Pathogens of Vet significance Flashcards
African Swine Fever Virus (ASFV) general info
Tick-borne and contagious, febrile, systemic viral disease of swine.
Stable and will survive over a wide range of pH. The virus will survive for 15 weeks in putrefied blood, three hours at 50ºC, 70 days in blood on wooden boards, 11 days in feces held at room temperature, 18 months in pig blood held at 4ºC, 150 days in boned meat held at 39ºF, and 140 days in salted dried hams.
Initially, domestic and wild pigs (Africa: warthog, bush pig, and giant forest hog; Europe: feral pig) were thought to be the only hosts of ASFV. Subsequently, researchers showed that ASFV replicates in Ornithodoros ticks and that there is transstadial, transovarial, and sexual transmission. ASF in wild pigs in Africa is now believed to cycle between soft ticks living in warthog burrows and newborn warthogs. Ornithodoros ticks collected from Haiti, the Dominican Republic, and southern California have been shown to be capable vectors of ASFV, but in contrast to the African ticks, many of the ticks from California died after being infected with ASFV. Because ASFV-infected ticks can infect pigs, ASFV is the only DNA virus that can qualify as an arbovirus. Even though the soft tick has been shown to be a vector (and in Africa probably the reservoir of ASFV), the primary method of spread from country to country has been through the feeding of uncooked garbage containing ASFV infected pork scraps to pigs. Aerosol transmission is not important in the spread of ASF. Because ASFV does not replicate in epithelial cells, the amount of virus shed by an ASF-infected pig is much less than the amount of virus shed by a hog-cholera-infected pig. The blood of a recently infected pig contains a very high ASFV titer.
African Swine Fever Virus (ASFV) Laboratory Safety and Containment Recommendations
Humans are not susceptible to ASFV infection. The greatest risk of working with the virus is the escape of the organism into a susceptible pig population, which would necessitate USDA emergency procedures to contain and eradicate the disease. ASF is considered a foreign animal disease in the United States. Due to the highly contagious nature of the agent and the severe economic consequences of disease in the United States, this organism should only be handled in vitro in a BSL-3 laboratory with enhancements as required by the USDA and in vivo in a USDA-approved BSL-3-Ag facility for loosely housed animals. Special consideration should be given to infected vector control.
African Horse Sickness Virus (AHSV) General
AHSV is a member of genus Orbivirus in the family Reoviridae. Nine serotypes, numbers 1 – 9, are recognized. AHSV grows readily in embryonated chicken eggs, suckling mice, and a variety of standard cell cultures. AHSV infects and causes viremia in equids. Most horses die from the disease, about half of donkeys and most mules survive, but zebras show no disease. Viremias may last up to one month despite the rapid development of neutralizing antibodies. AHSV may cause disease in dogs, but these are not thought to be important in the natural history of the disease.4,5 AHSV has been recognized in central Africa and periodically spreads to naive populations in South and North Africa, the Iberian Peninsula, the Middle East, Pakistan, Afghanistan, and India. AHSV is vectored by Culicoides species and perhaps by mosquitoes, biting flies, and ticks limiting viral spread to climates and seasons favorable to the vectors. At least one North American Culicoides species transmits AHSV. AHSV may infect carnivores that consume infected animals but these are not thought to be relevant to natural transmission to equids.
African Horse Sickness Virus (AHSV) Occupational Infections
Encephalitis and uveochorioretinitis were observed in four laboratory workers accidentally exposed to freeze-dried modified live vaccine preparations. Although AHSV could not be conclusively linked to disease, all four had neutralizing antibodies. Encephalitis was documented in experimentally infected monkeys.
African Horse Sickness Virus (AHSV) Lab safety and containment
Virus may be present in virtually any sample taken from an infected animal, but the highest concentrations are found in spleen, lung, and lymph nodes. The only documented risk to laboratory workers involves aerosol exposure to large amounts of vaccine virus. AHSV is unusually stable in blood or serum stored at 4°C. AHS is considered a foreign animal disease in the United States. Due to the severe economic consequences of disease presence in the United States, this organism should only be handled in vitro in a BSL-3 laboratory with enhancements as required by the USDA and in vivo in a USDA-approved ABSL-3 animal facility with enhancements. Blood, serum, or tissues taken from equids in areas where AHSV exists are potential means of transmitting the agent long distances. Special consideration should be given to infected vector containment.
Akabane Virus (AKAV) General
AKAV is a member of the genus Orthobunyavirus in the Simbu serogroup of the family Bunyaviridae. The Simbu serogroup also includes Aino, Peaton, and Tinaroo viruses that can cause similar disease. Experimental infection of pregnant hamsters leads to death of the fetus. This virus grows and causes disease in chick embryos. Isolated in suckling mice and hamster lung cell cultures, AKAV is an important cause of disease in ruminants. The virus does not cause overt disease in adults but infects the placenta and fetal tissues in cattle, sheep, and goats to cause abortions, stillbirths, and congenital malformations. The broad range of clinical signs in the fetus is related primarily to central nervous system damage that occurs during the first trimester of pregnancy.6,7 AKAV is not known to infect or cause disease in humans; concern focuses only on effects to agriculture and wildlife. Common names of disease include congenital arthrogryposis-hydranencephaly syndrome, Akabane disease, acorn calves, silly calves, curly lamb disease, curly calf disease, and dummy calf disease. The host range of naturally occurring Akabane disease appears limited to cattle, sheep, swine, and goats but other animals including swine and numerous wildlife species become infected. AKAV is an Old World virus, being found in Africa, Asia, and Australia. Disease is unusual in areas where the virus is common because animals generally become immune before pregnancy. AKAV spreads naturally only in gnat and mosquito insect vectors that become infected after feeding on viremic animals. Although it is virtually certain AKAV will grow and cause disease in New World livestock, it is not known if it will cause viremias in New World wildlife high enough to infect vectors, if it can be vectored by New World insects, or if it will cause disease in New World wildlife. Because fetal disease may not become evident until months after virus transmission, an introduction into a new ecosystem may not be recognized before the virus has become firmly entrenched.
Akabane Virus (AKAV) Laboratory Safety and Containment Recommendations
Present in blood, sera, and tissues from infected animals, as well as vectors from endemic regions.
Parenteral injection of these materials into naive animals and vector-borne spread to other animals represents a significant risk to agricultural interests.
Foreign animal disease in the United States.
In vitro in a BSL-3 laboratory with enhancements and in vivo in a USDA-approved ABSL-3 animal facility with enhancements. Special consideration should be given to infected vector containment.
Bluetongue Virus (BTV) General
BTV is a member of the family Reoviridae, genus Orbivirus. There are 24 recognized serotypes numbered 1 through 24. BTV is notable for causing disease in sheep and cattle and is very similar to other orbiviruses that cause disease in deer (epizootic hemorrhagic disease of deer virus) and horses (AHSV), and a few that cause disease in man (Colorado tick fever virus and others). These viruses have dsRNA genomes distributed amongst 10 segments, enabling efficient reassortment. Growth on a wide variety of cultured cells is usually cytocidal. Growth in animals results in viremia within three to four days that endures as long as 50 days despite the presence of high levels of neutralizing antibodies.8,9 BTV infects all ruminants, but bluetongue disease is unusual except in sheep and is unpredictable even in sheep. Disease is evidenced by fever, hyperemia, swelling, and rarely erosions and ulceration of the buccal and nasal mucosa. Hyperemia of the coronary bands of the hooves may cause lameness. In the worst cases, the disease progresses through weakness, depression, rapid weight loss, prostration, and death. Maternal transmission to the fetus may cause abortion or fetal abnormalities in the first trimester. Bluetongue disease also occurs in cattle but is rarely diagnosed. BTV may infect fetal calves and result in abortion or fetal brain damage. The full host range of BTV is still unknown but includes wild ruminants, neonatal mice, dogs, and chicken embryos. BTV infection occurs in tropical, subtropical, and temperate climates where the Culicoides vectors exist. Global warming may be expanding the geographic range of Culicoides, and therefore BTV, into higher latitudes. Most countries have a unique assortment of the 24 serotypes. For example, BTV serotypes 2, 10, 11, 13, and 17 are currently active in the United States, but serotypes 1, 3, 4, 6, 8, 12, and 17 were present in the Caribbean basin when last surveyed. Concern over the spread of individual serotypes by trade in animals and animal products has engendered costly worldwide trade barriers. The primary natural mode of transmission is by Culicoides midges. Only a few of more than 1,000 species of Culicoides transmit BTV. A strong correlation between the vector species and the associated BTV suggests these viruses may have adapted to their local vector. Thus, BTV does not exist in areas such as the Northeast United States where the local Culicoides fails to transmit BTV. Virus is present in semen at peak of viremia, but this is not considered a major route of transmission. Because of the prolonged viremia, iatrogenic transmission is possible. Only modified-live (attenuated) virus vaccines are available and a vaccine for only one serotype is currently available in the United States.
Bluetongue Virus (BTV) Laboratory Safety and Containment Recommendations
BTV is not known to cause disease in humans under any conditions.
BTV commonly enters the laboratory in blood samples. The virus is stable at -70°C and in blood or washed blood cells held at 4°C. Sera prepared from viremic animals may represent some risk if introduced parenterally into naive animals. Blood, sera, and bovine semen can carry BTV across disease control boundaries. The most significant threat from BTV occurs when virus is inoculated parenterally into naive animals. If appropriate Culicoides are present, virus can be transmitted to other hosts. Therefore, BTV-infected animals must be controlled for the two-month period of viremia and protected against Culicoides by physical means and/ or performing experiments at least two months before local Culicoides emerge. Thus, BTV exotic to the United States should only be handled in vitro in a BSL-3 laboratory with enhancements as required by the USDA and in vivo in a USDA-approved ABSL-3 with enhancements.
Special consideration should be given to infected vector containment.
Special containment is only needed when working with serotypes of BTV that are exotic to the country or locality.
Susceptible to 95% ethanol and 0.5% sodium hypochlorite solution.
Classical Swine Fever Virus (Hog Cholera) General
Classical swine fever is a highly contagious viral disease of swine that occurs worldwide in an acute, a subacute, a chronic, or a persistent form.10-12 In the acute form, the disease is characterized by high fever, severe depression, multiple superficial and internal hemorrhages, and high morbidity and mortality. In the chronic form, the signs of depression, anorexia, and fever are less severe than in the acute form, and recovery is occasionally seen in mature animals. Transplacental infection with viral strains of low virulence often results in persistently infected piglets, which constitute a major cause of virus dissemination to noninfected farms. Although minor antigenic variants of classical swine fever virus (CSFV) have been reported, there is only one serotype. Hog cholera virus is a lipid-enveloped pathogen belonging to the family Flaviviridae, genus Pestivirus. The organism has a close antigenic relationship with the bovine viral diarrhea virus (BVDV) and the border disease virus (BDV). In a protein-rich environment, hog cholera virus is very stable and can survive for months in refrigerated meat and for years in frozen meat. The virus is sensitive to drying (desiccation) and is rapidly inactivated by a pH of less than 3 and greater than 11. The pig is the only natural reservoir of CSFV. Blood, tissues, secretions and excretions from an infected animal contain virus. Transmission occurs mostly by the oral route, though infection can occur through the conjunctiva, mucous membrane, skin abrasion, insemination, and percutaneous blood transfer (e.g., common needle, contaminated instruments). Airborne transmission is not thought to be important in the epizootiology of classical swine fever. Introduction of infected pigs is the principal source of infection in classical swine fever-free herds. Farming activities such as auction sales, livestock shows, visits by feed dealers, and rendering trucks also are potential sources of contagion. Feeding of raw or insufficiently cooked garbage is a potent source of hog cholera virus. During the warm season, insect vectors common to the farm environment may spread hog cholera virus mechanically. There is no evidence, however, that hog cholera virus replicates in invertebrate vectors.
Classical Swine Fever Virus (Hog Cholera) Laboratory Safety and Containment Recommendations
Humans being are not susceptible to infection by CSFV. The greatest risk of working with these viruses is the escape of the organism into susceptible domestic or feral pig populations, which would necessitate USDA emergency procedures to contain and eradicate the diseases. The virus is considered cause of a foreign animal disease in the United States. Due to the highly contagious nature of the agent and the severe economic consequences of disease presence in the United States, this organism should only be handled in vitro in a BSL-3 laboratory with enhancements as required by the USDA and in vivo in a USDA-approved BSL-3-Ag facility for loosely housed animals. Laboratory workers should have no contact with susceptible hosts for five days after working with the agent.
Contagious Bovine Pleuropneumonia Agent (CBPP) General info
CBPP is a highly infectious acute, subacute, or chronic disease, primarily of cattle, affecting the lungs and occasionally the joints, caused by Mycoplasma mycoides. Contagious bovine pleuropneumonia is caused by M. mycoides mycoides small-colony type (SC type). M. mycoides mycoides large-colony type is pathogenic for sheep and goats but not for cattle. M. mycoides mycoides (SC type) survives well only in vivo and is quickly inactivated when exposed to normal external environmental conditions. The pathogen does not survive in meat or meat products and does not survive outside the animal in nature for more than a few days. Many of the routinely used disinfectants will effectively inactivate the organism.
CBPP is predominantly a disease of the genus Bos; both bovine and zebu cattle are naturally infected. There are many reported breed differences with respect to susceptibility. In general, European breeds tend to be more susceptible than indigenous African breeds. In zoos the infection has been recorded in bison and yak. Although it has been reported that the domestic buffalo (Bubalus bubalis) is susceptible, the disease is difficult to produce experimentally in this species.
CBPP is endemic in most of Africa. It is a problem in parts of Asia, especially India and China. Periodically, CBPP occurs in Europe, and outbreaks within the last decade have occurred in Spain, Portugal, and Italy. The disease was eradicated from the United States in the nineteenth century, and it is not present currently in the Western hemisphere.
CBPP is spread by inhalation of droplets from an infected, coughing animal. Consequently, relatively close contact is required for transmission to occur. Outbreaks usually begin as the result of movement of an infected animal into a naive herd. There are limited anecdotal reports of fomite transmission, but fomites are not generally thought to be a problem.
Contagious Bovine Pleuropneumonia Agent (CBPP) Lab Safety
Humans are not susceptible to infection by CBPP. The greatest risk of working with these mycoplasma is the escape of the organism into susceptible domestic bovine populations, which would necessitate USDA emergency procedures to contain and eradicate the diseases.
Contagious Caprine Pleuropneumonia Agent (CCPP) General
CCPP is an acute highly contagious disease of goats caused by a mycoplasma and characterized by fever, coughing, severe respiratory distress, and high mortality. The principal lesion at necropsy is fibrinous pleuropneumonia. The causative agent of CCPP is considered to be M. mycoides capri (type strain PG-3) or a new mycoplasma M. capricolum subsp. capripneumoniae (designated F-38). Neither of these agents occurs in North America.
M. mycoides mycoides has also been isolated from goats with pneumonia. This agent (the so-called large colony or LC variant of M. mycoides mycoides) usually produces septicemia, polyarthritis, mastitis, encephalitis, conjunctivitis, hepatitis, or pneumonia in goats. Some strains of this agent (LC variant) will cause pneumonia closely resembling CCPP, but the agent is not highly contagious and is not considered to cause CCPP. It does occur in North America. M. capricolum capricolum, a goat pathogen commonly associated with mastitis and polyarthritis in goats, can also produce pneumonia resembling CCPP, but it usually causes severe septicemia and polyarthritis. This agent (which does occur in the United States) is closely related to mycoplasma F-38 but can be differentiated from it using monoclonal antibodies.
CCPP is a disease of goats, and where the classical disease has been described, only goats were involved in spite of the presence of sheep and cattle. Mycoplasma F-38, the probable cause of the classic disease, does not cause disease in sheep or cattle. M. mycoides capri, the other agent considered a cause of CCPP, will result in a fatal disease in experimentally inoculated sheep and can spread from goats to sheep. It is however, not recognized as a cause of natural disease in sheep.
CCPP has been described in many countries of Africa, the Middle East, Eastern Europe, the former Soviet Union, and the Far East. It is a major scourge in many of the most important goat-producing countries in the world and is considered by many to be the world’s most devastating goat disease.
CCPP is transmitted by direct contact through inhalation of infective aerosols. Of the two known causative agents, F-38 is far more contagious. Outbreaks of the disease often occur after heavy rains (e.g., after the monsoons in India) and after cold spells. This is probably because recovered carrier animals start shedding the mycoplasmas after the stress of sudden climatic change. It is believed that a long-term carrier state may exist.
Contagious Caprine Pleuropneumonia Agent (CCPP)- Lab Safety
Humans are not susceptible to infection by the agent that causes CCPP. The greatest risk of working with this mycoplasma is the escape of the organism into susceptible domestic caprine populations, which would necessitate USDA emergency procedures to contain and eradicate the diseases.
Foot and Mouth Disease Virus (FMD) General
FMD is a severe, highly communicable viral disease of cloven-hoofed animals (cattle, swine, sheep, and goats), causing fever, malaise, vesicular lesions in affected livestock and in some cases death in young animals due to myocardial lesions.22 It can also affect a variety of wild ruminants (e.g., deer, bison). FMD is one of the most devastating diseases of livestock, causing large economic losses when introduced to FMD-free countries. The etiologic agent, FMD virus (FMDV), is a member of the aphtovirus genus, family picornaviridae with seven serotypes (A, O, C, Asia1, SAT1, SAT2 and SAT3).23 Humans are considered accidental hosts for FMDV and rarely become infected or develop clinical disease. Historically, humans have been exposed to large quantities of FMDV both during natural outbreaks among large herds of animals and in laboratory settings. Despite this, there has been an extremely low incidence of human infections reported and many have been anecdotal. Reports of fever, headaches and vesicles in the skin (especially at an accidental inoculation site) and oral mucosa have been associated with documented FMDV infections. The symptoms can be easily mistaken with those of Hand, Foot and Mouth Disease caused by coxsackie A viruses. On the other hand, humans have been shown to carry virus in their throats for up to three days after exposure to aerosols from infected animals, potentially making them carriers of FMDV. Humans and their clothing and footwear have been implicated as fomites for transmission of FMDV during outbreaks. Therefore, most FMDV laboratories impose a five day period of contact avoidance with susceptible species for personnel working with the viruses.
