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Pathogen Safety Data Sheet - African Horse Sickness


SECTION I: DISEASE / INFECTIOUS AGENT

SYNONYM / CROSS REFERENCE: Perdesiekte, Pestis Equorum, la Peste Equina, AHS (1).

ETIOLOGY / TAXONOMY:
Family: Reoviridae (2, 3)
Genus: Orbivirus (2, 3)

ORGANISM CHARACTERISTICS:

  • There are nine serotypes of AHS: serotype 1-8 are all highly pathogenic for horses and cause 90-95% of mortality but serotype 9 is slightly less pathogenic resulting in mortality rates of about 70% (3, 4).
  • The non-enveloped virus has seven structural proteins (VP1-7) organized in a two layered capsid (5, 6).
  • The genome, which is located within the core of the virus, consists of 10 double-stranded RNA segments of different sizes, three large, designated L1-L3, three medium, M4-M6, and four small, S7-S10 (5, 6).

SURVEILLANCE:

  • African Horse Sickness is a reportable disease in Canada. Animal owners, veterinarians and laboratories are required to immediately report the presence of an animal that is infected or suspected of being infected to a CFIA district veterinarian. Control or eradication measures will be applied immediately(http://laws.justice.gc.ca/en/H-3.3/fulltoc.html).

DISTRIBUTION:

  • The status of AHS in Canada is non-indigenous.
  • AHS occurs endemically in all parts of Africa south of the Sahara, with periodic spread further north. It has occurred in Egypt and the Middle East, extending to Pakistan and India in the early 1960s. Spread also occasionally occurs from North Africa to the Iberian peninsula (2, 3).
  • This distribution is primarily dictated by the presence of the principal insect vector, Culicoides spp (3).
  • Outbreaks in Botswana, Lesotho, South Africa, Zambia and Zimbabwe were confirmed between March and October 2004 (7).
  • Most recent outbreaks were in South Africa (May 2006) and Swaziland (January 2006) (7).

SECTION II: ANIMAL HEALTH HAZARD AND EPIDEMIOLOGY

CLINICAL DISEASE / PATHOGENESIS:
1) Clinical signs:

‘Pulmonary’ or peracute form (3):

  • This form is characterized by a short clinical course, fever 40°-41° C, severe respiratory distress and high mortality (up to 95%) (1).
  • Progressive, severe respiratory distress involves increased breathing rate, with the animal adopting a wide based stance, neck extended, nostrils dilated, forced expiration, profuse sweating, and sudden death.
  • Paroxysmal coughing develops, which becomes more frequent and severe as the disease progresses.
  • There are signs of abdominal pain and restlessness
  • Frothy white, sometimes blood-tinged, foam may flow from the nostrils of the moribund animal for several hours before death.
  • Death occurs 4-24 hours following onset of signs and is due to drowning in own exudate (1).

‘Cardiac, edematous’ or subacute form (3):

  • The first clinical sign is fever of 39-41°C persisting for 3-6 days. This form leads to mortality in 50%-70% of cases (1).
  • The longer clinical course is marked by fever and edematous swellings developing along the facial planes of muscles, particularly of the head and neck. Swelling of the area above the eye, the eyelids, lips and tongue and even the brisket, thorax and ventral abdomen is also seen, but generally not of the legs (important in differential diagnosis).
  • Bouts of abdominal discomfort, colic and rolling occur because of compromised blood supply and oxygen deficiency of the digestive tract.
  • Death may occur 4-8 days after onset of signs (1) .
  • Edema subsides in 3-8 days in animals that recover.

‘Horse sickness fever’ or mild form (3):

  • This mildest form of AHS is frequently subclinical and therefore easily overlooked in natural outbreaks (1).
  • Symptoms are similar to influenza and a transient fever up to 40°C can occur for 2-3 days.

2) infectious dose: unknown

3) incubation period:
‘Pulmonary’ or peracute form (3):

  • 3-5 days and onset of disease is marked by depression and high temperature (up to 42°C)

‘Cardiac, edematous’ or subacute form (3):

  • 7-21 days

‘Horse sickness fever’ or mild form (3):

  • variable period of 4-14 days

SOURCE / MODE OF TRANSMISSION / COMMUNICABILITY:

  • It is transmitted between susceptible animals by blood-sucking insects (biting midges of the family Culicoides).
  • It is not spread by aerosol or direct contact between infected and non-infected animals (3, 8).
  • There may be wind-borne spread of infected vectors (8).
  • Virus replication occurs mainly in the lungs, spleen and lymph nodes. The average duration of viremia after natural infection in theses species is about 4-8 days and rarely as long as 18 days (3).
  • Although virus is present in urine, milk and other body secretions of infected animals, no transmission of disease by contact, inhalation or ingestion of these materials is known (3).

VECTORS:

  • Biting midges of the family Culicoides imicola are the most significant vector (1, 3, 8).
  • Midges are able to transmit infection to other horses 7-13 days after feeding on an infected horse (3).
  • Experimentally, three species of mosquitoes, the brown dog tick and the camel tick have transmitted the virus (8).

HOST RANGE: (1, 2, 3)

  • Horses experience severest disease and highest mortality rates (3)
  • Mules
  • Donkeys
  • Zebras may be a long-term carrier - this has not been substantiated (3).
  • Camels have inapparent infections
  • Dogs

ZOONOTIC POTENTIAL:

  • African Horse Sickness virus cannot be transmitted to humans (8).

RESERVOIR: not known

Section III: DIAGNOSIS

NECROPSY / HISTOPATHOLOGY FINDINGS:

  • Respiratory form: edema of the lungs, hydropericardium hydrothorax, pleural effusion, edema of thoracic lymph nodes, petechial hemorrhages in pericardium, in mucosa of the small and large intestine, spleen, renal cortex (4).
  • Cardiac form: subcutaneous and intramuscular yellow gelatinous edema, hydropericardium, epicardial and endocardial ecchymosis, myocarditis, hemorrhagic gastritis (4).
  • Mixed form: lesions represent combination of those found in both the pulmonary and cardiac forms.

SAMPLE SUBMISSION:

  • Whole blood
  • Serum
  • Fixed and fresh tissues

All samples should be transported at 4°C.

For more information regarding the type of samples necessary for AHS diagnosis, please contact the National Centre for Foreign Animal Disease:

Diagnostic Co-ordinator
National Centre for Foreign Animal Disease
1015 Arlington Street
Winnipeg, Manitoba R3E 3M4
Telephone : ( 204 ) 789 - 2012
Fax: ( 204 ) 789 - 2038
Associate Diagnostic Co-ordinator
National Centre for Foreign Animal Disease
1015 Arlington Street
Winnipeg, Manitoba R3E 3M4
Telephone: ( 204 ) 789 - 2113
Fax: ( 204 ) 789 - 2143

LABORATORY DIAGNOSIS (3):

  • PCR
  • virus neutralization (serotyping)
  • ELISA
  • immunoblotting
  • virus isolation.
  • complement fixation (CF)- limited use.
  • hemagglutination inhibition

DRUG SUSCEPTIBILITY:

  • No treatment is available for animals.
  • One of the main measures used to control the 1987-90 outbreaks in Spain was a vaccination program for all susceptible equines in the outbreak area, using attenuated monovalent serotype AHS-4 vaccine (3).
  • The first inactivated AHS virus vaccines were prepared by adding formalin to infected horse tissue emulsion and have been used experimentally since 1929. More recently, this technique has been superseded by production of inactivated AHS virus vaccines using purified formalin-treated virus prepared in cell culture on an industrial scale (3).

DIFFERENTIAL DIAGNOSIS:
The following diseases may show clinical similarity to AHS:
Sudden Death:

  • Adverse drug reaction
  • Acute fulminating colitis
  • Snake bite
  • Pneumothorax
  • Toxic plants and chemicals
  • Endotoxemia
  • Monensin toxicity
  • Anthrax
  • Equine encephalosis

Peripheral edema:

  • Lymphatic obstruction
  • Trauma
  • Cellulitis
  • Parasitium
  • Vasculitis
  • Purpura haemorrhagica
  • Protein losing enteropathy
  • Phenylbutazone (PBZ) toxicity
  • Renal or heart failure
  • Equine viral arteritis
  • Equine infectious anaemia
  • Equine babesiosis

Respiratory distress:

  • Anaphylaxis
  • Pneumonia/pleuropneumonia
  • Choking
  • Tumor of respiratory tract

SECTION IV: DECONTAMINATION PROCEDURES

Select a registered disinfectant with a drug identification number (DIN). Use according to label directions for concentration and contact time. Consider organic load and temperature. It is recommended that laboratories evaluate the effectiveness of the disinfectant using a validated method (e.g. Quantitative Carrier Test). See table 1 to help select a registered disinfectant for use against AHS virus.

Table 1 : Active ingredients considered to be effective against AHS virus

ACTIVE INGREDIENT CONCENTRATION CONTACT TIME
Soaps and detergents:
(solids or liquids)
As appropriate 10 minutes (8)
Oxidising agents:
Sodium Hypochlorite
Calcium Hypochlorite
20,000-30,000 ppm (2-3%) 10-30 minutes (8)
Alkalis:
Sodium Hydroxide
2% (w/v) 10 minutes (8)
Acids:
Hydrochloric acids
Citric acid
2% (v/v)

0.2% (w/v)

10 minutes (8)

30 minutes (8)

Aldehydes:
Glutaraldehyde
2% (w/v) 10-30 minutes (8)

PHYSICAL INACTIVATION:

  • AHS virus is sensitive to autoclaving at 121°C for 15 minutes.
  • Optimal pH for survival is 6.5-8.5 (1, 8).
  • 99% of the AHS virus infectivity is inactivated within 15 minutes when pH is below 5.6 and above 10.9 (9).

SURVIVAL OUTSIDE OF HOST:

  • The AHS virus is very stable outside the host (3, 8).
  • Optimal pH for survival is 7.0-8.5; the virus is sensitive to acid pH values but is relatively resistant to alkaline pH conditions.
  • It is resistant to ether and other lipid solvents.
  • The virus is relatively heat stable and not inactivated by heating at 55-75°C for 10 minutes in presence of protein
  • It can be stored for at least six months at 4°C in saline containing 10% serum
  • It is not destroyed by putrefaction and may retain infectivity in putrid blood for more than 2 years. Virus can be recovered for 12 months from washed erythrocytes stored at 4°C.
  • Lyophilization may preserve infectivity for 40 years (1).

SECTION V: LABORATORY HAZARDS FOR HUMANS

LABORATORY-ACQUIRED INFECTIONS:
Four cases were reported over a period of 8 years at the vaccine -packing section of a veterinary research institute at Ondersterpoort in South Africa (10). Screening tests revealed antibody activity in the sera of 4 patients with cases of encephalitis and chorioretinitis, which suggests an infection with African horse sickness (AHS) virus. It is believed that the patients may have acquired aerosol infection with AHS virus as a results of accidental breakage of freeze-dried vaccine bottles. It must be stressed that the infection described above occurred under particular circumstances and that there is no evidence suggesting that AHS virus should ordinarily be considered a human pathogen (10).

BIOSAFETY PRECAUTIONS : none

SECTION VI: PHYSICAL AND OPERATIONAL REQUIREMENTS

CONTAINMENT REQUIREMENTS:
All physical containment and operational practices for containment level 3, non-indigenous agents, as per the Containment Standards for Veterinary Facilities must be met. The Standards can be accessed at : http://www.inspection.gc.ca/english/sci/lab/convet/convete.shtml

PROTECTIVE CLOTHING:
Laboratory:

  • Primary layer of protective clothing should include dedicated laboratory clothing (e.g. scrubs and headwear) and laboratory dedicated footwear.
  • Secondary layer of protective clothing (e.g. solid-front gowns with tight-fitting wrists, 2 pairs of gloves) should be worn over laboratory clothing when directly handling infectious materials.
  • A risk assessment should be conducted to determine if a respiratory protection is required when directly handling infectious material outside BSC.
  • A shower is required on exit.

Post Mortem:

  • Primary layer of protective clothing should include dedicated laboratory clothing (e.g. scrubs and headwear) and laboratory dedicated footwear.
  • Secondary layer of protective clothing (e.g. solid-front gowns with tight-fitting wrists, 2 pairs of gloves) should be worn over laboratory clothing when directly handling infectious materials.
  • Cut resistant gloves, adequate respiratory protection, steel toed/steel shanked rubber boots should also be worn when handling infectious materials.
  • A shower is required on exit.

HANDLING INFORMATION :
Spills in laboratory:

Spill protocol must be in place and include the following scenarios:

  • spills inside the Biological Safety Cabinet (BSC)
  • spills outside the BSC
  • spills while performing aerosol generating procedures
  • Consider entry and exit procedure modifications if necessary, appropriate PPE, disinfection of spill and surroundings including contact time, flow (pattern) of the clean up and disposal of contaminated materials.

Refer to Table 1 for disinfectant selection.

STORAGE: All cultures and infected material should be stored in leakproof, sealed containers that are accurately labeled and clearly identified as a biohazard risk. The access to infectious material should be controlled at all times. Records must be kept to describe the use, inventory and disposal of infectious material.

DISPOSAL: Decontaminate all infectious material prior to disposal. Use steam sterilization, incineration or chemical disinfection.

REFERENCES:

  1. Committee on Foreign Animal Diseases of the United States Animal Health Associatio. Foreign Animal Diseases. Revised 1998, Library of Congress Catalog Card Number, 17-12842, Pages 41-51.
  2. Radostits, O.M. Gay, C.C. Blood, D.C. & K.W. Hinchcliff. Veterinary Medecine, A Textbook of the Disease of Cattle, Sheep, Pigs, Goats and Horses. Ninth Edition. W.B. Saunders Company Ltd. 2000. Pages 1038-1039.
  3. Australian Veterinary Emergency plan, 1996, Disease Strategy, African Horse Sickness: http://www.aahc.com.au/ausvetplan/ahsfinal.pdf
  4. OIE, Animal Disease Data: http://www.oie.int/eng/maladies/fiches/a_A110.htm
  5. Roy P, Mertens PP, Casal I, African horse sickness virus structure. Comp Immunol Microbiol Infect Dis. 1994 Aug-Nov; 17(3-4):243-73.
  6. Roy P, Orbivirus Structure and Assembly, Virology 216, 1-11 (1996).
  7. OIE, Disease Information: http://www.oie.int/eng/info/hebdo/a_dsum.htm
  8. Australian Veterinary Emergency Plan. Operational Procedures Manual: Decontamination. 2000.
  9. Parker J, Inactivation of African horse-sickness virus by betapropiolactone and by pH . Arch Virol. 1975;47(4):357-65.
  10. Swanepoel R, Erasmus BJ, Williams R, Taylor MB. Encephalitis and chorioretinitis associated with neurotropic African horse sickness virus infection in laboratory workers. S Afr Med J. 1992 May 2;81(9):458-61.

LAST UPDATED (DATE): March 29, 2005
PREPARED BY: The Biohazard Containment and Safety Unit, CFIA

Disclaimer: Although the information and recommendations in this Pathogen Safety Data Sheet are compiled from reliable sources, there is no guarantee, warranty or any assurance that the information and recommendations are correct, accurate, sufficient, reliable or current and the Canadian Food Inspection Agency shall not be responsible for any loss or damage resulting from or in connection with the use of or reliance upon the information and recommendations.

The user assumes all risks and responsibility for and shall be liable for the use of and any reliance on the information and recommendations and the results thereof and any loss or damage resulting therefrom.