geriatric groups within hospitals.
Serogroup A rotavirus is responsible for ~95% of the rotavirus diarrhoea
6
cases worldwide ; however, serogroup B rotavirus has caused several
large outbreaks of gastroenteritis in adults in various parts of China, and has
also been associated with severe diarrheal illness in Bangladesh and India
2 .
HOST RANGE: Humans and experimentally infected animals (see SECTION

III: RESERVOIR for more detail).
MODE OF TRANSMISSION: The most common mode of transmission for

HRV is through faecal-oral spread, either from person-to-person or contact
3 4 6
with contaminated environmental surfaces . The possibility of
spread through faecally contaminated food and water also exists.
Transmission through respiratory droplets has also been suggested;
however, more investigation is required.
INCUBATION PERIOD: The incubation period for HRV infection is about 1-3
3 6
days .
COMMUNICABILITY: Person-to-person transmission appears to be fairly

common through the faecal-oral route. Rotavirus shedding rate is the
highest during the diarrhoeal stage of the disease, which occurs during the
3
first 2-5 days of illness .

RESERVOIR: Humans are the only reservoir for HRV; however, infection by
group A rotaviruses (GARVs) has been reported in calves, pigs, foals, cats,
dogs, and some birds. The GARVs found in animals appear to be very closely
8
related to HRV . Evidence for some interspecies infection by GARVs does
exist. More importantly, it has been suggested that reassortment and
interspecies transmission may generate novel human GARVs; and hence it is
important to consider these animals as relevant reservoirs for HRV.
ZOONOSIS: None.
VECTORS: None.

SUSCEPTIBILITY TO DISINFECTANTS: HRV, either in suspension or on

inanimate surfaces, is susceptible to glutaraldehyde (2%); chlorinated
disinfectants (>20,000 p.p.m. chlorine); iodinated disinfectants (>10,000
p.p.m. iodine); combinations of quaternary ammonium compounds with
alcohols (>40%), some acids (HCl), some bases (sodium metasilicate); and
9
combinations of phenolic compounds with strong anionic surfactants
10 . Longer exposure times are required for disinfecting contaminated
surfaces as compared to contaminated suspensions/solutions. HRV has also
been shown to be very susceptible to Lysol brand disinfectants (79% ethyl
11
alcohol, 0.1% o-phenylphenol) . Other disinfectants include formalin
(2%) and sodium hypochlorite (2%).
12
PHYSICAL INACTIVATION: HRV is susceptible to strong acidic pH (<3.0) .
It is also susceptible to heating above 50 °C (for 30 minutes), but is stabilized
13
in 2M magnesium sulphate .
SURVIVAL OUTSIDE HOST: HRV can survive ambient temperatures (30-35

14 3
°C) and can remain infectious on inanimate objects for up to 60 days
. They tend to be more stable at medium or low humidity levels.

SURVEILLANCE: Monitor for symptoms of disease. Electron microscopy is
still the gold standard diagnostic technique for HRV; however, it is slightly
3
less sensitive and more expensive than some new diagnostic techniques
6 . These include enzyme-linked immunosorbent assays (ELISAs) and latex
agglutination assays used for the detection of HRV (group A) antigen in stool
samples.
FIRST AID/TREATMENT: Supportive therapy is needed to prevent

3 6
dehydration by replacement of fluid and electrolyte losses . This can
15
be done using the World Health Organization (WHO) formulation or
other commercial formulations, or through intravenous fluids in cases of
severe diarrhoea, intractable vomiting, acidosis, and/or shock accompany
the illness. Resumption of normal diet should be promoted after rehydration
3 .
IMMUNISATION: In the past, the rhesus-human rotavirus reassortment-

tetravalent vaccine (Rotashield) had been recommended for use by the US
Advisory Committee on Immunization Practices (ACIP), but its use was
3
suspended in 1999 . Health Canada has approved RotaTeq and Rotarix
vaccines in Canada; however, they are not part of the routine immunization
16
programs that are currently available . RotaTeq is a live, oral, human-
bovine, reassortment rotavirus vaccine developed from a strain of bovine
rotavirus, approved by the US Food and Drug Administration (FDA). Rotarix
is a live, oral human rotavirus vaccine developed from the most common
strain of human rotavirus, also approved by FDA.
PROPHYLAXIS: None.

infection have been reported to date.
SOURCES/SPECIMENS: The main sources of HRV are intestinal mucosa and

8
stool extracts of infected humans . It has also been detected in rectal
7
swabs of infected humans .
PRIMARY HAZARDS: Ingestion of feces or stool samples and other

contaminated materials. Exposure of mucous membranes to contaminated
droplets. Importance of aerosol exposure may also present a primary
hazard.

17

18

18

18

18
STORAGE: The infectious agent should be stored in sealed containers that

14
are appropriately labelled, preferably at -20 °C . For long term (<1 year)
storage, it should be stored at -70 °C to -80 °C; however, the presence of a
18
cryoprotectant is not necessary .

and standards.

Canada.

Copyright ©
Canada
REFERENCES:
1 Mahy, B. W. J. (2008). The Dictionary of Virology (4th ed.). California,

USA: Academic Press.
2 Estes, M. K., & Kapikian, A. Z. (2007). Rotaviruses. In D. M. Knipe, P.

M. Howley, D. E. Griffin, R. A. Lamb, M. A. Martin, B. Roizman & S.
E. Straus (Eds.), Fields Virology (5th ed., pp. 1917-1958).
Philadelphia, USA: Lippincott Williams & Wilkins.
3 Leung, A. K., Kellner, J. D., & Davies, H. D. (2005). Rotavirus

gastroenteritis. Advances in Therapy, 22 (5), 476-487.
4 Gray, J., Vesikari, T., Van Damme, P., Giaquinto, C., Mrukowicz, J.,
Guarino, A., Dagan, R., Szajewska, H., & Usonis, V. (2008).
Rotavirus. Journal of Pediatric Gastroenterology and Nutrition, 46
Suppl 2 , S24-31. doi:10.1097/MPG.0b013e31816f78ee
5 Lynch, M., Lee, B., Azimi, P., Gentsch, J., Glaser, C., Gilliam, S.,
Chang, H. G., Ward, R., & Glass, R. I. (2001). Rotavirus and central
nervous system symptoms: cause or contaminant? Case reports
and review. Clinical Infectious Diseases : An Official Publication of the
Infectious Diseases Society of America, 33 (7), 932-938.
doi:10.1086/322650
6 Bernstein, D. I. (2009). Rotavirus overview. The Pediatric Infectious

Disease Journal, 28 (3 Suppl), S50-3.
doi:10.1097/INF.0b013e3181967bee
7 Rodrigues, A., de Carvalho, M., Monteiro, S., Mikkelsen, C. S., Aaby,

P., Molbak, K., & Fischer, T. K. (2007). Hospital surveillance of
rotavirus infection and nosocomial transmission of rotavirus
disease among children in Guinea-Bissau. The Pediatric Infectious
Disease Journal, 26 (3), 233-237.
8 Martella, V., Banyai, K., Matthijnssens, J., Buonavoglia, C., & Ciarlet,
M. (2010). Zoonotic aspects of rotaviruses. Veterinary Microbiology,
140 (3-4), 246-255. doi:10.1016/j.vetmic.2009.08.028
9 Springthorpe, V. S., Grenier, J. L., Lloyd-Evans, N., & Sattar, S. A.

(1986). Chemical disinfection of human rotaviruses: efficacy of
commercially-available products in suspension tests. The Journal of
Hygiene, 97 (1), 139-161.
10 Lloyd-Evans, N., Springthorpe, V. S., & Sattar, S. A. (1986). Chemical

disinfection of human rotavirus-contaminated inanimate surfaces.
The Journal of Hygiene, 97 (1), 163-173.
11 Ward, R. L., Bernstein, D. I., Knowlton, D. R., Sherwood, J. R., Young,

E. C., Cusack, T. M., Rubino, J. R., & Schiff, G. M. (1991). Prevention
of surface-to-human transmission of rotaviruses by treatment
with disinfectant spray. Journal of Clinical Microbiology, 29 (9), 1991-
1996.
12 Weiss, C., & Clark, H. F. (1985). Rapid inactivation of rotaviruses by

exposure to acid buffer or acidic gastric juice. The Journal of
General Virology, 66 ( Pt 12) (Pt 12), 2725-2730.
13 Estes, M. K., Graham, D. Y., Smith, E. M., & Gerba, C. P. (1979).

Rotavirus stability and inactivation. The Journal of General Virology,
43 (2), 403-409.
14 Fischer, T. K., Steinsland, H., & Valentiner-Branth, P. (2002).

Rotavirus particles can survive storage in ambient tropical
temperatures for more than 2 months. Journal of Clinical
Microbiology, 40 (12), 4763-4764.
15 World Health Organization. (2010). Guidelines for the safe

preparation, storage and handling of powdered infant formula.
Retrieved 11/24, 2010, from
www.who.int/foodsafety/publications/micro/pif2007/en/index.html
16 Health Canada. (2010). Questions and Answers - Porcine Circovirus

Found in Rotavirus Vaccines. Retrieved 11/24, 2010, from www.hc-
sc.gc.ca/dhp-mps/brgtherap/activit/fs-fi/rotavirus-questions-
eng.php#q5

2009, (2009).

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Human T-lymphotropic virus
(HTLV)

SUBSTANCES
NAME: Human T-lymphotropic virus (HTLV)
SYNONYM OR CROSS REFERENCE: HTLV, adult T-cell leukemia/lymphoma

(ATLL), HTLV-1-associated myelopathy/tropical spastic paraparesis
1 3 4
(HAM/TSP) , Sezary's disease .
CHARACTERISTICS: Human T-lymphotropic virus is a C-type retrovirus,

family Retroviridae, genus Deltaretrovirus, with a central, electron dense
1 5
nuclear core . Genetic material is in the form of two positively
charged single stranded RNA fragments. A reverse transcriptase is
contained within the virion. Virions are round with a diameter of
3 5 6
approximately 100 nm .

PATHOGENICITY/TOXICITY: Human T lymphotropic virus infection results
7
in a lifelong infection . There are two known pathogenic strains of HTLV,
HTLV-1 and HTLV-2. HTLV-1 primarily causes adult T-cell
leukemia/lymphoma and topical spastic parapareis/HTLV-1 associated
myelopathy. It also causes uveitis, infective dermatitis and lymphadenitis
3 5 7 10 . HTLV-2 is a less pathogenic strain and has been associated
with milder neurological disorders and chronic pulmonary infections. HTLV-3
and HTLV-4 have not been associated with specific illnesses. Acute HTLV
infection is rarely suspected or diagnosed. Adult T-cell leukemia or
lymphoma (ATLL) occurs in 1-2% of those infected. Symptoms present 20-30
1 2 7
years after infection . Of those who develop ATLL, more than two
11
thirds develop leukemia while the remainder develop lymphoma .
12
Prognosis is approximately 1 year after development of ATLL . ATLL has
five types: asymptomatic, pre-leukemic, chronic/smouldering, lymphoma,
7
and acute . The smouldering type presents with skin lesions and
involvement of the bone marrow. The chronic stage is associated with
elevated circulating leukemic cells and usually progresses to the acute type
within two years. The acute phase is an aggressive form of leukemia and is
accompanied by hypocalcaemia, elevated lactate dehydrogenase (LDH), skin
lesions, lymphadenopathy, lymphomatous meningitis, lytic bone lesions,
spleen or liver involvement and immunodeficiency. HTLV-1-associated
myelopathy/tropical spastic paraparesis (HAM/TSP) has a shorter latency
5 7
period than ATLL . HAM/TSP is a progressive and chronic
myelopathy, with preferential damage to the thoracic spinal cord. Symptoms
include muscle weakness of lower limbs, hyperreflexia, sphincter disorders,
impotence, sensory disturbances and lower back pain.
EPIDEMIOLOGY: Worldwide distribution, with an estimated 10-20 million

5 7
people carrying the human T-cell lyphotropic virus . Endemic regions
include southern Japan, Caribbean basin, central Africa, central and
southern America, Melanesian Islands and the aboriginal population of
Australia. Sporadic infections occur in at-risk groups, and metropolitan areas
of Europe and the United States.
HOST RANGE: Humans and animals, including rabbits, rats and non-human
7
primates .
MODE OF TRANSMISSION: Infections can occur from blood and mucosal

6
exposure . Virus is transmitted by sexual contact, intravenous drug
2 3 5 7 8 10
abuse and blood transfusions . Organ transplants,
childbirth and breast feeding are also effective modes of transmission.
INCUBATION PERIOD: Unknown
COMMUNICABILITY: Human-to-human transmission is possible. Human T-

lymphotropic virus is transmitted by sexual contact, intravenous drug abuse
2 3 5 7 8 10
and blood transfusions .

2 7 8
RESERVOIR: Humans .
13
ZOONOSIS: None .
VECTORS: None.

8
DRUG SUSCEPTIBILITY: No established therapy . Combination therapy
of Zidovudine (AZT) and interferon alpha (INF-α) is used with some success
to improve prognosis.
SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to 1% sodium

hypochlorite, 2% glutaraldehyde, 4% chlorhexidine, 70% ethanol, 0.3%
hydrogen peroxide, iodophores, phenolics, and quaternary ammonium
14
compounds .
PHYSICAL INACTIVATION: Can be inactivated by steam sterilization at

14
121ºC for a minimum of 15 minutes and UV light .
SURVIVAL OUTSIDE HOST: HTLV-1 and HTLV-2 can survive in stored blood
15
for 8-9 days .

SURVEILLANCE: Monitor for symptoms. HTLV is detected in blood serum by
identifying antibodies using ELISA. Other methods of detection include
5 6
particle agglutination assays and Western Blotting . For the
identification of specific viral sequences, PCR is used.
1
FIRST AID/TREATMENT: Limited therapy is available for HTLV infections .
ATL treated with chemotherapy. Zidovudine (AZT) and alpha interferon have
shown some response and improved the ATL prognosis. Other treatments
are currently under investigation including arsenic, trioxide, proteasome
inhibitors, retenoids, angiogenesis inhibitors and cellular immunotherapy.
Antiretroviral treatments using lamivudine and high dose interferon alpha
and interferon beta is used for HTLV-1-associated myelopathy/tropical
spastic parparesis. Uveitis is treated with topical and systemic corticoids to
improve sight. Infective dermatitis is treated with antibiotics.
IMMUNIZATION: None
PROPHYLAXIS: None

LABORATORY-ACQUIRED INFECTIONS: One reported infection with HTLV-1
of a physician after a syringe containing a blood sample pierced the foot
16 . One reported infection with HTLV of a nurse after accidental
17
inoculation of the finger with a needle containing a blood sample .
SOURCES/SPECIMENS: Blood samples and bodily fluids (ie. CSF, blood,etc)

6 .
PRIMARY HAZARDS: Exposure of mucous membranes and accidental

18 19
parenteral inoculation .

20
RISK GROUP CLASSIFICATION: Risk Group 3 pathogen .
CONTAINMENT REQUIREMENTS: Please refer to the Biosafety Directive for

Human Immunodeficiency Virus (HIV) and Human T-cell Lymphotropic Virus
Type 1 (HTLV-1)

20

covered with waterproof dressings. Additional precautions should be
18 20
considered with work involving animals or large scale activities .

18
DISPOSAL: Decontaminate all materials before disposal using steam

18 19
sterilization, incineration, and/or chemical disinfection
STORAGE: Infectious material should be stored in sealed, leak-proof

18 19
containers that are appropriately labelled .

and standards.

Copyright ©
Canada
REFERENCES:
REFERENCES:
1 Gessain, A., Dezzutti, C. S., Cowan, E. P., & Lal, R. B. (2007). Human
T-Cell Lymphotropic Virus Types 1 and 2. In P. M. Murray, E. J.
Baron, J. H. Jprgensen, M. L. Landry & M. A. Pfaller (Eds.), Manual of
Clinical Mircobiology (9th ed., pp. 1330). Washington, DC: ASM
Press.
2 Larson, C. J., & Taswell, H. F. (1988). Human T-cell leukemia virus

type I ( HTLV-I) and blood transfusion. Mayo Clinic
Proceedings.Mayo Clinic, 63(9), 869-875.
3 Ryan, K. J., & Ray, C. G. (Eds.). (2004.). Sherris Medical Microbiology:

An Introduction to Infectious Disease. (Fourth Edition. ed.). New
York.: McGraw-Hill.
4 Poiesz, B. J., Ruscetti, F. W., Reitz, M. S., Kalyanaraman, V. S., &

Gallo, R. C. (1981). Isolation of a new type C retrovirus ( HTLV) in
primary uncultured cells of a patient with Sezary T-cell leukaemia.
Nature, 294(5838), 268-271.
5 Verdonck, K., Gonzalez, E., Van Dooren, S., Vandamme, A. M.,

Vanham, G., & Gotuzzo, E. (2007). Human T-lymphotropic virus 1:
recent knowledge about an ancient infection. The Lancet Infectious
Diseases, 7(4), 266-281. doi:10.1016/S1473-3099(07)70081-6
6 Lairmore, M. D., & Franchini, G. (2007). Human T-cell Leukemia

Virus Types 1 and 2. In D. M. Knipe, & P. M. Howley (Eds.), Fields
Virology (5th ed., pp. 2071). Philadelphia: Lippincott Williams &
Wilkins.
7 Johnson, J. M., Harrod, R., & Franchini, G. (2001). Molecular biology

and pathogenesis of the human T-cell leukaemia/lymphotropic
virus Type-1 ( HTLV-1). International Journal of Experimental
Pathology, 82(3), 135-147.
8 Bagossi, P., Bander, P., Bozoki, B., & Tozser, J. (2009). Discovery
and significance of new human T-lymphotropic viruses: HTLV-3
and HTLV-4. Expert Review of Anti-Infective Therapy, 7(10), 1235-
1249. doi:10.1586/eri.09.97
9 Sutton, R. E., & Littman, D. R. (1996). Broad host range of human T-

cell leukemia virus type 1 demonstrated with an improved
pseudotyping system. Journal of Virology, 70(10), 7322-7326.
10 Koch, A. L. (2008). Stone age diseases and modern AIDS. Virology

Journal, 5, 93. doi:10.1186/1743-422X-5-93
11 Matutes, E. (2007). Adult T-cell leukaemia/lymphoma. Journal of

Clinical Pathology, 60(12), 1373-1377. doi:10.1136/jcp.2007.052456
12 Satou, Y., Nosaka, K., Koya, Y., Yasunaga, J. I., Toyokuni, S., &
Matsuoka, M. (2004). Proteasome inhibitor, bortezomib, potently
inhibits the growth of adult T-cell leukemia cells both in vivo and in
vitro. Leukemia: Official Journal of the Leukemia Society of America,
Leukemia Research Fund, U.K, 18(8), 1357-1363.
doi:10.1038/sj.leu.2403400
to Humans (3rd ed., pp. 1). Washington D.C.: ASM Press.
14 Disinfection, Sterilization, and Preservation (2001). In Block S. S.

(Ed.), (5th ed.). Philadelphia: Lippincott Williams & Wilkins.
15 Donegan, E., Lee, H., Operskalski, E. A., Shaw, G. M., Kleinman, S.

H., Busch, M. P., Stevens, C. E., Schiff, E. R., Nowicki, M. J., &
Hollingsworth, C. G. (1994). Transfusion transmission of
retroviruses: human T-lymphotropic virus types I and II compared
with human immunodeficiency virus type 1. Transfusion, 34(6),
478-483.
16 Kataoka, R., Takehara, N., Iwahara, Y., Sawada, T., Ohtsuki, Y.,
Dawei, Y., Hoshino, H., & Miyoshi, I. (1990). Transmission of HTLV-I
by blood transfusion and its prevention by passive immunization
in rabbits. Blood, 76(8), 1657-1661.
17 Menna-Barreto, M. (2006). HTLV-II transmission to a health care

worker. American Journal of Infection Control, 34(3), 158-160.
doi:10.1016/j.ajic.2005.12.002

19 Chosewood, L. C., & Decaudin, A. (Eds.). (2007). Biosafety in

Microbiological and Biomedical Laboratories (5th ed.). Washington:
US Government Printing Office.

2009, (2009).
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Influenza A virus subtypes H5, H7
and H9

SUBSTANCES
NAME: Influenza A virus subtypes H5, H7 and H9.
1 - 3
SYNONYM OR CROSS REFERENCE: Orthomyxovirus , influenza virus
1 - 3 1 - 3 1 - 3
type A , influenzavirus A , avian influenza , and
4
pandemic influenza .
CHARACTERISTICS: Influenza virus subtypes H5, H7 and H9 are members of

the Orthomyxoviridae family of segmented, negative sense single-stranded
RNA viruses. Type A influenza viruses are subdivided on the basis of the
antigenic nature of their membrane-bound surface glycoproteins,
haemagglutinin (HA) and neuraminidase (NA). To date, 16 HA, and 9 NA
5 - 9
subtypes have been detected in wild birds and poultry . Antigenic
alterations occur frequently in the antigenic sites of HA and NA and are the
mechanism for virus adaptation and survival. Small alterations are referred
to as antigenic drift, whereas larger alterations caused by reassortment are
referred to as antigenic shift. Influenza pandemics may occur as a result of
antigenic shifts if the virus is able to maintain efficient human-to-human
1 - 3
transmission .

PATHOGENICITY/TOXICITY: Avian influenza A viruses are referred to as low
pathogenic avian influenza (LPAI) and highly pathogenic avian influenza
(HPAI), based on the severity of illness caused in poultry. To date, only H5
and H7 subtypes have been shown to be HPAI, although not all H5 and H7
2 3 10
viruses are highly virulent . Furthermore, it appears that HPAI
viruses arise by mutation after LPAI viruses have been introduced to poultry
2 .
Human infections from influenza A virus subtypes H5, H7 and H9 range from
eye infections (conjunctivitis) to influenza-like illness (ILI) symptoms to
11 - 13
severe respiratory illness . Symptoms of H5N1 range from typical
flu-like symptoms (e.g., fever, sore throat, cough, and muscle aches) to
pneumonia, acute respiratory distress syndrome, multiple organ failure,
lymphopenia, elevated liver enzyme levels and abnormal clotting profiles,
diarrhoea, vomiting, abdominal pain, pleuritic pain, and bleeding from the
11 14 15
nose and gums .
EPIDEMIOLOGY: Influenza can occur in pandemics, epidemics, localized

outbreaks, and as sporadic cases. Many strains of avian influenza virus can
cause varying degrees of disease in domestic poultry. Avian influenza
usually does not make wild birds sick, but can cause serious illness and
10
death in poultry . HPAI is a fatal form of avian influenza that can spread
rapidly in flocks, causing high mortalities. Outbreaks of HPAI have led to
11
human infections, some of which resulted in deaths . Lack of previous
exposure to the virus and high virulence of avian influenza H5N1 is a key
11
determinant of the high fatality rate . LPAI can also cause disease in
humans. For example, H7N7 (1996, conjunctivitis); H9N2 (1999, ILI); H7N2
16
(2002, ILI); H9N2 (2003, ILI) and H7N2 (2003, ILI) . Continuous existence
of LPAI virus in an avian population may provide opportunities for the virus
2
to undergo mutation and convert to a highly pathogenic strain .
Animal influenza A virus subtypes that have infected humans include H5N1,
H7N2, H7N3, H7N7, H9N2, H10N7 and swine and avian H1 viruses.
Human cases of H5 were first reported in 1997 in Hong Kong, where avian-
to-human transmission of H5N1 resulted in 18 cases of human infection and
15 17
6 deaths . In 2003 another outbreak in Hong Kong led to 2 cases of
15 17
human infection and one death . In December 2003, a further
outbreak of H5N1 occurred among poultry in South Korea and then later in
Vietnam, Japan, Thailand, Laos, Cambodia, China, Indonesia and Malaysia
1 18 . Since the outbreak in 2003, the World Health Organization (WHO)
has reported a number of waves of avian-to-human transmission starting in
Southeast Asia and spreading to areas North and West of China reaching as
19 - 21
far as Eastern Europe and Northern Africa . The cumulative
number of human H5N1 cases reported to WHO from 2003 to May 6, 2010 is
21
498 cases with 294 deaths (59% mortality rate) .
H7 infection in humans is rare, but can occur in persons who have been in
12 22 23 24
direct contact with infected birds , or in one case, seals . In
2003, H7N7 was responsible for the death of a veterinarian and extensive
conjunctivitis among those employed in the disposal of diseased birds in the
12
Netherlands . An outbreak of H7N3 in 2004 also led to two cases of
23
human infection in British Columbia, Canada .
Since 1998, a number of human cases of H9N2 have been reported in Asia
25 26
and are generally associated with mild illness . Transmission of
26 27
H9N2 appears to be exclusively avian-to-human .
HOST RANGE: Domestic and wild avian species. H5 and H7 are generally
non-pathogenic in their natural waterfowl hosts but may become highly
3 15
pathogenic once introduced into domestic poultry . Viral
transmission of H5N1 to mammals has been reported in domestic cats,
1 20
dogs, tigers and also in a stone marten (reviewed in ).
MODE OF TRANSMISSION: Influenza A infections (H5, H7, H9) in humans

result predominantly from direct transmission of the virus from birds to
humans. Transmission occurs primarily through contact of the mucous
membranes with infectious secretions or excreta from infected wild birds or
poultry. Exposure to sick poultry and the butchering of birds is associated
28 29
with seropositivity for H5N1 . Slaughtering, de-feathering, or
preparing sick poultry for cooking, playing with or handling diseased or
dead poultry, handling fighting cocks or ducks that appear asymptomatic,
and consuming raw or uncooked poultry or poultry products, have all been
14 20
implicated as potential risk factors . Oral ingestion of contaminated
water during swimming and direct intranasal or conjunctival inoculation
during exposure to water are other potential modes of transmission, as is
contamination of hands from infected fomites and subsequent self-
20 28
inoculation . The widespread use of untreated poultry feces as
14
fertilizer is another possible risk factor . Non-sustained human-to-
30-32
human spread has only been documented in a few cases ; however,
the continued circulation of virulent influenza virus H5N1 increases the
potential for a new influenza virus to arise through reassortment with other
circulating influenza viruses, thus increasing the threat of an influenza virus
that is transmissible from person-to-person that could lead to a global
1 18 32
influenza pandemic .
INCUBATION PERIOD: Most cases of influenza A (H5N1) occurred within

15 18 - 20
two to four days after exposure . In clusters in which limited
human-to-human transmission may have occurred, the incubation period
appeared to be approximately 3 to 5 days, although in one cluster it was
30 31
estimated to be 8 to 9 days .
COMMUNICABILITY: Limited human-to-human transmission reported,

whereby transmission probably occurred during close unprotected contact
30 - 32
with a severely ill patient .

RESERVOIR: Wild aquatic birds, predominantly ducks, geese, and
shorebirds. Avian influenza viruses are generally non-pathogenic in wild
birds, sometimes causing significant morbidity and mortality upon
3
transmission to other species, including domestic birds and mammals
5 18 20 .
3 11 12 14 15 18 20
ZOONOSIS: Yes, from various avian species
23 28 31 .
3 5 18 20
VECTORS: Wild birds .

DRUG SUSCEPTIBILITY: Various subtypes of H5 (H5N1), H7 (H7N3, H7N7)
and H9 (N9N2) are susceptible to the neuraminidase inhibitors, oseltamivir
4 23 33 - 36 4 23 33 - 36
, zanamivir , and peramivir (RWJ-270201)
34 . In the past, influenza viruses have been shown to be sensitive to M2
inhibitors, amantadine and rimantadine, although to a lesser extent than
1 4 35
the neuraminidase inhibitors . There is evidence of increasing
1 4 35 36
resistance to M2 inhibitors by H5N1 .
SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to the following

disinfectants: 1% sodium hypochlorite, 70% ethanol, glutaraldehyde,
37
formalin and iodine compounds (reviewed in ). Also susceptible to a
37
number of commercially available disinfectants (reviewed in ).
PHYSICAL INACTIVATION: Incubation at 56ºC to 60ºC for 60 min will

37
inactivate various subtypes of H5, H7 and H9 (reviewed in ). Incubations
in low (1 to 3) or high (10 to 14) pH solutions has also been shown to be
effective at inactivating H5, H7 and H9, although the medium in which the
virus is suspended may interfere with the effect of pH on virus infectivity
37
(reviewed in ).
SURVIVAL OUTSIDE HOST: Influenza virus may remain infective in lake

2
water for 4 days, in water at 22ºC, and for 30 days at 0ºC . Survival in
feces is likely to be influenced by the strain of the virus, type of faeces and
37
temperature .

SURVEILLANCE: Identify potential exposure to H5, H7 or H9 through recent
1
travel to or from areas with known influenza activity . Monitor for
12 14 15 18 23
symptoms of influenza. Confirm by viral culture , RT-
12 14 15 18 20 22 23 31
PCR with strain specific primers ,
11
immunostaining (Western blot, ELISA) with subtype specific antibodies
15 17 27 28 30 31 30 31
, molecular sequencing , antiviral
30 27 30
resistance testing , and/or microneutralization .
FIRST AID/TREATMENT: Antivirals must be administered early after the

14 20
onset of symptoms to be effective . Oseltamivir is recommended
for the treatment of avian influenza viruses. Oseltamivir is an oral
preparation (capsule or liquid suspension), whereas zanamivir is delivered
4 20 35
by inhalation . Amantadine and rimantadine are also
administered in countries where they are licensed if oseltamivir and
1 35
zanamivir are unavailable .
IMMUNIZATION: A vaccine for humans against the H5N1 influenza virus

was approved by the Food and Drug Administration (FDA) in the United
States. The immunization consists of two intramuscular injections, given
38
approximately one month apart . A vaccine for H9N2 is currently in
1
clinical trials . It is a cold-adapted, live, attenuated virus vaccine
1
administered intranasally . There are currently no human vaccines for H7
viruses, although, avian vaccines for H7 viruses are being investigated as a
39 40
method to prevent outbreaks .
PROPHYLAXIS: Chemoprophylaxis with of oseltamivir once daily for 7 days

after the last known exposure is warranted for persons who have had a
4 35 38 41
possible unprotected exposure H5N1 . Zanamivir (10mg
1 4 35
twice daily) and the M2 inhibitors, amantadine (100 mg twice
1 4 35 1 4 35
daily) and rimantadine (100 mg twice daily are also
used; however, amantadine and rimantadine are documented to be less
1 4 35
effective as a first-line mono-therapy . The use of human or
humanized antibodies for prophylaxis and therapy are currently being
32
investigated .

LABORATORY-ACQUIRED INFECTIONS: None reported.
SOURCES/SPECIMENS: Tissues, secretions and/or excretions from infected

1 4 14 35
birds .
PRIMARY HAZARDS: Inhalation of virus from aerosols generated when

aspirating, dispensing, or mixing virus-infected samples from infected
1 4 14 35
animals, especially birds .
SPECIAL HAZARDS: Possible risk to people who have contact with surfaces
that have been contaminated with secretions or excretions from infected
1 20 28 1 20 28
birds . Accidental inoculation is also a risk .

RISK GROUP CLASSIFICATION: Risk Group 2 or 3, depending on specific
virus.

and operational practices for work involving clinical or diagnostic specimens.
Containment Level 3 facilities, equipment, and operational practices are
recommended for virus isolation and laboratory manipulation of highly
42
pathogenic H5, H7 and H9 strains of avian influenza
PROTECTIVE CLOTHING: Protective solid-front gowns, gloves, shoe covers,

1 42 43
eye protection with face seal, and N95 respiratory protection .
OTHER PRECAUTIONS: Manipulations with autopsy material or infectious

material in open vessels to be carried out in a certified biological safety
cabinet. Centrifugation of respiratory specimens or tissue samples to be
carried out using sealed centrifuge cups or rotors,both of which are to be
1 42 43
loaded and unloaded in a biological safety cabinet .

SPILLS: Allow aerosols to settle, and while wearing protective clothing,
gently cover the spill with paper towels and apply 1% sodium hypochlorite
or other proven effective disinfectant, starting at the perimeter and working
towards the centre. Allow sufficient contact time and then clean the area.
DISPOSAL: Decontaminate before disposal by steam sterilization, chemical

disinfection, or incineration.
43


Canada.

Copyright ©
Canada
REFERENCES:
1 Thomas, J. K., & Noppenberger, J. (2007). Avian influenza: A review.
American Journal of Health-System Pharmacy, 64(2), 149-165.
2 Alexander, D. J. (2007). An overview of the epidemiology of avian

influenza. Vaccine, 25(30), 5637-5644.
doi:10.1016/j.vaccine.2006.10.051
3 Hampson, A. W., & Mackenzie, J. S. (2006). The influenza viruses.

Medical Journal of Australia, 185(10 SUPPL.), S39-S43.
4 Harrod, M. E., Emery, S., & Dwyer, D. E. (2006). Antivirals in the

management of an influenza pandemic. The Medical Journal of
Australia, 185(10 Suppl), S58-61.
5 Fouchier, R. A. M., Munster, V., Wallensten, A., Bestebroer, T. M.,

Herfst, S., Smith, D., Rimmelzwaan, G. F., Olsen, B., & Osterhaus, A.
D. M. E. (2005). Characterization of a novel influenza A virus
hemagglutinin subtype (H16) obtained from black-headed gulls.
Journal of Virology, 79(5), 2814-2822.
6 World Health Organization (WHO). (1980). A revision of the system

of nomenclature for influenza viruses: a WHO memorandum.
Bulletin of the World Health Organization, 58(4), 585-591.
7 Hinshaw, V. S., Air, G. M., & Gibbs, A. J. (1982). Antigenic and

genetic characterization of a novel hemagglutinin subtype of
influenza A viruses from gulls. Journal of Virology, 42(3), 865-872.
8 Kawaoka, Y., Yamnikova, S., Chambers, T. M., Lvov, D. K., &

Webster, R. G. (1990). Molecular characterization of a new
hemagglutinin, subtype H14, of influenza A virus. Virology, 179(2),
759-767.
9 Röhm, C., Zhou, N., Süss, J., Mackenzie, J., & Webster, R. G. (1996).
Characterization of a novel influenza hemagglutinin, H15: Criteria
for determination of influenza A subtypes. Virology, 217(2), 508-
516.
10 Senne, D. A., Panigrahy, B., Kawaoka, Y., Pearson, J. E., Suss, J.,
Lipkind, M., Kida, H., & Webster, R. G. (1996). Survey of the
hemagglutinin (HA) cleavage site sequence of H5 and H7 avian
influenza viruses: amino acid sequence at the HA cleavage site as
a marker of pathogenicity potential. Avian Diseases, 40(2), 425-437.
11 Chan, P. K. (2002). Outbreak of avian influenza A(H5N1) virus

infection in Hong Kong in 1997. Clinical Infectious Diseases : An
Official Publication of the Infectious Diseases Society of America, 34
Suppl 2, S58-64. doi:10.1086/338820
12 Koopmans, M., Wilbrink, B., Conyn, M., Natrop, G., van der Nat, H.,
Vennema, H., Meijer, A., van Steenbergen, J., Fouchier, R.,
Osterhaus, A., & Bosman, A. (2004). Transmission of H7N7 avian
influenza A virus to human beings during a large outbreak in
commercial poultry farms in the Netherlands. Lancet, 363(9409),
587-593. doi:10.1016/S0140-6736(04)15589-X
13 Lin, Y. P., Shaw, M., Gregory, V., Cameron, K., Lim, W., Klimov, A.,
Subbarao, K., Guan, Y., Krauss, S., Shortridge, K., Webster, R., Cox,
N., & Hay, A. (2000). Avian-to-human transmission of H9N2
subtype influenza A viruses: relationship between H9N2 and H5N1
human isolates. Proceedings of the National Academy of Sciences of
the United States of America, 97(17), 9654-9658.
doi:10.1073/pnas.160270697
14 Beigel, J. H., Farrar, J., Han, A. M., Hayden, F. G., Hyer, R., de Jong,
M. D., Lochindarat, S., Nguyen, T. K., Nguyen, T. H., Tran, T. H.,
Nicoll, A., Touch, S., Yuen, K. Y., & Writing Committee of the World
Health Organization (WHO) Consultation on Human Influenza
A/H5. (2005). Avian influenza A (H5N1) infection in humans. The
New England Journal of Medicine, 353(13), 1374-1385.
doi:10.1056/NEJMra052211
15 Yuen, K. Y., Chan, P. K., Peiris, M., Tsang, D. N., Que, T. L.,
Shortridge, K. F., Cheung, P. T., To, W. K., Ho, E. T., Sung, R., &
Cheng, A. F. (1998). Clinical features and rapid viral diagnosis of
human disease associated with avian influenza A H5N1 virus.
Lancet, 351(9101), 467-471.
16 Alexander, D. J. (2006). Avian influenza viruses and human health.

Developments in Biologicals, 124, 77-84.
17 Peiris, J. S., Yu, W. C., Leung, C. W., Cheung, C. Y., Ng, W. F.,
Nicholls, J. M., Ng, T. K., Chan, K. H., Lai, S. T., Lim, W. L., Yuen, K. Y.,
& Guan, Y. (2004). Re-emergence of fatal human influenza A
subtype H5N1 disease. Lancet, 363(9409), 617-619.
doi:10.1016/S0140-6736(04)15595-5
18 Tran, T. H., Nguyen, T. L., Nguyen, T. D., Luong, T. S., Pham, P. M.,
Nguyen, V. C., Pham, T. S., Vo, C. D., Le, T. Q., Ngo, T. T., Dao, B. K.,
Le, P. P., Nguyen, T. T., Hoang, T. L., Cao, V. T., Le, T. G., Nguyen, D.
T., Le, H. N., Nguyen, K. T., Le, H. S., Le, V. T., Christiane, D., Tran, T.
T., Menno de, J., Schultsz, C., Cheng, P., Lim, W., Horby, P., Farrar, J.,
& World Health Organization International Avian Influenza
Investigative Team. (2004). Avian influenza A (H5N1) in 10 patients
in Vietnam. The New England Journal of Medicine, 350(12), 1179-
1188. doi:10.1056/NEJMoa040419
19 Chotpitayasunondh, T., Ungchusak, K., Hanshaoworakul, W.,

Chunsuthiwat, S., Sawanpanyalert, P., Kijphati, R., Lochindarat, S.,
Srisan, P., Suwan, P., Osotthanakorn, Y., Anantasetagoon, T.,
Kanjanawasri, S., Tanupattarachai, S., Weerakul, J., Chaiwirattana,
R., Maneerattanaporn, M., Poolsavathitikool, R., Chokephaibulkit,
K., Apisarnthanarak, A., & Dowell, S. F. (2005). Human disease from
influenza A (H5N1), Thailand, 2004. Emerging Infectious Diseases,
11(2), 201-209.
20 Writing Committee of the Second World Health Organization

Consultation on Clinical Aspects of Human Infection with Avian
Influenza A (H5N1) Virus, Abdel-Ghafar, A. N., Chotpitayasunondh,
T., Gao, Z., Hayden, F. G., Nguyen, D. H., de Jong, M. D.,
Naghdaliyev, A., Peiris, J. S., Shindo, N., Soeroso, S., & Uyeki, T. M.
(2008). Update on avian influenza A (H5N1) virus infection in
humans. The New England Journal of Medicine, 358(3), 261-273.
doi:10.1056/NEJMra0707279
21 World Health Organization (WHO). (2010). Cumulative Number of

Confirmed Cases of Avian Influenza A/(H5N1) Reported to WHO.
22 Kurtz, J., Manvell, R. J., & Banks, J. (1996). Avian influenza virus
isolated from a woman with conjunctivitis. Lancet, 348(9031), 901-
902. doi:10.1016/S0140-6736(05)64783-6
23 Tweed, S. A., Skowronski, D. M., David, S. T., Larder, A., Petric, M.,
Lees, W., Li, Y., Katz, J., Krajden, M., Tellier, R., Halpert, C., Hirst, M.,
Astell, C., Lawrence, D., & Mak, A. (2004). Human illness from avian
influenza H7N3, British Columbia. Emerging Infectious Diseases,
10(12), 2196-2199.
24 Webster, R. G., Geraci, J., Petursson, G., & Skirnisson, K. (1981).

Conjunctivitis in human beings caused by influenza A virus of
seals. The New England Journal of Medicine, 304(15), 911.
25 Peiris, M., Yuen, K. Y., Leung, C. W., Chan, K. H., Ip, P. L., Lai, R. W.,
Orr, W. K., & Shortridge, K. F. (1999). Human infection with
influenza H9N2. Lancet, 354(9182), 916-917.
26 Butt, K. M., Smith, G. J., Chen, H., Zhang, L. J., Leung, Y. H., Xu, K. M.,
Lim, W., Webster, R. G., Yuen, K. Y., Peiris, J. S., & Guan, Y. (2005).
Human infection with an avian H9N2 influenza A virus in Hong
Kong in 2003. Journal of Clinical Microbiology, 43(11), 5760-5767.
doi:10.1128/JCM.43.11.5760-5767.2005
27 Uyeki, T. M., Chong, Y. H., Katz, J. M., Lim, W., Ho, Y. Y., Wang, S. S.,
Tsang, T. H., Au, W. W., Chan, S. C., Rowe, T., Hu-Primmer, J., Bell, J.
C., Thompson, W. W., Bridges, C. B., Cox, N. J., Mak, K. H., &
Fukuda, K. (2002). Lack of evidence for human-to-human
transmission of avian influenza A (H9N2) viruses in Hong Kong,
China 1999. Emerging Infectious Diseases, 8(2), 154-159.
28 Bridges, C. B., Lim, W., Hu-Primmer, J., Sims, L., Fukuda, K., Mak, K.
H., Rowe, T., Thompson, W. W., Conn, L., Lu, X., Cox, N. J., & Katz, J.
M. (2002). Risk of influenza A (H5N1) infection among poultry
workers, Hong Kong, 1997-1998. The Journal of Infectious Diseases,
185(8), 1005-1010. doi:10.1086/340044
29 Schultsz, C., Nguyen, V. D., Hai le, T., Do, Q. H., Peiris, J. S., Lim, W.,
Garcia, J. M., Nguyen, D. T., Nguyen, T. H., Huynh, H. T., Phan, X. T.,
van Doorn, H. R., Nguyen, V. V., Farrar, J., & de Jong, M. D. (2009).
Prevalence of antibodies against avian influenza A (H5N1) virus
among Cullers and poultry workers in Ho Chi Minh City, 2005. PloS
One, 4(11), e7948. doi:10.1371/journal.pone.0007948
30 Kandun, I. N., Wibisono, H., Sedyaningsih, E. R., Yusharmen,

Hadisoedarsuno, W., Purba, W., Santoso, H., Septiawati, C.,
Tresnaningsih, E., Heriyanto, B., Yuwono, D., Harun, S., Soeroso, S.,
Giriputra, S., Blair, P. J., Jeremijenko, A., Kosasih, H., Putnam, S. D.,
Samaan, G., Silitonga, M., Chan, K. H., Poon, L. L., Lim, W., Klimov,
A., Lindstrom, S., Guan, Y., Donis, R., Katz, J., Cox, N., Peiris, M., &
Uyeki, T. M. (2006). Three Indonesian clusters of H5N1 virus
infection in 2005. The New England Journal of Medicine, 355(21),
2186-2194. doi:10.1056/NEJMoa060930
31 Ungchusak, K., Auewarakul, P., Dowell, S. F., Kitphati, R., Auwanit,

W., Puthavathana, P., Uiprasertkul, M., Boonnak, K.,
Pittayawonganon, C., Cox, N. J., Zaki, S. R., Thawatsupha, P.,
Chittaganpitch, M., Khontong, R., Simmerman, J. M., &
Chunsutthiwat, S. (2005). Probable person-to-person transmission
of avian influenza A (H5N1). The New England Journal of Medicine,
352(4), 333-340. doi:10.1056/NEJMoa044021
32 Sambhara, S., & Poland, G. A. (2010). H5N1 Avian influenza:

preventive and therapeutic strategies against a pandemic. Annual
Review of Medicine, 61, 187-198.
doi:10.1146/annurev.med.050908.132031
33 Leneva, I. A., Roberts, N., Govorkova, E. A., Goloubeva, O. G., &

Webster, R. G. (2000). The neuraminidase inhibitor GS4104
(oseltamivir phosphate) is efficacious against A/Hong
Kong/156/97 (H5N1) and A/Hong Kong/1074/99 (H9N2) influenza
viruses. Antiviral Research, 48(2), 101-115.
34 Govorkova, E. A., Leneva, I. A., Goloubeva, O. G., Bush, K., &

Webster, R. G. (2001). Comparison of efficacies of RWJ-270201,
zanamivir, and oseltamivir against H5N1, H9N2, and other avian
influenza viruses. Antimicrobial Agents and Chemotherapy, 45(10),
2723-2732. doi:10.1128/AAC.45.10.2723-2732.2001
35 World Health Organization (WHO). (2006). WHO Rapid Advice

Guidelines on Pharmacological Management of Humans Infected with
Avian Influenza A (H5N1) Virus. Retrieved from
http://www.who.int/medicines/publications/WHO_PSM_PAR_2006.6.pdf
36 World Health Organization Global Influenza Program Surveillance

Network. (2005). Evolution of H5N1 avian influenza viruses in Asia.
Emerging Infectious Diseases, 11(10), 1515-1521.
37 De Benedictis, P., Beato, M. S., & Capua, I. (2007). Inactivation of

avian influenza viruses by chemical agents and physical
conditions: a review. Zoonoses and Public Health, 54(2), 51-68.
doi:10.1111/j.1863-2378.2007.01029.x
38 Welliver, R., Monto, A. S., Carewicz, O., Schatteman, E., Hassman,

M., Hedrick, J., Jackson, H. C., Huson, L., Ward, P., Oxford, J. S., &
Oseltamivir Post Exposure Prophylaxis Investigator Group. (2001).
Effectiveness of oseltamivir in preventing influenza in household
contacts: a randomized controlled trial. JAMA : The Journal of the
American Medical Association, 285(6), 748-754.
Français
MENU 

Substances – Influenza virus (B and C)

SUBSTANCES
NAME: Influenza virus (B and C).
SYNONYM OR CROSS REFERENCE: Orthomyxovirus, grippe, pleural infusion,

1
pharyngitis, upper respiratory tract infection, and flu .
CHARACTERISTICS: Members of the Orthomyxoviridae family of segmented,

1 2
negative sense, single-stranded RNA viruses . Minor changes
(antigenic drift) in the surface antigenic configuration may occur in influenza
3
B and influenza C viruses, giving rise to variations in virus stain .
Comparisons of the sequence divergence among the genes of influenza
viruses belonging to type A, B and C suggest that, in humans, influenza B
viruses evolve more slowly than influenza A viruses and faster than C viruses
4 .

PATHOGENICITY/TOXICITY: Influenza B is an acute viral disease of the
upper respiratory tract characterized by acute fever, chills, headache,
myalgia, weakness, runny nose, sore throat, and cough (can be severe).
Nausea and vomiting are uncommon, except in children, and fatality is
1
generally low, except in those with chronic lung or heart conditions .
Recovery is usually rapid, but the cough may persist for some time.
Influenza B causes the same spectrum of disease as influenza A but does
not cause pandemics. Influenza C virus causes a mild upper respiratory tract
infection with fever, cough and rhinorrhea being the most common
3
symptoms .
EPIDEMIOLOGY: Influenza B can occur in epidemics, but serious disease

3
with influenza B is rare and is usually confined to the elderly . Influenza B
disease is common in children and young adults, and causes seasonal
5
epidemics every 2–4 years . Influenza B viruses were the most commonly
6
reported influenza type in Europe for the 20005-06 season . In Canada, in
the 2007-08 influenza season, it was reported that 42.1% of all influenza
7
detections were influenza b viruses . Influenza C has been associated
with sporadic cases and minor localized outbreaks, but has never been
associated with epidemic outbreaks and a large proportion of influenza C
1
infections are clinically unapparent .
HOST RANGE: Influenza B and C viruses are found almost exclusively in

humans; however, there are reports of the isolation of B virus from horses
1 8 9 1
and seals , and C virus from swine .
MODE OF TRANSMISSION: Transmission of influenza in humans can occur

via droplets (from coughing and sneezing) or from contact with
1 10
contaminated surfaces . Closed environments and crowds favour
1
transmission . Influenza virus can persist for 2 to 8 hours on stainless
10 11
steel surfaces and for a few minutes on paper tissues .
1
INCUBATION PERIOD: One to 3 days .
COMMUNICABILITY: Highly communicable, probably limited to 3 to 5 days

12
from clinical onset, and up to 7 days in young children .

RESERVOIR: Humans. There is no recognised zoonotic reservoir; however,
1
swine are suspected as sources of new human subtypes . In addition,
antibodies to influenza B and C viruses have been detected in horses and
1 1 8
dogs , and influenza B infection has been documented in seals
9 9
which are touted as a potential reservoir of influenza B .
ZOONOSIS: Transmission from animal to man is believed to be extremely

13
rare . Influenza C virus transmission has been reported to occur
14
between swine and humans .
VECTORS: None.

DRUG SUSCEPTIBILITY: The main antiviral agents to treat influenza B
available in the United States and Canada are the neuraminidase inhibitors,
15
zanamivir and oseltamivir . Oseltamivir is licensed in Canada for
treatment and post-exposure prophylaxis, and zanamivir for treatment and
16 17
prophylaxis ; however, oseltamivir is documented to be less
18
effective for influenza B viruses than for influenza A viruses . The M2
inhibitor amantadine, that is often used to treat influenza A, has no affect on
11 15 16
influenza B . Amantadine is no longer used in Canada due to
19
resistance that develops rapidly .
SUSCEPTIBILITY TO DISINFECTANTS: Not documented, but likely to be the

same as for influenza A subtypes, including sodium hypochlorite (freshly
made 1:10 dilution of bleach), 60 to 95% ethanol, 2% alkaline glutaraldehyde,
20
5 to 8% formalin, 3% lysol, and 5% phenol .
PHYSICAL INACTIVATION: Not documented, but likely to be the same as for

influenza A subtypes, including moist heat at 121ºC for 20 minutes or dry
heat at 170ºC for 1 hour, 160ºC for 2 hours, or 121ºC for at least 16 hours
20 .
SURVIVAL OUTSIDE HOST: Influenza B virus can survive for 24 to 48 hours

on hard, nonporous surfaces such as stainless steel and plastic, and 8 to 12
10
hours or less on cloth, paper and tissues .

1
SURVEILLANCE: Monitor for symptoms of influenza . Laboratory
confirmation of the virus is not routinely performed but consists of
inoculating cell cultures with swabs or washings taken from the nose during
the first days of illness. Point-of-care rapid testing, using commercially
available diagnostic test kits, may also be performed in order to distinguish
21
between influenza A and B, especially in out-of-season outbreaks .
FIRST AID/TREATMENT: Supportive. Oseltamivir and zanamivir used to treat

15
influenza B viruses , although oseltamivir is deemed to be less effective
18
against influenza B than it is against influenza A . These drugs are not
effective against influenza C.
IMMUNIZATION: The most effective strategy for reducing the impact of

influenza is through annual vaccination using a live attenuated influenza
15
vaccine (LAIV) or an inactivated influenza vaccine (TIV) . Both LAIV and
TIV contain strains of influenza viruses that are antigenically equivalent to
the annually recommended strains: 1 influenza A (H3N2) virus, 1 influenza A
15 16
(H1N1) virus and 1 influenza B virus . Each year, one or more virus
strains might be changed on the basis of global surveillance for influenza
15
viruses and the spread of new strains . LAIV is administered intranasally
by sprayer, whereas TIV is administered intramuscularly by injection. LAIV is
currently approved only for use among healthy persons aged 5 to 49 years
15 22
. The current vaccine does not protect against influenza C . LAIV is
not available in Canada.
15
PROPHYLAXIS: Vaccines that protect against influenza B are available
16 ; however, chemoprophylactic drugs must not be overlooked in the
control or prevention of influenza. Antiviral prophylaxis must be initiated
within 3 days of the detected illness of the index cases to be effective in
23
slowing transmission . Available drugs for prophylaxis are the
15 16
neuraminidase inhibitors, zanamivir and oseltamivir .

LABORATORY-ACQUIRED INFECTIONS: Unknown.
SOURCES/SPECIMENS: Respiratory tissues, human secretions, and infected

1
animals .

1
aspirating, dispensing, or mixing virus-infected samples .
SPECIAL HAZARDS: Genetic manipulation of virus has unknown potential

for altering host range, pathogenicity, or for introducing into man
24
transmissible viruses with novel antigenic composition .

25
CONTAINMENT REQUIREMENTS: Containment Level 2 practices and

containment are required when receiving and inoculating routine diagnostic
26
circulating human specimens ; however, additional operational
precautions are required to reduce the possibility of direct transmission and
re-assortment in humans. Any work involving the intentional co-infection of
human and animal influenza viruses in animal models requires a
Containment Level 3 facility and operational procedures with rigorous
adherence to additional respiratory protection and clothing change
16
protocols .
PROTECTIVE CLOTHING: Wear protective solid-front gowns, gloves and N95

respiratory protection. Manipulations that may produce aerosols should be
26
carried out in a certified biological cabinet .
OTHER PRECAUTIONS: Centrifugation of respiratory and tissue specimens

should be carried out using sealed centrifuge cups or rotors, both of which
26
are to be unloaded in a biological safety cabinet .

cover spill with paper towels and apply 1% sodium hypochlorite, starting at
16 20
(30 minutes) before clean up .

20 26

26
that are appropriately labelled. .

and standards.

Canada.

Copyright ©
Canada
REFERENCES:
1 Acha, P. N., & Szyfres, B. (2003). In Pan American Health

Organization (Ed.), Zoonoses and Communicable Diseases Common
to Man and Animals (3rd ed.). Washington DC: PAHO HQ library.
2 Hampson, A. W., & Mackenzie, J. S. (2006). The influenza viruses.

Medical Journal of Australia, 185(10 SUPPL.), S39-S43.
3 Cunha, B. A. (2004). Influenza: Historical aspects of epidemics and

pandemics. Infectious Disease Clinics of North America, 18(1), 141-
155.
4 Yamashita, M., Krystal, M., Fitch, W. M., & Palese, P. (1988).

Influenza B virus evolution: Co-circulating lineages and
comparison of evolutionary pattern with those of influenza A and
C viruses. Virology, 163(1), 112-122.
5 Belshe, R. B. (2010). The need for quadrivalent vaccine against

seasonal influenza. Vaccine, 28 Suppl 4, D45-53.
doi:10.1016/j.vaccine.2010.08.028
6 Center for Disease Control and Prevention. (June 2006). Update:

Influenza Activity-United States and Worldwide, 2005-06 Season, and
Composition of the 2006-07 Influenza VaccineMorbidity and
Mortality Weekly Report (MMWR).
7 Reyes F., Aziz S., Winchester B., Li Y., Vaudry W., JBettinger J.,
Huston P., King A. (July 2008). Canada Communicable Disease
Report. Public Health Agency of Canada.
8 Osterhaus, A. D. M. E., Rimmelzwaan, G. F., Martina, B. E. E.,

Bestebroer, T. M., & Fouchier, R. A. M. (2000). Influenza B virus in
seals. Science, 288(5468), 1051-1053.
9 Ohishi, K., Ninomiya, A., Kida, H., Park, C. -., Maruyama, T., Arai, T.,
Katsumata, E., Tobayama, T., Boltunov, A. N., Khuraskin, L. S., &
Miyazaki, N. (2002). Serological evidence of transmission of human
influenza A and B viruses to Caspian seals (Phoca caspica).
Microbiology and Immunology, 46(9), 639-644.
10 Bean, B., Moore, B. M., & Sterner, B. (1982). Survival of influenza

viruses on environmental surfaces. Journal of Infectious Diseases,
146(1), 47-51.
11 Nicholson, K. G., Wood, J. M., & Zambon, M. (2003). Influenza.

Lancet, 362(9397), 1733-1745.

13 Hay, A. J., Gregory, V., Douglas, A. R., & Yi, P. L. (2001). The
evolution of human influenza viruses. Philosophical Transactions of
the Royal Society B: Biological Sciences, 356(1416), 1861-1870.
14 Kimura, H., Abiko, C., Peng, G., Muraki, Y., Sugawara, K., Hongo, S.,
Kitame, F., Mizuta, K., Numazaki, Y., Suzuki, H., & Nakamura, K.
(1997). Interspecies transmission of influenza C virus between
humans and pigs. Virus Research, 48(1), 71-79.
15 Advisory Committee on Immunization Practices, Smith, N. M.,

Bresee, J. S., Shay, D. K., Uyeki, T. M., Cox, N. J., & Strikas, R. A.
(2006). Prevention and Control of Influenza: recommendations of
the Advisory Committee on Immunization Practices (ACIP).
MMWR.Recommendations and Reports : Morbidity and Mortality
Weekly Report.Recommendations and Reports / Centers for Disease
Control, 55(RR-10), 1-42.
16 Public Health Agency of Canada. (2006). The Canadian Pandemic

Influenza Plan for the Health Sector. www.phac-aspc.gc.ca/cpip-
pclcpi/pdf-e/CPIP-2006_e.pdf
17 Public Health Agency of Canada. (2009). The Canadian Pandemic

Influenza Plan for the Health Sector Annex E: The Use of Antiviral
Drugs During a Pandemics.
18 Kawai, N., Ikematsu, H., Iwaki, N., Kawashima, T., Maeda, T.,
Mitsuoka, S., Kondou, K., Satoh, I., Miyachi, K., Yamaga, S.,
Shigematsu, T., Hirotsu, N., & Kashiwagi, S. (2007). Longer virus
shedding in influenza B than in influenza A among outpatients
treated with oseltamivir. Journal of Infection, 55(3), 267-272.
19 Publich Health Agency of Canada. National Influenza Treatment

Guidelines: Interim Options for Clinicians Considering Influenza
Antivirals in the Context of Changing Patters of Resistance, 2008-09
Season

Instructions for Monitoring Health of Laboratory Workers and for
Destroying Influenza A (H2N2)
Samples.http://www2a.cdc.gov/HAN/ArchiveSys/ViewMsgV.asp?
AlertNum=00228
21 Heymann, D. L. (2008). Control of Communicable Diseases Manual

Association.
22 Ryan, K. J., & Ray, C. G. (Eds.). (2004.). Sherris Medical Microbiology:

York.: McGraw-Hill.
23 Longini Jr., I. M., Halloran, M. E., Nizam, A., & Yang, Y. (2004).
Containing Pandemic Influenza with Antiviral Agents. American
Journal of Epidemiology, 159(7), 623-633.
24 De Jong, J. C., Rimmelzwaan, G. F., Fouchier, R. A. M., & Osterhaus,

A. D. M. E. (2000). Influenza virus: A master of metamorphosis.
Journal of Infection, 40(3), 218-228.

2009, (2009).

Guidelines (3rd ed.). Canada.
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Influenza virus type A

SUBSTANCES
SECTION 1 - INFECTIOUS AGENT
NAME: Influenza virus type A (excluding 1918 influenza A (H1N1) strain and
subtypes H5, H7 and H9).
SYNONYM OR CROSS REFERENCE: Orthomyxovirus , grippe, and flu(1).
CHARACTERISTICS: Members of the Orthomyxoviridae family of segmented,

negative sense, single-stranded RNA viruses(1,2). Type A influenza viruses are
subdivided on the basis of the antigenic nature of their membrane-bound
surface glycoproteins, haemagglutinin (HA) and neuraminidase (NA). To
date, 16 HA, and 9 NA subtypes have been detected in wild birds and
poultry, of which subtypes H1N1 and H3N2 are currently circulating among
humans in seasonal influenza outbreaks(3,4,5,6,7). Antigenic alterations occur
frequently in influenza HA and NA antigenic sites and are the mechanism for
virus adaptation to the host and survival. Small alterations are referred to as
antigenic drift, whereas larger alterations caused by reassortment are
referred to as antigenic shift. Influenza pandemics may occur as a result of
antigenic shifts if the mutation of the virus leads to efficient human-to-
human transmission(2,8). Only three haemagglutinin subtypes (H1, H2, H3)
and two neuraminidase subtypes (N1 and N2) have established stable
lineages in the human population since 1918(9).
SECTION 2 – HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: An acute viral disease of the upper respiratory
tract characterized by fever (temperature 37.8ºC or above), headache,
myalgia, malaise, sore throat, non-productive cough, sneezing and nasal
discharge(10). Among children, otitis media, nausea and vomiting are
commonly reported(11). Pulmonary complications of influenza include
pneumonia (viral and bacterial), croup, asthma and bronchitis. Myocarditis
and pericarditis are occasional cardiac complications. Fatality due to
influenza is generally low, except in those with chronic lung or heart
conditions(1). Secondary bacterial pneumonia after influenza is a leading
cause of mortality worldwide(12).
EPIDEMIOLOGY: Influenza caused approximately 36,000 deaths per year in

the United States between 1990 and 1999, and approximately 226,000
hospitalizations between 1979 and 2001(13,14).
Influenza can occur in pandemics and epidemics, localized outbreaks, and as

sporadic cases(1). In temperate climates, epidemics of influenza typically
occur during the late fall and winter seasons(2,11), whereas in tropical and
subtropical regions influenza epidemics occur throughout the year(11).
Historical evidence suggests that more severe, world wide pandemics have
occurred at 10 to 40 year intervals since the 16th century(2).
A pandemic that occurred in 1957-1958 (Asian flu) was caused by influenza

virus A subtype H2N2, that resulted from the reassortment of circulating
human H1N1 and avian H2N2 viruses(15), and is estimated to have caused
70,000 deaths in the United States(16).
Another influenza pandemic that occurred in 1968-1969 (Hong Kong flu),

was caused by an H3N2 strain of influenza that was the result of a
reassortment between circulating human H2N2 and avian H3(15) viruses and
is estimated to have caused 34,000 deaths in the United States(16). Together,
the Asian and Hong Kong flu pandemics resulted in 1 to 2 million deaths
worldwide(17).
Since the Hong Kong flu (H3N2) pandemic, the number of influenza-
associated hospitalizations has typically been greater during seasonal
influenza epidemics caused by influenza A/H3N2 viruses than during
seasons in which other influenza A virus subtypes have predominated(18).
During the summer of 2002, an epidemic of respiratory illness with 22,646

cases and a 3% case- mortality affected Madagascar and was attributed to a
strain of H3N2(9).
The 2009 H1N1 pandemic resulted in rates of infection ranging from 11%
(New Zealand) to 21% (Pittsburgh, USA) of the population, depending on
location(19,20) . As of March 13, 2010, the U.S. Centers for Disease Control and
Prevention estimate that in the United States 60 million people were
infected with 2009 H1N1, resulting in 270,000 hospitalizations and 12,270
deaths(21). Overall mortality rate was less than 0.5%, and morbidity and
mortality were predominant in young adults and less common for adults
over 60 years old(22,23,24).
Influenza A subtypes H1N1 and H3N2 are still currently circulating in the
human population(25) and are included in current vaccines(11).
HOST RANGE: Humans, swine, horses, domestic and wild avian species
(predominantly ducks), geese, and shorebirds(1,2).
INFECTIOUS DOSE: Unknown for specific influenza A subtypes. The

infectious dose for the influenza A variant, Influenza A2, is greater than 790
organisms via the nasopharyngeal route(26). Influenza A (subtype not
specified) is more infectious by aerosol inhalation (50% human infectious
dose (HID50) = 0.6 – 3.0 median tissue culture infectious doses (TCID50)) than
by intranasal drop inoculation (HID50 = 127 – 320 TCID50)(27).
MODE OF TRANSMISSION: Transmission of influenza in humans can occur

via respiratory infection by aerosols and droplets (from coughing and
sneezing) or from contact transmission from contaminated surfaces(1,9,28).
Closed environment and crowds favour transmission(1). Transmission of
influenza virus from donors who are shedding large amounts of virus can be
infective for 2 to 8 hours via stainless steel surfaces and for a few minutes
via paper tissues(9,28,29).
INCUBATION PERIOD: Short, usually 1 to 3 days(1,16,28).
COMMUNICABILITY: Highly communicable. Infected persons can shed

detectable amounts of influenza virus the day before symptoms begin(18,30).
Adults usually shed the virus for 3 to 5 days, and up to 7 days in young
children(18,28,30).
SECTION 3 - DISSEMINATION
RESERVOIR: Humans are the principle reservoir of human influenza A
viruses. The avian reservoir of influenza A viruses is wild birds,
predominantly ducks, geese, and shorebirds. Animal reservoirs are
suspected as sources of new human subtypes. Influenza A viruses are also
frequently isolated in pigs and horses(31). Swine have been demonstrated to
have receptors for both human and avian influenza viruses and as such are
considered potential mixing vessel for human and avian viruses(31,32). This
could result in a reassortment which may be infectious to man with
antigenic characteristics for which the human population is immunologically
naïve(31).
ZOONOSIS: Transmission from pigs to man has been demonstrated(33).

There are documented cases of human infections with swine influenza
viruses, and zoonotic infection may occur frequently in those involved
directly or indirectly in swine farming; however, the illness is mild and
person-to-person transmission is very limited(33). In the case of pandemic
H1N1 influenza, the person-to-person transmission measured by basic
reproduction number (R0) was almost the same (R0 = 1.4 to 1.6) as seasonal
influenza (R0 = 0.9 to 2.1), and the disease may in a range from mild to
acute(34,35).
VECTORS: None.
SECTION 4 – STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: Seasonal influenza viruses are sensitive to the
neuraminidase inhibitors oseltamivir (Tamiflu), and zanamivir (Relenza), and
to amantadine, and rimantadine, which inhibit the M2 ion channel protein
activity and block viral uncoating(36). The 2009 H1N1 virus is susceptible to
neuraminidase inhibitors, including oseltamivir (Tamiflu) and zanamivir
(Relenza), but usually resistant to amantadine and rimantadine(35,37,38,39).
Sporadic instances of oseltamivir-resistant 2009 H1N1 viruses have been
documented(22,35). Oseltamivir is licensed in Canada for treatment and post-
expose prophylaxis, zanamivir for treatment alone, and amantadine for
prophylaxis alone(40). Rimantadine is not currently licensed for use in
Canada(40).
DRUG RESISTANCE: A significant increase in resistance to oseltamivur,

adamantanes (amantadine, and rimantadine) has been observed
recently(41).
SUSCEPTIBILITY TO DISINFECTANTS: Influenza A is susceptible to

disinfectants, including sodium hypochlorite (freshly made 1:10 dilution of
bleach), 60 to 95% ethanol, 2% alkaline glutaraldehyde, 5 to 8% formalin, and
5% phenol(42).
PHYSICAL INACTIVATION: Susceptible to moist heat at 121ºC for 20

minutes or dry heat at 170ºC for 1 hour, 160ºC for 2 hours, or 121ºC for at
least 16 hours(42).
SURVIVAL OUTSIDE HOST: Influenza A virus can survive for 24 to 48 hours

on hard, nonporous surfaces such as stainless steel and plastic and for
approximately 8 to 12 hours on cloth, paper and tissues(29).
SECTION 5 – FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms of influenza(1,9). Confirm diagnosis
with RT-PCR (favoured) or point-of-care testing and give appropriate
antiviral treatment(43). Laboratory confirmation of the virus is not routinely
performed, occurring only during an epidemic and consists of inoculating
cell cultures with swabs or washings taken from the nose during the first
days of illness(1).
FIRST AID/TREATMENT: Fluids and rest. Antiviral agents (mainly

oseltamivir) can be employed to treat influenza A(11,12,16). Antibiotic
treatment (in combination with antiviral treatment) may also be used to
prevent or treat secondary bacterial pneumonia(12).
IMMUNIZATION: The most effective strategy for reducing the effect of

influenza is through annual vaccination using a live, attenuated influenza
vaccine (LAIV) or an inactivated influenza vaccine (TIV)(11). Both LAIV and
TIV contain strains of influenza viruses that are antigenically equivalent to
the annually recommended strains: 1 influenza A (H3N2) virus, 1 influenza A
(H1N1) virus and 1 influenza B virus(11,40). Each year, one or more virus
strain might be changed on the basis of global surveillance for influenza
viruses and the spread of new strains(11). LAIV is administered intranasally
by sprayer, whereas TIV is administered intramuscularly by injection. LAIV is
currently approved only for use among healthy persons aged 5 to 49
years(11). During the 2009 H1N1 pandemic, an adjuvanted inactivated
vaccine was developed by Glaxo Smith Kline (Pandemrix), which was
authorized for use by the European Commission, with priority given to at
risk populations, pregnant women, health care workers, and those in close
contact with immunocompromised individuals(38). The FDA approved 4
vaccines against the novel 2009 H1N1 for use in the United States on
September 15, 2009: inactivated vaccines manufactured by Sanofi Pasteur,
Novartis Vaccines and Diagnostics Limited, and CSL Limited; and a live
attenuated intranasal vaccine manufactured by Medimmune LLC(36). In
Canada an adjuvanted monovalent inactivated vaccine manufactuered by
GlaxoSmithKline and an unadjuvanted inactivated vaccine (Panvax),
manufactured by CSL Biotherapies, were approved for use by Health Canada
during the 2009 H1N1 pandemic. A LAIV intranasal vaccine has also recently
been approved for use in Canada(44).
PROPHYLAXIS: Vaccines are available for influenza A subtypes H1N1 and

H3N2(11); however, chemoprophylactic drugs must not be overlooked in the
control or prevention of influenza. Antiviral prophylaxis must be initiated
within 3 days of the detected illness of the index cases to be effective in
slowing transmission(16). Available drugs for prophylaxis are the
neuraminidase inhibitors, zanamivir (10mg twice daily for 5 days) and
oseltamivir (75mg once daily for 7 to 10 days)(11). The M2 inhibitor,
amantadine can also be used for chemoprophylaxis during outbreaks of
seasonal influenza.
SECTION 6 - LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: Fifteen reported cases up to
1974(45). Animal- associated infections are not reported; however, risk is
high from infected ferrets(46).
SOURCES/SPECIMENS: Respiratory tissues, human secretions, and infected

animals. In addition, the virus may be present in the intestines and cloacae
of infected avian species. Influenza A may be disseminated in multiple
organs in infected animal species(47).

aspirating, dispensing, or mixing virus-infected samples (tissues, faeces,
secretions) from infected animals(47). Laboratory infection can also occur
from direct inoculation of mucous membranes via virus contaminated
gloves following the handling of tissues, faeces and/or secretions from
infected animals(47).
SPECIAL HAZARDS: Genetic manipulation of virus has an unknown potential

for altering host range, pathogenicity, and/or for introducing transmissible
viruses with novel antigenic composition into humans(47).
SECTION 7 – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2(48). This risk group applies to
the species as a whole, and may not apply to every strain.

infectious materials and cultures. These containment requirements apply to
the species as a whole, and may not apply to each strain within the species.
A detailed risk assessment should be conducted for activities involving
animal work to determine whether additional operational practices should
be considered.
PROTECTIVE CLOTHING: For diagnostic work: Lab coat. Gloves when direct
skin contact with infected materials or animals is unavoidable. Eyes
exposure to splashes(49).

should be strictly limited(49). Additional precautions should be considered
with work involving animals or large scale activities(49).
SECTION 8 - HANDLING AND STORAGE

cover spill with paper towels and apply suitable disinfectant, starting at
perimeter and working towards the centre. Allow sufficient contact time (30
minutes) and then clean the area(49).
DISPOSAL: Decontaminate before disposal by steam sterilization, chemical

disinfection, or incineration(49).
STORAGE: In sealed containers that are appropriately labelled(49).
SECTION 9 – REGULATORY AND OTHER INFORMATION

and standards.

Canada.

Copyright ©
Canada
REFERENCES:
1. Acha, P. N., & Szyfres, B. (2003). Zoonoses and Communicable Diseases
Common to Man and Animals (3rd ed., ). Washington, D.C.: Pan American
Health Organization.
2. Hampson, A. W., & Mackenzie, J. S. (2006). The influenza viruses. Medical
Journal of Australia, 185 (10 SUPPL.), S39-S43.
3. World Health Organization (WHO). (1980). A revision of the system of
nomenclature for influenza viruses: a WHO memorandum. Bulletin of the
World Health Organization, 58 (4), 585-591.
4. Hinshaw, V. S., Air, G. M., & Gibbs, A. J. (1982). Antigenic and genetic
characterization of a novel hemagglutinin subtype of influenza A viruses
from gulls. Journal of Virology, 42 (3), 865-872.
5. Kawaoka, Y., Yamnikova, S., Chambers, T. M., Lvov, D. K., & Webster, R. G.
(1990). Molecular characterization of a new hemagglutinin, subtype H14,
of influenza A virus. Virology, 179 (2), 759-767.
6. Ro hm, C., Zhou, N., Su ss, J., Mackenzie, J., & Webster, R. G. (1996).
Characterization of a novel influenza hemagglutinin, H15: Criteria for
determination of influenza A subtypes. Virology, 217 (2), 508-516.
7. Fouchier, R. A. M., Munster, V., Wallensten, A., Bestebroer, T. M., Herfst,
S., Smith, D., Rimmelzwaan, G. F., Olsen, B., & Osterhaus, A. D. M. E.
(2005). Characterization of a novel influenza A virus hemagglutinin
subtype (H16) obtained from black-headed gulls. Journal of Virology, 79
(5), 2814-2822.
8. Thomas, J. K., & Noppenberger, J. (2007). Avian influenza: A review.
American Journal of Health-System Pharmacy, 64 (2), 149-165.
9. Nicholson, K. G., Wood, J. M., & Zambon, M. (2003). Influenza. Lancet, 362
(9397), 1733-1745.
10. Nicholson, K. G. (1992). Clinical features of influenza. Seminars in
Respiratory Infections, 7(1), 26-37.
11. Fiore, A. E., Shay, D. K., Haber, P., Iskander, J. K., Uyeki, T. M., Mootrey, G.,
Bresee, J. S., & Cox, N. J. (2007). Prevention and control of influenza.
Recommendations of the Advisory Committee on Immunization
Practices (ACIP), 2007. MMWR.Recommendations and Reports : Morbidity
and Mortality Weekly Report.Recommendations and Reports / Centers for
Disease Control, 56 (RR-6), 1-54.
12. McCullers, J. A. (2004). Effect of antiviral treatment on the outcome of
secondary bacterial pneumonia after influenza. Journal of Infectious
Diseases, 190 (3), 519-526.
13. Thompson, W. W., Shay, D. K., Weintraub, E., Brammer, L., Cox, N.,
Anderson, L. J., & Fukuda, K. (2003). Mortality associated with influenza
and respiratory syncytial virus in the United States. Journal of the
American Medical Association, 289 (2), 179-186.
14. Thompson, W. W., Shay, D. K., Weintraub, E., Brammer, L., Bridges, C. B.,
Cox, N. J., & Fukuda, K. (2004). Influenza-associated hospitalizations in
the United States. Journal of the American Medical Association, 292 (11),
1333-1340.
15. Lindstrom, S. E., Cox, N. J., & Klimov, A. (2004). Genetic analysis of human
H2N2 and early H3N2 influenza viruses, 1957-1972: Evidence for genetic
divergence and multiple reassortment events. Virology, 328 (1), 101-119.
16. Longini Jr., I. M., Halloran, M. E., Nizam, A., & Yang, Y. (2004). Containing
Pandemic Influenza with Antiviral Agents. American Journal of
Epidemiology, 159 (7), 623-633.
17. Beveridge, W. I. (1991). The chronicle of influenza epidemics. History and
Philosophy of the Life Sciences, 13 (2), 223-234.
18. Morris, J. A. (1966). Immunity to influenza as related to antibody levels.
N. Engl. J. Med., 274 (10), 527-535.
19. Writing Committee of the WHO Consultation on Clinical Aspects of
Pandemic (H1N1) 2009 Influenza, Bautista, E., Chotpitayasunondh, T.,
Gao, Z., Harper, S. A., Shaw, M., Uyeki, T. M., Zaki, S. R., Hayden, F. G.,
Hui, D. S., Kettner, J. D., Kumar, A., Lim, M., Shindo, N., Penn, C., &
Nicholson, K. G. (2010). Clinical aspects of pandemic 2009 influenza A
(H1N1) virus infection. The New England Journal of Medicine, 362 (18),
1708-1719. doi:10.1056/NEJMra1000449
20. Tang, J. W., Shetty, N., & Lam, T. T. (2010). Features of the new pandemic
influenza A/H1N1/2009 virus: virology, epidemiology, clinical and public
health aspects. Current Opinion in Pulmonary Medicine, 16 (3), 235-241.
doi:10.1097/MCP.0b013e3283375727
21. Center for Disease Control and Prevention. (2010). CDC Estimates of 2009
H1N1 Cases and Related Hospitalizations and Death from April 2009
through March 13, 2010, By Age Group.
www.cdc.gov/h1n1flu/pdf/graph_March%202010.pdf
22. Franco-Paredes, C., Hernandez-Ramos, I., Del Rio, C., Alexander, K. T.,
Tapia-Conyer, R., & Santos-Preciado, J. I. (2009). H1N1 influenza
pandemics: comparing the events of 2009 in Mexico with those of 1976
and 1918-1919. Archives of Medical Research, 40 (8), 669- 672.
doi:10.1016/j.arcmed.2009.10.004
23. Guarner, J., & Falcon-Escobedo, R. (2009). Comparison of the pathology
caused by H1N1, H5N1, and H3N2 influenza viruses. Archives of Medical
Research, 40 (8), 655-661. doi:10.1016/j.arcmed.2009.10.001
24. Halasa, N. B. (2010). Update on the 2009 pandemic influenza A H1N1 in
children. Current Opinion in Pediatrics, 22 (1), 83-87.
doi:10.1097/MOP.0b013e3283350317
25. Kobasa, D., & Kawaoka, Y. (2005). Emerging influenza viruses: Past and
present. Current Molecular Medicine, 5 (8), 791-803.
26. Collins, C. H., & Kennedy, D. A. (1999). Laboratory-acquired Infections (4th
ed.). Woburn, WA: Reed Educational and Professional Publishing Ltd.
27. Tellier, R. (2006). Review of aerosol transmission of influenza A virus.
Emerging Infectious Diseases, 12 (11), 1657-1662.
28. Heymann, D. L. (2004). An Official Report of the American Public Health
Association. In D. L. Heymann (Ed.), Control of Communicable Diseases
Manual. (18th ed., pp. 35-37). Washington, D.C.: American Public Health
Association.
29. Bean, B., Moore, B. M., & Sterner, B. (1982). Survival of influenza viruses
on environmental surfaces. Journal of Infectious Diseases, 146 (1), 47-51.
30. Murphy, B. R., Chalhub, E. G., & Nusinoff, S. R. (1973). Temperature
sensitive mutants of influenza virus. III. Further characterization of the
ts 1[E] influenza A recombinant (H3N2) virus in man. Journal of Infectious
Diseases, 128 (4), 479-487.
31. Scholtissek, C., & Naylor, E. (1988). Fish farming and influenza
pandemics. Nature, 331 (6153), 215.
32. Zhou, N. N., Senne, D. A., Landgraf, J. S., Swenson, S. L., Erickson, G.,
Rossow, K., Liu, L., Yoon, K. -., Krauss, S., & Webster, R. G. (1999). Genetic
reassortment of avian, swine, and human influenza A viruses in
American pigs. Journal of Virology, 73 (10), 8851-8856.
33. Olsen, C., Brammer, L., Easterday, B. C., Arden, N., Belay, E., Baker, I., &
Cox, N. J. (2002). Serological evidence of H1 swine influenza virus
infection in swine farm residents and employees. Emerg. Infect. Dis., 8
(8), 814-819.
34. Coburn, B., Wagner, B., & Blower, S. (2009). Modeling influenza
epidemics and pandemics: insights into the future of swine flu (H1N1).
BMC Medicine, 7 (1), 30. Retrieved from www.biomedcentral.com/1741-
7015/7/30
35. Writing Committee of the WHO Consultation on Clinical Aspects of
Pandemic (H1N1) 2009 Influenza, Bautista, E., Chotpitayasunondh, T.,
Gao, Z., Harper, S. A., Shaw, M., Uyeki, T. M., Zaki, S. R., Hayden, F. G.,
Hui, D. S., Kettner, J. D., Kumar, A., Lim, M., Shindo, N., Penn, C., &
Nicholson, K. G. (2010). Clinical aspects of pandemic 2009 influenza A
(H1N1) virus infection. The New England Journal of Medicine, 362 (18),
1708-1719. doi:10.1056/NEJMra1000449
36. Sym, D., Patel, P. N., & El-Chaar, G. M. (2009). Seasonal, avian, and novel
H1N1 influenza: prevention and treatment modalities. The Annals of
Pharmacotherapy, 43 (12), 2001-2011. doi:10.1345/aph.1M557
37. Krauss, H., Weber, A., Appel, M., Enders, B., Isenberg, H. D., Schiefer, H.
G., Slenczka, W., von Graevenitz, A., & Zahner, H. (2003). Zoonoses.
Infectious Diseases Transmissible from Animals to Humans. Third Edition .
38. Patel, M., Dennis, A., Flutter, C., & Khan, Z. (2010). Pandemic (H1N1) 2009
influenza. British Journal of Anaesthesia, 104 (2), 128-142.
doi:10.1093/bja/aep375
39. Narain, J. P., Kumar, R., & Bhatia, R. (2009). Pandemic (H1N1) 2009:
epidemiological, clinical and prevention aspects. The National Medical
Journal of India, 22 (5), 242-247.
40. Public Health Agency of Canada. (2006). The Canadian Pandemic
Influenza Plan for the Health Sector. http://www.phac-aspc.gc.ca/cpip-
pclcpi/index-eng.php
41. CDC. (2008). Influenza Antiviral Drug Resistance. Retrieved 11/22, 2010,
from www.cdc.gov/flu/about/qa/antiviralresistance.htm
42. Centers for Disease Control and Prevention (CDC). (2006). Instructions
for Monitoring Health of Laboratory Workers and for Destroying Influenza A
(H2N2) Samples. www2a.cdc.gov/HAN/ArchiveSys/ViewMsgV.asp?
AlertNum=00228
43. Lee, B. Y., McGlone, S. M., Bailey, R. R., Wiringa, A. E., Zimmer, S. M.,
Smith, K. J., & Zimmerman, R. K. (2010). To test or to treat? An analysis of
influenza testing and antiviral treatment strategies using economic
computer modeling. PloS One, 5 (6), e11284.
doi:10.1371/journal.pone.0011284
44. Public Health Agency of Canada. (2009). Guidance Document on the Use of
Pandemic Influenza A (H1N1) 2009 Inactivated Monovalent Vaccine
www.phac-aspc.gc.ca/alert-alerte/h1n1/vacc/monovacc/intro-
eng.php#n3
45. Collins, C. H., & Kennedy, D. A. (1999). Laboratory acquired infections.
Laboratory acquired infections: History, incidence, causes and prevention
(4th ed., pp. 1-37). Woburn, MA: BH.
46. Herlocher, M. L., Truscon, R., Elias, S., Yen, H. -., Roberts, N. A., Ohmit, S.
E., & Monto, A. S. (2004). Influenza viruses resistant to the antiviral drug
oseltamivir: Transmission studies in ferrets. Journal of Infectious Diseases,
190 (9), 1627-1630.
Français
MENU 

Substances – Lassa virus

SUBSTANCES
NAME: Lassa virus.
SYNONYM OR CROSS REFERENCE: Lassa fever, Lassa fever virus, viral

1 2 3
haemorrhagic fever (VHF) .
CHARACTERISTICS: Double-segmented, single-stranded RNA virus,

belonging to the genus Arenavirus , family Arenaviridae . The viral fragment
may occupy several distinct shapes (pleomorphic) measuring 80 to 150nm in
1 4
diameter . The surface of the virion lipid envelope is studded with
glycoproteins that consist of tetrameric complexes of the viral glycoproteins
4
GP1 and GP2 .

3
PATHOGENICITY/TOXICITY: Acute viral illness of 1 to 4 weeks duration .
1 3
Disease may be asymptomatic to mild (80 % of cases), severe, or fatal
5 6 7 . Early symptoms include gradual onset of fever, nausea,
abdominal pain, severe sore throat, cough, conjunctivitis, ulceration of
1
buccal mucosa, exudative pharyngitis, and cervical lymphadenopathy
3 5 7 8 . Late symptoms include severe swelling of head and neck,
8 9
pleural and pericardial effusions . Twenty-five percent of cases result
1 3 5 7 10
in deafness and/or (transient) alopecia . The disease is
3 10
severe in pregnancy, resulting in foetal loss in 80 % of cases . Death
1
as a result of infection with Lassa virus is usually due to cardiac arres .
Fatality rate is 15 to 20 % of hospitalized patients and 1 to 2 % of infected
1 3 7
individuals in general .
EPIDEMIOLOGY: Endemic in West Africa. Between 10,000 and 300,000

1 3 6 10
infections occur annually with 5,000 deaths . Outbreaks have
occurred in Guinea, Liberia (1972), Sierra Leone (1970-72, 1973-75, and 1996-
97), areas of Nigeria (first cases in 1969, further outbreaks in 1970, 1974, and
1975), Central African Republic, Democratic Republic of Congo, Mali,
1
Senegal, Benin, Burkina Faso, Cameroon, Ghana, Ivory Coast and Sudan
3 . Approximately 20 cases of imported Lassa fever have been recorded
11 12
worldwide .
HOST RANGE: Mastomys natalensis (an African rodent also known as the
1 3 4 7
multimammate mouse or multimammate rat) and humans
10 .
13
INFECTIOUS DOSE: One to 10 aerosolized organisms .
MODE OF TRANSMISSION: Transmission from the multimammate rat to

humans occurs via aerosols; or by direct contact with rat excretions, or with
food and water contaminated with excretions(1,3,6). Infection may occur
through cuts and sores or when infected rats are prepared as food(1,4,6).
Person-to-person transmission can cause epidemics with a high mortality
rate, or be achieved by nosocomial outbreaks involving blood (contaminated
needles), pharyngeal secretions and urine or contaminated medical
equipment(1,2,3,6,7,15). Lassa virus can also be transmitted via sexual
contact or via contact with skin lesions.
1 3 7 8
INCUBATION PERIOD: Five to 21 days .
COMMUNICABILITY: Person-to-person spread may occur during the acute

3
febrile phase when the virus is present in the throat . Lassa virus can be
excreted in urine for 3-9 weeks from the onset of illness. Male patients
should refrain from unprotected sex until the semen is virus- free for 3
2 9
months .

RESERVOIR: The primary reservoir is the multimammate rat ( Mastomys
1 2 3 7
natalensis ) .
1
ZOONOSIS: Yes, transmission from the multimammate rat to humans
3 7 .
9
VECTORS: Rodents .

1 3 10 16
DRUG SUSCEPTIBILITY: Ribavirin .
SUSCEPTIBILITY TO DISINFECTANTS: Lassa virus is susceptible to 0.5 %

sodium hypochlorite, phenolic compounds, 3 % acetic acid (pH 2.5), lipid
solvents and detergents such as SDS, formaldehyde and paraformaldehyde
1 3 4 17
fixation, formaldehyde fumigation, and β- propiolactone
18 19 .
PHYSICAL INACTIVATION: Lassa virus can be inactivated by heating serum

for 1 hour at 60oC, gamma irradiation (1.2 x10 6 rads to 1.27 x10 6 rads),
3 4 7 17 19
UV irradiation, autoclaving, incineration, and/or boiling .
SURVIVAL OUTSIDE HOST: The virus is stable as an aerosol, particularly at

low relative humidity (30 % RH). The biological half-live at both 24°C and
20
32°C ranges from 10.1 to 54.6 minutes .

SURVEILLANCE: Definitive diagnosis is reached mainly upon laboratory
testing (i.e. RT-PCR or serological testing) of virus isolation from blood
1 2 3
samples, pharyngeal washings, pharyngeal swabs, and/or urine
7 .
FIRST AID/TREATMENT: Ribavirin, which is most effective within the first 6

1 3 7 9 13 15 16
to 7 days of illness, and supportive care .
7 9 13
IMMUNIZATION: None .
1 9 16
PROPHYLAXIS: Ribavirin may reduce mortality after infection .

LABORATORY-ACQUIRED INFECTIONS: Two cases, one fatal, occurred
1 21
among staff at a research institute in the United States . Laboratory
3
infections have also occurred in hospital environments
SOURCES/SPECIMENS: Blood, respiratory and pharyngeal secretions, urine,

3 7 21
semen, tissues from human or animal hosts, and rodent excreta .
PRIMARY HAZARDS: Respiratory exposure to infectious aerosols, mucous

membrane exposure to infectious droplets, and accidental parenteral
15 21
inoculation are the primary hazards .
SPECIAL HAZARDS: Work with, or exposure to rodents that are naturally or

experimentally infected represents a risk of human infection.

22

PROTECTIVE CLOTHING: Personnel entering the laboratory must remove

street clothing, including undergarments, and jewellery, and change into
dedicated laboratory clothing and shoes, or don full coverage protective
clothing (i.e., completely covering all street clothing). Additional protection
may be worn over laboratory clothing when infectious materials are directly
handled, such as solid-front gowns with tight fitting wrists, gloves, and
respiratory protection. Eye protection must be used where there is a known
23
or potential risk of exposure to splashes .

conducted in a biological safety cabinet (BSC) in combination with a positive
pressure suit, or within a class III BSC line. Centrifugation of infected
materials must be carried out in closed containers placed in sealed safety
cups, or in rotors that are loaded or unloaded in a biological safety cabinet.
The integrity of positive pressure suits must be routinely checked for leaks.
The use of needles, syringes, and other sharp objects should be strictly
limited. Open wounds, cuts, scratches, and grazes should be covered with
waterproof dressings. Additional precautions should be considered with
23
work involving animal activities .

23
DISPOSAL: Patient excreta, sputum, blood and all objects with which a
patient has had contact with, including laboratory equipment used for
testing, should be disinfected with 0.5 % sodium hypochlorite solution or
0.5 % phenol with detergent, followed by autoclaving, incineration or boiling
3 . Decontaminate all materials for disposal from the containment
laboratory by steam sterilization, chemical disinfection, incineration or by
gaseous methods. Contaminated materials include both liquid and solid
23
wastes .
STORAGE: In sealed leak-proof containers that are appropriately labelled

23

and standards.

Canada.

Copyright ©
Canada
REFERENCES:
2 Drosten, C., Go ttig, S., Schilling, S., Asper, M., Panning, M.,
Schmitz, H., & Gu nther, S. (2002). Rapid detection and
quantification of RNA of Ebola and Marburg viruses, Lassa virus,
Crimean-Congo hemorrhagic fever virus, Rift Valley fever virus,
dengue virus, and yellow fever virus by real-time reverse
transcription-PCR. Journal of Clinical Microbiology, 40 (7), 2323-
2330.
3 Heymann, D. L. (2008). Control of Communicable Diseases

Manual (19th Edition ed.). Washington, D.C.: American Public
Health Association.
4 Knipe, D. M., & Howley, P. M. (Eds.). (2001). Fields Virology (4th ed.).
5 McCormick, J. B., King, I. J., & Webb, P. A. (1987). A case-control

study of the clinical diagnosis and course of Lassa fever. Journal of
Infectious Diseases, 155 (3), 445-455.
6 McCormick, J. B., Webb, P. A., & Krebs, J. W. (1987). A prospective

study of the epidemiology and ecology of Lassa fever. Journal of
7 Richmond, J. K., & Baglole, D. J. (2003). Lassa fever: Epidemiology,

clinical features, and social consequences. British Medical Journal,
327 (7426), 1271-1275.
8 Khan, S. H., Goba, A., Chu, M., Roth, C., Healing, T., Marx, A., Fair, J.,
Guttieri, M. C., Ferro, P., Imes, T., Monagin, C., Garry, R. F., &
Bausch, D. G. (2008). New opportunities for field research on the
pathogenesis and treatment of Lassa fever. Antiviral Research,
78 (1), 103-115.
9 Borio, L., Inglesby, T., Peters, C. J., Schmaljohn, A. L., Hughes, J. M.,
Jahrling, P. B., Ksiazek, T., Johnson, K. M., Meyerhoff, A., O'Toole, T.,
Ascher, M. S., Bartlett, J., Breman, J. G., Eitzen Jr., E. M., Hamburg,
M., Hauer, J., Henderson, D. A., Johnson, R. T., Kwik, G., Layton, M.,
Lillibridge, S., Nabel, G. J., Osterholm, M. T., Perl, T. M., Russell, P.,
& Tonat, K. (2002). Hemorrhagic fever viruses as biological
weapons: Medical and public health management. Journal of the
American Medical Association, 287 (18), 2391- 2405.
10 Fisher-Hoch, S. P., Hutwagner, L., Brown, B., & McCormick, J. B.

(2000). Effective vaccine for lassa fever. Journal of Virology, 74 (15),
6777-6783.
11 Imported Lassa fever - New Jersey, 2004. (2004). Morbidity and

Mortality Weekly Report, 53 (38), 894-897.
12 Schmitz, H., Ko hler, B., Laue, T., Drosten, C., Veldkamp, P. J., Gu
nther, S., Emmerich, P., Geisen, H. P., Fleischer, K., Beersma, M. F.
C., & Hoerauf, A. (2002). Monitoring of clinical and laboratory data
in two cases of imported Lassa fever. Microbes and Infection, 4(1),
43-50.
13 Franz, D. R., Jahrling, P. B., McClain, D. J., Hoover, D. L., Byrne, W.

R., Pavlin, J. A., Christopher, G. W., Cieslak, T. J., Friedlander, A. M.,
& Eitzen E.M., J. (2001). Clinical recognition and management of
patients exposed to biological warfare agents. Clinics in Laboratory
Medicine, 21 (3), 435-473.
14 Heymann, D. L. (Ed.). (2008). Control of Communicable Diseases

Manual (19th Edition ed.). Washington, DC: American Public Health
Association.
15 Update on Lassa fever in West Africa. (2005). Releve

Epidemiologique Hebdomadaire / Section d'Hygiene Du Secretariat De
La Societe Des Nations = Weekly Epidemiological Record / Health
Section of the Secretariat of the League of Nations, 80 (10), 86-88.
16 McCormick, J. B., King, I. J., & Webb, P. A. (1986). Lassa fever:

Effective therapy with ribavirin. New England Journal of Medicine,
314 (1), 20-26.
17 Elliott, L. H., McCormick, J. B., & Johnson, K. M. (1982). Inactivation

of Lassa, Marburg, and Ebola viruses by gamma
irradiation. Journal of Clinical Microbiology, 16 (4), 704-708.
18 Mitchell, S. W., & McCormick, J. B. (1984). Physicochemical

inactivation of Lassa, Ebola, and Marburg viruses and effect on
clinical laboratory analyses. Journal of Clinical Microbiology, 20 (3),
486-489.
19 Mahanty, S., Kalwar, R., & Rollin, P. E. (1999). Cytokine

measurement in biological samples after physicochemical
treatment for inactivation of biosafety level 4 viral agents. Journal
of Medical Virology, 59 (3), 341-345.
20 Stephenson, E. H., Larson, E. W., & Dominik, J. W. (1984). Effect of

environmental factors on aerosol-induced Lassa virus
infection. Journal of Medical Virology, 14 (4), 295-303.
21 arboviruses and related zoonotic viruses. (1999). In J. Y. Richmond,

& R. W. McKinney (Eds.), Biosafety in Microbiological and Biomedical
Laboratories (BMBL) (5th ed., pp. 183- 199). Washington, D.C.:
Centers for Disease Control and Prevention.

2009, (2009).

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Lymphocytic choriomeningitis
virus

SUBSTANCES
1
NAME: Lymphocytic choriomeningitis virus .
2- 13 14- 18
SYNONYM OR CROSS REFERENCE: LCMV , LCM , benign
14 15
(or serous) lymphocytic meningitis , and Armstrong's disease .
CHARACTERISTICS: As member of the family Arenaviridae, genus Arenavirus

9 15 , LCMV is an enveloped, round, oval, or pleomorphic virion,
measuring roughly 110 nm to 130 nm in diameter with a bipartite single-
6, 15
stranded RNA genome . The virion interior contains granules
resembling grains of sand, which are characteristic of the family
15
Arenaviridae, while the surface has hollow golf-club shaped projections .

PATHOGENICITY/TOXICITY: Acquired LCM (Postnatal): LCMV infection in
immunocompetent adults may be asymptomatic (nearly one third of all
2 8
infections or limited to a non-specific, self-limited viral syndrome
with symptoms such as fever, cough, malaise, myalgia, headache,
2 8 9
photophobia, nausea, vomiting, adenopathy, and sore throat
15 19 . The illness can progress to include meningitis or
6 8 14
meningoencephalitis , and other less common neurologic
2 6 8
symptoms such as paralysis, sensorineural hearing loss , and
8
Guillain-Barré type syndrome . Uncommon non-neurologic
2 2 8
manifestations of illness include pancreatitis , orchitis , arthritis,
8 2
pericarditis, parotitis pneumonitis, and rash . Acquired LCMV
infection is usually non-fatal, with a mortality rate of less than 1%, and
recovery from even severe disease occurs without sequelae in most cases
5 6 14 .
Congenital LCM: LCMV infection can produce a spectrum of pathologic

effects, from minimal to severe, depending on the developmental stage of
12
the foetus at the time of infection . In some cases, infection may result in
2 9
abortion , hydrocephalus, chorioretinitis, and/or mental retardation
6
of the infant . The mortality rate of infants diagnosed with congenital
16
LCMV is approximately 35% . Among survivors of congenital LCMV
infection, two thirds have long-term neurologic abnormalities, including
microcephaly, mental retardation, cerebral palsy, seizures, and visual
2 8 16
impairment .
Transplantation associated LCM: Recently LCMV infection has been identified

in individuals who received solid organ transplants from donors who died of
7 20
apparent non-infectious aetiologies . These cases were uniformly
fatal with the exception of one recipient who underwent ribavirin treatment
when LCMV infection was suspected.
EPIDEMIOLOGY: The first identified Arenavirus, LCMV was isolated in 1933

1
from a woman thought to have St. Louis encephalitis . Unlike other
Arenaviruses, which have limited geographic distribution, LCMV is found in
Europe, the Americas, and Asia, primarily in areas where mice co-habitate
15
with humans . The largest outbreak occurred between 1973 and 1974 in
19
the United States with 181 cases and no deaths . Other recognised
9
outbreaks have been recorded in Germany and France . The number of
acquired LCM cases is underestimated since most cases are mild or
12
asymptomatic and such individuals rarely seek medical attention .
Greater awareness and improved methods of detection may be contributing
6
to increased prevalence . Approximately 5% of humans show evidence of
previous infection with LCMV (5). Congenital LCM was first recognised in
3 6
1955, and since then there have been 54 reported cases worldwide
21 6
, 63% of them since 1993 . It is not known whether the actual
number of cases is significantly higher than this since only the most severe
13
cases are reported , and congenital LCM can produce a spectrum of
12
pathological effects from minimal to severe .
2- 4 6 8 9 12- 17 2 3 6 14
HOST RANGE: Humans , mice
15 3 4 15 17 18
, hamsters , guinea pigs, rats, monkeys, dogs,
17
rabbits, and chickens .
MODE OF TRANSMISSION: Mice infected in utero asymptomatically shed

2, 3 8 14
LCMV in their faeces, urine, saliva, breast milk, and semen
15 , and transmit the virus to humans (and other rodents, such as
2 3 14
hamsters) by direct contact , through damaged skin or mucous
14 15 2 3 8 14
membranes , inhalation of aerosolised virus ,
8 9 14 15 9 14
ingestion of virus contaminated food or dust ,
8 15 2 14
through rodent bites , or by contact with infected fomites .
Transmission is also possible through organ transplantation from LCMV
4 7
infected donors , and vertically from an infected mother to her foetus
3 .
9 14
INCUBATION PERIOD: Approximately 8 to 13 days and 15 to 21
14 15
days before any meningeal symptoms appear .
14
COMMUNICABILITY: No evidence of human-to-human transmission ,
with the exception of vertical transmission from an infected mother to her
3
foetus during pregnancy , and through solid organ transplantation from
4 7
infected donors .

2 5 14- 16
RESERVOIR: Primarily the house mouse (Mus. musculus) ,
17
but the Syrian hamster is also a possibility .
ZOONOSIS: Yes, LCMV is spread mainly through contact with contaminated

2 5 14 15 18
rodent secretions/excretions .
VECTORS: LCMV has been isolated from fleas, Culicoides flies, several species
of Aedes mosquitoes, ticks and cockroaches, but it is deemed unlikely that
15
arthropods play a role in LCMV transmission .

DRUG SUSCEPTIBILITY: Ribavirin has been shown to inactivate arenaviruses
5 7 21
in vitro and may improve symptoms under clinical conditions .
SUSCEPTIBILITY TO DISINFECTANTS: Bleach (sodium hypochlorite) or other

11
common household disinfectants will inactivate LCMV .
10
PHYSICAL INACTIVATION: LCMV is inactivated by UV light and heat
1
(55°C for at least 20 minutes) .
SURVIVAL OUTSIDE HOST: Unless it is preserved at -80°C, LCMV is quickly

9
inactivated outside its host . LCMV will retain its infectivity for at least 206
1
days if stored in 50% glycerine and 0.85% saline at 4-10°C .

SURVEILLANCE: Monitor for symptoms. Diagnosis is confirmed by serology,
2- 4 8 9 15 3 4 15 9 15
ELISA , RT-PCR , Western blot ,
4 17 17
immunohistochemical staining , neutralisation assay ,
8 9
immunofluorescent antibody test , and viral culture from blood or
4 9
cerebrospinal fluid . The widely available complement fixation test,
however, is deemed to be insensitive and its use is no longer recommended
6 8 .
FIRST AID/TREATMENT: Treatment is symptomatic and generally supportive

12 15 . Ribavirin is effective in vitro, and may be effective for treatment of
5 7 21
LCM .
14
PROPHYLAXIS: None.

LABORATORY-ACQUIRED INFECTIONS: LCMV infection is a well known
occupational risk for those working with rodents, especially hamsters and
22
mice. 76 cases were reported up until 1978 , including 3 outbreaks
between 1973 and 1975 among laboratory workers who had handled
18 19
hamsters that had tumour grafts containing LCMV . Further cases
have occurred since then, notably in an outbreak associated with nude mice,
in which 9% of 82 animal care workers were found to be seropositive for
23
LCMV .
1 14 18 1 8 14
SOURCES/SPECIMENS: Blood , cerebrospinal fluid
18 1 17 18 15 18
, urine , transplantable tumours , secretions of the
8 14 15 18 8 14 15
nasopharynx , faeces , and infected tissues
5
from animals and humans .
5
PRIMARY HAZARDS: Aerosols , and direct contact of mucous membranes
14 15
with virus .
SPECIAL HAZARDS: Transplantable tumour lines represent a potential

14 15
hazard .

24
RISK GROUP CLASSIFICATION: Risk Group 3 . This risk group applies to
the species as a whole, and may not be representative of all strains and
clonal isolates.

infectious materials, animals, or cultures. These containment levels apply to
the species as a whole, and may not be representative of all strains and
clonal isolates.

25

25

SPILLS: Allow aerosols to settle and, wear protective clothing, gently cover
before clean up.

chemical disinfection, and/or incineration.
STORAGE: In sealed containers that are appropriately labelled.

and standards.

Canada.

Copyright ©
Canada
REFERENCES:
REFERENCES:
1 Armstrong, C., & Lillie, R. D. (1934). Experimental lymphocytic
choriomeningitis of monkeys and mice produced by a virus
encountered in studies of the 1933 St. Louis encephalitis epidemic.
Pub. Health Rep., 49, 1019-1027.
2 Barton, L. L., & Mets, M. B. (2001). Congenital lymphocytic

choriomeningitis virus infection: Decade of rediscovery. Clinical
3 Barton, L. L., Mets, M. B., & Beauchamp, C. L. (2002). Lymphocytic

choriomeningitis virus: emerging fetal teratogen. American Journal
of Obstetrics and Gynecology, 187(6), 1715-1716.
4 Center for Disease Control and Prevention. (2005). Lymphocytic

Choriomeningitis Virus Infection in Organ Transplant Recipients-
Massachusetts, Rhode Island. MMWR, 54, 537.
5 Peters, C. J. (2006). Lymphocytic choriomeningitis virus - An old

enemy up to new tricks. New England Journal of Medicine, 354(21),
2208-2211.
6 Jamieson, D. J., Kourtis, A. P., Bell, M., & Rasmussen, S. A. (2006).

Lymphocytic choriomeningitis virus: An emerging obstetric
pathogen? American Journal of Obstetrics and Gynecology, 194(6),
1532-1536.
7 Fischer, S. A., Graham, M. B., Kuehnert, M. J., Kotton, C. N.,

Srinivasan, A., Marty, F. M., Comer, J. A., Guarner, J., Paddock, C. D.,
DeMeo, D. L., Shieh, W. -., Erickson, B. R., Bandy, U., DeMaria Jr., A.,
Davis, J. P., Delmonico, F. L., Pavlin, B., Likos, A., Vincent, M. J.,
Sealy, T. K., Goldsmith, C. S., Jernigan, D. B., Rollin, P. E., Packard,
M. M., Patel, M., Rowland, C., Helfand, R. F., Nichol, S. T., Fishman, J.
A., Ksiazek, T., & Zaki, S. R. (2006). Transmission of lymphocytic
choriomeningitis virus by organ transplantation. New England
Journal of Medicine, 354(21), 2235-2249.
8 Barton, L. L., & Mets, M. B. (1999). Lymphocytic choriomeningitis

virus: pediatric pathogen and fetal teratogen. The Pediatric
Infectious Disease Journal, 18(6), 540-541.
9 Rousseau, M. C., Saron, M. F., Brouqui, P., & Bourgeade, A. (1997).

Lymphocytic choriomeningitis virus in southern France: Four case
reports and a review of the literature. European Journal of
10 Gairin, J. E., Joly, E., & Oldstone, M. B. A. (1991). Persistent infection

with lymphocytic choriomeningitis virus enhances expression of
MHC class I glycoprotein on cultured mouse brain endothelial
cells. Journal of Immunology, 146(11), 3953-3957.
11 Centers for Disease Control and Prevention. (2005). Update:

Interim Guidance for Minimizing Risk for Human Lymphocytic
Choriomeningitis Virus Associated with Pet Rodents. MMWR, 54,
799.
12 Bonthius, D. J., Wright, R., Tseng, B., Barton, L., Marco, E., Karacay,
B., & Larsen, P. D. (2007). Congenital lymphocytic choriomeningitis
virus infection: Spectrum of disease. Annals of Neurology, 62(4),
347-355.
13 Bonthius, D. J., & Perlman, S. (2007). Congenital viral infections of

the brain: Lessons learned from lymphocytic choriomeningitis
virus in the neonatal rat. PLoS Pathogens, 3(11), 1541-1550.
14 Control of Communicable Diseases Manual: An Official Report of

the American Public Health Association. (2004). In D. L. Heymann
(Ed.), (18th ed., pp. pp. 321-322). Washington, D.C.: American
Public Health Association.

16 Wright, R., Johnson, D., Neumann, M., Ksiazek, T. G., Rollin, P.,
Keech, R. V., Bonthius, D. J., Hitchon, P., Grose, C. F., Bell, W. E., &
Bale Jr., J. F. (1997). Congenital lymphocytic choriomeningitis virus
syndrome: a disease that mimics congenital toxoplasmosis or
Cytomegalovirus infection. Pediatrics, 100(1)
17 Parker, J. C., Igel, H. J., Reynolds, R. K., Lewis, A. M., & Rowe, W. P.
(1967). Lymphocytic choriomeningitis virus infection in foetal,
newborn, and young adult Syrian hamsters. Infection and
Immunity, 13(3), 967-981.
18 Bowen, G. S., Calisher, C. H., & Winkler, W. G. (1975). Laboratory

studies of a lymphocytic choriomeningitis virus outbreak in man
and laboratory animals. American Journal of Epidemiology, 102(3),
233-240.
19 Gregg, M. B. (1975). Recent outbreaks of lymphocytic

choriomeningitis in the United States of America. Bulletin of the
World Health Organization, 52(4-5 6), 549-553.
20 Paddock, C., Ksiazek, T., Comer, J. A., Rollin, P. N., S., & Shieh, W. J.
(2005). Pathology of fatal lymphocytic choriomeningitis virus
infection in multiple organ transplant recipients from a common
donor. Modern Pathology: An Official Journal of the United States and
Canadian Academy of Pathology, Inc, 18, 263A-264A.
21 Greenhow, T. L., & Weintrub, P. S. (2003). Neonate with

hydrocephalus. Pediatric Infectious Disease Journal, 22(12),
1099+1111-1112.
22 Collins, C. H., & Kennedy, D. A. (1999). laboratory acquired

infections. Laboratory-Acquired Infections: History, Incidence, Causes
and Prevention. . . (4th Edn ed., pp. 1-37 27) Buttersworth, London,
UK.
23 Dykewicz, C. A., Dato, V. M., Fisher-Hoch, S. P., Howarth, M. V.,

Perez-Oronoz, G. I., Ostroff, S. M., Gary Jr., H., Schonberger, L. B., &
McCormick, J. B. (1992). Lymphocytic choriomeningitis outbreak
associated with nude mice in a research institute. Journal of the
American Medical Association, 267(10), 1349-1353.

2009, (2009).

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Marburg virus

SUBSTANCES
NAME: Marburg virus
SYNONYM OR CROSS REFERENCE: Marburg disease, Marburg

haemorrhagic fever, African haemorrhagic fever, and green monkey disease
1 2 .
CHARACTERISTICS: Marburg virus is a member of the Filoviridae family, and

is an elongated filamentous molecule, highly variable in length, but typically
2 3
around 1000 nm long with a uniform diameter of 80 nm . The viral
fragment is pleomorphic, and may appear in the shape of a "6", a "U", or a
2 3
circle, and it is contained within a lipid membrane . Each virion
contains one molecule of single-stranded, negative-sense viral genomic
1 4 1 4
RNA< , complexed with the proteins NP, VP35, VP30, and L .

PATHOGENICITY/TOXICITY: A rare, severe haemorrhagic fever in humans
1
and non-human primates , characterised by a sudden onset with high
fever, chills, headache, myalgia, and maculopapular rash, possibly followed
2
by vomiting, chest pain, sore throat, abdominal pain, and diarrhoea .
Symptoms become increasingly severe and may include inflammation of the
pancreas, jaundice, severe weight loss, delirium, shock, liver failure, massive
haemorrhage, and multi-organ dysfunction. Marburg disease has a fatality
1 2
rate of approximately 25 % .
EPIDEMIOLOGY: Occurrence of Marburg haemorrhagic fever has been

primarily limited to countries in sub-Saharan Africa.
In 1967, simultaneous outbreaks in Marburg, Frankfurt (Germany), and

Belgrade (Yugoslavia, now Serbia) were reported following the handling of
viscera, body fluids, and/or kidney tissue cultures from African green
monkeys imported from Uganda. Thirty-one cases and 9 deaths were
1 2 4 5 6
reported . Between 1975 and 1987, isolated cases were
reported in South Africa (originating from Zimbabwe), Kenya, Zimbabwe,
1 2 4 6
Kenya, and the Democratic Republic of Congo . The large long
running outbreak occurred between 1998 and 2000 in the Democratic
7 6 8
Republic of Congo , resulting in 149 cases and 123 deaths . The
largest outbreak to date occurred in 2004 and 2005 centered in Uige, Angola
6 8
where 252 cases were reported with 227deaths . Since 2007, a
number of cases have been reported in Uganda, some of which have been
diagnosed into other countries (i.e. USA, Netherlands) in individuals
6 9 10
returning from Uganda .
HOST RANGE: Humans and non-human primates (e.g. the African green
1 2
monkey) .
5
INFECTIOUS DOSE: One to 10 aerosolized organisms .
MODE OF TRANSMISSION: Primary mode of transmission appears to be via

close personal contact with an infected individual or their body fluids(1). In
the laboratory, the virus displays some capability of infection through small-
particle aerosols; however, airborne spread among humans has not been
clearly demonstrated(2). Individuals handling the infected monkeys or their
fluids and cell cultures of Marburg virus have become ill.
1
INCUBATION PERIOD: Three to 10 days .
COMMUNICABILITY: Person-to-person transmission can occur via close

1
personal contact between an infected individual or their body fluids .
1 2
Communicable as long as blood and secretions contain the virus .
Semen can contain the virus for 3 months and is infective until semen is
1 2
virus-free . Mother-to-child transmission while nurturing has also
7
been documented .

2
RESERVOIR: The natural reservoir is unknown , but is likely African fruit
bats (Rousettus aegyptiacus), and/or other fauna of the goldmine area in
8 11 12 13
Congo . Monkeys are susceptible but are incidental hosts .
ZOONOSIS: Yes, via contact with monkeys or bats, or handling their viscera
1 2 4 5
and/or body fluids .
VECTORS: Unknown, but it is suggested that the index case in South Africa
(1975) had been bitten by arthropods while sleeping outdoors in Zimbabwe
2 .

8
DRUG SUSCEPTIBILITY: Unknown .
4
SUSCEPTIBILITY TO DISINFECTANTS: Sodium hypochlorite , β-
4 14 15
propiolactone , 3 % acetic acid (pH 2.5) , phenolic disinfectants
4 16 17
, formaldehyde and paraformaldehyde , 1 % glutaraldehyde ,
1 4 17
formalin , lipid solvents , and detergents such as SDS . Note:
Decontamination requires specific, controlled use of virus-inactivating
4
agents .
4 15
PHYSICAL INACTIVATION: Heating for 30 minutes to 60 minutes at
17 6
60°C, boiling for 5 minutes , gamma irradiation (1.2 x10 rads to 1.27
6 4 14 15 17 14
x10 rads) , and UV radiation .
SURVIVAL OUTSIDE HOST: Can survive for up to 4 to 5 days on

18
contaminated surfaces , and can survive in liquid or dried material for a
3 19 20 21
number of days .

SURVEILLANCE: Monitor for symptoms. Diagnosis can be confirmed by
1 2 4 7
virus isolation , ELISA to detect viral antigens or patient
1 7 1
antibodies , serum or organ homogenates , RT- PCR,
1
immunohistochemistry , and electron microscopy of tissue sections
1 2
and/or biopsies .
2
Other tests include indirect immunofluorescence to detect virus , or
1
antiviral antibodies . Laboratory studies are extremely hazardous and
1
should be performed in a Containment Level 4 facility .
4 6 20
FIRST AID/TREATMENT: No anti-viral therapy currently available
. Supportive therapy should be provided to maintain renal function, fluid and
electrolyte balance, oxygen status and blood pressure, replace lost blood
4 21
and clotting factors, and complicating infections . Transfusion of
4
convalescent serum may be beneficial . Ribavirin has poor in vitro and in
21
vivo activity against filoviruses .
20
22
PROPHYLAXIS: None .

LABORATORY-ACQUIRED INFECTIONS: In 1967 in Marburg, Frankfurt
(Germany), and Belgrade (Yugoslavia, now Serbia), there were 25 reported
primary cases with 7 deaths. The cases arose from contact and accidents
1 2 4 5
with blood and tissues from infected African green monkeys
23 . Six secondary cases (medical personnel, one spouse) developed from
2
the primary cases .
SOURCES/SPECIMENS: Blood(1,21); serum(2); secretions(21), including

respiratory and throat secretions(7); semen(1,2,7,21); urine; and various
tissues and organs from human or animal hosts, or their
homogenates(2,19,22).
PRIMARY HAZARDS: Accidental parenteral inoculation, respiratory exposure

to infectious aerosols, and mucous membrane exposure to infectious
20
droplets .

24


25

25

25
DISPOSAL: Decontaminate all materials for disposal from the containment

laboratory by steam sterilization, chemical disinfection, incineration or by
gaseous methods. Contaminated materials include both liquid and solid
25
wastes .

25

and standards.

Canada.

Copyright ©
Canada
REFERENCES:
1 (2004). In D. L. Heymann (Ed.), Control of Communicable Diseases
Manual (18th ed., pp. 180-182). Washington, D.C.: American Public
Health Association.
2 Acha, P. N., & Szyfres, B. (2003). Chlamydioses, Rickettsioses, and

Viruses. Zoonoses and communicable diseases common to man and
animals (3rd ed., pp. 205-208). Washington, D.C.: Pan American
Health Organization.
3 Burke, R. (2006). Counter-terrorism for emergency

responders. Counter-terrorism for emergency responders (CRC
press, ed., pp. 163) Boca Raton, FL.
4 Sanchez, A., Khan, A. S., Zaki, S. R., Nabel, G. J., Ksiazek, T. G., &
Peters, C. J. (2001). Filoviridae : Marburg and Ebola viruses. In D. M.
Knipe, & P. A. Howley (Eds.), (4th ed., pp. 1279-1304). Philadelphia,
PA: Lippincott Williams & Wilkins.

& Eitzen, E. M.,Jr. (2001). Clinical recognition and management of
Medicine, 21 (3), 435-473.
6 Bausch, D. G., Sprecher, A. G., Jeffs, B., & Boumandouki, P. (2008).

Treatment of Marburg and Ebola hemorrhagic fevers: a strategy
for testing new drugs and vaccines under outbreak
conditions. Antiviral Research, 78 (1), 150-161.
7 Borchert, M., Muyembe-Tamfum, J. J., Colebunders, R., Libande, M.,

Sabue, M., & Van Der Stuyft, P. (2002). Short communication: a
cluster of Marburg virus disease involving an infant. Tropical
Medicine & International Health, 7 (10), 902-906.
8 World Health Organization. (2005). WHO update on current reported

Marburg cases in Angola. Retrieved 4/30, 2010

Imported case of Marburg hemorrhagic fever - Colorado,
2008. MMWR.Morbidity and Mortality Weekly Report, 58 (49), 1377-
1381.
10 Timen, A., Koopmans, M. P., Vossen, A. C., van Doornum, G. J.,

Gunther, S., van den Berkmortel, F., Verduin, K. M., Dittrich, S.,
Emmerich, P., Osterhaus, A. D., van Dissel, J. T., & Coutinho, R. A.
(2009). Response to imported case of Marburg hemorrhagic fever,
the Netherland. Emerging Infectious Diseases, 15 (8), 1171-1175.
11 Towner, J. S., Pourrut, X., Albarino, C. G., Nkogue, C. N., Bird, B. H.,
Grard, G., Ksiazek, T. G., Gonzalez, J. P., Nichol, S. T., & Leroy, E. M.
(2007). Marburg virus infection detected in a common African
bat. PLoS ONE [Electronic Resource], 2 (1), e764.
12 Swanepoel, R., Smit, S. B., Rollin, P. E., Formenty, P., Leman, P. A.,
Kemp, A., Burt, F. J., Grobbelaar, A. A., Croft, J., Bausch, D. G., Zeller,
H., Leirs, H., Braack, L. E., Libande, M. L., Zaki, S., Nichol, S. T.,
Ksiazek, T. G., Paweska, J. T., & International Scientific and
Technical Committee for Marburg Hemorrhagic Fever Control in
the Democratic Republic of,Congo. (2007). Studies of reservoir
hosts for Marburg virus. Emerging Infectious Diseases, 13(12), 1847-
1851.
13 Nakazibwe, C. (2007). Marburg fever outbreak leads scientist to

suspected disease reservoir. Bulletin of the World Health
Organization, 85 (9), 654-656.
14 Elliott, L. H., McCormick, J. B., & Johnson, K. M. (1982). Inactivation

of Lassa, Marburg, and Ebola viruses by gamma
irradiation. Journal of Clinical Microbiology, 16 (4), 704-708.
15 Mitchell, S. W., & McCormick, J. B. (1984). Physicochemical

inactivation of Lassa, Ebola, and Marburg viruses and effect on
clinical laboratory analyses. Journal of Clinical Microbiology, 20 (3),
486-489.
16 Mahanty, S., Kalwar, R., & Rollin, P. E. (1999). Cytokine

measurement in biological samples after physicochemical
treatment for inactivation of biosafety level 4 viral agents. Journal
of Medical Virology, 59 (3), 341-345.
17 Kurata, T., Hondo, R., Sato, S., Oda, A., Aoyama, Y., & McCormick, J.
B. (1983). Detection of viral antigens in formalin-fixed specimens
by enzyme treatment. Annals of the New York Academy of Sciences,
420 , 192-207.
18 Belanov, E. F., Muntianov, V. P., Kriuk, V. D., Sokolov, A. V.,

Bormotov, N. I., P'iankov, O. V., & Sergeev, A. N. (1996). [Survival of
Marburg virus infectivity on contaminated surfaces and in
aerosols]. Voprosy Virusologii, 41 (1), 32-34.
19 Frolov, V. G., & Gusev, I. (1996). [Stability of Marburg virus to

lyophilization process and subsequent storage at different
temperatures]. Voprosy Virusologii, 41 (6), 275-277.
20 Bray, M. (2003). Defense against filoviruses used as biological

weapons. Antiviral Research, 57 (1-2), 53-60.
21 US Army Medical Research Institute of Infectious Diseases. (2004).

Medical Management of Biological Casualties Handbook. Medical
Management of Biological Casualties Handbook. (5th ed.,). USA: US
Army Medical Research Institute of Infectious Diseases.
22 Fisher-Hoch, S. P. (2005). Lessons from nosocomial viral

haemorrhagic fever outbreaks. British Medical Bulletin, 73-74 , 123-
137.

and prevention (4th ed., pp. 27). London, UK: Buttersworth.

2009, (2009).

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 
Pathogen safety data sheets: Infectious

substances - Norovirus
On this page
Section VII: Exposure controls and personal protection
References

Name: Norovirus
Synonym or cross reference: Norwalk virus, Norwalk-like virus, winter

vomiting disease, acute nonbacterial gastroenteritis, acute diarrhoeal
illness, Southampton virus, Desert Shield virus, Cruise Ship virus, Snow
Mountain virus, Mexico virus, White River Lordsdale virus, Camberwell virus,
1 2 3
Toronto virus, Hawaii virus .
Characteristics: Noroviruses are a group of viruses belonging to the

14
Norovirus genus and the Caliciviridae family . Based on the sequence of
the major capsid protein, these viruses are further divided into 6
15
genogroups (GI-GVI), consisting of numerous genotypes . GI, GII and
GIV are the only genogroups known to infect humans. GIII infect cattle; GV
16
infect mice . Porcine noroviruses belong to GII, although porcine and
17
human noroviruses belong to different genotypes within GII . GII is the
most prevalent Norovirus genotype circulating in humans populations,
15
accounting for more than 95% of all infections . Noroviruses are slightly
smaller than other viruses in the Caliciviridae family, with a diameter of
5
approximately 27 nm . The edges of the virus, when viewed by electron
microscopy, are not well defined. The virus is round, non-enveloped, and has
1 2
single-stranded, positive-sense, polyadenylated RNA . Norovirus
recombination and antigenic drift results in replacement of circulating
dominant viruses every 2-3 years, with the new variants able to re-infect
15
hosts immune to previous viruses .

Pathogenicity: Norovirus infection causes acute gastroenteritis,
characterized by rapid onset of nausea, vomiting, diarrhea, abdominal
1
cramps, abdominal pain, mucus in stool, malaise, headache, and fever
5 . The infection is usually resolved within 12 to 60 hours, although it can
last longer in elderly, young children or immunocompromised individuals
1 2 3 5 , and these groups are at greatest risk for mortality and
1
increased morbidity . Up to 30% of Norovirus infections are
16
asymptomatic, however, these individuals are able to transmit the virus .
Epidemiology: Worldwide distribution. Noroviruses infect humans of all

ages. Most outbreaks occur in hospitals, nursing homes, dining locations,
1 4
schools, daycare centres, and vacation venues . Outbreaks occur
1
throughout the year, but have a distinct winter seasonality . Because of
persistence of Norovirus in the environment, outbreaks can last a long time
1
and have been reported to last over 3 months . Noroviruses are
responsible for 60-95% of outbreaks of nonbacterial acute infectious
1
diarrhea .
17
Host range: Humans, pigs, cattle, mice .
2
Infectious dose: Less than 10 virions .
Mode of transmission: Norovirus transmission is usually person to person

6
through the fecal-oral route . It can also be transmitted through the
4
environment, contaminated surfaces, food, water, fomites, and aerosols
6 .
Incubation period: Onset of symptoms usually takes 15-48 hours from the
2
time of infection .
Communicability: Individuals can spread virus particles without showing

2
symptoms of disease . Those who have recovered from symptoms and
those who are asymptomatic can shed infectious virus particles up to three
2
weeks after exposure .

1
Reservoir: Shellfish, Humans
Zoonosis: None
Vectors: None

Drug susceptibility: No specific antivirals.
Susceptibility to disinfectants: Formulation R-82 for 10 minutes, 0.25-

0.50% sodium hypochlorite for 10-20 minutes, peracetic acid or
1 2 7
glutaraldehyde for 5 minutes . Recurrent outbreaks on cruise
ships and in tropical resorts have been related to improper decontamination
8 9
procedures .
Physical inactivation: Noroviruses are inactivated by temperatures of

10 10
71.3°C for 1 minute . It can survive at pH 2.7 for at least 3 hours . UV
10
radiation may have intermediate effect .
Survival outside host: Norwoviruses have a protein capsid protecting it

2
from the environment . They can survive in seawater, groundwater, fresh
water, soil, and inanimate surfaces for an unknown period of time. Norwalk
virus cannot be cultivated under laboratory conditions as of yet. Feline
calicivirus, another member of this family, with similar structure, can survive
on glass surfaces for 21-28 days at room temperature and for longer periods
11 11
at 4°C . At 37°C, feline calcinivirus survives over 24 hours .

1
Surveillance: Monitor for symptoms and confirm clinically . Viral RNA can
10
be detected in stool samples using reverse transcription PCR . ELISA is
3
also available for identifying noroviruses .
 Note: All diagnostic methods are not necessarily available in all

countries.
First aid/treatment: No specific therapy other than rest, oral rehydration

2
and intravenous electrolyte replacement .
1
Immunization: None
Prophylaxis: None

Laboratory-acquired infections: None reported as of 2010.
1 6
Source/specimens: Faeces, aerosolized vomit .
Primary hazards: Ingestion, exposure of mucous membranes to infective

6
aerosols .
Special hazards: None
Section VII: Exposure controls and personal

protection
12
Risk group classification: Risk Group 2 .
Containment requirements: Containment Level 2 facilities, equipment, and

operational practices for work involving infectious or potentially infectious
Protective clothing: Lab coat. Gloves when direct skin contact with infected
13
Other precautions: All procedures that may produce aerosols, or involve

13

Spills: Allow aerosols to settle and, wearing protective clothing, gently cover
13
before clean up .
Disposal: Decontaminate all wastes that contain or have come in contact

13
Storage: The infectious agent should be stored in leak-proof containers that

13
are appropriately labelled .

and standards.
Updated: March 2017
Prepared by: Centre for Biosecurity, Public Health Agency of Canada

Copyright© Public Health Agency of Canada, 2017 Canada
References
1 Goodgame, R. (2006). Norovirus gastroenteritis. Current

Gastroenterology Reports, 8(5), 401-408.
2 Hutson, A. M., Atmar, R. L., & Estes, M. K. (2004). Norovirus

disease: changing epidemiology and host susceptibility factors.
Trends in Microbiology, 12(6), 279-287.
doi:10.1016/j.tim.2004.04.005
3 Kesson, A. M., Benwell, N., & Elliott, E. J. (2010). Norovirus

diarrhoeal disease in infants and children. The Medical Journal of
Australia, 192(2), 108-109.
4 Gospodarek, E., & Zalas-Wiecek, P. (2009). Noroviruses--tactic of

spread. [Norowirusy--taktyka rozprzestrzeniania sie] Przeglad
Epidemiologiczny, 63(1), 5-9.
5 Murray, P. R., Baron, E. J., Jorgensen, J. H., Landry, M. L., & Pfaller,
M. A. (Eds.). (2007). Manual of Clinical Microbiology (9th ed.).
Washington: ASM Press.
6 Jimenez, L., & Chiang, M. (2006). Virucidal activity of a quaternary

ammonium compound disinfectant against feline calicivirus: a
surrogate for norovirus. American Journal of Infection Control,
34(5), 269-273. doi:10.1016/j.ajic.2005.11.009
7 Magulski, T., Paulmann, D., Bischoff, B., Becker, B., Steinmann, E.,
Steinmann, J., Goroncy-Bermes, P., & Steinmann, J. (2009).
Inactivation of murine norovirus by chemical biocides on stainless
steel. BMC Infectious Diseases, 9, 107. doi:10.1186/1471-2334-9-
107
8 Wikswo, M. E., Cortes, J., Hall, A. J., Vaughan, G., Howard, C.,
Gregoricus, N., & Cramer, E. H. (2011). Disease transmission and
passenger behaviors during a high morbidity Norovirus outbreak
on a cruise ship, January 2009. Clinical Infectious Diseases : An
Official Publication of the Infectious Diseases Society of America,
52(9), 1116-1122. doi:10.1093/cid/cir144
9 Domenech-Sanchez, A., Juan, C., Perez, J. L., & Berrocal, C. I. (2011).

Unmanageable norovirus outbreak in a single resort located in the
Dominican Republic. Clinical Microbiology and Infection : The
Official Publication of the European Society of Clinical
Microbiology and Infectious Diseases, 17(6), 952-954.
doi:10.1111/j.1469-0691.2010.03411.x; 10.1111/j.1469-
0691.2010.03411.x
10 Duizer, E., Bijkerk, P., Rockx, B., De Groot, A., Twisk, F., &
Koopmans, M. (2004). Inactivation of caliciviruses. Applied and
Environmental Microbiology, 70(8), 4538-4543.
doi:10.1128/AEM.70.8.4538-4543.2004
11 Rzezutka, A., & Cook, N. (2004). Survival of human enteric viruses

in the environment and food. FEMS Microbiology Reviews, 28(4),
441-453. doi:10.1016/j.femsre.2004.02.001

2009, (2009).

14 International Committee on Taxonomy of Viruses (ICTV). Available

online at http://ictvonline.org
15 White, P.A. (2014) Evolution of norovirus. Clinical Microbiology and

Infection, 20(8):741-745.
16 Morillo, S.G.; Timenstsky, M. D. (2011) Norovirus: an overview.

Revista da Associaçao Medica Brasileira, 57(4): 453-458.
17 Mattison, K.; Shukla, A.; Cook, A.; Pollari, F.; Friendship, R.; Kelton,
D.; Bidawid, S.; Farber, J.M. (2007) Human Noroviruses in Swine
and Cattle, Emerging Infectious Diseases 13(8): 1184-1188.
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Parvovirus B19

SUBSTANCES
1 - 4
NAME: Parvovirus B19 .
SYNONYM OR CROSS REFERENCE: Erythrovirus B19, B19V, fifth disease,

human parvovirus (HPV), human serum parvovirus-like virus, erythaema
infectiosum, slapped-cheek disease, hydrops foetalis, "gloves and socks"
1 - 7
syndrome, and "Nakatani virus" in Japan .
CHARACTERISTICS: Parvovirus 19 is a member of the family Parvoviridae,

4
sub-family Parvovirinae, and genus Erythrovirus . It is classified into three
genotypes: genotype 1 (classical B19 strains), genotype 2 (prototype K71-
5 8
and A6-like strains), and genotype 3 (prototype V9 virus) . Parvovirus
B19 is an icosahedral (20 to 25 nm diameter), non- enveloped, single-
2 5 9
stranded DNA virus . The virus targets rapidly growing erythroid
progenitor cells, which are found in human bone marrow, foetal liver,
6
human umbilical cord, and peripheral blood . The virus is also found in
platelets, and tissues from the heart, liver, lung, kidney, endothelium, and
10
synovium .

PATHOGENICITY/TOXICITY: Many persons with parvovirus B19 infection
are asymptomatic (about 25% of adults and children during outbreak), or
exhibit mild, non-specific, cold-like symptoms that are never linked to the
1 - 4 6
virus . The clinical conditions associated with the infection
include erythema infectiosum (Fifth Disease), arthropathy, transient aplastic
crisis, chronic red cell aplasia, hydrops foetalis, and papular, purpuric
eruptions on the hands and feet ("gloves and socks" syndrome).
Complications t hought to be associated with parvovirus B19 infection
include encephalopathy, epilepsy, meningitis, myocarditis, dilated
1 6
cardiomyopathy, and autoimmune hepatitis .
Erythema infectiosum (Fifth Disease) is the most recognizable presentation

of parvovirus B19 infection. It consists of a rash that generally affects
children between 4 and 10 years of age, although a less-pronounced rash
can occur in adults. Prodromal symptoms are mild, and include fever,
coryza, headache, and nausea. The first stage of the rash presents as
erythaema of the cheeks ("slapped-cheek" rash). After 1 to 4 days, t he
second stage appears as a maculopapular rash of the extremities and trunk.
Central clearance of the rash is possible, giving it a lacy, reticular pattern.
The second-stage rash usually lasts 1 to 6 weeks. The third stage may
continue for the following 1 to 3 weeks and resolves spontaneously with no
6
permanent sequelae .
Arthropathy may be a complication of erythaema infectiosum or a primary

presentation of infection. Approximately 8% of children infected with the
virus have arthralgia; however, it is more common in adolescents and
adults, affecting up to 60% of those infected. The pattern of arthropathy
differs between adults and children. In children, the pattern can be
symmetric or asymmetric and usually involves the knees (82% of patients)
and ankles. In adults, the pattern is 2 symmetric and polyarticular and
usually involves the proximal interphalangeal and metacarpophalangeal
joints. Arthropathy generally resolves within three weeks but can last from
months to years, especially in women(Footnote 6).
Transient aplastic crisis as a result of parvovirus B19 infection may occur in

persons with decreased erythrocytes, for example due to iron deficiency
anaemia, sickle cell disease, HIV, spherocytosis, or thalassaemia. Chronic red
cell aplasia may occur in immunocompromised persons infected with
6
parvovirus B19 in the absence of rashes and arthropathy .
In young adults, infection can be associated with papular, purpuric, "gloves

and socks" syndrome, which presents as symmetric, painful erythaema and
oedema of the feet and hands. A hallmark of the syndrome is a sharp
demarcation of the rash at the wrists and ankles, although other areas (e.g.,
cheeks, elbows, knees, inner thighs, glans of the penis, buttocks, or vulva)
may also be involved. Patients may experience fever, arthralgia, or both.
6
Symptoms usually resolve within 1 to 3 weeks without scarring .
A major concern with foetal infection is the development of foetal anaemia.

Thrombocytopenia may be present in addition to anaemia. Infection in the
first trimester may result in foetal loss or miscarriage. Infection in the
second and third trimester may result in foetal anaemia, myocarditis, high
output cardiac failure, hydrops foetalis, and stillbirth. Foetal death may
11
occur in up to 10% of infected foetuses .
EPIDEMIOLOGY: Persons with blood group P antigen (the receptor for B19
2
erythroid cells) are universally susceptible to Parvovirus B19 . Virus
strains are found in Western Europe, United States, and Brazil, with a lower
prevalence of genotype 1 strain compared to the other strains. Genotype 3
5
is endemic in Ghana, West Africa . Infection can occur in sporadic or
epidemic forms, and can occur in any month of the year, and. In temperate
climates, epidemic manifestations are more common in late winter, spring,
and early summer, with epidemic peaks every 3 to 7 years in a given
community. Over a 2 to 6 months observed outbreak period, the
susceptibility rates are 50% in household contacts, and 10% to 60% in the
day care or school settings. In the United States, 50 to 60% of adults have
2
serological evidence of past infection, depending on age and location
4 6
. Arthropathy appears to affect women twice as often as men . The
prevalence of IgG antibodies directed against B19 ranges from 2 to 15% in
children 1 to 5 years old, 15 to 60% in children 6 to 19 years old, 30 to 60% in
1
adults, and more than 85% in the geriatric population . The
infectiousness of the virus has also been observed in the occupational
2 3 12 13
setting among hospital staff and research laboratories .
1 - 5
INFECTIOUS DOSE: Unknown. In a study of B19 seronegative plasma pool-

recipients, it was shown that only those recipients who received plasma
containing greater than 10Footnote 7 genome copies/ml became infected or
seroconverted(Footnote 14,Footnote 15); however, it has also been
proposed that products with much lower virus DNA concentrations (e.g.,
10Footnote 1 geq/ml or even lower) would transmit the virus(Footnote 16)
MODE OF TRANSMISSION: Transmission occurs most commonly by

personal contact, via aerosols, respiratory secretions, or saliva droplets. It
can also be transmitted vertically from mother to foetus or via transfusion of
blood and contaminated blood products (especially pooled factor VIII and
factor IX concentrates), and organ transplantation (iatrogenic nosocomial
2 - 5 10 17
infections) . The risk of vertical transmission to the foetus is
11
approximately 33% .
2
INCUBATION PERIOD: Four to 14 days, but can last as long as 21 days .
COMMUNICABILITY: Illness is most communicable before the onset of rash

in people with rash illness alone, and probably not communicable thereafter
6
because viraemia has been cleared by this point . Patients are highly
contagious during aplastic crisis and should be isolated to prevent
6
transmission of the virus . Individuals with aplastic crisis are
communicable up to 1 week after onset of symptoms. Immunosuppressed
people with chronic infection and severe anaemia may be infectious for
2
months to years .

2 18
RESERVOIR: Humans .
ZOONOSIS: None.
VECTORS: None.

18
DRUG SUSCEPTIBILITY: None currently available .
SUSCEPTIBILITY TO DISINFECTANTS: Treatment with formaldehyde or β-

12
propiolactone destroys the antigenicity of the virus . Parvovirus B19 may
be sensitive to a 5 minute contact at room temperature with sodium
hypochlorite (3,000 to 5,000 ppm free chlorine), and accelerated hydrogen
19 - 21
peroxide (5,000 ppm) .
PHYSICAL INACTIVATION: Unknown. The physical properties contribute to

viral resistance to various factors such as heat (80°C for 72 hours), solvent,
4 7
and detergent treatments .
SURVIVAL OUTSIDE HOST: It is difficult to cultivate in vitro. Serum samples

containing the virus can be stored for short periods at 4°C and for longer
4
periods at -70°C for virus detection .

SURVEILLANCE: If erythaema infectiosum is present, a clinical diagnosis can
6
be made without laboratory testing . Serum IgM testing is recommended
to diagnose acute viral infection in immunocompetent patients. Elevated
IgM antibodies will remain detectable for 2 to 3 months after acute
infection. IgG testing is less useful because it only indicates previous
infection and immunity. Viral DNA testing is crucial for the diagnosis of
infection in patients in transient aplastic crisis or in immunocompromised
6 22
patients with chronic infection . PCR assays are preferred over less
6
sensitive nucleic acid hybridization assays . ELISA- and
haemagglutination-based assays have been developed to detect viral
14
antigen during blood screening . Other methods such as detection of
B19 protein production by immunofluorescence staining and quantitative
23
PCR methods have been developed for laboratory diagnosis .
FIRST AID/TREATMENT: Erythaema infectiosum is usually self-limited and

6
does not require treatment . Generally, no specific therapy is required for
10
parvovirus B19 infection in immunocompetent individuals . Treatment of
symptoms such as fever, pain, or itching may be required. Adults with joint
pain and swelling may require rest and anti-inflammatory drugs, such as
1
non-steroidal anti-inflammatory drugs (NSAIDs), to relieve symptoms .
Pure red-cell aplasia and the underlying persistent infection may be
terminated by discontinuing immunosuppressive therapy, or by instituting
3
antiretroviral drug therapy in patients with AIDS . Patients in transient
aplastic crisis may require erythrocyte transfusions. Chronic red cell aplasia,
if severe, may require intravenous immunoglobulin therapy. This treatment
may improve the symptoms of anaemia, but it may precipitate a rash or
arthropathy. Intravenous immunoglobulin G (IVIG) therapy has also been
2 6 10
used in other cases of severe illness .
IMMUNISATION: A vaccine has been developed, but is not yet available for
1 2 6 18
use .
PROPHYLAXIS: Pregnant women with sick children at home are advised to

2
wash hands frequently and to avoid sharing eating utensils . Isolation of
infected persons is impractical, with the exception of hospitalized patients
3 . Health care workers should be advised of the importance of following
2
good infection control measures .

LABORATORY-ACQUIRED INFECTIONS: Many cases of laboratory-acquired
infection have been reported, and occupational exposure to infectious
aerosols in laboratories is suspected. Infectious aerosols can be generated
by centrifugation, during the resuspension of virus pellets, or in washing
stages of solid phase immunoassays. It is suggested that parvovirus
infection will remain a problem in the laboratory unless the antigen is
inactivated beforehand or, as a minimum precaution, aerosols are contained
12 13 .
SOURCES/SPECIMENS: Parvovirus B19 has been found in blood (serum or

plasma), respiratory secretions (e.g., saliva, sputum, or nasal mucus), bone
marrow aspirates, cord blood samples, amniotic fluid cells and biopsy
specimens of placenta, foetal tissues, synovial fluid, cells and tissue of
affected joints, and skin tissue from systemic sclerosis that is used for B19
4 6 10 22 - 24
DNA detection .
PRIMARY HAZARDS: Exposure to infectious aerosols and needlestick

2 9 12
injuries .

25

26

26

gently cover the spill with paper towels and apply appropriate disinfectant
26

26
chemical disinfection, and incineration .
26

and standards.
UPDATED: November 2010.

Canada.

Copyright ©
Canada
REFERENCES:
1 Heegaard, E. D., & Brown, K. E. (2002). Human parvovirus B19.
2 Heymann, D. L. (2004). In American Public Health Association (Ed.),

Control of Communicable Diseases Manual (18th ed., pp. 196-199).
Washington, D.C.: American Public Health Association.
3 Young, N. S., & Brown, K. E. (2004). Mechanisms of disease:

Parvovirus B19. New England Journal of Medicine, 350 (6), 586-597.
4 Zerbini, M., & Musiani, M. (2003). Human Parvoviruses. In P. R.

Murray, E. J. Baron, J. H. Jorgensen, M. A. Pfaller & R. H. Yolken
(Eds.), Manual of Clinical Microbiology (8th ed., pp. 1534-1543).
5 Parsyan, A., & Candotti, D. (2007). Human erythrovirus B19 and

blood transfusion - An update. Transfusion Medicine, 17 (4), 263-
278.
6 Servey, J. T., Reamy, B. V., & Hodge, J. (2007). Clinical presentations

of parvovirus B19 infection. American Family Physician, 75 (3), 373-
376+377.
7 Clewley, J. P. (1984). Biochemical characterization of a human

parvovirus. Journal of General Virology, 65 (1), 241-245.
8 Servant, A., Laperche, S., Lallemand, F., Marinho, V., De Saint Maur,
G., Meritet, J. F., & Garbarg-Chenon, A. (2002). Genetic diversity
within human erythroviruses: Identification of three genotypes.
Journal of Virology, 76 (18), 9124-9134.
9 Kerr, J. R. (2000). Pathogenesis of human parvovirus B19 in

rheumatic disease. Annals of the Rheumatic Diseases, 59 (9), 672-
683.
10 Corcoran, A., & Doyle, S. (2004). Advances in the biology, diagnosis

and host-pathogen interactions of parvovirus B19. Journal of
Medical Microbiology, 53 (6), 459-475.
11 Ramirez, M. M., & Mastrobattista, J. M. (2005). Diagnosis and

management of human parvovirus B19 infection. Clinics in
Perinatology, 32 (3), 697-704.
12 Cohen, B. J., & Brown, K. E. (1992). Laboratory infection with

human parvovirus B19 [7]. Journal of Infection, 24 (1), 113-114.
13 Cohen, B. J., Couroucé, A. M., Schwarz, T. F., Okochi, K., &

Kurtzman, G. J. (1988). Laboratory infection with parvovirus B19.
Journal of Clinical Pathology, 41 (9), 1027-1028.
14 Brown, K. E. (2004). Detection and quantitation of parvovirus B19.

Journal of Clinical Virology, 31 (1), 1-4.
15 Brown, K. E., Young, N. S., Alving, B. M., & Barbosa, L. H. (2001).

Parvovirus B19: Implications for transfusion medicine. Summary
of a workshop. Transfusion, 41 (1), 130-135.
16 Blu mel, J., Schmidt, I., Effenberger, W., Seitz, H., Willkommen, H.,
Brackmann, H. H., Lo wer, J., & Eis-Hu binger, A. M. (2002).
Parvovirus B19 transmission by heat-treated clotting factor
concentrates. Transfusion, 42 (11), 1473-1481.
17 Eid, A. J., Brown, R. A., Patel, R., & Razonable, R. R. (2006).

Parvovirus B19 infection after transplantation: A review of 98
cases. Clinical Infectious Diseases, 43 (1), 40-48.
18 Broliden, K., Tolfvenstam, T., & Norbeck, O. (2006). Clinical aspects

of parvovirus B19 infection. Journal of Internal Medicine, 260 (4),
285-304.
19 Collins, C. H., & Kennedy, D. A. (1999). Decontamination.

Laboratory acquired infections: History, incidence, causes and
preventions (4th ed., pp. 160-186). Woburn, MA: Butterworth-
Heinemann.
20 Omidbakhsh, N., & Sattar, S. A. (2006). Broad-spectrum

microbicidal activity, toxicologic assessment, and materials
compatibility of a new generation of accelerated hydrogen
peroxide-based environmental surface disinfectant. American
Journal of Infection Control, 34 (5), 251-257.
21 Favero, M. S., & Arduino, M. J. (2006). Decontamination and

Disinfection. In D. O. Fleming, & D. L. Hunt (Eds.), Biological Safety:
Principles and Practices (4th ed., pp. pp. 373-381). Washington, D.C.:
ASM Press.
22 Weir, E. (2005). Parvovirus B19 infection: Fifth disease and more.

Canadian Medical Association Journal, 172 (6), 743.
23 Wong, S., & Brown, K. E. (2006). Development of an improved

method of detection of infectious parvovirus B19. Journal of Clinical
Virology, 35 (4), 407-413.
24 Ohtsuka, T., & Yamazaki, S. (2004). Increased prevalence of human

parvovirus B19 DNA in systemic sclerosis skin. British Journal of
Dermatology, 150 (6), 1091-1095.

2009, (2009).

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Rabies virus

SUBSTANCES
NAME: Rabies virus.
SYNONYM OR CROSS REFERENCE: Rabies, hydrophobia, lyssavirus(1-9).
CHARACTERISTICS: As a member of the Lyssavirus genus, in the family

Rhabdoviridae(1,3, 5), rabies virus is a bullet-shaped, enveloped virus of
approximately 75 nm in diameter by 180 nm in length, and has a single-
stranded, negative-sense RNA genome(3). The Lyssavirus genus has 7
members, of which only serotype 1 commonly infects humans, while the
other 6 are rare causes of human disease(4).

PATHOGENICITY/TOXICITY: Rabies virus can cause an acute infection,
marked by progressive encephalomyelitis, and is usually fatal(10). The initial
symptoms of rabies resemble those of other systemic viral infections,
including fever, headache, malaise, and upper respiratory and
gastrointestinal tract disorders(1,4,7). This prodromal phase typically lasts
about 4 days, but can last as long as 10 days before specific symptoms
develop(1-4). Almost all cases of clinical rabies are fatal(1,2). Human rabies is
typically seen in 2 forms: furious and paralytic (or dumb)(3).
Furious rabies : Accounts for 80% of rabies cases, is dominated by

encephalitis, and presents with hydrophobia, delirium, and agitation(1,3).
Hydrophobia is the symptom most identified with rabies; patients have
severe difficulty in swallowing and can become fearful at the sight of water
despite an intense thirst. Other manifestations of furious rabies include
hyperactivity, seizures, and aerophobia(4). Hyperventilation is frequently
present, presumably reflecting brain stem infection. Patients then fall into a
coma and typically die within 1 to 2 weeks, despite maximal intensive
care(3).
Paralytic (dumb) rabies: In contrast to furious rabies, paralytic rabies patients

lack signs of cortical irritation, instead presenting with ascending paralysis
or symmetrical tetraparalysis(3). As the condition progresses, the patient
becomes confused and death preceded by a coma may ensue(3).
EPIDEMIOLOGY: Rabies occurs throughout the world except in Antarctica,

and a few island nations(2,3,5). The vast majority of cases occur in areas of
uncontrolled domestic dog rabies(3). Rabies is divided into two types for
epidemiological purposes: urban and sylvan(1,4).
Urban rabies : Found predominately in developing countries in Asia and

Africa(4).
Sylvan rabies : Mostly seen in developed countries in the northern

hemisphere(4).
Rabies is estimated to cause 55,000 worldwide human deaths per year, the
vast majority of which are in Africa and Asia(6,10). Several countries, most of
which are islands, are rabies-free, including the British Isles, New Zealand,
Japan, Taiwan, many of the Caribbean islands, Sweden, Norway, and Spain.
These countries remain rabies-free due to the stringency of their quarantine
laws for imported animals. Australia was at one time believed to be rabies
free, but bat-transmitted rabies is now endemic there(2). In Canada, a total
of 23 people have died of rabies since 1924, and two fatal cases were
observed in 2000 and 2003, which were the first cases of rabies in the
country since 1985(11).
HOST RANGE: Humans, and many mammals, most commonly wild and
domestic canids (e.g. dogs, foxes, coyotes), mustelids (e.g. skunks, badgers,
martens), viverids (e.g. mongooses, civets, genets), procyonids (e.g.
racoons), and insectivorous and haematophagous bats(1,3,4,8,9).
MODE OF TRANSMISSION: Rabies is most commonly transmitted to

humans via the bite of a rabies-infected animal(2-4,7). Bites to the head,
neck, and arms are the most likely to lead to transmission(1). The amount of
virus reaching the lesion is also a factor in transmission; for example, when
a bite has to penetrate clothing, the saliva may be retained in the fabric and
be prevented from entering the wound(2-4). Potential non-bite modes of
transmission include contamination of a pre-existing wound, contact of
mucous membrane or respiratory tract with the saliva of an infected animal,
exposure to aerosolised rabies virus in the laboratory (or from bats), or via
organ transplantation from an infected donor(1-4,7).
INCUBATION PERIOD: Varies from days to more than 7 years, with 75% of
patients becoming ill within 90 days of exposure(1,3-5).
COMMUNICABILITY: Direct human-to-human transmission is theoretically

possible but rare and has only been documented in cases of transplants
(corneal, kidney, liver, blood vessel)(1,4-7, 9,10).

RESERVOIR: Urban rabies: stray dogs(1,4). Sylvan rabies; dogs, foxes,
coyotes, wolves, jackals, skunks, racoons, mongooses, and other biting
mammals such as bats(1,5).
ZOONOSIS: Yes, from the bite of an infected animal(1-9).
VECTORS: None known.

DRUG SUSCEPTIBILITY: Ribavirin (virazole) has shown some efficacy against
rabies virus in vitro, and interferon-γ was shown to be modestly effective in
treating rabies-infected cynomolgus monkeys(12,13).
SUSCEPTIBILITY TO DISINFECTANTS: Rabies virus is inactivated by

exposure to 70% ethanol, phenol, formalin, ether, trypsin, β-propiolactone,
and some other detergents(3).
PHYSICAL INACTIVATION: Rabies virus does not tolerate pH below 3 or

above 11, and is inactivated by ultraviolet light(3).
SURVIVAL OUTSIDE HOST: This virus does not survive well outside its host
(in dried blood and secretions) as it is susceptible to sunlight and
desiccation(3,9).

SURVEILLANCE: Monitoring for symptoms is inadequate since, by the time
symptoms are apparent, rabies is invariably fatal. No diagnostic methods
are available during the incubation period(3). Following the incubation
period, methods of detection include viral isolation, RT- PCR, and direct
immunofluorescence of clinical specimens(1,4-7).
FIRST AID/TREATMENT: First aid for rabies begins with good wound care,
which can reduce the risk of rabies by up to 90%. Wash the wound with a
soap solution, followed by 70% ethanol or an iodine containing solution(1,3-5).
Following wound care, the clinician must decide whether to institute passive
and/or active immunization(3).
There is no established treatment for rabies once symptoms have begun;

almost all patients succumb to the disease or its complications within a few
weeks of onset(1,3). Supportive therapy includes intubation, sedation,
mechanical ventilation, fluid and electrolyte management, nutrition, and
management of intercurrent illnesses and complications(3).
IMMUNISATION: Pre-exposure immunization of individuals at high risk for

exposure (e.g. laboratory workers, veterinarians, and animal handlers) can
be done using Imovax Rabies, a human diploid cell vaccine (HDCV), or
RabAvert, a purified chick embryo cell vaccine (PCECV)(2,8). Currently, both
have been approved for use in Canada, and may be used as a pre- and post-
exposure prophylaxis(14).
PROPHYLAXIS: Post-exposure rabies prophylaxis with HDCV or PCECV

together with the administration of rabies immunoglobulin (RIG) is highly
effective(14), although this should not be used in persons who have
previously received complete vaccine regimens (pre-exposure vaccination)
who require vaccination only(8).

LABORATORY-ACQUIRED INFECTIONS: Two cases of laboratory-acquired
rabies infections have been reported and are thought to have been acquired
via aerosolized virus across mucous membranes(7,15). No cases of
laboratory-acquired infections have been reported in the last several
decades. Pre-exposure vaccination is necessary for any individuals working
in the laboratory with live virus or diagnostic specimens.
SOURCES/SPECIMENS: Saliva, cerebrospinal fluid, brain tissue, conjunctival

or corneal imprints, throat washings, urine, blood, skin biopsies of infected
individuals or animals(1,4,6,7).
PRIMARY HAZARDS: Infectious droplets and aerosols containing rabies

virus(1-6).
SPECIAL HAZARDS: Fixed tissue preparations can still be infectious so

extreme care is needed when handling them(4).
SECTION VII - EXPOSURE CONTROLS / PERSONAL PROTECTI ON



street clothing and jewelry, and change into dedicated laboratory clothing
exposure to splashes(17).

be considered with work involving animals or large scale activities(17).

gently cover the spill with paper towels and apply appropriate disinfectant

chemical disinfection, and/or incineration(17).

and locked in a Containment Level 3 laboratory(17).

and standards.

Canada.

Copyright ©
Canada
REFERENCES:
1. Takayama, N. (2008). Rabies: a preventable but incurable disease.
Journal of Infection & Chemotherapy, 14 (1), 8-14.
2. Hankins, D. G., & Rosekrans, J. A. (2004). Overview, prevention, and
treatment of rabies. Mayo Clinic Proceedings, 79 (5), 671-676.
3. Bleck, T. P. (2006). Rabies. In R. L. Guerrant, D. H. Walker & P. F. Weller
(Eds.), Tropical Infectious Diseases: Principles, Pathogens, and Practice (2nd
ed., pp. 839-851). Philadelphia, PA: Elsevier Churchill Livingston.
G., Slenczka, H. G., von Graevenitz, A., & Zahner, H. (2003). Viral
Zoonoses. Zoonoses: Infectious diseases transmissible from animals to
humans (3rd ed., pp. 113-119). Washington, D.C.: ASM Press.
5. (2004). In D. L. Heymann (Ed.), Control of Communicable Diseases Manual
(18th ed., pp. 438-447). Washington, D.C.: American Public Health
Association.
6. Plotkin, S. (2000). Rabies. Clinical Infectious Diseases, 30 (1), 4-12.
Retrieved from dx.doi.org/10.1086/313632
7. Anderson, L. J., Nicholson, K. G., Tauxe, R. V., & Winkler, W. G. (1984).
Human rabies in the United States, 1960 to 1979: epidemiology,
diagnosis, and prevention. Annals of Internal Medicine, 100 (5), 728-735.
8. Human rabies prevention--United States, 1999. Recommendations of
the Advisory Committee on Immunization Practices (ACIP).[Erratum
appears in MMWR Morb Mortal Wkly Rep 2000 Aug 18;49(32):737].
(1999). Morbidity & Mortality Weekly Report.Recommendations &
Reports, 48 (RR-1), 1-21.
9. Rupprecht, C. E., & Gibbons, R. V. (2004). Clinical practice. Prophylaxis
against rabies. New England Journal of Medicine, 351 (25), 2626-2635.
10. Heymann, D. L. (2008). Control of Communicable Diseases Manual (19th
Edition ed.). Washington, D.C.: American Public Health Association.
11. Public Health Agency of Canada. (2007). Vaccine-Preventable Diseases -
Rabies. Retrieved 11/24, 2010, from www.phac-aspc.gc.ca/im/vpd-
mev/rabies-eng.php
12. Bussereau, F., & Ermine, A. (1983). Effects of heteropolyanions and
nucleoside analogues on rabies virus: In vitro study of syntheses and
viral production. Annales De Virologie, 134 (4), 487-506.
13. Weinmann, E., Majer, M., & Hilfenhaus, J. (1979). Intramuscular and/or
intralumbar postexposure treatment of rabies virus-infected
cynomolgus monkeys with human interferon. Infection and Immunity, 24
(1), 24-31.
14. Public Health Agency of Canada. (2007). Canadian Immunization Guide
Seventh Edition - 2006 - Part 4: Active Immunizing Agents. Retrieved 11/24,
2010, from www.phac-aspc.gc.ca/publicat/cig-gci/p04-rabi-rage-
eng.php#approve
15. Collins, C. H., & Kennedy, D. A. (1999). Laboratory acquired infections.
Laboratory acquired infections: History, incidence, causes and prevention
(4th ed., pp. 28). London, UK: Buttersworth.
16. Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of
Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009,
(2009).
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Respiratory syncytial virus

SUBSTANCES
NAME: Respiratory syncytial virus
SYNONYM OR CROSS REFERENCE: RSV, Pneumovirus
CHARACTERISTICS: Respiratory syncytial virus (RSV) is classified as a member

of the genus Pneumovirus in the family Paramyxoviridae(1-4). Virus particles
are enveloped and pleomorphic, occurring as irregular spherical particles
that are 100 to 350 nm in diameter, and as long filamentous fibres that are
60 to 200 nm in diameter and 10 mm in length(2). The virion consists of eight
structural proteins(1-4). Three proteins are associated with the nucleocaspid
and include nucleoprotein (N), phosphoprotein (P), and polymerase or large
protein (L). The other five viral proteins are contained within the virus
envelope and include nonglycosylated matrix protein (M), M2, fusion protein
(F), glycoprotein (G), and short hydrophobic protein (SH). RSV lacks
haemagglutinin and neuraminidase activity. The viral genome consists of a
linear, single- stranded, negative-sense, nonsegmented RNA (~15.2 kb).

PATHOGENICITY/TOXICITY: RSV primarily infects human epithelial cells
within the nasopharynx; however, it can also infect other types of cells,
including cell lines, but with much lower efficacy(1,2). Infection may lead to
the formation of syncytia within the infected cell. Primary infection with RSV
is generally exhibited as lower respiratory tract disease, pneumonia,
bronchiolitis, tracheobronchitis, or upper respiratory tract illness(1-4).
Common clinical symptoms include rhinorrhea, sneezing, cough,
pharyngitis, bronchitis, headache, fatigue, and fever. In some cases, otitis
media may occur(4). RSV infections usually begin with upper respiratory
tract disease, which has the tendency to progress to lower respiratory tract
disease (in ~50% cases)(1,2). Severe infection (involving pneumonia) may
develop among elderly patients with underlying respiratory conditions.
Children and immunocompromised individuals are more susceptible to
developing severe disease.
EPIDEMIOLOGY: RSV occurs worldwide and is the most common cause of

bronchiolitis and pneumonia among infants and young children(1-4). Within
USA, 100,000 hospitalizations and 4,500 deaths annually are attributed to
RSV infections(1,2). RSV is also a major cause of nosocomial infections.
Morbidity and mortality is highest among children with underlying illness
and individuals with immunodeficiency or immunosuppression. Virtually all
children are infected by age 2 to 3(1-3). Repeated infections are common,
particularly in young children with up to 5 or 6 infections per year(4).
Although all individuals can be infected with RSV, those at high risk include
premature infants, young children, elderly, immunocompromised(1-4), and
children under age 2 with chronic lung conditions. Other factors that may
predispose to RSV infection include: crowding (schools and day care
centers), exposure to tobacco and smoke, low socioeconomic status, and
family history of atopy and asthma. Infection among healthy and
immunocompetent individuals tends to be less severe. RSV follows a
seasonal pattern(1,2). Annual outbreaks occur during fall, winter, and early
spring among urban centres. In the Northern hemisphere, epidemics peak
in February and March, and may last up to 5 months. In tropical and
subtropical regions, most outbreaks occur during the rainy season. RSV
outbreaks involving lower respiratory illness have been reported in nursing
homes and institutions(1).
HOST RANGE: Humans(1,2); however, various animal species can be

experimentally infected with RSV including cotton rats, mice, ferrets, guinea
pigs, hamsters, marmosets, lambs, and nonhuman primates(2).
INFECTIOUS DOSE: The infectious dose for RSV is > 160 - 640 viral units,
administered through intranasal spray, as listed by the National Institutes of
Health(5).
MODE OF TRANSMISSION: RSV is most likely transmitted through direct

contact with infectious secretions (via fomites) and/or large-particle
aerosols(1,2); however, close contact with infected individuals, or significant
exposure of nasal or conjunctival mucosa with contaminated hands is
required for transmission(2). Transmission via small-particle aerosols is less
likely(1,2).
INCUBATION PERIOD: Incubation period for RSV infection ranges from 2 to

8 days(1).
COMMUNICABILITY: Communicable during the period of active disease.

The disease is likely not readily transmitted from person-to-person, since
significant and prolonged contact is required with infected individuals(1).
Children are known to shed virus for long periods (up to weeks) even after
clinical recovery(1,2).

RESERVOIR: Humans(1,6).
ZOONOSIS: None(6).
VECTORS: None.

DRUG SUSCEPTIBILITY: RSV has been shown to be susceptible to ribavirin,
which has been used to treat severe RSV infections; however, recent studies
suggest that its use produces no significant benefit(1,2,4).
SUSCEPTIBILITY TO DISINFECTANTS: RSV has been shown to be susceptible

to ether, chloroform, and a variety of detergents, including 0.1% sodium
deoxycholate, sodium dodecyl sulphate, and Triton X-100(1). It may also be
sensitive to hypochlorites (1% sodium hypochlorite), formaldehyde (18.5
g/L; 5% formalin in water), 2% glutaraldehyde, and iodophores (1% iodine)
(7).
PHYSICAL INACTIVATION: RSV is sensitive to heating above 55 °C for 5

minutes (up to 90% decrease in infectivity)(1). It is also sensitive to freezing
and thawing (~90% loss in infectivity following each freeze-thaw cycle). It is
also sensitive to acidic media (pH<7).
SURVIVAL OUTSIDE HOST: RSV is generally very vulnerable to

environmental changes, particularly temperature and humidity(1). It is
sensitive to high and low temperature, and to drying; i.e., low humidity
levels. It loses up to 90% infectivity at room temperature after 48 hours and
up to 99% at 1 °C after 7 days. The optimal pH is 7.5. It may survive for about
3 to 30 hours on nonporous surfaces at room temperature.

SURVEILLANCE: Monitor for symptoms(4). Other than monitoring for
symptoms, there are four main techniques for diagnosing RSV, including
virus cultures, serology, immunofluorescence and/or antigen detection, and
nucleic acid based tests. Being labour- intensive and time consuming, the
first two techniques are rarely employed for diagnostic purposes in
epidemiological studies. Rapid diagnostic techniques for viral antigen
detection, including immunofluorescent-antibody assay, optical
immunoassay, enzyme immunoassay, and chromatographic immunoassay
are preferred(1). Most are commercially available, easy to perform and
produce rapid results. Nucleic acid tests (such as RT-PCR) are generally more
sensitive(4).
FIRST AID/TREATMENT: Treatment is mainly supportive for infants with

mild disease; however, children with severe disease, people with underlying
illness, and/or immunocompromised individuals may require
hospitalization(1,2,4). Aerosolized ribavirin may be administered to
immunocompromised patients with severe illness; however, recent studies
suggest that its use produces no significant benefit(1,2). Palivizumab
prophylactic treatment, in combination with aerosolized ribavirin, may also
be considered for high-risk children. Another approach is to consider the
use of anti-inflammatory drugs; however, their efficacy is yet to be
determined(4).
IMMUNISATION: None.
PROPHYLAXIS: Palivizumab prophylactic treatment has been shown to

reduce the rate of hospitalization in children by up to 55%; however,
convincing results on its therapeutic efficacy following an infection have not
been observed(1,2,4). Palivizumab is a humanized monoclonal antibody that
is administered as prophylaxis to high-risk infants for RSV infection. Other
monoclonal antibodies are also available(2).

LABORATORY-ACQUIRED INFECTIONS: 1 case of a laboratory-acquired
infection with RSV was reported up to 1976(8).
SOURCES/SPECIMENS: The main sources for RSV include nasal secretions,

nasal swabs, nasopharyngeal swabs, and nasopharyngeal aspirates(1,4).
PRIMARY HAZARDS: Droplet or aerosol exposure of mucous membranes

and accidental inoculation(2).





chemical disinfection, before disposal(10).
STORAGE: The infectious agent should be stored in sealed containers that

are appropriately labelled(10). Storage conditions for RSV can be improved by
flash freezing in an alcohol and by addition of stabilizing agents (glycerine or
sucrose)(10).

and standards

Canada.

Copyright ©
Canada
REFERENCES:
1. Tang, Y. W., & Crowe JR, J. E. (207). Respiratory Syncytial Virus and
Human Metapneumovirus. In P. R. Murray, E. J. Baron, J. H. Jorgensen,
M. L. Landry & M. A. Pfaller (Eds.), Manual of Clinical Microbiology (9th
ed., pp. 1361-1373). Washington, USA: ASM Press.
2. Collins, P. L., & Crowe JR, J. E. (2007). Respiratory Syncytial Virus and
Metapneumovirus. In D. M. Knipe, P. M. Howley, D. E. Griffin, R. A. Lamb,
M. A. Martin, B. Roizman & S. E. Straus (Eds.), Fields Virology (5th ed., pp.
1601-1636). Philadelphia, USA: Lippincott Williams & Wilkins.
3. Ogra, P. L. (2004). Respiratory syncytial virus: the virus, the disease and
the immune response. Paediatric Respiratory Reviews, 5 Suppl A , S119-26.
4. Tregoning, J. S., & Schwarze, J. (2010). Respiratory viral infections in
infants: causes, clinical symptoms, virology, and immunology. Clinical
Microbiology Reviews, 23 (1), 74-98. doi:10.1128/CMR.00032-09
5. Collins, C. H., & Kennedy, D. A. (1999). Exposure, sources and route of
infection. Laboratory-acquired Infection: History, incidence, causes and
preventions (pp. 38-53). Oxford, UK: Butterworth-Heinemann.
D., Slenczka, W., Graevenitz, A., & Zahner, H. (2003). Viral Zoonoses.
Zoonoses: Infectious Disease Transmissible from Animals to Humans (3rd
ed., pp. 123). Washington, USA: ASM Press.
7. Disinfection and Sterilization. (1993). Laboratory Biosafety Manual (2nd
ed., pp. 60-70). Geneva: WHO.
8. Pike, R. M. (1976). Laboratory associated infections: summary and
analysis of 3921 cases. Health Laboratory Science, 13 (2), 105-114.
9. Human Pathogens and Toxins Act. S.C. 2009, c. 24, (2009).
10. Public Health Agency of Canada. (2004). In Best B., Graham M. L., Leitner
R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd
ed.). Canada: Public Health Agency of Canada.
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Rhinovirus

SUBSTANCES
NAME: Rhinovirus
SYNONYM OR CROSS REFERENCE: Acute viral rhinitis, acute coryza,

common cold virus, RhV.
CHARACTERISTICS: Rhinovirus, part of the Picornaviridae family and

discovered in 1956, are small, icosahedral, non-enveloped viruses around 27
nm in diameter, and contain one positive-strand RNA(1,2). Over 100
antigenically distinct serotypes have been identified, which are divided into
RhV A and RhV B groups, with RhV A2 and RhV C subclasses, based on their
sequence similarity and cell entry receptors(3).

PATHOGENICITY/TOXICITY: Human rhinovirus (HVR) infections are the
cause of about 50% of all common colds and asthma, and chronic
obstructive pulmonary diseases (COPD) exacerbations(4). Most infections are
mild and self-limited, and generally affect the sinuses, although it has been
speculated to occur in the middle ear as well(5). Symptoms may include
runny nose and nasal congestion, headache, cough, sneezing, sore throat,
rhinorrhea, croup in infants, tracheitis, and malaise that may last from 1 - 2
weeks(5-8), and fever may occur in infants and young children. Replication of
the virus is optimized at 33° - 35 °C, thus it is commonly found in the upper
respiratory tract, where it can cause persistent bronchospastic cough, and
can also lead to secondary bacterial infections such as sinusitis and otitis
media(8). Although infrequent, it is also the second most recognized means
of lower respiratory tract infections such as pneumonia and bronchiolitis in
young children and immuno-compromised adults, and can also cause
bronchitis and bronchopneumonia(3). Grayish white vesicles may appear in
the posterior region of the palate, uvula, and the tonsillar pillars(9).
Contracting infection can further exacerbate pre-existing respiratory
diseases such as cystic fibrosis(3).
EPIDEMIOLOGY: Worldwide - accounts for more than 80% of common colds

during high prevalence seasons in autumn between September to
November in temperate climates although it is present in the community
year-round and can affect persons of all ages(3,7). Epidemiological studies
have shown that children under 7 years of age are more susceptible than
adults, with almost all children having experienced this infection by the age
of 2 years. Individuals with asthma are more susceptible to infection(10).
HOST RANGE: Humans(11).
INFECTIOUS DOSE: The infectious dose depends on the strain/type of the

virus, and ranges from 0.032 - 0.4 TCID50 when inoculated as nasal spray,
and 0.68 TCID50 through aerosol particles(12,13).
MODE OF TRANSMISSION: Airborne transmission of aerosols and droplets

is the major route of dissemination of the virus, which can enter the body
through the respiratory tract by the nose and mouth(14,15). Transmission
through direct and indirect contact also occurs and is most common via the
hand-nose-hand route, followed by self-inoculation of nasal/conjunctival
mucosa present on one's hands(8).
INCUBATION PERIOD: Generally between 48-72 hours(8).
COMMUNICABILITY: While symptomatic, and while the virus can be

detected on their hands and nasal mucosa(16).

RESERVOIR: Humans(11).
ZOONOSIS: None.
VECTORS: None.

DRUG SUSCEPTIBILITY: No single antiviral treatment is effective for
Rhinovirus infections as there are a great number of different serotypes;
however, a combined antiviral and antimediator treatment may be effective
as intranasal interferon-α2b and ipratropium and oral naproxen together
can reduce symptoms, rhinorrhea, cough, and malaise . Dextromethorphan
and hydrocodone can relieve cough in adults(7). Topical (intranasal), oral
nasal decongestants, and topical ipratropium (a prescription anticholinergic)
can relieve nasal symptoms in adults. Antihistamines alone or in
combination with decongestant therapy are effective but side effects have
been observed.
DRUG RESISTANCE: Resistance has been shown for antiviral pleconaril,

chalcone, dichloroflavan, and disoxaril(18,19).
SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to disinfectants such as

Lysol Disinfectant Spray (0.1% o-phenylphenol and 79% ethanol) after 1 - 10
minutes, domestic bleach (800 ppm free chlorine diluted from 6% sodium
hypochlorite) after 10 minutes, 7.05% quaternary ammonium diluted in
water, 14.7% phenol diluted in water(20), 2% glutaraldehyde(21), and 1%
iodine has virucidal activity for up to 1 hour on hands(22).
PHYSICAL INACTIVATION: Inactivate by heating in a 56°C water bath for 16

minutes(23), and at pH 6 or at pH 3 for rapid and complete inactivation(13).
Applying virucides (mixture of 3.5 mg citric acid, 1.7 mg malic acid, and 0.7
mg sodium lauryl sulphate) to paper tissues prevents the virus expelled
through the nasal passage from reaching the hands, and thus prevents its
spread(15).
SURVIVAL OUTSIDE HOST: Virus can survive on formica, stainless steel,

varnished wood, nylon, acetate, orlon, Dacron, wool, and silk for up to 3
hours; on cotton, rayon, facial tissue, and paper towel for up to 1 hour; and
in nasal mucous up to 24 hours(24). Drying has little effect on viability.

SURVEILLANCE: Monitor for symptoms. Diagnosis of rhinovirus infections
can be done using reverse-transcription polymerase chain reactions (RT-
PCR) assay, with probes that target the non-coding region of the virus(3).
Identification by cell culture has been utilized traditionally; however, this
method is less sensitive compared to RT-PCR.
FIRST AID/TREATMENT: Administer appropriate drug therapy for

symptomatic relief if necessary. Humidified air, fluid intake, bed rest, nasal
decongestants, cough suppressants, and warm saline gargles can be
effective in relieving symptoms(7,8).
IMMUNISATION: No vaccines against rhinovirus are currently available.
PROPHYLAXIS: Studies on human volunteers have shown zinc gluconate

lozenges to be an effective treatment in reducing clinical signs of rhinovirus
infection(25), as well as human interferon α2 (HuIFN- α2), which is easy to
self-administer and can produce a protective effect against infection(26).
Antivirals have proven ineffective when used alone, and thus can only be
protective when administered with other antimediators(17). Good personal
hygiene can limit the risk of infection.

LABORATORY-ACQUIRED INFECTIONS: No incidents have been reported to
date.
SOURCES/SPECIMENS: Nasal and throat swabs(27).
PRIMARY HAZARDS: Exposure to particle aerosols or droplets of mucous

membranes carrying the infectious virus, contact via hand-to-hand route(16).
SECOND VII - EXPOSURE CONTROLS / PERSONAL PROTECTION




SPILLS: Allow aerosols to settle. Wear protective clothing and cover spill with
absorbent paper towel. Apply appropriate disinfectant, and starting from
perimeter and wipe towards the center. Allow sufficient contact time with
the detergent before cleaning up(29).

disinfection, gamma irradiation, or incineration(29).
STORAGE: Properly labelled and sealed containers(29).

and standards.

Canada

Pathogen Data Sheet are compiled from sources believed to be reliable, we
accept no responsibility for the accuracy, sufficiency, or reliability or for any
loss or injury resulting from the use of the information. Newly discovered
date.
Copyright ©
Canada
REFERENCES:
1. Hadfield, A. T., Lee, W., Zhao, R., Oliveira, M. A., Minor, I., Rueckert, R. R.,
& Rossmann, M. G. (1997). The refined structure of human rhinovirus 16
at 2.15 A resolution: implications for the viral life cycle. Structure (London,
England : 1993), 5 (3), 427-441.
2. Kapikian, A. Z., Almeida, J. D., & Stott, E. J. (1972). Immune electron
microscopy of rhinoviruses. Journal of Virology, 10 (1), 142-146.
3. Hayden, F. G. (2004). Rhinovirus and the lower respiratory tract. Reviews
in Medical Virology, 14 (1), 17-31. doi:10.1002/rmv.406
4. Palmenberg, A. C., Rathe, J. A., & Liggett, S. B. (2010). Analysis of the
complete genome sequences of human rhinovirus. The Journal of
Allergy and Clinical Immunology, 125 (6), 1190-9; quiz 1200-1.
doi:10.1016/j.jaci.2010.04.010
5. Pitkaranta, A., & Hayden, F. G. (1998). Rhinoviruses: important
respiratory pathogens. Annals of Medicine, 30 (6), 529-537.
6. Sanu, A., & Eccles, R. (2008). The effects of a hot drink on nasal airflow
and symptoms of common cold and flu. Rhinology, 46 (4), 271-275.
7. Simasek, M., & Blandino, D. A. (2007). Treatment of the common cold.
American Family Physician, 75 (4), 515-520.
8. George, R. B., Light, R. W., Matthay, M. A., & Matthay, R. A. (Eds.). (2005).
Chest Medicine - Essentials of Pulmonary and Critical Care Medicine (5th
ed.). Philadelphia, PA: Lippincott Williams & Wilkins.
9. Shih, S. R., Chen, S. J., Hakimelahi, G. H., Liu, H. J., Tseng, C. T., & Shia, K.
S. (2004). Selective human enterovirus and rhinovirus inhibitors: An
overview of capsid-binding and protease-inhibiting molecules. Medicinal
Research Reviews, 24 (4), 449-474. doi:10.1002/med.10067
10. Hershenson, M. B., & Johnston, S. L. (2006). Rhinovirus infections: more
than a common cold. American Journal of Respiratory and Critical Care
Medicine, 174 (12), 1284-1285. doi:10.1164/rccm.200609-1387ED
11. Gern, J. E. (2010). The ABCs of rhinoviruses, wheezing, and asthma.
Journal of Virology, 84 (15), 7418-7426. doi:10.1128/JVI.02290-09
12. Couch, R. B., Cate, T. R., Douglas, R. G.,Jr, Gerone, P. J., & Knight, V.
(1966). Effect of route of inoculation on experimental respiratory viral
disease in volunteers and evidence for airborne transmission.
Bacteriological Reviews, 30 (3), 517-529.
13. Fields, B. N., Knipe, D. M., & Howley, P. M. (Eds.). (2007). Fields' Virology
(5th ed.). Philadelphia, PA: Lippincott William's & Wilkins.
14. Bischoff, W. E. (2010). Transmission Route of Rhinovirus Type 39 in a
Monodispersed Airborne Aerosol. Infection Control and Hospital
Epidemiology : The Official Journal of the Society of Hospital Epidemiologists
of America, doi:10.1086/655022
15. Hayden, G. F., Gwaltney, J. M.,Jr, Thacker, D. F., & Hendley, J. O. (1985).
Rhinovirus inactivation by nasal tissues treated with virucide. Antiviral
Research, 5 (2), 103-109.
16. Gwaltney, J. M.,Jr, Moskalski, P. B., & Hendley, J. O. (1978). Hand-to-hand
transmission of rhinovirus colds. Annals of Internal Medicine, 88 (4), 463-
467.
17. Gwaltney, J. M.,Jr. (1992). Combined antiviral and antimediator
treatment of rhinovirus colds. The Journal of Infectious Diseases, 166 (4),
776-782.
18. Dearden, C., al-Nakib, W., Andries, K., Woestenborghs, R., & Tyrrell, D. A.
(1989). Drug resistant rhinoviruses from the nose of experimentally
treated volunteers. Archives of Virology, 109 (1-2), 71-81.
19. Rotbart, H. A. (2000). Antiviral therapy for enteroviruses and
rhinoviruses. Antiviral Chemistry & Chemotherapy, 11 (4), 261-271.
20. Sattar, S. A., Jacobsen, H., Springthorpe, V. S., Cusack, T. M., & Rubino, J.
R. (1993). Chemical disinfection to interrupt transfer of rhinovirus type
14 from environmental surfaces to hands. Applied and Environmental
Microbiology, 59 (5), 1579-1585.
21. Laboratory Safety Manual (1993). (2nd ed.). Geneva: World Health
Organization.
22. Hendley, J. O., Mika, L. A., & Gwaltney, J. M.,Jr. (1978). Evaluation of
virucidal compounds for inactivation of rhinovirus on hands.
Antimicrobial Agents and Chemotherapy, 14 (5), 690-694.
23. Hughes, J. H., Mitchell, M., & Hamparian, V. V. (1979). Rhinoviruses:
kinetics of ultraviolet inactivation and effects of UV and heat on
immunogenicity. Archives of Virology, 61 (4), 313-319.
24. Hendley, J. O., Wenzel, R. P., & Gwaltney, J. M.,Jr. (1973). Transmission of
rhinovirus colds by self-inoculation. The New England Journal of Medicine,
288 (26), 1361-1364.
25. Al-Nakib, W., Higgins, P. G., Barrow, I., Batstone, G., & Tyrrell, D. A.
(1987). Prophylaxis and treatment of rhinovirus colds with zinc
gluconate lozenges. The Journal of Antimicrobial Chemotherapy, 20 (6),
893-901.
26. Phillpotts, R. J., Scott, G. M., Higgins, P. G., Wallace, J., Tyrrell, D. A., &
Gauci, C. L. (1983). An effective dosage regimen for prophylaxis against
rhinovirus infection by intranasal administration of HuIFN-alpha 2.
Antiviral Research, 3 (2), 121-136.
27. GWALTNEY, J. M.,Jr, & JORDAN, W. S.,Jr. (1964). Rhinoviruses and
Respiratory Disease. Bacteriological Reviews, 28 , 409-422.
28. Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of
Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009,
(2009).
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Rubella virus

SUBSTANCES
NAME: Rubella virus
1 - 5
SYNONYM OR CROSS REFERENCE: German measles , 3 day measles
4 1 - 5
, congenital rubella syndrome (CRS) .
CHARACTERISTICS: Family Togaviridae, Genus Rubivirus. Each virion is 55-89

nm and contains one positive stranded RNA molecule. Genetic material is
enveloped in an isometric nucleocapsid. The capsid consists of multiple
copies of one virus-specific protein, surrounded in a lipid bilayer containing
two virus-specific glycoproteins.

PATHOGENICITY/ TOXICITY: Rubella: Mild infection characterized by rash
starting on the face and gradually spreading to the feet, fever,
lymphadenopathy, and other flu-like symptoms such as coughing, sore
2 3
throat, and sneezing . Older children and adults may experience joint
2
involvement and purpuric rash . Rare complications include encephalitis,
thrombocytopenia with hemorrhagic manifestations, neuritis, conjunctivitis,
3
and ochitis .
Congenital rubella syndrome: Women in their first trimester who contract

rubella have an increased risk of passing the infection to the developing
3
foetus . When contracted during the first trimester the effects on the
child are most marked. Ocular, cardiovascular, and central nervous system
defects are common, along with deafness and intrauterine growth
retardation. Contraction of rubella later in pregnancy reduces the risk and
severity of symptoms. Second trimester infections are associated with
deafness, retinopathy, microcephaly, and mental retardation, while third
trimester infections are associated with intrauterine growth retardation.
1 3
EPIDEMIOLOGY: Worldwide . Epidemics occurred roughly every 6-9
years but immunisation programmes have greatly reduced the number of
1 3
cases in developed countries . Infections peaks in late winter and
3
spring .
1 5
INFECTIOUS DOSE: Thirty viral units subcutaneously, >10 viral units by

6
pharyngeal spray, and 60 units by nasal drops are sufficient for infection .
MODE OF TRANSMISSION: The virus is transmitted by aerosols from the

7
respiratory tract in infected individuals . Transmission may also occur via
nasal and respiratory tract secretions carried on hands that come in contact
with nasal mucosa.
INCUBATION PERIOD: The incubation period is 14-17 days with a range of

8
14-21 days . Rash is the first symptoms to appear. Rash appears 2 weeks
1 3
after infection .
COMMUNICABILITY: Carrier is infectious for 7 days before appearance of

2 3
rash and for 5-7 days after the appearance of the rash . Transmission
7
requires close person-to-person contact .

3 5
RESERVOIR: Humans
ZOONOSIS: None
VECTORS: None

DRUG SUSCEPTIBILITY: Susceptibility to antiviral drugs has not been
1
reported .
SUSCEPTIBILITY TO DISINFECTANTS: Rubella virions are susceptible to

ether, chloroform, sodium dodecyl sulphate (SDS), saponin, formaldehyde,
1
ethylene oxide and beta- propiolactone . 1% sodium hypochlorite and
7
70% ethanol are also effective disinfectants .
PHYSICAL INACTIVATION: Temperatures exceeding 56 °C for 2-20 minutes,

1
37°C for 48 hours, or -20 °C will inactivate the Rubella virus . Virions are
also susceptible to UV light. Virions are not stable at a pH less than 6.8 or
1
greater than 8.0 .
SURVIVAL OUTSIDE HOST: Rubella has a half life of 1 hour at 37 °C outside

9
of the host . The mean survival time is 0.9 days.

SURVEILLANCE: Monitor for symptoms. Confirm diagnosis with serological
1
testing . Enzyme-linked immunosorbent assays (ELISA),
hemagglutination inhibition test (HI), and immunofluorescent antibody
assay (IFA) are common methods used. Serologic testing can also be used to
confirm congenital rubella syndrome in an infant, which may yield more
harm than the rubella virus itself.
1
FIRST AID/TREATMENT: Treatment for rubella is supportive . There have
been no reports of successful treatment with antiviral drugs.
IMMUNISATION: Vaccine available; vaccine is combined with measles and

mumps vaccines and is known as the measles, mumps and rubella (MMR)
2 5 16
vaccine . Vaccination for women is suggested 1 month before
3
conception if not previously vaccinated . Recent studies show any risk to
foetus during the first month of pregnancy from the vaccine is negligible.
PROPHYLAXIS: Vaccination of females of child bearing age decreases the

1 3
risk of CRS . Immune globulin given soon after exposure to rubella
may modify or suppress symptoms but is not certain to prevent infection,
including congenital infection and thus is not recommended for routine use
10 .

LABORATORY-ACQUIRED INFECTIONS: Two cases of Rubella in laboratory
workers were reported as of 1985, and the source of these infections may
11
have been from the community . Health care workers have been known
12
to carry the virus and act as a source of infection to in larger community
.
SOURCES/SPECIMENS: Blood, faeces, urine, and nasopharyngeal secretions

2
contain the viral agent during the course of infection .
PRIMARY HAZARDS: Inhalation of aerosols during manipulation of

infectious samples or cultures are the primary hazards associated with the
6 13
Rubella virus . Splashing of infectious samples in the eye also poses
risk of infection.
14
SPECIAL HAZARDS: Rubella is a teratogen . Based on the outcomes of a
local risk assessment, mitigation measures should be put in place to protect
pregnant women, and women trying to become pregnant, from possible
exposures when working in a laboratory where Rubella virus is handled.

15

13

13

SPILLS: Allow all aerosols to settle, and, while wearing protective clothing,
cover the spill gently with paper towel and apply appropriate disinfectant,
starting at the edges of the spill zone and working inward. Allow an
13
appropriate contact time before clean up .
DISPOSAL: Decontamination using steam sterilization, chemical disinfection,

13
or incineration must be performed before disposal of infectious waste .
STORAGE: All infectious materials should be stored in sealed containers

13
bearing the appropriate labelling .

and standards.
UPDATED: March 2017

Copyright ©
Canada
REFERENCES:
1 Chantler, J., Wolinsky, J. S., & Tingle, A. (2001). Rubella Virus. In D.

M. Knipe, & P. M. Howley (Eds.), Fields Virology (4th ed., pp. 963-
990). Philidelphia: Lippincott Williams & Wilkins.
2 Edlich, R. F., Winters, K. L., Long, W. B.,3rd, & Gubler, K. D. (2005).

Rubella and congenital rubella (German measles). Journal of Long-
Term Effects of Medical Implants, 15 (3), 319-328.
3 De Santis, M., Cavaliere, A. F., Straface, G., & Caruso, A. (2006).

Rubella infection in pregnancy. Reproductive Toxicology (Elmsford,
N.Y.), 21 (4), 390-398. doi:10.1016/j.reprotox.2005.01.014
4 Frey, T. K., & Abernathy, E. S. (1993). Identification of strain-specific

nucleotide sequences in the RA 27/3 rubella virus vaccine. The
Journal of Infectious Diseases, 168 (4), 854-864.
5 Ilkow, C. S., Willows, S. D., & Hobman, T. C. (2010). Rubella virus

capsid protein: a small protein with big functions. Future
Microbiology, 5 (4), 571-584. doi:10.2217/fmb.10.27
6 Collins, C. H., & Kennedy, D. A. (1999). Exposure, sources and

routes of infections. Laboratory acquired infections: History
incidences, cases and prevention (4th ed., pp. 38-52, 53). Oxford, UK:
Butterworth Heinmann.

Williams & Wilkins.

Association.
9 Walther, B. A., & Ewald, P. W. (2004). Pathogen survival in the

external environment and the evolution of virulence. Biological
Reviews of the Cambridge Philosophical Society, 79 (4), 849-869.

Guide. Retrieved 11/02, 2010, from www.phac-
aspc.gc.ca/publicat/cig-gci/index-eng.php
11 Grist, N. R., & Emslie, J. (1985). Infections in British clinical

laboratories, 1982-3. Journal of Clinical Pathology, 38 (7), 721-725.
12 Sepkowitz, K. A. (1996). Occupationally acquired infections in

health care workers. Part II. Annals of Internal Medicine, 125 (11),
917-928.

14 Collins, C. H., & Kennedy, D. A. (1999). The laboratory worker.

Laboratory acquired infections: History, incidence, causes and
preventions (4th ed., pp. 187-198). Oxford, UK: Butterworth
Heinemann.

2009, (2009).

2009, (2009).
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Severe acute respiratory
syndrome (SARS) associated coronavirus
On this page
More information
Section I – Infectious agent
Characteristics
Section II – Hazard identification
Host range
Section III – Dissemination
Section IV – Stability and viability
Section V – First aid/medical
Section VII - Exposure controls/personal protection
Section IX – Regulatory and other information
References
More information
For more information on SARS-CoV, see the following:
Biosafety advisories/notifications/directives: Severe Acute Respiratory

Syndrome Interim Guidelines, March 25, 2003
Government of Canada Diseases and Conditions facts: SARS - Severe
Acute Respiratory Syndrome - Diseases and Conditions - Health Canada

Name: Severe acute respiratory syndrome (SARS)-related coronavirus
Agent type: Virus
Taxonomy
Family: Coronaviridae
Genus: Betacoronavirus
Species: Severe acute respiratory syndrome-related coronavirus
1 2 3 3 4
Synonym or cross reference: SARS-CoV , SCV , SCoV ,
5
CoV , formerly "atypical pneumonia" in China before SARS was identified
2 6 7 8 9 10 9 10
.
Characteristics
7 8
Brief description: First isolated in 2003 , and originating from
Guangdon province of southern China, SARS-CoV is a novel coronavirus that
is phylogenetically distinct and only distantly related to other human
6 9
coronaviruses . SARS-CoV is a spherical enveloped virion measuring
1 7
80 to 140 nm in diameter , with a single-stranded, linear, non-
1 2 9 11
segmented, positive-sense RNA genome 30 kb in size .
Properties: Unlike most coronaviruses with narrow host ranges, SARS-CoV

is able to infect cell cultures other than the natural host species and closely
6 9
related species .

Pathogenicity and toxicity: Most common initial symptoms include a fever
1 2
greater than 38°C , often accompanied by myalgia, malaise, chills,
headache, diarrhea, a non-productive cough, shortness of breath, and rigor
1 7 8 12 . After 2 to 7 days, this is followed by respiratory symptoms
1
such as a dry cough, shortness of breath, difficulty breathing, or hypoxia
2 12 . In some cases, the respiratory symptoms become increasingly
1
severe, and patients require oxygen support and mechanical ventilation
12 . Similar to other cases of atypical pneumonia, physical signs upon
chest examination are minimal compared with radiological findings, which
1
typically show ground-glass opacities and focal consolidations . Diarrhea
13
is the most common extra-pulmonary manifestation , followed by
hepatic dysfunction, dizziness, abnormal urinalysis, petechiae, myositis,
1
neuromuscular abnormalities, and epileptic fits . The case-fatality rate is
2 12 14
9.6% ; however, in patients over 65 years of age, this rate
6 12 15
exceeds 50% . Attack rates, defined as the proportion of those
who become ill in an exposed population initially free from disease, of over
16 17
50% have been reported in hospitals . While infections in children
18
appear to be milder than those in adults , SARS in pregnant women
19 20
carries a significant risk of mortality .
Since coronavirus infection is generally host-specific, natural animal hosts

do not reportedly display overt signs of disease when infected with SARS-
4 21 22
CoV . Animal pathogenicity is derived mainly from experimental
data. Animal models infected with human isolates of SARS-CoV experience
less severe symptoms of disease such as mild lung pathology, lethargy,
fever, diarrhea, and conjunctivitis, with some animals recovering on their
3 21 23 24
own . Respiratory distress and temporary skin rash have
21
also been reported in a few experimentally infected Rhesus macaques .
Although coronavirus infection in domestic animals does occur,
experimental infection with a SARS-CoV human isolate did not produce
clinical signs of disease or pathology in pigs, chickens, geese, Pekin ducks,
turkeys, or quail despite viral RNA detection in swab specimens, and blood
25 26
and tissue samples .
20
Predisposing factors: Pregnant women and those 65 years or older
6 15 are at an increased risk of more severe disease.
Communicability: Person-to-person transmission (direct mucous

membrane contact (eyes, nose, and mouth) with infectious respiratory
droplets and/or direct contact with infected body fluids) and/or through
7 10 27 28
exposure to contaminated fomites . The virus preferably
27 29
spreads via respiratory droplets over a close distance . Other
possible modes of transmission include through inhalation of infectious
27 28
aerosols, blood transfusions, or by sharps injuries .
Communicability is at its greatest in severely ill patients or those
experiencing rapid clinical deterioration. Transmission usually occurs after
onset of clinical signs and symptoms (on or after the 5th day of illness on
average), which coincides with peak viral load in nasopharyngeal secretions
1 12 13
around the 10th day of illness . The maximum period of
12
communicability is 21 days .
Non-inoculated cats housed with experimentally infected cats and ferrets

also became infected with SARS-CoV, although no elaboration was provided
3
on the possible mode of transmission . Mice, golden hamsters, and non-
human primates have been used to study SARS-CoV infection but virus
transmission within members of the same species or between these animal
30
models has not been reported .
Epidemiology: SARS-CoV is a novel virus that caused the first major

7 8 31
pandemic of the new millennium . The earliest known cases
were identified in mid-November 2002 in the Guangdong Province of South-
5 6 32
East China . The index case was reported in Foshan, a city 24 km
1 5
from Guangzhou . Retrospective analysis revealed severe cases of
the disease in 5 cities around Guangzhou over a period of 2 months, with
many of the cases having had epidemiological links to the live-animal
5
market trade . A serological study on the prevalence of antibodies to
SARS-CoV in civets from the Xinyuan Live Animal Market in Guangzhou and
farms in different regions of Guangdong, Henan, and Hunan Provinces was
performed. The results revealed a seroprevalence of 78% in the Xinyuan Live
Animal Market, compared to an overall prevalence of ~10% for farms in the
various regions, pointing towards a specific outbreak originating in
33
Guangzhou .
Subsequent to its introduction to Hong Kong in mid-February 2003, the virus

spread to Vietnam, Singapore, Canada, the Philippines, the United Kingdom,
1
the United States, and then back again to China . By the end of July
2003, SARS had spread to affect a reported 8,098 people in over 30 countries,
2 14 31
across 5 continents, killing 774 people . Over half of these
infections can be traced back to 1 index patient who arrived in Hong Kong
14
on February 21, 2003, and 21% of all cases were healthcare workers
31 . Although the World Health Organization declared the end of
the SARS epidemic in early July 2003, sporadic outbreaks of SARS occurred in
34 35 36
late 2003 and early 2004, due to laboratory incidents , and
37
community-acquired SARS in the city of Guangzhou, China .
Host range
Natural host(s): Natural hosts include humans, Himalayan palm civets
(Paguma larvata), racoon dogs (Nyctereutes procyonoides), Chinese ferret
3 4 38 39
badgers (Melogale moschata), cats, and pigs .
Other host(s): Experimental hosts include non-human primates, poultry,

25 26 38
ferrets, golden hamsters, guinea pigs, mice, and rats .
Infectious dose: Experimental infection with 105 PFU of recombinant

mouse-adapted SARS-CoV in mice resulted in development of significant
40
clinical disease including labored breathing and death . In another
study, 107 PFU of recombinant SARS-CoV isolates obtained from human and
41
zoonotic strains were inoculated in cynomolgus macaques, producing
42
radiological changes without development of overt clinical symptoms ;
however, the precise infectious dose remains unknown for humans and
animals alike.
Incubation period: The incubation period of SARS ranges from 2 to 16 days,

2 6 15
with a maximum of 10 days as the best estimate . The rate of
viral shedding from nasopharynx, stool, and urine samples progressively
13
declines from day 10 to 21 after onset of symptoms . The viral load in
1 12
nasopharyngeal secretions peaks around day 10 .

43
Reservoir: Bats are the origin and natural reservoir for SARS-CoV .
Research is ongoing to identify the specific reservoir species, although the
Chinese Horseshoe Bat (Rhinolophus spp.) is considered the most likely
candidate since SARS-CoV-like viruses having a high degree of sequence
38 39 44 45
homology with SARS-CoV were found in these animals
46 . On the other hand, the horseshoe bat angiotensin-converting enzyme
2 (ACE2) was found in one study to be unable to act as a receptor for
47
human SARS-CoV, unlike its human equivalent . Rhinolophus sinicus
(Chinese Rufous Horseshoe Bat) and Myotis daubentoni (Daubenton's Bat)
were found to be susceptible to SARS-CoV infection in this same study.
Zoonosis/Reverse zoonosis: Yes, most likely from Himalayan palm civets

4 38
(Paguma larvata) to humans . Progenitor SARS-CoV in the bat
reservoir is unlikely to be able to infect humans. Rapid viral evolution in an
intermediate host, such as the civet, is believed to occur in order for the
38
virus to adapt and infect humans .
Vectors: None.

Drug susceptibility: Unknown.
Drug resistance: Unknown.
Susceptibility to disinfectants: Inactivated by common disinfection

28
measures such as a 5 minute contact with household bleach , ice-cold
acetone (90 seconds), ice-cold acetone/methanol mixture (40:60, 10
minutes), 70% ethanol (10 minutes), 100% ethanol (5 minutes),
48
paraformaldehyde (2 minutes), and glutaraldehyde (2 minutes) .
Commonly used brands of hand disinfectants also inactivate SARS-CoV (30
48
seconds) .
48
Physical inactivation: Sensitive to heat (60°C for 30 minutes) ,
49
and UV radiation (60 minutes) .
Survival outside host: Can survive for 4 days in diarrheal stool samples with
12 28 48
an alkaline pH , more than 7 days in respiratory secretions at
room temperature, for at least 4 days in undiluted urine, feces and human
28 49
serum at room temperature , up to 9 days in suspension, 60 hours
in soil/water, more than a day on hard surfaces such as glass and metal
48 49 6
, up to 48 hours on plastic surfaces , and 6 days in dried state
48 . The virus does not survive well after drying on paper, but lasts longer
28
on disposable, compared to cotton, gowns .
Human coronavirus 229E can remain infectious on high-touch

environmental surfaces (polyvinylchloride, laminate, wood, stainless steel)
for at least 7 days at ambient temperature (24°C) and relative humidity
50
conditions (~50%) . As a human coronavirus with comparable genetic
characteristics, SARS-CoV may also survive outside the host under similar
conditions.

Surveillance: None of the symptoms of SARS can be used to
differentiate SARS from other causes of pneumonia or respiratory illness;
1 51
therefore, laboratory confirmation is the only form of diagnosis .A
positive viral culture from a respiratory, fecal, urine, or tissue specimen, or a
fourfold rise in neutralising antibody titer taken upon admission and 28 days
1
afterward is the most definitive evidence of SARS infection . Rapid
detection of nucleic acid by RT-PCR or antigen by ELISA can be used as
34 52 37
alternatives . Immunofluorescence, microneutralisation ,
18 31
electron microscopy, and chest radiography can also be used to
diagnose SARS-CoV. Epidemiological features such as exposure to known
SARS case-patients or SARS-affected areas may help in early recognition of
51
infection .

First aid/treatment: Clinical management of SARS relies largely upon

1
supportive care . Ribavirin, corticosteroids, lopinavir, ritonavir, type 1
interferon, intravenous immunoglobulin, and SARS convalescent plasma
have all been used by physicians to treat SARS, but it is not possible to
determine whether the treatments actually benefited patients during
53
the SARS outbreak . There are no reports of treatment undertaken for
infected animals.

should come from the post-exposure response plan, which should be
developed as part of the medical surveillance program. More information on
the post-exposure response plan can be found in the CBH.
Immunization: Several inactivated vaccine candidates have been developed

but they are not currently available for human use due to major safety
2
concerns . Some vaccines in development have only been tested in
54
animal models without clear evidence of protection from disease .
Other vaccines have proven successful in reducing viral replication in animal
models; however, these animals do not express all of the clinical signs and
55 56
lethality of SARS-CoV observed in infected humans .
More information on the medical surveillance program can be found in the

CBH, and by consulting the Canadian Immunization Guide.
2 57
Prophylaxis: No known post-exposure prophylaxis .

program can be found in the CBH.

Laboratory-acquired infections: Four incidents have been reported to
date. The first case occurred in Singapore in September 2003 when a 27 year
old graduate student contracted SARS while working with West Nile virus in
34
a culture laboratory where SARS-CoV was being maintained . The
second case occurred in December 2003 in Taiwan when a 44 year old
researcher contracted the disease while testing herbal remedies
35
against SARS-CoV . The third and fourth cases occurred in China in late-
March to mid-April 2004 when 2 CDC workers developed SARS after
36
improperly inactivating a batch of SARS virus in the laboratory . Each
case was attributed to poor understanding or lack of safety procedures
while working with SARS-CoV.
Please consult the Canadian Biosafety Standard (CBS) and CBH for
additional details on requirements and guidelines for reporting exposure
incidents.
Sources/specimens: Respiratory secretions, faeces, blood, urine, lung

1 8 27 31 52
biopsy tissue, and tears of infected individuals .
Primary hazards: Droplet exposure of the mucous membranes of the eye,

1 10
nose and/or mouth, inhalation of infectious aerosols, and ingestion
.
Special hazards: None.
Section VII - Exposure controls/personal

protection
Risk group classification: Severe acute respiratory syndrome-related
58
coronavirus is considered to be a Risk Group 3 Human Pathogen and
Risk Group 1 Animal Pathogen. SARS-CoV is a Security Sensitive Biological
Agent (SSBA).
Containment requirements: The applicable CL3 requirements outlined in

the CBS and in the Biosafety Advisory for Severe Acute Respiratory Syndrome
should be followed. Note that there are additional security requirements,
such as obtaining a Human Pathogens and Toxins Act Security Clearance, for
work involving SSBAs.
Protective clothing: The applicable CL3 requirements for personal

protective equipment and clothing outlined in the CBS should be followed.
Based on a local risk assessment, appropriate hand, foot, head, body,

eye/face, and respiratory protection should be identified, and the PPE
requirements for the containment zone should be documented in Standard
Operating Procedures.
Other precautions: All activities involving open vessels of infectious

material or toxins to be performed in a certified BSC or other appropriate
primary containment device.

Spills: Allow aerosols to settle. Wearing protective clothing, gently cover the
spill with absorbent paper towel and apply suitable disinfectant, starting at
before clean up.
Disposal: All materials/substances that have come in contact with the

infectious agent should be completely decontaminated before they are
removed from the containment zone. This can be achieved by using a
decontamination method that has been demonstrated to be effective
decontamination.
Storage: The applicable CL3 requirements for storage outlined in the CBS
should be followed. Containers of infectious material or toxins stored
outside the containment zone should be labelled, leakproof, impact
resistant, and kept in locked storage equipment and within an area with
59
limited access .

and standards.
Work with SARS-CoV requires a Human Pathogens and Toxins Licence,

issued by the Public Health Agency of Canada.
Updated: 2018
PREPARED by: Centre for Biosecurity, Public Health Agency of Canada.
Although the information, opinions, and recommendations contained in this

Copyright©Public Health Agency of Canada, 2019, Canada
References
1 Cheng, V. C. C., S. K. P. Lau, P. C. Y. Woo, and Y. Y. Kwok. 2007.

Severe acute respiratory syndrome coronavirus as an agent of
emerging and reemerging infection. Clin. Microbiol. Rev. 20:660-
694.
2 Feng, Y., and G. F. Gao. 2007. Towards our understanding of

SARS-CoV, an emerging and devastating but quickly conquered
virus. Comp. Immunol. Microbiol. Infect. Dis. 30:309-327.
3 Martina, B. E. E., B. L. Haagmans, T. Kuiken, R. A. M. Fouchier,

G. F. Rimmelzwaan, G. Van Amerongen, J. S. M. Peiris, W. Lim,
and A. D. M. E. Osterhaus. 2003. SARS virus infection of cats and
ferrets. Nature. 425:915.
4 Guan, Y., B. J. Zheng, Y. Q. He, X. L. Liu, Z. X. Zhuang, C. L.

Cheung, S. W. Luo, P. H. Li, L. J. Zhang, Y. J. Guan, K. M. Butt, K.
L. Wong, K. W. Chan, W. Lim, K. F. Shortridge, K. Y. Yuen, J. S. M.
Peiris, and L. L. M. Poon. 2003. Isolation and characterization of
viruses related to the SARS coronavirus from animals in Southern
China. Science. 302:276-278.
5 Zhong, N. S., B. J. Zheng, Y. M. Li, L. L. M. Poon, Z. H. Xie, K. H.

Chan, P. H. Li, S. Y. Tan, Q. Chang, J. P. Xie, X. Q. Liu, J. Xu, D. X.
Li, K. Y. Yuen, J. S. M. Peiris, and Y. Guan. 2003. Epidemiology
and cause of severe acute respiratory syndrome (SARS) in
Guangdong, People's Republic of China, in February, 2003. Lancet.
362:1353-1358.
6 Berger, A., C. Drosten, H. Doerr, M. Stürmer, and W. Preiser.

2004. Severe acute respiratory syndrome (SARS)—paradigm of an
emerging viral infection. Journal of Clinical Virology. 29:13-22.
7 Peiris, J. S. M., S. T. Lai, L. L. M. Poon, Y. Guan, L. Y. C. Yam, W.

Lim, J. Nicholls, W. K. S. Yee, W. W. Yan, M. T. Cheung, V. C. C.
Cheng, K. H. Chan, D. N. C. Tsang, R. W. H. Yung, T. K. Ng, and K.
Y. Yuen. 2003. Coronavirus as a possible cause of severe acute
respiratory syndrome. Lancet. 361:1319-1325.
8 Drosten, C., S. Günther, W. Preiser, S. Van der Werf, H. -. Brodt,

S. Becker, H. Rabenau, M. Panning, L. Kolesnikova, R. A. M.
Fouchier, A. Berger, A. -. Burguière, J. Cinatl, M. Eickmann, N.
Escriou, K. Grywna, S. Kramme, J. -. Manuguerra, S. Müller, V.
Rickerts, M. Stürmer, S. Vieth, H. -. Klenk, A. D. M. E. Osterhaus,
H. Schmitz, and H. W. Doerr. 2003. Identification of a novel
coronavirus in patients with severe acute respiratory syndrome. N.
Engl. J. Med. 348:1967-1976.
9 Rota, P. A., M. S. Oberste, S. S. Monroe, W. A. Nix, R.

Campagnoli, J. P. Icenogle, S. Peñaranda, B. Bankamp, K.
Maher, M. -. Chen, S. Tong, A. Tamin, L. Lowe, M. Frace, J. L.
DeRisi, Q. Chen, D. Wang, D. D. Erdman, T. C. T. Peret, C. Burns,
T. G. Ksiazek, P. E. Rollin, A. Sanchez, S. Liffick, B. Holloway, J.
Limor, K. McCaustland, M. Olsen-Rasmussen, R. Fouchier, S.
Günther, A. D. H. E. Osterhaus, C. Drosten, M. A. Pallansch, L. J.
Anderson, and W. J. Bellini. 2003. Characterization of a novel
coronavirus associated with severe acute respiratory syndrome.
Science. 300:1394-1399.
10 Seto, W., D. Tsang, R. Yung, T. Ching, T. Ng, M. Ho, L. Ho, J.

Peiris, and Advisors of Expert SARS group of Hospital
Authority. 2003. Effectiveness of precautions against droplets and
contact in prevention of nosocomial transmission of severe acute
respiratory syndrome (SARS). The Lancet. 361:1519-1520.
11 Marra, M. A., S. J. M. Jones, C. R. Astell, R. A. Holt, A. Brooks-

Wilson, Y. S. N. Butterfield, J. Khattra, J. K. Asano, S. A. Barber,
S. Y. Chan, A. Cloutier, S. M. Coughlin, D. Freeman, N. Girn, O. L.
Griffith, S. R. Leach, M. Mayo, H. McDonald, S. B. Montgomery,
P. K. Pandoh, A. S. Petrescu, A. G. Robertson, J. E. Schein, A.
Siddiqui, D. E. Smailus, J. M. Stott, G. S. Yang, F. Plummer, A.
Andonov, H. Artsob, N. Bastien, K. Bernard, T. F. Booth, D.
Bowness, M. Czub, M. Drebot, L. Fernando, R. Flick, M. Garbutt,
M. Gray, A. Grolla, S. Jones, H. Feldmann, A. Meyers, A. Kabani,
Y. Li, S. Normand, U. Stroher, G. A. Tipples, S. Tyler, R. Vogrig,
D. Ward, B. Watson, R. C. Brunham, M. Krajden, M. Petric, D. M.
Skowronski, C. Upton, and R. L. Roper. 2003. The genome
sequence of the SARS-associated coronavirus. Science. 300:1399-
1404.
12 Heymann, D. L. 2008. Control of Communicable Diseases Manual.

American Public Health Association, Washington, D.C.
13 Peiris, J. S. M., C. M. Chu, V. C. C. Cheng, K. S. Chan, I. F. N.

Hung, L. L. M. Poon, K. I. Law, B. S. F. Tang, T. Y. W. Hon, C. S.
Chan, K. H. Chan, J. S. C. Ng, B. J. Zheng, W. L. Ng, R. W. M. Lai,
Y. Guan, and K. Y. Yuen. 2003. Clinical progression and viral load
in a community outbreak of coronavirus-associated SARS
pneumonia: A prospective study. Lancet. 361:1767-1772.
14 Anonymous 2004. Summary of Probable SARS Cases with Onset

of Illness from 1 November 2002 to 31 July 2003.
15 Anonymous 2003. Update 49 SARS case fatality ratio, incubation

period, July 3rd 2003.
16 Encyclopedia Britannica, S. Pettygrove, and K. Rogers. March

15, 2016. Attack Rate: Epidemiology.
17 Goh, D. L., B. W. Lee, K. S. Chia, B. H. Heng, M. Chen, S. Ma, and

C. C. Tan. 2004. Secondary household transmission of SARS,
Singapore. Emerg. Infect. Dis. 10:232-234.
Français
MENU 

Substances – St. Louis Encephalitis Virus
PATHOGEN SAFETY DATA SHEET – INFECTIOUS

SUBSTANCES
NAME: St. Louis Encephalitis Virus
SYNONYM OR CROSS REFERENCE: SLE, SLEV, St. Louis encephalitis virus,

mosquito-borne encephalitis, arthropod-borne encephalitis, arbovirus, viral
1 2
encephalitis .
CHARACTERISTICS: SLEV belongs to the family Flaviviridae, genus Flavivirus

3 4
(formerly grouped with family Togaviridae) and is a member of
5 6
Japanese encephalitis virus (JEV) serocomplex . SLEV is an arthropod-
borne, positive-sense ssRNA, enveloped, icosahedral virus with a genome of
5 6 6
approximately 11 Kb . They are 40-50 nm in diameter .

PATHOGENICITY/TOXICITY: Most infections are asymptomatic or result in
mild malaise of short duration, especially in young or middle-aged
1
individuals . Clinical disease as a result of infection can include
encephalitis, meningoencephalitis, encephalomyelitis, high fever, altered
consciousness, neurologic dysfunction, aseptic meningitis, stiff neck,
headache, myalgia, tremors, nausea, vomiting and urinary tract infection
1 3 7 - 9 1 3 7
. Onset of symptoms is often acute , and may
1
resolve spontaneously . The severity of clinical illness and fatality rate,
but not rate of infection, increase with age and are most prevalent in the
1 7 - 13 11 12
over-60 population . Hypertension and vascular
12
disease may be risk factors for infection. Based on observations with
other members of the Flavivirus genus, immunocompromised individuals
14 15
may also be at greater risk of severe illness . The fatality rate is 5-
1
20% , and acute illness may be followed by prolonged convalescence in
1 3
30-50% of cases .
EPIDEMIOLOGY: St. Louis encephalitis virus is distributed in Northern,

1
Southern and Central America . Several outbreaks have occurred, and
16
the average number of reported cases is slightly more than 100 . The
greatest number of reported cases was between 1974 and 1976, when more
than twelve outbreaks resulted in more than 2000 officially reported cases in
10 16
Canada and the United States . Cases occur primarily in mid-to-late
summer or early fall in temperate areas, and can occur year-round in milder
1
climates . Higher temperatures may increase the length of the
transmission season, and areas with the greatest abundance of mosquitoes
relative to number of residents (i.e. rural areas) may be at greater risk of
1
infection .
HOST RANGE: Humans, bats, wild birds, domesticated fowl, killer whale,
1 2 6 8 12 15 17
rodents, and possibly other mammals . Wild
birds are the primary vertebrate host, and develop an immediate viremic
response sufficient to infect the mosquito vector, but do not develop
apparent illness following infection.
MODE OF TRANSMISSION: The primary source of human infections is the

mosquito-wild birds transmission cycle. Infected mosquitoes transmit the
virus by biting an infected animal host and then biting a human host (or
other animal host). Principal mosquito species known to transmit SLE virus
are Culex pipiens, Culex quinquefasciatus, Culex, nigripalpus and Culex tarsalis
1 9 10 13 .
1 9
INCUBATION PERIOD: 4 – 21 days .
COMMUNICABILITY: Person-to-person transmission has not been

documented. Virus is not demonstrated in the blood of humans after the
onset of disease; however, the viremia response in infected birds is typically
detected 1-5 days after infection, depending on the viral strain and bird
species (1, 18). Mosquitoes are infected for life.

1
RESERVOIR: Primary reservoirs are wild birds, domestic fowl, and bats
19 19 20
. Overwinter survival is possible in bats , birds , and
1
mosquitoes or mosquito eggs .
ZOONOSIS: Yes. SLEV can be transmitted from infected animals to humans

1 3 10
via mosquitoes. Infected animals are typically asymptomatic .
VECTORS: The principal vectors are mosquitoes of the Culex spp., including
1 10 13
C. pipiens, C. tarsalis, C, quinquefasciatus, C. nigripalpus .

DRUG SUSCEPTIBILITY: No known drug susceptibility.
SUSCEPTIBILITY TO DISINFECTANTS: SLEV is susceptible to disinfectants

including 3–8% formaldehyde, 2% glutaraldehyde, 2–3% hydrogen peroxide,
500–5000-ppm available chlorine, alcohol, 1% iodine, and phenol iodophors
21 .
PHYSICAL INACTIVATION: SLEV is completely inactivated at 56°C for 30 min

22 23 7
and is sensitive to UV and gamma irradiation. At 50 °C, 50% of
21 22
infectivity is lost in 10 minutes and SLEV is stable at 4°C .
SURVIVAL OUTSIDE HOST: SLEV is stable in liquid aerosol form for at least 6
hours at room temperature and 23-80% humidity, and in freeze-dried form
21
almost indefinitely at room temperature .

SURVEILLANCE: Monitor for symptoms and confirm by serology. SLEV
antibody titre can be determined through serological testing or lumbar
puncture, and seroprevalence rates in free-ranging birds or sentinel
1 18 22
chickens can be useful for monitoring transmission activity .
Passive surveillance of suspected human SLEV infection, as well as active
monitoring of high-risk populations may provide indications of human
1
involvement . Effective vector control is the only mechanism for reducing
1
virus amplification and human infections .
FIRST AID/TREATMENT: There are no vaccines or antiviral agents for SLEV

3 . Symptoms and complications as a result of infection are treated with
supportive care.
IMMUNIZATION: None currently available.
PROPHYLAXIS: No specific prophylaxis available; however, measures to

reduce the likelihood of mosquito bites may be effective (i.e. protective
clothing, insect repellents).

LABORATORY-ACQUIRED INFECTIONS: One laboratory-acquired infection
24 25
by percutaneous exposure was reported in 1950 and another
three of non-aerosol source were reported in a 1979 survey of laboratories
26
in the United States .
1 12 17 9
SOURCES/SPECIMENS: Blood , CSF , urine and exudates .
Post-mortem, SLEV has been isolated from the CNS, liver, spleen, and kidney
9 17 27 - 29 .
PRIMARY HAZARDS: Exposure to aerosols of infectious solutions or infected

animal blood or urine (i.e. from animal bedding), accidental perenteral
27
inoculation, or broken skin contact .
SPECIAL HAZARDS: None known.

30

infectious material, infected animals, or cultures.

31

31

cover spill with paper towels and apply appropriate disinfectant, starting at
before clean up .
DISPOSAL: Decontaminate before disposal, steam sterilization, and

31
incineration .
STORAGE: In sealed containers that are appropriately labelled in a

31
Containment Level 3 laboratory .

and standards.

Canada.

Copyright ©
Canada
REFERENCES:
1 Reisen, W. K. (2003). Epidemiology of St. Louis encephalitis

virus. Advances in Virus Research, 61, 139-183.
2 Ciota, A. T., Jia, Y., Payne, A. F., Jerzak, G., Davis, L. J., Young, D. S.,
Ehrbar, D., & Kramer, L. D. (2009). Experimental passage of St.
Louis encephalitis virus in vivo in mosquitoes and chickens reveals
evolutionarily significant virus characteristics. PloS One, 4(11),
e7876. doi:10.1371/journal.pone.0007876
3 Gould, E. A., & Solomon, T. (2008). Pathogenic flaviviruses. Lancet,

371(9611), 500-509. doi:10.1016/S0140-6736(08)60238-X
4 Collett, M. S., Anderson, D. K., & Retzel, E. (1988). Comparisons of

the pestivirus bovine viral diarrhoea virus with members of the
flaviviridae. The Journal of General Virology, 69 ( Pt 10)(Pt 10), 2637-
2643.
5 May, F. J., Li, L., Zhang, S., Guzman, H., Beasley, D. W., Tesh, R. B.,
Higgs, S., Raj, P., Bueno, R.,Jr, Randle, Y., Chandler, L., & Barrett, A.
D. (2008). Genetic variation of St. Louis encephalitis virus. The
Journal of General Virology, 89(Pt 8), 1901-1910.
doi:10.1099/vir.0.2008/000190-0
6 Buck, C., Paulino, G. P., Medina, D. J., Hsiung, G. D., Campbell, T.

W., & Walsh, M. T. (1993). Isolation of St. Louis encephalitis virus
from a killer whale.Clinical and Diagnostic Virology, 1(2), 109-112.
7 Jones, S. C., Morris, J., Hill, G., Alderman, M., & Ratard, R. C. (2002).
St. Louis encephalitis outbreak in Louisiana in 2001. The Journal of
the Louisiana State Medical Society : Official Organ of the Louisiana
State Medical Society, 154(6), 303-306.
8 Spinsanti, L. I., Diaz, L. A., Glatstein, N., Arselan, S., Morales, M. A.,
Farias, A. A., Fabbri, C., Aguilar, J. J., Re, V., Frias, M., Almiron, W. R.,
Hunsperger, E., Siirin, M., Da Rosa, A. T., Tesh, R. B., Enria, D., &
Contigiani, M. (2008). Human outbreak of St. Louis encephalitis
detected in Argentina, 2005. Journal of Clinical Virology : The Official
Publication of the Pan American Society for Clinical Virology, 42(1),
27-33. doi:10.1016/j.jcv.2007.11.022
9 Gubler, D. J., Kuno, G., & Markoff, L. (2007). Flaviviruses. In D. M.

Knipe, D. E. Griffin, R. A. Lamb, S. E. Staus, P. M. Howley, M. A.
Martin & B. Roizman (Eds.), Fields Virology (5th ed., pp. 1153).
Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer
Business.
10 Monath, T. P., & Tsai, T. F. (1987). St. Louis encephalitis: lessons

from the last decade. The American Journal of Tropical Medicine and
Hygiene, 37(3 Suppl), 40S-59S.
11 Bleed, D. M., Marfin, A. A., Karabatsos, N., Moore, P., Tsai, T., Olin,
A. C., Lofgren, J. P., Higdem, B., & Townsend, T. E. (1992). St. Louis
encephalitis in Arkansas. The Journal of the Arkansas Medical
Society, 89(3), 127-130.
12 Marfin, A. A., Bleed, D. M., Lofgren, J. P., Olin, A. C., Savage, H. M.,
Smith, G. C., Moore, P. S., Karabatsos, N., & Tsai, T. F. (1993).
Epidemiologic aspects of a St. Louis encephalitis epidemic in
Jefferson County Arkansas, 1991. The American Journal of Tropical
Medicine and Hygiene, 49(1), 30-37.
13 Reimann, C. A., Hayes, E. B., DiGuiseppi, C., Hoffman, R., Lehman, J.

A., Lindsey, N. P., Campbell, G. L., & Fischer, M. (2008).
Epidemiology of neuroinvasive arboviral disease in the United
States, 1999-2007. The American Journal of Tropical Medicine and
Hygiene, 79(6), 974-979.
14 Roukens, A. H., & Visser, L. G. (2008). Yellow fever vaccine: past,

present and future. Expert Opinion on Biological Therapy, 8(11),
1787-1795. doi:10.1517/14712598.8.11.1787
15 Diamond, M. S., Mehlhop, E., Oliphant, T., & Samuel, M. A. (2009).

The host immunologic response to West Nile encephalitis
virus. Frontiers in Bioscience : A Journal and Virtual Library, 14, 3024-
3034.
16 Centers for Disease Control and Prevention. (2009).
Confirmed and Probable St. Louis Encephalitis Virus Neuroinvasive

Disease Cases, Human, United States, 1964-2008, By State (as of
4/7/2009)
17 Siirin, M. T., Duan, T., Lei, H., Guzman, H., da Rosa, A. P., Watts, D.
M., Xiao, S. Y., & Tesh, R. B. (2007). Chronic St. Louis encephalitis
virus infection in the golden hamster (Mesocricetus auratus). The
18 Patiris, P. J., Oceguera, L. F.,3rd, Peck, G. W., Chiles, R. E., Reisen, W.

K., & Hanson, C. V. (2008). Serologic diagnosis of West Nile and St.
Louis encephalitis virus infections in domestic chickens. The
19 Herbold, J. R., Heuschele, W. P., Berry, R. L., & Parsons, M. A.

(1983). Reservoir of St. Louis encephalitis virus in Ohio
bats. American Journal of Veterinary Research, 44(10), 1889-1893.
20 Reisen, W. K., Lothrop, H. D., Chiles, R. E., Cusack, R., Green, E. G.,
Fang, Y., & Kensington, M. (2002). Persistence and amplification of
St. Louis encephalitis virus in the Coachella Valley of California,
2000-2001. Journal of Medical Entomology, 39(5), 793-805.
21 Gritsun, T. S., Lashkevich, V. A., & Gould, E. A. (2003). Tick-borne

encephalitis. Antiviral Research, 57(1-2), 129-146.
22 Fang, Y., Brault, A. C., & Reisen, W. K. (2009). Comparative

thermostability of West Nile, St. Louis encephalitis, and western
equine encephalomyelitis viruses during heat inactivation for
serologic diagnostics. The American Journal of Tropical Medicine and
Hygiene, 80(5), 862-863.
23 Parquet, M. C., Kumatori, A., Hasebe, F., Mathenge, E. G., & Morita,
K. (2002). St. Louis encephalitis virus induced pathology in
cultured cells. Archives of Virology, 147(6), 1105-1119.
doi:10.1007/s00705-002-0806-6
24 Mediannikov, O. I., Likhoded, L. I., Penkina, G. A., Manzeniuk, O. I.,

Fatalieva, S. F., & Tarasevich, I. V. (2005). Bartonella and
bartonellosis--emerging and re-emerging infections:
epidemiology, clinical course, diagnosis. Zhurnal Mikrobiologii,
Epidemiologii, i Immunobiologii, (1), 83-89.
25 Taye, A., Chen, H., Duncan, K., Zhang, Z., Hendrix, L., Gonzalez, J., &
Ching, W. (2005). Production of recombinant protein Pap31 and its
application for the diagnosis of Bartonella bacilliformis
infection. Annals of the New York Academy of Sciences, 1063, 280-
285.
26 Zeaiter, Z., Fournier, P. -., Greub, G., & Raoult, D. (2003). Diagnosis
of Bartonella endocarditis by a real-time nested PCR assay using
serum. Journal of Clinical Microbiology, 41(3), 919-925.
27 Brooks, T. J., & Phillpotts, R. J. (1999). Interferon-alpha protects

mice against lethal infection with St Louis encephalitis virus
delivered by the aerosol and subcutaneous routes. Antiviral
Research, 41(1), 57-64.
28 Luby, J. P., Stewart, W. E.,2nd, Sulkin, S. E., & Sanford, J. P. (1969).

Interferon in human infections with St. Louis encephalitis
virus. Annals of Internal Medicine, 71(4), 703-709.
29 Coleman, P. H., Lewis, A. L., Schneider, N. J., & Work, T. H. (1968).

Isolations of St. Louis encephalitis virus from post-mortem tissues
of human cases in the 1962 Florida epidemic. American Journal of

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Vaccinia Virus

SUBSTANCES
NAME: Vaccinia Virus
SYNONYM OR CROSS REFERENCE: Poxvirus, smallpox vaccine, VACV, VV
CHARACTERISTICS: The vaccinia virus is a linear, double stranded DNA virus

1 2
that is a member of the Poxviridae family . It is usually 320-380 by
3
260-340 nm in size .

PATHOGENICITY/TOXICITY: VV normally has no serious health effects in
humans, although it can cause disease of the skin when used to inoculate
1
against the smallpox virus . Vaccinia virus is usually injected in the
dermis where a localized lesion appears (a "take"), and then scabs over and
4
heals in about 10-14 days . The vaccination is accompanied by fever,
rash, lymphadenopathy, fatigue, myalgia and headaches in some patients
4 5 . Accidental infection with the virus can occur through contact
between the vaccination lesion and broken skin (inadvertent inoculation)
6 . Serious complications such as ocular vaccinia, myopericarditis, eczema
vaccinatum (a papular, vesicular and pustular rash that is very infectious, 38
cases per million doses), progressive vaccinia (progressive necrosis at the
vaccination site, 3 cases per million doses), postvaccinial CNS disease
(headache, lethargy, seizures and coma, 12 cases per million doses), foetus
malformations and abortion (very rare) sometimes occur after vaccination
5 7 8 . Complications are more serious in immunosuppressed
individuals and the smallpox vaccine usually causes one death for every
5 6
million doses . Contraindications to vaccine are their use in
immunocompromised individuals, individuals with certain skin (e.g.,
24
eczema) and cardiac diseases, and pregnant women .
EPIDEMIOLOGY: Routine vaccination is not recommended due to the

5 9
eradication of smallpox by 1980 . US military and laboratory and
health personnel working with the vaccine or other orthopox viruses still
5
receive the vaccine .
HOST RANGE: Several mammals, including humans, rabbits, cows and river
6 10
buffalo have been shown to contain the virus .
INFECTIOUS DOSE: Unknown. Vaccine titre is usually 108 pock-forming units

11
per ml .
MODE OF TRANSMISSION: The virus can be spread through the contact of a

9
recently vaccinated individual with an unvaccinated person . Contact of a
vaccinia virus lesion and broken skin is the most common mode of
transmission between humans, although it has been shown that human-to-
cattle and cattle-to-human transmission can occur, usually by touching the
9 12
cow's teats .
INCUBATION PERIOD: As this is an immunizing agent, there is no

incubation period; rather the time it takes to become immune is usually 7-14
7
days after vaccination .
COMMUNICABILITY: Vaccinia virus transmission between humans occurs

9 10
through direct contact . Vaccinee-to-cattle and cattle-to-human
transmission has been shown, particularly due to contact with cow's teats
9 12 .

RESERVOIR: Vaccinated humans.
ZOONOSIS: Occurs by contact with broken skin, from cattle to humans and
12
vice-versa .
VECTORS: None.

DRUG SUSCEPTIBILITY: None known
SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to 0.02% sodium

hypochlorite, 30% isopropanol, 40% ethanol, 0.02% glutaraldehyde, 0.01%
benzalkonium chloride, 0.0075% iodine, 30% Sanytex and 0.12% ortho
13 14
phenylphenol . The virus is however resistant to solvent/detergent
combinations (TNBP/Triton X-100 and TNBP/ Tween 80) and longer
incubation periods (between 10 minutes and 24h depending on the
15
solvent/detergent used) are necessary to inactivate the virus .
PHYSICAL INACTIVATION: The virus is inactivated by dry heat at 95 ºC for 2

16
hours . The heat-sensitive fraction of the virus is inactivated by moist
heat at 60 ºC while the heat-resistant fraction may take higher temperatures
17
to fully inactivate it . The virus in its aerosol form is also sensitive to UV
18
light (254 nm) .
SURVIVAL OUTSIDE HOST: The dried virus can survive up to 39 weeks at

19
6.7% moisture and 4ºC .

SURVEILLANCE: Monitor for symptoms and confirm using PCR, electron
7 9
microscopy and histology .
FIRST AID/TREATMENT: Vaccinia immune globulin and cidofovir can be

used to treat more serious complications such as eczema vaccinatum and
5
progressive vaccinia . Supportive care should be given to patients with
5
postvaccinial CNS disease .
IMMUNIZATION: Smallpox vaccination is recommended for laboratory

personnel working with the vaccinia virus (the smallpox vaccine and tissues,
materials or animals that may be infected) or other orthopoxviruses
23
because the virus can be spread to non-vaccinated individuals .
PROPHYLAXIS: None

LABORATORY-ACQUIRED INFECTIONS: 9 laboratory acquired infections
2
were reported between 1986 and 2005 .
SOURCES/SPECIMENS: Lesion fluids or crusts, respiratory secretions and

20
infected tissues containing the virus .
PRIMARY HAZARDS: Ingestion, parenteral inoculation, droplet or aerosol

exposure to mucous membranes, and exposure to broken skin are the
20
primary hazards when working with this agent .
SPECIAL HAZARDS: Certain poxviruses are stable at ambient temperature

20
when dried .

21
RISK GROUP CLASSIFICATION: Risk group 2 .

and operational practices are recommended when working with the vaccine
20 22 . Viable materials should be manipulated in a biological safety
20
cabinet .
22

22
work involving animals or large scale activities . Laboratory personnel
23
working with the agent should consider up-to-date vaccination .




and standards.

Canada.

Copyright ©
Canada
REFERENCES:
Brock, T. D., Madigan, M. T., Martinko, J. M., & Parker, J. (2000).

1
Biology of Microorganisms (9th ed.). New Jersey, USA: Prentice-Hall,
Inc.
Fleming D & Hunt D (Ed.). (2006). Biological Safety Principles and

2
Practices (4th ed.). Washington: ASM Press.
Malkin, A. J., McPherson, A., & Gershon, P. D. (2003). Structure of

3
intracellular mature vaccinia virus visualized by in situ atomic
force microscopy. Journal of Virology, 77(11), 6332-6340.
Ryan, K. J., & Ray, C. G. (Eds.). (2004.). Sherris Medical Microbiology:

4
York.: McGraw-Hill.
Bronze, M.S., and Greenfield, R.A (Ed.). (2005). Biodefence Principles

5
and Pathogens horizon bioscience.
Knipe, D. M., & Howley, P. M. (Eds.). (2001). Fields Virology (4th ed.).
6
Krauss, H., Weber, A., Appel, M., Enders, B., Isenberg, H. D.,
7
Schiefer, H. G., Slenczka, W., von Graevenitz, A., & Zahner, H.
(Eds.). (2003). Zoonoses Infectious Diseases Transmissible from
Animals to Humans (3rd ed.). Washington: ASM press.
Bray, M. (2003). Pathogenesis and potential antiviral therapy of

8
complications of smallpox vaccination. Antiviral Research, 58(2),
101-114.
Silva, D. C., Moreira-Silva, E. A., Gomes Jde, A., Fonseca, F. G., &
9
Correa-Oliveira, R. (2010). Clinical signs, diagnosis, and case
reports of Vaccinia virus infections. The Brazilian Journal of
Infectious Diseases : An Official Publication of the Brazilian Society of
Fleming, D. O., Richardson, J. H., Tulis, J. J., & Vesley, D. (Eds.).

10
(1995). Laboratory Safety Principles and Practices (2nd ed.).
Washington: American Society for Microbiology.
Belongia, E. A., & Naleway, A. L. (2003). Smallpox vaccine: the

11
good, the bad, and the ugly. Clinical Medicine & Research, 1(2), 87-
92.
Murray, P. R., Baron, E. J., Jorgensen, J. H., Landry, M. L., & Pfaller,
12
M. A. (Eds.). (2007). Manual of Clinical Microbiology (9th ed.).
Washington: ASM Press.
Block, S. S. (Ed.). (2001). Disinfection, Sterilization, and Preservation

13
(5th ed.). Philidelphia: Lippincott Williams & Wilkins.
Ferrier, A., Garin, D., & Crance, J. M. (2004). Rapid inactivation of

14
vaccinia virus in suspension and dried on surfaces. The Journal of
Hospital Infection, 57(1), 73-79. doi:10.1016/j.jhin.2004.01.012
Roberts, P. (2000). Resistance of vaccinia virus to inactivation by

15
solvent/detergent treatment of blood products. Biologicals :
Journal of the International Association of Biological Standardization,
28(1), 29-32. doi:10.1006/biol.1999.0236
Sauerbrei, A., & Wutzler, P. (2009). Testing thermal resistance of

16
viruses. Archives of Virology, 154(1), 115-119. doi:10.1007/s00705-
008-0264-x
KAPLAN, C. (1958). The heat inactivation of vaccinia virus. Journal

17
of General Microbiology, 18(1), 58-63.
McDevitt, J. J., Milton, D. K., Rudnick, S. N., & First, M. W. (2008).

18
Inactivation of poxviruses by upper-room UVC light in a simulated
hospital room environment. PloS One, 3(9), e3186.
doi:10.1371/journal.pone.0003186
Sparkes, J. D., & Fenje, P. (1972). The effect of residual moisture in

19
lyophilized smallpox vaccine on its stability at different
temperatures. Bulletin of the World Health Organization, 46(6), 729-
734.
Richmond, J. Y., & McKinney, R. W. (Eds.). (1999). Biosafety in

20
Microbiological and Biomedical Laboratories (4th ed.). Washington:
CDC-NIH.
Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of

21
2009, (2009).

22
Guidelines (3rd ed.). Canada:
Public Health Agency of Canada. (2018). Canadian Immunization

23
page=18#approve
Handley, L., Buller, R. M., Frey, S. E., Bellone, C., & Parker, S. (2009).
24
The new ACAM2000 vaccine and other therapies to control
orthopoxvirus outbreaks and bioterror attacks.Expert Review of
Vaccines, 8(7), 841-850. doi : 10.1586/erv.09.55
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Varicella-zoster virus

SUBSTANCES
NAME: Varicella-zoster virus
SYNONYM OR CROSS REFERENCE: VZV , chickenpox , shingles , Human

herpesvirus 3 , Herpes Zoster.
CHARACTERISTICS: Varicella-Zoster virus belongs to the subfamily

alphaherpesviridae in the Herpesviridae family, genus Varicellovirus. The
Varicella-Zoster virus has a diameter of 150-200 nm and contains a linear,
double stranded DNA (125 kbp) genome, enclosed within an icosahedral
capsid, surrounded by a phospholipid envelope. VZV grows slowly in human
diploid fibroblasts cells, and will remain attached to the host cell, resulting in
less circulating viral particles.

PATHOGENICITY/TOXICITY: Varicella (Chickenpox) and Zoster (shingles)
are the two different manifestations of the Varicella-Zoster virus.
Chickenpox: Varicella/chickenpox is a primary infection with VZV. It occurs

mainly in children and is characterized by generalized itchy, vesicular
eruptions/rash and fever. The lesions usually first appear on the back of the
head and ears, and then spread to the face, neck, trunk and proximal
extremities. The number of lesions may vary from 10 to several hundred.
Progressive, generalized varicella, associated with viremia, visceral
dissemination of the virus, pneumonia, hepatitis, and CNS complications
such as encephalitis, transient ataxia, aseptic meningitis, and transverse
myelitis may occur, particularly in immunocompromised children and adults.
Thirty percent of children with leukemia develop disseminated varicella, and
the accompanying mortality rate is 7%. Arthritis, glomerulonephritis,
myocarditis, and purpura fulminans are other less common complications
associated with varicella. Following acute infection, the virus becomes latent
in sensory ganglia neurons and may persist indefinitely.
Shingles: Shingles/Zoster is due to reactivation of latent VZV. The risk of

acquiring zoster infection increases with age, especially after 50 years of
age. It is characterized by a painful eruption of vesicular lesions along with
inflammation in the skin area supplied by the associated dorsal root or
cranial nerve sensory ganglia. Postherpetic neuralgia, characterized by
persistent pain in the dermatome for many months or years after the
resolution of the infection, may occur. Disseminated infection involving
visceral organs may occur in immunosuppressed patients.
EPIDEMIOLOGY: Varicella-zoster infections occur worldwide.

Varicella/chickenpox is more common in temperate climates than in tropical
countries. Before the introduction of VZV vaccine in 1995, an estimated 4
million cases of varicella and 1 million cases of zoster occurred annually in
the United States. Most of the varicella cases occurred in children <15 years
of age. The disease, however, is more severe in the low percentage of adults
who became affected. The incidence of varicella in the United States has
declined substantially (overall decrease of 90% between 1995 and 2005, with
a 74% decrease among adults), since the introduction of the varicella
vaccination program. Varicella-related morbidity and mortality have also
declined since the introduction of the vaccine. Herpes zoster is caused by
reactivation of the latent virus, and affects mainly adults. Risk factors for
zoster infection include age >50 years, spinal trauma, irradiation, HIV
infection, corticosteroid therapy and cancer. The incidence of herpes zoster
declined by 55% among varicella vaccinated children < than 10 years of age,
between the years 2001-2006, in the United States. The incidence of herpes
zoster among adolescents and adults has remained stable or increased
since 1995.
HOST RANGE:Humans are the only natural host.
MODE OF TRANSMISSION: The main route of transmission is through

aerosols carrying cell-free enveloped VZV particles. Transmission occurs
from the skin vesicles of infected persons to the respiratory tract of
susceptible person. Transmission can also occur through direct contact with
infectious vesicular fluid from an infected person. In utero infection can also
occur as a result of transplacental passage of virus during maternal varicella
infection.
INCUBATION PERIOD: 10-21 days, with an average of 14 days.
COMMUNICABILITY: VZV is highly contagious. Highly infectious cell-free

VZV, produced in the skin vesicles of patients, are responsible for high
degree of contagiousness of this virus. Chickenpox is communicable 1-2
days before onset of rash and approximately 3-4 days after the appearance
of rash, until all the vesicles are crusted over. Zoster is less communicable
than varicella, but patients with zoster can transmit the virus to susceptible
persons.

RESERVOIR: Humans are the only natural host.
ZOONOSIS: None.
VECTORS: None.

DRUG SUSCEPTIBILITY: Acyclovir has been shown to inhibit viral replication.
Some strains resistant to acyclovir have been reported, mainly in HIV
infected patients.
SUSCEPTIBILITY TO DISINFECTANTS: Varicella-Zoster virus is easily

inactivated by lipid solvents, detergents, and proteases. Although not much
information is available on disinfectants specific for VZV, most herpes
viruses are susceptible to 30% ethanol, 20% propanol, 200 ppm sodium
hypochlorite, 0.12 % orthophenyl phenol, and 0.04% glutaraldehyde.
PHYSICAL INACTIVATION: It is a very fragile virus and can be easily

inactivated by heating at 60oC, prolonged storage at a temperature of -70oC
and above, extremes of pH (< 6.2 or >7.2), and ultrasonic disruption.
SURVIVAL OUTSIDE HOST: Labile outside host cell. It survives in the

external environment for a few hours and occasionally for a day or two.

SURVEILLANCE: Monitor for symptoms. Varicella presents with a vesicular
rash. Zoster presents with distinct unilateral vesicular rash with dermatomal
distribution. Direct examination by EM of skin lesions for virus is the most
rapid and sensitive method of identification. Direct examination may be
performed using direct fluorescent antibody (DFA) test, PCR of viral DNA.
Viral culture is also used from isolated of skin lesions and human diploid
fibroblasts cells. Other methods employ serological test such as enzyme-
linked immunosorbent assay.
FIRST AID/TREATMENT: Varicella is a mild and self-limited illness in healthy

children; treatment with antiviral agents is not recommended. Non-specific
methods such as frequent bathing, calamine lotion, and oatmeal bath can
be used for symptomatic relief. Acetaminophen may be given to control
fever. Acyclovir (ACV) has been recommended for treatment in healthy
patients 12 years or older. Intravenous ACV is used for children, and adults
with severe VZV infection or at a risk of developing serious infection such as
immunocompromised patients. ACV is also used for treating herpes zoster
in healthy patients, but is not very effective in immunocompromised
patients. Oral famciclovir is more effective for treating zoster infection in
adults, but is not approved for children or treatment of varicella. Infections
resistant to ACV are treated with intravenous foscarnet.
IMMUNIZATION: A live attenuated vaccine, developed from the Japanese

Oka strain, is recommended for use in healthy children after 12 months of
age. The vaccine can also be used for immunocompetent adults, especially
those at occupational risk of acquiring the disease. In Canada, herpes zoster
vaccine, has also been recommended for immunization of
immunocompetent adults >60 years of age.
PROPHYLAXIS: Passive immunization with intravenous immune globulin,

varicella-zoster immune globulin (VZIG) or VariZIG™ (similar to VZIG, and
produced in Canada), if given within 96 hours of exposure, is effective in
preventing infection or reducing the severity of disease in susceptible
individuals.

SOURCE/SPECIMENS: Vesicular fluids, vesicular lesions, respiratory

secretions.
PRIMARY HAZARDS: Direct contact with clinical material or viral isolates,

inhalation of concentrated aerosolized materials, droplet exposure of
mucous membranes of the eyes, nose, or mouth, ingestion, accidental
parenteral inoculation are the primary hazards associated with herpes
viruses.


where there is a known or potential risk of exposure to splashes.

work involving animals or large scale activities. Women who are or may
become pregnant, if seronegative, should consider being vaccinated and
restricted from working with this agent.




and standards.

Canada

Pathogen Safety Data sheet are compiled from sources believed to be
Copyright ©
Canada
REFERENCES:
American Academy of Pediatrics.Committee on Infectious Diseases.
(2009). Red book (28th ed.). Elk Grove Village, IL: American Academy of
Pediatrics. Retrieved from http://online.statref.com/document.aspx?
Broyer, M., Tete, M. J., Guest, G., Gagnadoux, M. F., & Rouzioux, C. (1997).
Varicella and zoster in children after kidney transplantation: Long-term
results of vaccination. Pediatrics, 99(1), 35-39.
Civen, R., Chaves, S. S., Jumaan, A., Wu, H., Mascola, L., Gargiullo, P., &
Seward, J. F. (2009). The incidence and clinical characteristics of herpes
zoster among children and adolescents after implementation of
varicella vaccination. Pediatric Infectious Disease Journal, 28(11), 954-959.
Cohen, J. I., Straus, S. E., & Arvin, A. M. (2007). Varicella-zoster virus:
Replication, pathogenesis and management. In D. M. Knipe, & P. M.
Howley (Eds.), Fields of virology (5th ed., pp. 2773-2818). Philadelphia, PA:
Lippincott Williams & Wilkins.
Collins, C. H., & Kennedy, D. A. (1999). The laboratory worker. Laboratory
acquired infections: History, incidence, causes and preventions (4th ed., pp.
187-198). Oxford, UK: Butterworth Heinemann.
Creed, R., Satyaprakash, A., & Ravanfar, P. (2009). Varicella zoster
vaccines. Dermatologic Therapy, 22(2), 143-149.
Drew, W. L. (2004). Herpesviruses. In K. J. Ryan, & C. G. Ray (Eds.), Sherris
medical microbiology: An introduction to infectious diseases (4th ed., pp.
555-576). USA: McGraw Hill.
Gershon, A. A., Chen, J., Larussa, P., & Steinberg, S. P. (2007). Varicella-
zoster virus. In P. R. Murray (Ed.), Manual of clinical microbiology (9th ed.,
pp. 1537-1548). Washington, D.C.: ASM Press.
Gershon, A. A. (2008). Varicella-zoster virus infections. Pediatrics in
Review, 29(1), 5-11.
Guris, D., Jumaan, A. O., Mascola, L., Watson, B. M., Zhang, J. X., Chaves,
S. S., . . . Seward, J. F. (2008). Changing varicella epidemiology in active
surveillance sites--united states, 1995-2005. Journal of Infectious Diseases,
197(Suppl 2), S71-5.
Marin, M., Watson, T. L., Chaves, S. S., Civen, R., Watson, B. M., Zhang, J.
X., . . . Seward, J. F. (2008). Varicella among adults: Data from an active
surveillance project, 1995-2005. Journal of Infectious Diseases, 197(Suppl
2), S94-S100.
Mustafa, M. B., Arduino, P. G., & Porter, S. R. (2009). Varicella zoster
virus: Review of its management. Journal of Oral Pathology & Medicine,
38(9), 673-688.
National Advisory Committee on Immunization (NACI)†. (2010).
Statement on the recommended use of herpes zoster vaccine.36
Oxman, M. N., Levin, M. J., Johnson, G. R., Schmader, K. E., Straus, S. E.,
Gelb, L. D., . . . the Shingles Prevention Study Group,. (2005). A vaccine to
prevent herpes zoster and postherpetic neuralgia in older adults. The
New England Journal of Medicine, 352(22), 2271-2284.
doi:10.1056/NEJMoa051016
Prince, H. N., & Prince, D. L. (2001). Principles of viral control and
preservation (5th ed., pp. 543-571). Philadelphia, PA: Lippincott Williams
& Wilkins.
Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory biosafety
guidelines (3rd ed.). Canada: Public Health Agency of Canada.
Reynolds, M. A., Chaves, S. S., Harpaz, R., Lopez, A. S., & Seward, J. F.
(2008). The impact of the varicella vaccination program on herpes zoster
epidemiology in the united states: A review. Journal of Infectious
Diseases, 197(Suppl 2), S224-7.
Viral agents: Human herpes virus. (1999). In J. Y. Richmond, & R. W.
Mckinney (Eds.), Biosafety in microbiological and biomedical laboratories
(BMBL) (4th ed., pp. 161). Washington, D.C.: CDC & NIH.
Walther, B. A., & Ewald, P. W. (2004). Pathogen survival in the external
environment and the evolution of virulence. Biological Reviews of the
Cambridge Philosophical Society, 79(4), 849-869.
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Variola virus

SUBSTANCES
1 2
NAME: Variola virus .
SYNONYM OR CROSS REFERENCE: Smallpox, VARV, and variola minor virus

1 2 3
strains (alastrim, amass, or kaffir viruses) .
CHARACTERISTICS: A member of the family Poxviridae, subfamily

Chordopoxvirinae, genus Orthopoxvirus. Virions are shaped like bricks on
2
electron micrographs and measure approximately 300 x 250 x 200 nm
4 . Orthopoxviruses have an outside envelope and a second membrane
underneath. Instead of a capsid, poxviruses have a nucleosome which
5
contains DNA, and is surrounded by its own membrane . They contain
single, linear, double-stranded DNA molecules of 130 to 375 kb pairs and
4
replicate in the cell cytoplasm . Variola virus is the most complex of the
6 7
orthopoxvirus genus, having many different strains .

PATHOGENICITY/TOXICITY: Smallpox is an acute, contagious disease with
two main forms, variola major and variola minor, both of which cause
1
similar lesions . There are 4 types of variola major infection
presentations.
Ordinary variola major: The most common form, which accounts for more
than 90% of cases and has a fatality rate of approximately 30% among
8
unvaccinated individuals, and 3% for vaccinated individuals . The cause of
death is usually bronchopneumonia, although in about 3% of cases, fatal
haemorrhages occur. The prodromal phase consists of sudden onset of
influenza-like symptoms, characterized by fever, malaise, headache,
prostration, severe back pain, and sometimes abdominal pain and vomiting.
Two to 3 days later, the temperature falls and the patient feels somewhat
better, at which time a characteristic rash appears, first on the face (starting
as small red spots) then on the tongue, mouth, nose, and hands. After a few
days, the rash progresses to the trunk where fewer lesions occur. Lesions in
the mucous membranes of the nose and mouth ulcerate quickly, releasing
large amounts of virus into the mouth and throat. Lesions progress from
macules to papules to vesicles to pustules, and at 8 to14 days, the pustules
form scabs which leave depressed depigmented scars upon healing. All
1 8
lesions in a given area progress through these stages together .
The milder or "modified" variola major: Accounts for 2% of cases in

unvaccinated persons and for 25% in previously vaccinated persons. Cases
are rarely fatal with fewer, smaller, and more superficial lesions than those
4
in patients with the ordinary type .
Haemorrhagic variola major: A rare form of variola major which is always

fatal and involves haemorrhages in the mucous membranes and the skin
1 4 .
Flat variola major: Another rare form of variola major that is almost always
fatal and is characterized by lesions that do not develop to the pustular
2 4
stage, but remain soft and flat .
Variola minor: The other main form of smallpox (also known as alastrim),
1
which is a milder illness with a fatality rate of less than 1% .
Another type of smallpox, variola sine eruptione , occurs in previously

vaccinated contacts or in infants with maternal antibodies. Affected persons
are asymptomatic or have a brief rise in temperature, headache, and
present influenza-like symptoms. The transmission of clinical smallpox has
4
not been documented with variola sine eruptione . Overall, 65% to 80% of
1
smallpox survivors have pockmarks, mostly on the face .
EPIDEMIOLOGY: As a result of a successful worldwide vaccination program,

smallpox was eradicated, with the last natural infection occurring in Somalia
1 8
in 1977 .
1 8
HOST RANGE: Humans . Monkeys are also susceptible to infection .
INFECTIOUS DOSE: Viruses in an aerosol suspension can spread widely, and

8 9 10
infect at a very low dose (10 to 100 organisms) .
MODE OF TRANSMISSION: Transmission occurs via respiratory droplets

(primary route of transmission), or via fine-particle aerosol, or skin
inoculation. The conjunctiva or placenta may be occasional portals of entry
1 . Respiratory droplets (i.e., coughing, sputum, and saliva) have a range of
likely no more than 2 metres and are, therefore, a threat only to persons in
11
the immediate vicinity of the affected patient .
12
INCUBATION PERIOD: Can range from 7-19 days . Typically, onset of
illness occurs after 10-14 days and 2-4 more days for onset of rash to occur
4 9 12 .
COMMUNICABILITY: The highest risk of transmission is during the

appearance of the earliest lesions; however, the period of communicability is
from the development of the earliest lesions to the disappearance of all
1
scabs (about a 3 week period) . Some infected people shed the virus
5
without ever showing signs of illness .

RESERVOIR: No known animal or environmental reservoir. Currently, the
virus isolates are maintained only in World Health Organization (WHO)
1
designated laboratories .
ZOONOSIS: None.
VECTORS: None.

DRUG SUSCEPTIBILITY: The acyclic nucleoside phosphonate analogue
cidofovir has been shown to have activity against variola virus in cell culture,
and in animal models, including animals where therapy was delayed until
13 14
the first signs of smallpox .
SUSCEPTIBILITY TO DISINFECTANTS: Inactivation can be achieved using

apolar lipophilic solvents (chloroform) and quaternary ammonia compounds
15 . Other disinfectants used for standard hospital infection control such
as 0.5% or 200 ppm hypochlorite, 40% ethanol, 30% isopropyl alcohol,
formalin, formaldehyde, phenol, cresol, surface-active detergents (e.g. 100
ppm benzalkonium chloride), chlorobenzene mixtures, and 75 ppm
15 16 17 18 19
iodophor may be effective .
PHYSICAL INACTIVATION: Inactivated by heat (incineration and

18
autoclaving) .
SURVIVAL OUTSIDE HOST: The virus can be propagated in a monkey kidney

17
cell line . Specimens of blood, scrapings from skin lesions, saliva,
pustular fluid, and crusts can be transported and stored for short periods
without refrigeration. Materials from smallpox patients (dried fluid and
crusts) containing virus remain infectious at room temperature for
approximately 1 year. The infectivity of the virus is maintained at 4°C for
15
several months and at -20 to -70°C for years . Based on the behaviour of
vaccinia virus, it is believed that aerosolized variola can retain its infectivity
for up to 24 hours if not exposed to UV light, and if temperatures are cool
(10°C to 11°C) and humidity low (20%). Variola can be almost completely
destroyed within 6 hours in an atmosphere of high temperature (31°C to
33°C) and humidity (80%). At cooler temperatures (26°C), variola virus has
survived for 8 weeks at high relative humidity and 12 weeks at a relative
humidity less than 10%. Virus has been isolated from scabs that had been
9
sitting on a shelf for 13 years . It was also found to be viable in bread,
salad, sausages and gauze bandages stored at 4°C for up to 2 weeks, and in
5
storm water kept at 4.5 °C for up to 166 days . Samples of freeze-dried
20
virus in a laboratory have been revived after storage for 20 years .

SURVEILLANCE: In the past, smallpox was sometimes confused with
chickenpox. The centrifugal distribution of lesions, mostly on the face and
extremities than on the trunk, is a distinctive diagnostic feature of smallpox
which serves to distinguish it from chickenpox, which is characterized by
much more superficial lesions that are concentrated mostly on the trunk, as
1 8
opposed to the face and extremities .
There are several methods for confirming the diagnosis. Some are specific
for variola virus, and others are for orthopoxviruses in general.
Haemadsorption with susceptible chicken erythrocytes is an early detection
method for infection with smallpox virus. Giemsa-stained smears of material
from skin lesions may show Guarnieri inclusion bodies. The soluble antigens
in blood, vesicle fluid, pustule fluid, and saline extracts from crusts or
scrapings in certain stages of disease can be detected via complement
fixation, haemagglutination inhibition, immunofluorescence, and
Ouchterlony techniques. Serologic response is variable in partially immune
15
patients, who may present clinically with variola sine eruptione .
Specimens such as vesicular or pustular fluids or scabs can be examined
directly for the presence of virions by electron microscopy, and viral antigen
can be identified by immunohistochemical studies. Isolation of the virus in
live-cell cultures, followed by PCR, or growth on chorioallantois, is
4
confirmatory; however, PCR diagnostic techniques are more accurate .
The results of serologic testing do not differentiate among orthopoxvirus
species, and paired serum samples are required to distinguish recent
infection from vaccination in the remote past. Newer methods, that detect
IgM responses, may enhance the sensitivity and specificity of serological test
4 . Other diagnostic methods such as immunodiffusion technique, ELISA,
restriction fragment-length polymorphisms, and in situ hybridization have
been suggested by various laboratories for confirming the presence of
1 8 9 21
Variola .
FIRST AID/TREATMENT: If possible, a suspected case of smallpox should be

managed in a negative-pressured room, and the patient should be
vaccinated, particularly in an early stage of illness. Strict respiratory and
contact isolation is imperative. When there are many patients, an isolation
hospital or other facility should be designated. Penicillinase-resistance
antimicrobial agents should be used if smallpox lesions are secondarily
infected, if bacterial infection endangers the eyes, or if the eruption is very
dense and widespread. Daily eye rinsing is required in severe cases. Patients
need adequate hydration and nutrition. Topical idoxuridine should be
considered for the treatment of corneal lesions, although its efficacy is
4 15
unproved for smallpox . Leukocyte transfer from immuno-
compromised persons, and methisazone have been used to treat Vaccinia
gangrenosa (or progressive vaccinia), which is characterized by a slowly
progressive enlargement and necrosis or gangrene of the skin at the site of
smallpox vaccination that can be fatal if treated with non-specific measures
22
only (antibiotics or steroids alone) .
IMMUNIZATION: The vaccine consists of a live Vaccinia virus , which is a

"pox"-type virus related to smallpox. There are significant side effects and
risks associated with this vaccine, such as skin complications (eczema
vaccinatum) which may occur in people with pre-existing eczema, allergic
reactions at site of vaccination, vaccinia gangrenosa (or progressive
vaccinia), eye infections (spread of virus from site of vaccination),
15
postvaccinal encephalitis, intrauterine vaccinia, and viremia . Thus
vaccination should be administered only to those exposed to the virus or
4
facing a high probability of exposure . A successful primary vaccination
confers full immunity to smallpox in more than 95% of persons for perhaps
5 to 10 years, and successful revaccination probably provides protection for
4 23
10 to 20 years or more .
The recently recognised risk of myopericarditis with both first and second
generation vaccinia vaccines serves as a reminder that larger-scale studies
of newer vaccines are necessary to further define their safety profiles and
24
relative roles in protection against smallpox . Two attenuated vaccine
strains have also been isolated and tested: modified vaccinia Ankara (MVA),
which has been effectively used in more than 1900 people with few adverse
25
effects ; and a Japanese strain (LC16m8), which is licensed in Japan, and
26
was safely used on more than 50,000 children in the 1970 .
PROPHYLAXIS: Vaccination very early in the incubation period (within 3 to 4

days of exposure) can markedly attenuate or even prevent clinical
manifestations of smallpox. Full protection occurs after successful
4
vaccination . Vaccination at 4 to 7 days after exposure likely offers some
23
protection from disease or may modify the severity of disease . Unless
directly exposed, the vaccine is not advised for groups of people at greater
risk for serious side effects, including pregnant and nursing women,
children younger than 12 months of age, immuno-compromised patients,
4 23
HIV patients, or patients with a history of eczema . Vaccinia immune
globulin has also been administered (0.6 ml/kg IM) within 3 days of
4 10
exposure .

LABORATORY-ACQUIRED INFECTIONS: Except for a laboratory-associated
smallpox death at the University of Birmingham, England, in 1978, no
further cases have been identified. All known variola virus stocks are held
under security at WHO collaborating centers located at Centers for Disease
Control and Prevention, Atlanta, United States, or the State Research Centre
1 4
of Virology and Biotechnology, Koltsovo, Novosibirsk Region, Russia .
The possession and use of variola viruses are restricted to the WHO
27
collaborating centers .
SOURCES/SPECIMENS: Scrapings of skin lesions, scab materials, papular,

vesicular, or pustular fluid, crusts, bodily fluids including blood and urine,
1 4 8 19
respiratory secretions, pharyngeal and tonsillar swabbings
27 .
PRIMARY HAZARDS: Ingestion, parenteral inoculation, and droplet or

aerosol exposure of mucous membranes or broken skin with infectious
27
fluids or tissues .
SPECIAL HAZARDS: Genetically engineered recombinant vaccinia viruses

pose a potential risk to laboratory personnel, through direct contact or
8 27
contact with clinical materials from infected volunteers or animals .

28


29

29

29

29
STORAGE: In leak-proof containers that are appropriately labelled and

29
locked in a Containment Level 4 laboratory .

and standards.

Canada.

Copyright ©
Canada
REFERENCES:
1 Heymann, D. L. (Ed.). (2004). Control of Communicable Diseases
Manual (18th Edition. ed.). Washington, D.C.: American Public
Health Association.
2 Damon, I. K., & Esposito, J. J. (2003). Poxviruses that infect humans.

In P. R. Murray (Ed.), Manual of clinical microbiology (8th ed., pp.
1583-1591). Washington, D.C.: ASM Press.
3 Essbauer, S., Meyer, H., Porsch-Ozcurumez, M., & Pfeffer, M.

(2007). Long-lasting stability of vaccinia virus (orthopoxvirus) in
food and environmental samples. Zoonoses & Public Health, 54 (3-
4), 118-124.
4 Breman, J. G., & Henderson, D. A. (2002). Diagnosis and

management of smallpox. New England Journal of Medicine, 346
(17), 1300-1308.
Schiefer, H. G., Slenczka, H. G., von Graevenitz, A., & Zahner, H.
(2003). Viral Zoonoses: zoonoses caused by pox viruses. Zoonoses:
Infectious diseases transmissible from animals to humans (3rd ed.,
pp. 151-153). Washington, D.C.: ASM Press.
6 Foster, D. (2003). Smallpox as a biological weapon: implications for

the critical care clinician. DCCN - Dimensions of Critical Care Nursing,
22 (1), 2-7.
7 Sulaiman, I. M., Tang, K., Osborne, J., Sammons, S., & Wohlhueter,
R. M. (2007). GeneChip resequencing of the smallpox virus
genome can identify novel strains: a biodefense application.
Journal of Clinical Microbiology, 45 (2), 358-363.

& Eitzen, E. M.,Jr. (2001). Clinical recognition and management of
Medicine, 21 (3), 435-473.
9 Henderson, D. A. (1999). Smallpox: clinical and epidemiologic

features. Emerging Infectious Diseases, 5 (4), 537-539.
10 Rosenbloom, M., Leikin, J. B., Vogel, S. N., & Chaudry, Z. A. (2002).

Biological and chemical agents: a brief synopsis. American Journal
of Therapeutics, 9 (1), 5-14.
11 Weiss, M. M., Weiss, P. D., Mathisen, G., & Guze, P. (2004).

Rethinking smallpox. Clinical Infectious Diseases, 39 (11), 1668-1673.

Association.
13 De Clercq, E. (2002). Cidofovir in the therapy and short-term

prophylaxis of poxvirus infections. Trends in Pharmacological
Sciences, 23 (10), 456-458.
14 Griffiths, P. D. (2004). Smallpox: the old and the new. Reviews in

Medical Virology, 14 (5), 273-274.
15 Klietmann, W. F., & Ruoff, K. L. (2001). Bioterrorism: implications

for the clinical microbiologist. Clinical Microbiology Reviews, 14 (2),
364-381.
16 Henderson, D. A., Inglesby, T. V., Bartlett, J. G., Ascher, M. S., Eitzen,

E., Jahrling, P. B., Hauer, J., Layton, M., McDade, J., Osterholm, M.
T., O'Toole, T., Parker, G., Perl, T., Russell, P. K., & Tonat, K. (1999).
Smallpox as a biological weapon: medical and public health
management. Working Group on Civilian Biodefense. JAMA, 281
(22), 2127-2137.
17 Tanabe, I., & Hotta, S. (1976). Effect of disinfectants on variola virus

in cell culture. Applied & Environmental Microbiology, 32 (2), 209-
212.
18 Guide D - Specimen Collection and Transport Guidelines. (2003).

Retrieved 4, 2010, 2010, from
19 Guide F - Environmental Control of Smallpox Virus. (2003). Retrieved

4, 30, 2010, from
20 Ambrose, C. T. (2005). Osler and the infected letter. Emerging

21 Nuovo, G. J., Plaza, J. A., & Magro, C. (2003). Rapid diagnosis of

smallpox infection and differentiation from its mimics. Diagnostic
Molecular Pathology, 12 (2), 103-107.
22 Rajagopalan, S. (1965). Vaccinia gangrenosa. Indian Journal of

Pediatrics, 32 (207), 123-127.
23 Rotz, L. D., Dotson, D. A., Damon, I. K., Becher, J. A., & Advisory
Committee on Immunization, P. (2001). Vaccinia (smallpox)
vaccine: recommendations of the Advisory Committee on
Immunization Practices (ACIP), 2001. Morbidity & Mortality Weekly
Report.Recommendations & Reports, 50 (RR-10), 1-25.
24 Artenstein, A. W. (2008). New generation smallpox vaccines: a

review of preclinical and clinical data. Reviews in Medical Virology,
18 (4), 217-231.
25 Kennedy, J. S., & Greenberg, R. N. (2009). IMVAMUNE: modified

vaccinia Ankara strain as an attenuated smallpox vaccine. Expert
Review of Vaccines, 8 (1), 13-24. doi:10.1586/14760584.8.1.13
26 Kenner, J., Cameron, F., Empig, C., Jobes, D. V., & Gurwith, M.
(2006). LC16m8: an attenuated smallpox vaccine. Vaccine, 24 (47-
48), 7009-7022. doi:10.1016/j.vaccine.2006.03.087
27 Restricted animal pathogens. (1999). In J. Y. Richmond, & R. W.

Mckinney (Eds.), Biosafety in microbiological and biomedical
laboratories (BMBL) (4th ed., pp. 220-221). Washington, D.C.: CDC &
NIH.

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Vesicular stomatitis virus (VSV)
Pathogen Safety Data Sheet - Infectious

Substances
SECTION 1 - Infectious Agent
NAME: Vesicular stomatitis virus (VSV)
SYNONYM OR CROSS REFERENCE: Vesiculovirus(1,2), vesicular

stomatitis(1,2,3,4,5), VS(1,2,3,4,5,6), vesicular stomatitis virus disease(3,7), vesicular
stomatitis fever, and Indiana fever (3).
CHARACTERISTICS: A member of the Vesiculovirus genus, in the family

Rhabdoviridae(3,6). VSV is a bullet-shaped, enveloped virus, approximately 70
nm in diameter and 170 nm in length(3), and has a single-stranded, negative-
sense RNA genome(5,8).VSV has eight main serotypes: Indiana, New Jersey,
Cocal, Alagoas, Isfahan, Chandipura, Maraba, and Piry (1,2,3,5,6,8,9).
SECTION 2 – Hazard Identification

PATHOGENICITY/TOXICITY: Most human infections with Indiana and New
Jersey VSV serotypes appear to be subclinical(1,6,8). In patients that show
clinical manifestations, the initial symptom is high fever that is often
biphasic. Subsequent symptoms are “flu-like” including severe malaise,
headaches, myalgia, arthralgia, retrosternal pain, eye aches, and nausea
(1,3,6,7). Vesicle formation on the oral mucosa, lips, and nose is possible, but
these are rare symptoms of vesicular stomatitis (VS) (3,6,7). Human
infections with Cocal virus have not been documented (6), whereas Alagoas
virus infections in humans have only been reported in Brazil, with flu-like
symptoms that resolved within 3-4 days (10). Chandipura virus has only
been reported in India, where it mostly infects children. Symptoms include
fever, sensory disorders, convulsions, vomiting, diarrhoea, and encephalitis
leading to coma and death (11). Reports on the pathogenicity of Piry virus in
humans are inconsistent and virtually absent from the primary literature;
however, Piry virus is closely related to Chandipura virus, based on
glycoprotein sequence analysis (12). The pathogenicity of Maraba virus in
humans is also not known. Isfahan virus was associated with human
infections in Iran; however, the virus has not been definitively linked to
human illness(13). In the laboratory, VSV has been engineered to target
cancer cells or to stimulate immunity against diseases such as AIDS or
influenza(8).
EPIDEMIOLOGY: VS exists in North and South America, Africa and Asia but
not in central Europe(6). Serological surveys indicate that the prevalence of
infection may be high among some populations in enzootic areas. For
example, in a rural locality in Panama, more than 90% of the adult
population is affected (3); however, the precise frequency of VS is not well
established, as the disease often goes unnoticed due to its benign course.
HOST RANGE: Humans (except for Maraba and Cocal viruses) (1,2,4,5,6,8),
horses(2,4,6,8), cattle, pigs, mules(2,6), sand flies(5,6), grasshoppers(4), and
rodents(2).
MODE OF TRANSMISSION: Bite of an infected sand fly(1,5,7,8); by direct

contact with abrasions on the skin; by contact with infected domestic
animals; or by inhaling aerosols via the nasopharyngeal route(1,3). The virus
has also been transmitted via accidental autoinoculation or inhalation of
aerosols in a laboratory setting(3,8).
INCUBATION PERIOD: A wide range of incubation periods have been

reported from 30 hours(1,6) to 6 days(7).
COMMUNICABILITY: There is no documented evidence of person-to-person

transmission of VSV.
SECTION 3 - Dissemination
RESERVOIR: The main reservoir is the sand fly, although arboreal rodents
and non-human primates may also harbour VSV (7). Grasshoppers have also
been implicated as a potential reservoir for VSV(4).
ZOONOSIS: Yes, humans can contract VSV through direct contact with
infected animals, or indirectly through the bite of an infected fly (1,5,7,8).
VECTORS: Sand fly (Phlebotomus spp.) appears to be the most important

vector for VSV(2,6,8). Black flies (Simuliidae)(2,5,6), midges (Culicoides spp.),
mosquitoes (Aedes spp.)(2,5,8) and other diptera(2,5,6) have also been
implicated.
SECTION 4 – Stability and Viability

SUSCEPTIBILITY TO DISINFECTANTS: VSV is inactivated by 1% cresylic acid,

phenolics, chlorinated phenol, 2.5% phenol, 0.4% HCl, 2% sodium
orthophenylphenate (14), and sodium hypochlorite(1,14).
PHYSICAL INACTIVATION: Inactivated at low pH (1.5) (14), and immediately

upon heating to 60 °C (15,16). VSV in stroma-free haemoglobin can also be
inactivated by phototreatment (for example, with red light-emitting diode
(655 nm), 1,9-dimethylmethylen blue (DMMB), or methylen blue (MB)) (16).
SURVIVAL OUTSIDE HOST: VSV can survive for 3 to 4 days in infected saliva
on milking pails, mangers and hay(1).
SECTION 5 – First Aid / Medical

SURVEILLANCE: Monitor for symptoms. Human VSV infections are
confirmed by virus isolation from throat swabs or blood (1,2,6). Other
methods of detection include PCR (1,2,6), ELISA(1,2), neutralisation(2),
compliment fixation, immunofluorescence, and electron microscopy(1).
FIRST AID/TREATMENT: No specific therapy is currently available.

Symptomatic treatment and prevention of secondary infections is important
(6).
IMMUNIZATION: None currently available for use in humans.
PROPHYLAXIS: Good hygiene is usually sufficient to prevent the spread of

VSV(6).
SECTION 6 - Laboratory Hazards

LABORATORY-ACQUIRED INFECTIONS: 46 recorded cases with New Jersey
and Indiana viruses (with no deaths) until 1980 (17). 13 cases of laboratory
infections (no deaths) due to Piry virus were also reported before 1980(18).
No LAIs associated with Chandipura, Cocal, Maraba or Isfahan viruses have
been reported to date.
SOURCES/SPECIMENS: Blood(3,4,6), throat secretions(1,3,6), saliva(1,3,4),

exudates, or epithelium from open vesicles(1,3,4).
PRIMARY HAZARDS: Exposure of skin and mucous membranes to VSV by

direct contact or bite by an infected sand fly.
SPECIAL HAZARDS: Handling infected livestock is a well documented

hazard (1,2,3,6,7).
SECTION 7 – Exposure Controls / Personal Protection

RISK GROUP CLASSIFICATION: Chandipura and Piry viruses are classified as
Risk Group 3 human pathogens. Indiana, Cocal, Alagoas, New Jersey, Isfahan
and Maraba viruses are classified as Risk Group 2 human pathogens.
Vesicular Stomatitis Virus is classified as Risk Group 3 since the species
includes Risk Group 3 serotypes.
CONTAINMENT REQUIREMENTS: Chandipura and Piry viruses:Containment

Level 3 facilities, equipment, and operational practices for work involving
infectious or potentially infectious materials, animals, or cultures. Indiana,
Cocal, Alagoas, New Jersey, Isfahan and Maraba viruses: Containment Level
2 facilities, equipment, and operational practices for work involving
infectious or potentially infectious materials, animals, or cultures.
PROTECTIVE CLOTHING: In Containment Level 3 laboratories: Personnel

entering the laboratory should remove street clothing and jewellery, and
change into dedicated laboratory clothing and shoes, or don full coverage
protective clothing (i.e., completely covering all street clothing). Additional
protection may be worn over laboratory clothing when infectious materials
are directly handled, such as solid-front gowns with tight fitting wrists,
gloves, and respiratory protection. Eye protection must be used where there
is a known or potential risk of exposure to splashes(19). In Containment Level
2 laboratories: Lab coat. Gloves when direct skin contact with infected
there is a known or potential risk of exposure to splashes.
OTHER PRECAUTIONS: In Containment Level 3 laboratories: All activities

with infectious material should be conducted in a biological safety cabinet
(BSC) or other appropriate primary containment device in combination with
personal protective equipment. Centrifugation of infected materials must be
carried out in closed containers placed in sealed safety cups, or in rotors
that are loaded or unloaded in a biological safety cabinet. The use of
needles, syringes, and other sharp objects should be strictly limited. Open
wounds, cuts, scratches, and grazes should be covered with waterproof
dressings. Additional precautions should be considered with work involving
animals or large scale activities (19). In Containment Level 2 laboratories: All
procedures that may produce aerosols, or involve high concentrations or
large volumes should be conducted in a biological safety cabinet (BSC). The
use of needles, syringes, and other sharp objects should be strictly limited.
Additional precautions should be considered with work involving animals or
large scale activities.
SECTION 8 - Handling and Storage

SPILLS:Allow aerosols to settle and, wearing protective clothing, gently
before clean up (30 min) (19).

chemical disinfection, and/or incineration (19).
STORAGE: Chandipura and Piry viruses: In sealed, leak-proof containers that

are appropriately labelled and locked in a Containment Level 3
laboratory(19). Indiana, Cocal, Alagoas, New Jersey, Isfahan and Maraba
viruses: In sealed containers that are appropriately labeled (19).
SECTION 9 – Regulatory and Other Information

and standards.
UPDATED: January 2012.

Canada.

Copyright ©
Canada
References:
1. Letchworth, G. J., Rodriguez, L. L., & Barrera, J. D. C. (1999). Vesicular
stomatitis. Veterinary Journal, 157(3), 239-260.
2. de Mattos, C. A., de Mattos, C. C., & Rupprecht, C. E. (2001).
Rhabdoviruses. In D. M. Knipe, & P. A. Howley (Eds.), (4th ed., pp. 1245-
3. Acha, P. N., & Szyfres, B. (2003). Vesicular Stomatitis. Zoonoses and
Communicable Diseases Common to Man and Animals (3rd ed., pp. 347-
355). Washington D.C.: Pan American Health Organization.
4. Nunamaker, R. A., Lockwood, J. A., Stith, C. E., Campbell, C. L., Schell, S.
P., Drolet, B. S., Wilson, W. C., White, D. M., & Letchworth, G. J. (2003).
Grasshoppers (Orthoptera: Acrididae) Could Serve as Reservoirs and
Vectors of Vesicular Stomatitis Virus. Journal of Medical Entomology,
40(6), 957-963.
5. Rodríguez, L. L. (2002). Emergence and re-emergence of vesicular
stomatitis in the United States. Virus Research, 85(2), 211-219.
6. Krauss, H., Schiefer, H. G., Weber, A., Slenczka, W., Appel, M., Graevenitz,
A. V., Enders, B., Zahner, H., & Isenberg, H. D. (2003). Viral Zoonoses.
Zoonoses: Infectious Disease Transmissible from Animals to Humans (3rd
ed., pp. 119-121). Washington D.C.: ASM Press.
7. (2004). In D. L. Heymann (Ed.), Control of Communicable Diseases Manual
(18th ed., pp. 50-52). Washington, D.C.: American Public Health
Association.
8. Lichty, B. D., Power, A. T., Stojdl, D. F., & Bell, J. C. (2004). Vesicular
stomatitis virus: Re-inventing the bullet. Trends in Molecular Medicine,
10(5), 210-216.
9. Travassos da Rosa, A. P., Tesh, R. B., Travassos da Rosa, J. F., Herve, J. P.,
& Main, A. J.,Jr. (1984). Carajas and Maraba viruses, two new
vesiculoviruses isolated from phlebotomine sand flies in Brazil. The
10. Tesh, R. B., Boshell, J., Modi, G. B., Morales, A., Young, D. G., Corredor, A.,
Ferro de Carrasquilla, C., de Rodriguez, C., Walters, L. L., & Gaitan, M. O.
(1987). Natural infection of humans, animals, and phlebotomine sand
flies with the Alagoas serotype of vesicular stomatitis virus in Colombia.
The American Journal of Tropical Medicine and Hygiene, 36(3), 653-661.
11. Mullen, G. R., & Durden, L. (Eds.). (2009). Medical and Veterinary
Entomology (2nd ed.). USA: Academic Press.
12. Brun, G., Bao, X., & Prevec, L. (1995). The relationship of Piry virus to
other vesiculoviruses: a re-evaluation based on the glycoprotein gene
sequence. Intervirology, 38(5), 274-282.
13. Marriott, A. C. (2005). Complete genome sequences of Chandipura and
Isfahan vesiculoviruses. Archives of Virology, 150(4), 671-680.
doi:10.1007/s00705-004-0452-2
14. Wright, H. S. (1970). Test method for determining the viricidal activity of
disinfectants against vesicular stomatitis virus. Applied Microbiology,
19(1), 92-95.
15. Huang, Y., Takeoka, S., Sakai, H., Abe, H., Hirayama, J., Ikebuchi, K., Ikeda,
H., & Tsuchida, E. (2002). Complete deoxygenation from a hemoglobin
solution by an electrochemical method and heat treatment for virus
inactivation. Biotechnology Progress, 18(1), 101-107.
doi:10.1021/bp0101233
16. Hirayama, J., Abe, H., Kamo, N., Ikebuchi, K., & Ikeda, H. (2001).
Comparison of the effects of different antiviral treatments on the
antioxidant systems of stroma-free hemoglobin. Photochemistry and
Photobiology, 74(3), 461-464.
17. Scherer, W. F., Eddy, G. A., & Monath, T. P. (1980). Laboratory safety for
arboviruses and certain other viruses of vertebrates. American Journal of
Tropical Medicine and Hygiene, 29(6), 1359-1381.
18. Tesh, R. B., & and Johnson, K. M. (Eds.). (1975). Diseases transmitted from
animals to man. Vesicular Stomatitis. (6th ed.). Springfield: C.C. Thomas.
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – West Nile virus (WNV)

SUBSTANCES
NAME: West Nile virus (WNV)
SYNONYM OR CROSS REFERENCE: WNV(1,2,3,4,5,6,7,8,9,10,11,12,13>), West Nile

fever(6), West Nile encephalitis, WN fever(1,10), West Nile disease(12), and West
Nile neuroinvasive disease(10).
CHARACTERISTICS: A member of the genus Flavivirus, and Flavivirida e

family(1,3,4,6). West Nile virus is an icosahedral, enveloped virus of 40 to 50
nm in diameter(1,5,10) and has a single-stranded, positive-sense RNA
genome(1,5,6,12). WNV belongs to the Japanese encephalitis antigenic
complex(14).

PATHOGENICITY/TOXICITY: Most individuals infected with WNV remain
asymptomatic(4,10,12). West Nile (WN) fever is typically a mild illness lasting 3
to 6 days(1,4,12). The main symptoms are sudden onset of fever with chills,
rash, malaise, headache, backache, arthralgia, myalgia and eye pain(1,4,10).
Other non-specific manifestations include nausea, vomiting, anorexia,
diarrhoea, rhinorrhoea, sore throat, and cough(1,10). In some patients there
is generalised lymphadenopathy, and an erythematous macular, papular, or
morbilliform eruption involving the entire body(1,4,10).
Meningitis, encephalitis, and/or acute flaccid paralysis develop in less than

1% of WNV-infected individuals(2,10,14). Patients with neurological disease
typically have a febrile prodrome of 1 to 7 days, which may be biphasic,
before they develop neurological symptoms(1). Typically, neurological
patients will present with a fever, stiff neck, headache, weak muscles,
gastrointestinal symptoms, disorientation, tremors, convulsions, and
paralysis(1,4,10).
A New York serological survey revealed that, of those infected,

approximately 20% developed West Nile fever(14). The overall case fatality
rate ranges from 4% to 14% in individuals exhibiting neuroinvasive disease,
with a higher incidence of severe presentation and higher fatality rates in
older populations(2,14).
EPIDEMIOLOGY: WNV was first discovered in 1937 from the blood of a

febrile woman in the West Nile region of Uganda(5,9,10). WNV is now known
to be enzootic in most of Africa, southern Europe, India, the Middle East,
western and southeast Asia, Australia (known as Kunjin virus), and North
America(1,8,9,15). WNV was first detected in North America in 1999,
following an outbreak in New York City(8). The virus spread westwards
across the United States, southward into Central America and the Caribbean,
and northward into Canada(8,10,11), resulting in the largest epidemics of
neuroinvasive WNV fever ever known(8,10). In temperate and subtropical
regions, most infections in humans occur in summer or early fall when;
whereas, infections in tropical regions tend to coincide with the rainy season
when mosquito populations are most abundant(16).
HOST RANGE: Humans(1,2,3,4,5,6,7,8,9,10,11,12,13,17),

mosquitoes(1,3,4,5,6,7,8,9,10,12), ticks(7,8), birds (particularly passerine
species)(1,3,5,6,8,9,17), horses(1,6), alligators (Alligator mississippiensis )(6),
tree squirrels (Sciurus spp.)(3), eastern chipmunks (Tamias striatus ), eastern
cottontail rabbits (Sylvilagus floridanus ), lake frogs ( Rana ridibunda ); as
well as a broad range of common North American wild and domestic
mammals, such as dogs, deer, feral swine, coyotes, foxes, opossums,
raccoons skunks, bats and other small rodents.
INFECTIOUS DOSE: One viral unit (via the intramuscular route)(18).
MODE OF TRANSMISSION: The main route of infection is via the bite of a

mosquito that has been infected by feeding on WNV infected birds(1,3,6,9).
Humans and most other mammals are regarded as dead-end hosts, since
they do not produce sufficient viraemia to infect mosquitoes and thus do
not significantly contribute to the transmission cycle(10,12).
Other possible routes include blood transfusion, vertical transmission,

breast milk, organ transplantation(11), contact of the conjunctiva with
contaminated bodily secretions of infected birds(17), and laboratory
accidents involving injury with sharps(13).
INCUBATION PERIOD: Ranges from 2 to 6 days, but may extend to 14 days,

or as long as 21 days for patients following organ transplantation(1,14).
COMMUNICABILITY: Human-to-human transmission can occur via infected

breast milk, organ transplantation, blood transfusion, and via vertical
transmission (from mother to child during pregnancy)(11).

RESERVOIR: Birds, particularly passerine species (jays, finches, grackles,
sparrows, and crows)(3,6,11).
ZOONOSIS: Yes. Humans can contract WNV from the exposure of

conjunctival membranes(17) and/or percutaneous injury to the body fluids or
tissues of WNV infected birds(13), as well as indirectly by the bite of an
infected mosquito(4,15,16).
VECTORS: The main vectors are Culex mosquitoes(1,3,4,9,10).

In North America: C. pipiens , C. restuans , C. salinarius , C. quinquefasciatus ,
and C. tarsalis(3,9,10).
In Africa and the Middle East: C. univittatus(5,9).
In Asia: C. vishnui(5).
In Europe: C. pipiens , C. modestus , and Coquillettidia richiardii(9).
Other mosquito species such as Culex nigripalpus , Aedes albopictus , Aedes
vexans , and
Ochlerotatus triseriatus , may also be of importance in the transmission of
WNV(3).

DRUG SUSCEPTIBILITY: Ribavirin and interferon can inhibit WNV in
vitro(10,11).
SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to disinfectants such as 3

to 8% formaldehyde, 2% glutaraldehyde, 2 to 3% hydrogen peroxide, 500 to
5,000 ppm available chlorine, alcohol, 1% iodine, and phenol iodophors(19).
PHYSICAL INACTIVATION: Inactivated by heat (50 to 60°C for at least 30

minutes), ultraviolet light, and gamma irradiation(19).
SURVIVAL OUTSIDE HOST: Low temperatures preserve infectivity, with

stability being greatest below -60°C(19). When added to ELISA wash buffer
there is a 10-fold decrease in titre per 24 hour period at 28°C(20).

SURVEILLANCE: Monitor for symptoms. Confirmation is via virus isolation
from blood(1,2,4,11) or cerebrospinal fluid(1,2,10,11) during the viraemic phase.
Other methods of detection include PCR(2,3,4,13,18), haemagglutinin
inhibition(1,12,17), plaque reduction neutralization(1,12), compliment fixation,
indirect immunofluorescence assay(12), and IgM capture ELISA(1,2,3,10,12,17).
FIRST AID/TREATMENT: Currently there is no treatment of proven efficacy

for WNV fever(10,11). Supportive therapy for encephalitis cases includes
intravenous fluid, electrolyte management, assisted respiration if needed,
anticonvulsants, management of cerebral oedema, and prevention of
secondary bacterial infections(1,2). Studies have assessed ribavirin,
interferon, osmotic agents, gamma globulins, and steroids for treatment of
WN fever in open trials, but more definitive evidence is needed to determine
their efficacy(1,2,4).
IMMUNIZATION: None currently available. An inactivated vaccine is

available for horses, but human vaccines are unlikely to be available for
several years(4,12), although a number of candidates are in clinical trials(10,12).
PROPHYLAXIS: None currently available. The most effective preventative

measure it to avoid mosquito bites(2,3,4,8,10). There are no chemoprophylactic
measures for individuals suspected of being in contact with WNV. To prevent
transmission of WNV through blood transfusion and organ donations, blood
products are screened for WNV in the United States(11).

LABORATORY-ACQUIRED INFECTIONS: Eighteen cases were reported up
until 1980(21), with no deaths. Recently two more cases were reported of
workers who acquired WNV following percutaneous inoculation whilst
handling fluids and tissues infected with WNV(13).
SOURCES/SPECIMENS: Blood(2,3,10,12), cerebrospinal fluid(1,2,3,10,11,12),

tissues(2,3,11,12,17), infected arthropods(1,2,3,4,5,6,7,8,9,10,11,12,13), oral and cloacal
swabs, and feather pulp(3).
PRIMARY HAZARDS: Needlestick injuries, droplets, and aerosols(6,13,17).
SPECIAL HAZARDS: Faecal secretions of infected birds may present a hazard

to humans(4,17).



protection must be used where there is a known or potential risk to
splashes(23).

covered with waterproof dressings. The use of needles, syringes and other
sharp objects should be strictly limited. Additional precautions should be
considered with work involving animals or large scale activities(23).

before clean up (30 min).

chemical disinfection, and/or incineration(23).

and locked in a Containment Level 3 laboratory(23).

and standards.

Canada.

Copyright ©
Canada
REFERENCES:
1. Watts, D. M. (2006). Japanese Encephalitis and West Nile and Other
Flavivirus Infections. In R. Guerrant, D. Walker & P. Weller (Eds.), Tropical
Infectious Diseases: Principles, Pathogens, and Practice (2nd ed., pp. 823-
830). Philadelphia, PA: Elsevier Churchill Livingston.
2. Watson, J. T., & Gerber, S. I. (2004). West Nile Virus: A brief review.
Pediatric Infectious Disease Journal, 23 (4), 357-358.
3. Trevejo, R. T., & Eidson, M. (2008). West Nile virus. Journal of the American
Veterinary Medical Association, 232 (9), 1302-1309.
4. Petersen, L. R., Marfin, A. A., & Gubler, D. J. (2003). West Nile Virus. JAMA:
The Journal of the American Medical Association, 290 (4), 524-528.
doi:10.1001/jama.290.4.524
5. Van Der Meulen, K. M., Pensaert, M. B., & Nauwynck, H. J. (2005). West
Nile virus in the vertebrate world. Archives of Virology, 150 (4), 637-657.
6. Briese, T., & Bernard, K. A. (2005). West Nile virus - An old virus learning
new tricks? Journal of Neurovirology, 11 (5), 469-475.
7. Glaser, A. (2004). West Nile virus and North America: An unfolding story.
OIE Revue Scientifique Et Technique, 23 (2), 557-568.
8. Hayes, E. B., Komar, N., Nasci, R. S., Montgomery, S. P., O'Leary, D. R., &
Campbell, G. L. (2005). Epidemiology and transmission dynamics of West
Nile virus disease. Emerging Infectious Diseases, 11 (8), 1167-1173.
9. Mackenzie, J. S., Gubler, D. J., & Petersen, L. R. (2004). Emerging
flaviviruses: The spread and resurgence of Japanese encephalitis, West
Nile and dengue viruses. Nature Medicine, 10 (12 SUPPL.), S98-S109.
10. Davis, L. E., DeBiasi, R., Goade, D. E., Haaland, K. Y., Harrington, J. A.,
Harnar, J. B., Pergam, S. A., King, M. K., DeMasters, B. K., & Tyler, K. L.
(2006). West nile virus neuroinvasive disease. Annals of Neurology, 60 (3),
286-300.
11. Hayes, E. B., & O'Leary, D. R. (2004). West Nile Virus Infection: A Pediatric
Perspective. Pediatrics, 113 (5 I), 1375-1381.
12. Dauphin, G., & Zientara, S. (2007). West Nile virus: Recent trends in
diagnosis and vaccine development. Vaccine, 25 (30 SPEC. ISS.), 5563-
5576.
13. From the Centers for Disease Control and Prevention. Laboratory-
acquired West Nile virus infections--United States, 2002. (2003). JAMA :
The Journal of the American Medical Association, 289 (4), 414-415.
14. Peterson, L. R., & Marfin, A. A. (2002). West Nile Virus: A Primer for the
Clinician. Annals of Internal Medicine, 137 (3), E-173-E-179.
15. Heymann, D. L. (2008). Control of Communicable Diseases Manual (19th
Edition ed.). Washington, D.C.: American Public Health Association.
16. Campbell, G. L., Marfin, A. A., Lanciotti, R. S., & Gubler, D. J. (2002). West
Nile virus. The Lancet Infectious Diseases, 2 (9), 519-529.
17. Fonseca, K., Prince, G. D., Bratvold, J., Fox, J. D., Pybus, M., Preksaitis, J. K.,
& Tilley, P. (2005). West Nile virus infection and conjunctival exposure
[8]. Emerging Infectious Diseases, 11 (10), 1648-1649.
18. Collins, C. H., & Kennedy, D. A. (1999). Exposure, sources and routes of
infection. Laboratory-Acquired Infections: History, incidence, causes and
prevention (4th ed., pp. 52). Oxford U.K.: Butterworth Heinemann.
19. Burke, D. S., & Monath, T. P. (2001). Flaviviruses . In D. M. Knipe, & P. A.
Howley (Eds.), (4th ed., pp. 1043-1125). Philadelphia, PA: Lippincott
Williams & Wilkins.
20. Mayo, D. R., & Beckwith III, W. H. (2002). Inactivation of West Nile virus
during serologic testing and transport. Journal of Clinical Microbiology, 40
(8), 3044-3046.
21. Scherer, W. F., Eddy, G. A., & Monath, T. P. (1980). Laboratory safety for
arboviruses and certain other viruses of vertebrates. American Journal of
Tropical Medicine and Hygiene, 29 (6), 1359-1381.
22. Human pathogens and toxins act. S.C. 2009, c. 24, Second Session,
Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy
Français
MENU 

Substances – Yellow fever virus

SUBSTANCES
NAME: Yellow fever virus
1 1 2 3 1
SYNONYM OR CROSS REFERENCE: YFV , YF yellow fever
2 3 4 5 6 7 8 9 10 1
, and black vomit .
CHARACTERISTICS: A member of the genus Flavivirus , and Flaviviridae

2 6
family . YFV is a spherical, enveloped virus of 40 to 50 nm in diameter
1 5 1 4 5
, and has a single-stranded, positive- sense RNA genome .

PATHOGENICITY/TOXICITY: It is estimated that 15 to 50 % of people
infected with YF develop illness, beginning abruptly with fever, chills and
5
headache . Of those that develop illness, approximately 57 to 85 % will
abort their infection and recover without developing classic YF. Classic YF is
characterised by three clinical illness stages: infection, remission, and
intoxication.
Infection : This stage typically lasts 3 or 4 days and is characterised by

intense viraemia with symptoms including fever, chills, malaise, headache,
2
lower back pain, knee pain, generalised myalgia, nausea, and dizziness
4 5 6 . On examination, the patient has a heart rate lower than would
be expected for a fever (Faget sign), and congestion and erythaema of the
conjunctivae, tongue and face. Most infections resolve at this stage.
Temperatures up to 40.5°C are associated with severe illness and poor
5
outcome .
Remission : This stage is typified by an abatement of fever and other

constitutional symptoms for a period of about 48 hours. Viraemia may still
4 > 5
be present but it is usually waning .
Intoxication : Approximately 15 to 25 % of people who develop any clinical

symptoms (or 10 % of all infected people) progress to this stage, which
generally occurs 3 to 6 days after the onset of illness and can last for 3 to 8
days. During this period, viraemia disappears, and antibodies, along with the
4 5
classic signs of YF (jaundice, renal failure and haemorrhage), appear .
Common symptoms of this stage include fever, relative bradycardia,
vomiting, nausea, epigastric pain, jaundice, oliguria and haemorrhagic
manifestations (melena, haematuria, non-menstrual uterine bleeding,
petechiae, ecchymoses, epistaxis, and oozing of blood from the gums and
2 5
needle puncture sites) . Many patients will progress to multi-organ
failure dominated by hepatic, renal, haematological and cardiovascular
5
involvement .
The case fatality rate of patients who develop hepatic and renal failure is 20
5 6
to nearly 50 % . Death is typically preceded by profound hypotension
4 5
and shock that is difficult to manage with fluids and vasopressors .
EPIDEMIOLOGY: YF occurs only in tropical regions of Africa and South

4 5 7
America . Approximately 200,000 cases of yellow fever occur
1 1 7
annually , 90 % of them in Africa . Up to 5,000 cases of YF in Africa
and 300 in South America are reported annually, but the true incidence is
4
believed to be 10 to 50-folds higher than official reports .
Three distinct transmission cycles exist. A sylvatic (jungle) cycle occurs in the
rainforests of Africa and South America whereby YFV is transmitted between
5
non-human primates and mosquitoes . Human cases are rare and usually
occur in people who are occupationally exposed in forested or transitional
areas. An urban human-mosquito-human transmission cycle occurs in both
Africa and South America; and a savannah cycle that occurs only in Africa
involves transmission of YFV among monkeys, mosquitoes and humans.
1 2 5 6 1 2 5
HOST RANGE: Humans , non-human primates ,
5
hedgehogs, and golden hamsters .
MODE OF TRANSMISSION: YFV is transmitted to humans from infected

non-human primates and other humans by the bite of Aedes and
2 4 5 6 8
Haemagogus mosquitoes .
2 4 5 6
INCUBATION PERIOD: 3 to 6 days .
COMMUNICABILITY: No evidence for direct human-to-human transmission.

RESERVOIR: In urban areas: humans and mosquitoes (Aedes aegypti); in
areas of rainforest: monkeys and mosquitoes; and in savannah areas:
1 2 5 8
humans, monkeys and mosquitoes .
ZOONOSIS: Yes, indirectly from mosquitoes infected by non-human

1 5 6
reservoir hosts (sylvatic and savannah YF transmission) .
VECTORS: The principal arthropod vectors of YF differ depending on their

5
geographical location .
5 6
Urban YF : Aedes aegypti in both South America and Africa .
Sylvatic YF : Aedes africanus in Africa and members of the Haemagogus
5 6
species in South America .
Savannah YF : Aedes furcifer, Aedes vittatus, Aedes luteocephalus , and Aedes
africanus in West Africa, and Aedes africanus and Aedes simpsoni in East Africa
5 .

DRUG SUSCEPTIBILITY: Ribavirin has activity against YF virus at high
5
(potentially cytotoxic) concentrations in vitro .
SUSCEPTIBILITY TO DISINFECTANTS: Inactivated by 3 to 8 % formaldehyde,

2 % glutaraldehyde, 2 to 3 % hydrogen peroxide, 500 to 5,000 ppm available
11
chlorine, alcohol, 1 % iodine, and phenol iodophors .
PHYSICAL INACTIVATION: Inactivated by heat (50 to 60°C for at least 30

11
minutes), ultraviolet light, and gamma irradiation .
SURVIVAL OUTSIDE HOST: Low temperatures preserve infectivity, with

11
stability being greatest below -60°C .

SURVEILLANCE: Monitor for symptoms. Confirmation is via virus isolation
1 2 6 2
from blood or cerebrospinal fluid during the viraemic phase.
1 2 6
Other methods of detection include immunofluorescence , PCR
2 6 2
, real-time PCR , compliment fixation, haemagglutinin inhibition,
1 1 2 6
neutralization , and IgM capture ELISA .
FIRST AID/TREATMENT: Treatment is supportive and symptomatic, however

2
it may vary as infection is highly case-dependent . Treatments and care
may include maintenance of nutrition and prevention of hypoglycaemia,
nasogastric suction to prevent gastric distension and aspiration, intravenous
cimetidine to prevent gastric bleeding, treatment of hypotension by fluid
replacement and vasoactive drugs, administration of oxygen, correction of
metabolic acidosis, treatment of bleeding with fresh frozen plasma, dialysis
if indicated by renal failure, and treatment of secondary infections by
4
antibiotics .
IMMUNIZATION: There are 2 attenuated live YF virus vaccines available: the

2 2 5 6 7 8
neurotropic French Dakar vaccine and the 17D strain ,
the latter being the only preparation approved for use in Canada. Immunity
develops 10 days after primary immunization and persists for more than 10
12
years . Only designated Yellow Fever Vaccination Centre clinics approved
13
by PHAC can administer YF immunization , which should then be
recorded on an appropriately validated International Certificate of
Vaccination.
PROPHYLAXIS: Immunisation is required legally for travelers visiting areas

of endemicity or traveling from areas of endemicity into counties that are
2
free of YF . Also, passive antibody, interferon, and interferon inducers can
3
be effective if given before YF infection or during incubation . Most often
they are used when it is clear that the individual has been exposed to YFV
4 5
(i.e. in a laboratory setting) . Travelers should also take precautions
against mosquito bites when in areas with yellow fever transmission.

LABORATORY-ACQUIRED INFECTIONS: Thirty-eight cases were reported up
14
until 1980 with 8 deaths .
1 4 5 6 6
SOURCES/SPECIMENS: Blood , liver tissue , and
2
cerebrospinal fluid .
9 10
PRIMARY HAZARDS: Contact with infected blood and/or tissues .
SPECIAL HAZARDS: Direct or indirect exposure to aerosols of concentrated

8
YF 17D vaccine . Evidence also exists of transmission of YFV from the
9
infected blood of a patient to a caregiver , from infected monkey and
10
mouse tissues, and from handling infected laboratory animals .

15


16

16

before clean up (30 min).

16

16

and standards.
UPDATED: October 2010.

Canada.

Copyright ©
Canada
REFERENCES:
1 Acha, P. N., & Szyfres, B. (2003). Yellow Fever. Zoonoses and

Communicable Diseases Common to Man and Animals (3rd ed., pp.
377-387). Washington D.C.: Pan American Health Organization.
to Humans (3rd ed., pp. 52-57). Washington D.C.: ASM Press.
3 Monath, T. P. (2008). Treatment of yellow fever. Antiviral Research,

78 (1), 116-124.
4 Monath, T. P. (2001). Yellow fever: An update. Lancet Infectious

Diseases, 1 (1), 11-20.
5 Marfin, A. A. (2006). Yellow Fever. In R. Guerrant, D. Walker & P.

Weller (Eds.), Tropical Infectious Diseases: Principles, Pathogens, and
Practice (2nd ed., pp. 797-812). Philadelphia, PA: Elsevier Churchill
Livingston.
6 (2004). In D. L. Heymann (Ed.), Control of Communicable Diseases

Manual (18th ed., pp. 595-600). Washington, D.C.: American Public
Health Association.
7 Barnett, E. D. (2007). Yellow fever: Epidemiology and prevention.

Clinical Infectious Diseases, 44 (6), 850-856.
8 Cetron, M. S., Marfin, A. A., Julian, K. G., Gubler, D. J., Sharp, D. J.,
Barwick, R. S., Weld, L. H., Chen, R., Clover, R. D., Deseda-Tous, J.,
Marchessault, V., Offit, P. A., & Monath, T. P. (2002). Yellow fever
vaccine. Recommendations of the Advisory Committee on
Immunization Practices (ACIP), 2002. MMWR. Recommendations
and Reports: Morbidity and Mortality Weekly
Report.Recommendations and Reports / Centers for Disease
Control, 51 (RR-17), 1-11; quiz CE1.
9 Cook, G. C. (1994). Fatal yellow fever contracted at the Hospital for

Tropical Diseases, London, UK, in 1930. Transactions of the Royal
Society of Tropical Medicine and Hygiene, 88 (6), 712-713.
10 Berry, G. P., & Kitchen, S. F. (1931). Yellow Fever Accidentally

Contracted in the Laboratory: A Study of Seven Cases. American
Journal of Tropical Medicine and Hygiene, s1-11 (6), 365-434.
11 Burke, D. S., & Monath, T. P. (2001). Flaviviruses . In D. M. Knipe, &

P. A. Howley (Eds.), (4th ed., pp. 1043-1125). Philadelphia, PA:
Lippincott Williams & Wilkins.
12 Public Health Agency of Canada. (2010). Yellow Fever. Retrieved 09-

09-2010, 2010, from www.phac-aspc.gc.ca/tmp-pmv/info/yf-fj-
eng.php
13 Public Health Agency of Canada. (2010). Yellow Fever Vaccination

Centres in Canada. Retrieved 09-09-2010, 2010, from www.phac-
aspc.gc.ca/tmp-pmv/yf-fj/index-eng.php

American Journal of Tropical Medicine and Hygiene, 29 (6), 1359-
1381.

Contact us
All contacts
About government
Social media
Mobile applications
About Canada.ca
Privacy

Virology Compilation For Final Exam Guide

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Virology Compilation For Final Exam Guide

Uploaded by

Copyright:

Available Formats

Français

Canada.ca  Health  Health risks and safety  Biosafety and biosecurity

 Pathogen Safety Data Sheets

Pathogen safety data sheet: Infectious

PATHOGEN SAFETY DATA SHEET - INFECTIOUS

SYNONYM OR CROSS REFERENCE: Adenovirus Species F, enteric

CHARACTERISTICS: Human adenoviruses are members of the family

SECTION II - HAZARD IDENTIFICATION

EPIDEMIOLOGY: Enteric adenovirus is a common cause of acute

HOST RANGE: Humans.

INFECTIOUS DOSE: Unknown.

MODE OF TRANSMISSION: The virus is transmitted via the fecal-oral

INCUBATION PERIOD: 3 to 10 days(1).

COMMUNICABILITY: Low communicability between close contacts in the

SECTION III - DISSEMINATION

SECTION IV - STABILITY AND VIABILITY

SUSCEPTIBILITY TO DISINFECTANTS: Adenoviruses are resistant to lipid

PHYSICAL INACTIVATION: Adenoviruses are highly resistant to

SECTION V - FIRST AID / MEDICAL

FIRST AID/TREATMENT: Illness is generally self-limiting. Treatment is

SECTION VI - LABORATORY HAZARDS

SOURCES/SPECIMENS: Fecal samples(1,4).

PRIMARY HAZARDS: Ingestion of virus(1), accidental parenteral inoculation,

SPECIAL HAZARDS: None.

SECTION VII - EXPOSURE CONTROLS / PERSONAL PROTECTION

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment,

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve

SECTION VIII - HANDLING AND STORAGE

DISPOSAL: Decontaminate before disposal by steam sterilization,

STORAGE: In locked, leak-proof containers that are appropriately labelled

SECTION IX - REGULATORY AND OTHER INFORMATION

UPDATED: November 2010

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of

Although the information, opinions and recommendations contained in this

Report a problem or mistake on this page  Share this page

Date modified: 2011-04-19

Public Health Agency of Canada

Jobs Culture, history and sport

Immigration and citizenship Policing, justice and emergencies

Travel and tourism Transport and infrastructure

Business Canada and the world

Benefits Money and finance

Health Science and innovation

Taxes Indigenous peoples

Environment and natural resources Veterans and military

National security and defence Youth

Terms and conditions

Canada.ca  Health  Health risks and safety  Biosafety and biosecurity

 Pathogen Safety Data Sheets

Pathogen Safety Data Sheets: Infectious

SECTION I - INFECTIOUS AGENT

SYNONYM OR CROSS REFERENCE: Acute respiratory disease (ARD),

CHARACTERISTICS: Human adenoviruses are members of the family

SECTION II - HAZARD IDENTIFICATION

Childhood febrile illness and pharyngoconjunctival fever – 1, 2, 3, 5, 7

General infections are commonly observed in young children, particularly by

EPIDEMIOLOGY: Adenovirus is of worldwide prevalence, and is ubiquitous

HOST RANGE: Humans.

INFECTIOUS DOSE: Inhalation of as few as 5 adenovirus particles can cause

MODE OF TRANSMISSION: Respiratory and fecal-oral routes. Infection can

COMMUNICABILITY: Children shed non enteric adenovirus in throat and

SECTION III - DISSEMINATION

SECTION IV - STABILITY AND VIABILITY