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222 Cards in this Set
- Front
- Back
What are the tools for prevention, control, eradication of zoonotic diseases?
|
minimize contact with infected
vaccination sanitation and hygiene test and remove infected vector control import/export restrictions |
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What are everyday issues for the veterinary profession in regards to public health?
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impact of animals on the environment
food safety zoonotic diseases occupational hazards |
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What is the definition of a zoonotic disease?
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those diseases and infections that are naturally transmitted between vertebrate animals and man with or without an arthropod intermediate
|
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What are emerging diseases?
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1. those that have not previously occurred in humans
2. those that are now seen beyond previous boundaries 3. those that have occurred over history but only recently as a distinct disease |
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What factors promote emerging diseases?
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- increased human population (increased human/animal interaction)
- transportation of man and animals into new areas - changes in environment and husbandry - increasing immuno-compromised populations - better disease recognition - discovery of previously unrecognized organisms - xenotransplantation - bioterrorism |
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What are the three categories of bioterrorist agents?
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Category A- highest risk to nation's population
Category B- moderate risk Category C- emerging pathogens that could be engineered |
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What are re-emerging diseases?
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diseases that were major health problems, went through a period of decline, but now have increase in prevallence
|
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What are the requirements to be a category A agent of bioterrorism?
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easily disseminated and or transmitted from person to person
high mortality rates and potential for health impact may cause panic requires special action in preparedness |
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What agents are currently category A agents in bioterrorism?
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anthrax
botulism plague smallpox tularemia viral hemorrhagic fevers |
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What are the requirements to be a category B agent of bioterrorism?
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moderate risk
moderately easy to disseminate cause moderate morbidity and low mortality require specific enhancements of diagnostic capabilities and surveillance |
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What are the current category B agents of bioterrorism?
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brucella species
clostridium perfringens salmonella, E. coli, shigella Glanders Meliodiosis Psittacosis Q-fever |
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What are the requirements for a category C agent of bioterrorism?
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could be engineered in the future because of:
availability ease of production and dissemination potential for high morbidity and mortality |
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What agents are currently category C bioterrorism agents?
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nipah virus
hantavirus tick-borne hemorrhagic fevers tick-borne encephalitis viruses yellow fever multi-drug resistant tuberculosis |
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What areas does the veterinary profession contribute to public health protection?
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food safety and security
protecting environmental health bioterrorism prevention of infectious diseases contributing to medical science |
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How does the veterinarian contribute to public health protection?
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zoonotic disease and animal bite prevention
early detection of unusual diseases disease surveillance animal health emergency readiness surge capacity for human response client education risk communication |
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What is the plague?
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an infectious disease of animals and humans caused by yersinia pestis
|
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When was the last plague epidemic in the US?
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1924-1925 in Los Angeles
|
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How many plague cases are reported per year by WHO?
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1000-3000 human cases
|
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Where are plague infections currently seen in the US?
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small rodents and their predators in the western states in rural settings
|
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What is the causative agent of plague?
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yersinia pestis
primarily rodent pathogen survivors become carriers facultative anaerobic, intracellular gram-negative bacillus easy to culture survives poorly in environment |
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What is the epidemiology of rodent exposure to plague?
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fleas bite an infected rodent and ingest the bacillus
bacillus multiplies in esophagus and foregut so when flea bites gain it expels bacteria into the new host |
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What is the primary vector of rodent plague?
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Xenopsylla cheopis- the oriental rat flea
|
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What is the epidemiology of human exposure to plague?
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flea-borne when infected flea bites a human
direct contact- handling sick or dead animals air-borne by respiratory droplets from infected cats or humans Human exposure increases following epizootics in rodents |
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What species causes the most human exposures to plague?
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the rock squirrel
|
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What carnivore is responsible for the most human exposures to the plague?
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domestic cats
|
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What is the sylvatic cycle of plague?
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the plague is circulating in wild rodents like prarie dogs, man enters the rodents' domain
sporadic outbreaks are associated with wild rodent fleas |
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What is the Urban cycle of plague?
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plague is circulating in rats living in proximity to man
Pandemics and epidemics are associated with urban cycle and the rat flea |
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Sporadic outbreaks of plague are associated with...
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the sylvatic cycle in wild rodents
|
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Pandemics and epidemics of plague are associated with....
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the urban cycle of plague
|
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What are the clinical signs of feline plague?
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high fever (106)
lethargy lymphadenitis abscess secondary pneumonia >50% mortality |
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What are the 3 forms of human plague?
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bubonic- lymph node
septicemic- throughout body pneumonic- lung |
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What parts of the body are associated with bubonic plague and what are the symptoms?
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regional lymph nodes
incubation of 2-6 days swollen, painful lymph node |
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What is the primary site of septicemic plague and what are the clinical signs?
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bacilli spread through the body from lymph node or directly from flea bite
internal organs including lungs are involved thrombosis in extremities leading to gangrene (black plague) |
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What is the primary site of infection for pneumonic plague and what are the clinical signs?
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lungs
primary if through aerosol route, secondary if extension of septicemia poor prognosis >50% mortality incubation 1-3 days high fever, chills, cough, bloody sputum can infect others via aerosol nearly all human cases in past 85 yrs in US associated with cats with "pneumonia" |
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What are the important factors in plague prevention and control?
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environmental management (fleas and rats)
public health education preventative drug therapy |
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What are appropriate preventative measures for the plague?
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avoid areas known to harbor infected hosts
use insecticides to kill fleas eliminate food and shelter for rodents report sick and dead rodents to local health dept treat pets for fleas once per week |
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When are preventative antibiotics indicated for the plague?
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if exposed to:
wild rodent fleas during an outbreak tissues or fluids of infected animals person or pet with pneumonic plague |
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What is cat scratch disease?
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a condition characterized by swollen regional lymph nodes in people following cat scratches
|
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What is the agent that causes cat scratch disease?
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bartonella henselae, a rickettsia
gram-negative, pleomorphic very slow growing and sensitive to antibiotics |
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What cats have the highest likelihood of being bacteremic with bartonella henselae?
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cats <1 yr old
with fleas with high titers |
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What is the progress of cat scratch disease in cats?
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self-limiting infection causes febrile illness for 2-3 days followed by a chronic, asymptomatic bacteremia in younger cats lasting 2 months and as much as several years in others
|
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How is bartonella henselae transmitted among cats?
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by the cat flea and by the IV and IM inoculation of blood
|
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What describes the typical cat scratch disease human patient?
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male
<21 years old seasonally between Sept-March |
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What is the course of cat-scratch disease in humans?
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small skin lesion 3-10 days following bite or scratch
regional lymph nodes become swollen and painful in 1-2 weeks typically resolves itself without treatment in 2-5 months in healthy people but some enlarged lymph nodes persist for 2 years |
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What are possible complications of cat-scratch disease in immunocompromised humans?
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persistent or relapsing fever
anorexia and weight loss bacillary angiomatosis, bacillary peliosis hepatitis ophthalmic manifestation- Parinaud Ocular Glandular Syndrome |
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How should you prevent and control cat scratch disease?
|
1. minimize opportunity for scratches and bites
2. promptly clean wounds 3. control fleas on cats 4. pets of immuno-compromised should be sero-negative 5. antibiotic treatment of bacteremic cats may not clear infection |
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What is the etiological agent of murine typhus?
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reckettsia typhi
gram-negative obligate intracellular bacterium survives well in the environment |
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What is the distribution of murine typhus?
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endemic regions on all continents except antarctica
|
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Where are the most case reports of murine typhus?
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Hawaii, Texas gulf-coast, and southern California
|
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What are the primary reservoir of murine typhus?
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rats- primary reservoir and host while remaining asymptomatic
|
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What is the significance of murine typhus?
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it is second only to malaria as a cause of febrile illness in US troops in vietnam
|
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What is the vector of murine typhus?
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fleas- Xenopsylla cheopis (rat flea)
becomes infected when feeding on infected rats not harmful to flea, but flea infected for life with fecal shedding |
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How does man become infected with murine typhus?
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when infected fleas deposit contaminated feces while feeding. scratching in response to the bite allows entry of the bacteria
|
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When and where are most murine typhus cases reported?
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highest incidence in the summer and most cases from southern states
nearly all associated with large rat populations in urban areas |
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What are the clinical signs of murine typhus in humans?
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incubation of 1-2 weeks
fever, chills, malaise, headache, joint pain, loss of appetite |
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How do you treat humans with murine typhus?
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tetracyclines and doxycycline
|
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How should you prevent and control murine typhus?
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1. reduce the flea population with residual insecticides
2. reduce commensal rat populations 3. education of the public |
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What is a definitive host?
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parasite reaches sexual maturity
|
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What is an intermediate host?
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it is required for parasite maturation, does not reach sexual maturity here
|
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What is a paratenic host?
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not required for parasite maturation
|
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What is a transport host?
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paratenic host that moves the nematode around and protects it
|
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What is a direct life cycle in terms of parasitic infection?
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infects another definitive host directly- can use paratenic hosts but they are not required
|
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What is an indirect life cycle in terms of parasitic infection?
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required to pass through an intermediate host to become infective
|
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What is an example of a direct life cycle not involving paratenic hosts?
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fecal-oral transmission
|
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What is fecal-oral transmission of parasites?
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eggs pass into the environment and are directly ingested by the direct host
the parasite egg or oocyst must survive environmental conditions |
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What does a parasite gain from a paratenic host?
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homeostasis with regards to ambient temperature and humidity
transport leading to ingestion up the food chain into another area |
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How does Toxacara use a paratenic host?
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dog defecates toxacara eggs
earthworm or insect ingests soil with eggs, slugs, snails rodent/bird eats the earthworm dog eats rodent or insect and becomes infected with toxacara |
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What is the process of an indirect life cycle in parasites?
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mature parasite in DH passes eggs that infect the IH, DH becomes infected by the IH, parasite matures in the DH
|
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What is the purpose of the organ that a parasite attachks?
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infection in the eyes, CNS, muscles can increase the chance of predation, meaning transmission for the parasite
|
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How is toxacara canis transmitted?
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transplacental transmission
transmammary transmission direct paratenic host |
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What is the most common way toxacara canis is transmitted?
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transplacental transmission 98%
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What do toxacara eggs look like?
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symmetrical, cell wall with uniform thickness, organized inside
|
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What is the benefit of cortication of toxacara eggs?
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thick outer coating allows eggs to stick in one place, protects, insulates
|
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What are paratenic hosts used in toxacara?
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earthworms, snails (least likely), slugs, insects
rodents, birds consume and are consumed |
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What percentage of puppies are born with in utero exposure to toxacara?
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98%
|
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When are toxacara eggs shed by puppies?
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early as 21 days postpartum, peak by 3 mo (b/c of immunity), decline with age of dog
|
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How many eggs can one female toxacara canis produce each day?
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>200,000
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How long can toxacara eggs remain viable in the environment?
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>10 years
|
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How do kids get infected with toxacara?
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playing in soil where infective eggs are located
usually back yards |
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What are the symptoms of visceral larval migrans of toxacara canis in humans?
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fever, malaise, abdominal pain
Leukocytosis, eosinophilia Titer done by CDC |
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What is a common misdiagnosis of ocular larval migrans of toxacara canis?
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retrobulbar tumor
|
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What are the age differences for cases of VLM and OLM in toxacara canis/catii?
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VLM: 1-5 yrs
OLM: 5-10yrs |
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What is the second leading cause of blindness in children?
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Ocular Larval Migrans of toxacara canis
|
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How should you prevent toxacara canis zoonotic infections as a veterinarian?
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Assume all puppies and kittens are infected
treat at 2,4,6,8 weeks, Htwm at 10 weeks tell client why to clean feces from yards, parks |
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What can you do to prevent toxacara canis during gestation?
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Selamectin can be applied ad d40 of gestation before the larvae move to fetus, apply again ad d10 postpartum for transmammary reduction
|
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What other ascarids can cause OLM and VLM?
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Toxacara cati of felids from yards, sandboxes, counter tops
Baylisascaris procyonis of racoons worse than T. canis |
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How can you clean surfaces to kill toxacara canis/ cati?
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1% Clorox to clean- removes the proteinaceous cover
|
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How are hookworms transmitted?
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transmammary
direct- larvae in the environment percutaneous |
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What parasite causes cutaneous larval migrans?
|
hookworms of cats and dogs
|
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How do hookworm larvae get under skin?
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they produce variations of collagenase
|
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How do people become infected with cutaneous larval hookworms?
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by lying on contaminated ground (sand) or walking barefoot
|
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What type of infection do hookworms cause in aberrant hosts?
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they cannot digest collagen efficiently enough to get to the GI tract, so they end up wandering and leaving irritating, painful serpentine tracks
|
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How can you control cutaneous larval migrans of hookworms?
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-deworm cats and dogs so no eggs are shed
-pick up the feces -feral animals are an issue - wear shoes |
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What types of meat is trichinella spiralis associated with?
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eating pork and bear meat b/c they are omnivores
|
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What is the life cycle of trichinella spiralis?
|
carnivore ingests infected meat
larvae from meet get into stomach lining and become adults adults mate and females produce larvae in lining of small intestine larvae pass through lymphatics into blood and are distributed to muscles paralysis of muscle develops infected animal eaten |
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What are the principle muscles infected by trichinella spiralis?
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diaphragm
hypoglossal masseters |
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How are trichinella spiralis an exception to the rule of indrect life cycle?
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it can use any animal (not always carnivore) as a definitive, then intermediate host
|
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How can you kill trichinella spiralis in pork?
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freeze at -15 C for 21 days
|
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What are the sources of toxoplasmosis infection?
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oocytes: from cat feces
tachyzoites: in tissues in acute phase bradyzoites: in tissue in chronic phase |
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Which stage of toxoplasmosis infects the fetus in a pregnant woman?
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tachyzoites
|
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What are the two forms of toxoplasma in cats?
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systemic
intestinal |
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Which form of toxoplasmosis in cats causes them to shed eggs to the environment?
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the intestinal form
|
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What are clinical signs of systemic toxoplasmosis in cats?
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• Usually subclinical
• Fever, myalgia, weight loss • Pneumonia or respiratory distress • Anterior uveitis, blindness, retinitis • Seizures, shifting neurologic deficits • Cardiomyopathy • Abortions, Congenital Defects |
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What is the source of toxoplasmosis in the kitchen?
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Handling raw pork or lamb without properly washing hands
|
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What is the major source of toxoplasmosis outside?
|
feral kittens that defecate in sandboxes, gardens, feed bins
|
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What is the source for toxoplasmosis in farm animals?
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barn cats or their litters that defecate in the feed bin or the hay
|
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What recommendations should be made to an owner trying to avoid toxoplasmosis?
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don't adopt a kitten during pregnancy
cats indoors-only during pregnancy do not feed raw scraps automatic scooper freeze meat >48 hours |
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What is the seroprevalence of toxoplasmosis in cats in the US?
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30-40%
|
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What do IgM and IgG indicate on toxoplasmosis titer?
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IgM+ means recent infection
IgG/IgM is active infection IgG is past infection |
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What livestock species are commonly infected with toxoplasmosis?
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pigs
sheep/goats- suffer abortion during acute phase |
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What are the clinical signs of cryptosporidium in humans?
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self-limiting diarrhea
|
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How are cryptosporidium and giardia spread?
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by ingestion of cyst or oocyst from environment
|
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What is the infectious dose of cryptosporidium vs giardia?
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30 cryptosporidium or 1 giardia cyst
|
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What can lead to cryptosporidium or giardia outbreak in municiple water systems?
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surface water contamination or sewage overflow- normal chlorination methods do not kill it
|
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What are classes of giardia?
|
assemblages
|
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What giardia assemblages are zoonotic?
|
A and B
C and D canid only E hoofstock F and G cats and rats |
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What are the 2 subgroups of cryptosporidium parvum?
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Genotype I: C. hominis
Genotype II: C. parvum- zoonotic |
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How can you prevent cryptosporidium and giardia?
|
stay out of wading pools
observe boil water orders beware of mountain stream water |
|
What are 3 types of tapeworms?
|
Taenia saginata (Beef tapeworm)
T. solium (Neural Cysticercosis) Echinococcus (Hydatid disease) |
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What is the tapeworm life cycle?
|
Indirect
they use intermediate hosts, occasionally debilatating them to increase chance of predation, to infect the definitive host |
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What are the forms of toxacara in the intermediate host?
|
eggs hatch and become a cysticercus (vertebrate) or cysticercoid (arthropod) with a single scolex
|
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What is a cysticercus?
|
semitransparent
opalescent white contains scolex (head) fills with fluid space occupying lesion |
|
What are the parts of a tapeworm's body?
|
scolex= head
body/bladder= strobila proglottids= egg packets |
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What is the life cycle of taenia saginata?
|
feedlot workers defecate in pens/ feed troughs
cattle ingest eggs or proglottids cysticerca in cattle muscles man eats undercooked beef |
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What is the life cycle of taenia solium?
|
Humans- DH
Pigs- IH- form cyst in muscle Humans eat cyst in pork Humans become IH if they eat eggs |
|
What is the leading cause of adult-onset epilepsy in Mexico?
|
Neural cysticercosis of tapeworms
|
|
What is neural cysticercosis in tapeworms?
|
when human becomes an intermediate host
cysts form in weird places can be brain and eye lesions |
|
Historically who has been effected by taenia solium?
|
Orthodox Jewish Community on East Coast--> Guatamalan housekeeper
high prevalence outside US |
|
What causese Ecchinococcus infection?
|
Echinococcus granulosus (canid DH)
E. multilocularis (felid DH) – both present in US |
|
What is the life cycle of ecchinococcus?
|
DH passes eggs in feces
IH becomes infected- cysts (Hyatid) enlarges to incapacitate host |
|
What are the cycles of echinococcus?
|
wolf-moose, sylvatic, sheepdog-sheep, domestic
|
|
What species are involved in the life cycle of E. granulosis?
|
Foxes, coyotes, stray dogs, rabbits
|
|
What species are involved in the life cycle of E. multilocularis?
|
Barn cat-rodent cycle
|
|
Where do hydatid cysts of echinococcus grow?
|
liver and lungs
|
|
What species are intermediate hosts for echinococcus?
|
rabbits, deer, humans, sheep
|
|
What is the process of echinococcus infection in humans?
|
Eggs ingested fecal-oral
hatch and embryos travel to organs cause space-occupying lesion asymptomatic in lung and liver enlarge over time complications if rupture |
|
Where is echinococcus very endemic?
|
Africa and the Sudan and Ethiopia
|
|
For what parasites are humans a definitive host?
|
Taenia saginata
Taenia solium |
|
For what parasites are humans an intermediate host?
|
Echinococcus
Taenia solium |
|
What is a dead-end host?
|
animal becomes infected, but not enough pathogen develops so the vectors do not become infected
Lyme disease in deer |
|
What type of ticks transmit Rocky Mountain Spotted Fever?
|
Dermacentor ticks
|
|
What type of ticks transmit Lyme disease?
|
Ixodes ticks
|
|
What are tick-borne diseases?
|
RMSF
Lyme disease Human Granulocytic Erlichiosis Relapsing Fever Tick-borne Encephalitis Anaplasmosis |
|
What are the 4 genera of hard ticks (Ixodid) in North America?
|
Dermacentor, Amblyomma, Rhipicephalus, Ixodes
|
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What are soft ticks?
|
Argasid ticks- feed on birds
|
|
What is the tick life cycle?
|
adult female lays eggs then dies
eggs hatch into larva, feed on blood-meal and molt into nymphs nymphs feed on blood meal and molt into adults adults quest for blood meal on larger mammals or birds |
|
How are pathogens passed in arthropods?
|
transovarian from adult female to eggs
transtadial means a larval stage becomes infected and remains infected when maturing to nymph or adult |
|
What is Dermacenter variabilis and what disease does it transmit?
|
American Dog Tick
Rocky Mountain Spotted Fever |
|
What is the causative agent of RMSF?
|
Rickettsia rickettsii
|
|
How is Dermacentor passed within ticks?
|
transtradial and transovarian
|
|
What is the disease RMSF causes in humans?
|
acute vasculitis causing petechia on skin
bleeding in many organs (CNS and kidney) mortalities from 2-10% of infected humans |
|
What is the pathogenesis of RMSF in canines?
|
enters circulatory system after bite
invades endothelial cells causing vasculitis Prevents apoptosis replicates and spreads hemorrhage and shock end-arterial organs most affected |
|
What is the reservoir for lyme disease?
|
white footed mouse
|
|
What is the life cycle of Ixodes (deer tick)?
|
2 years from hatching to adult
No transovarian transmission larvae hatch and feed on infected Peromyscus and remain infected until adulthood |
|
What are the requirements for epidemiology of lyme disease in Ixodes ticks?
|
habitat where white-tailed deer and white-footed mouse overlap
|
|
What is the deadliest tick-borne disease in North America?
|
Rocky Mountain Spotted Fever
|
|
What percentage of the US population is colonized with S. aureus?
|
32%
|
|
What is the leading cause of identifiable skin and soft tissue infections in US emergency rooms?
|
community-associated MRSA
|
|
What birds are the reservoir of West Nile Virus?
|
blue jays, american crows, grackles, house finches, and house sparrows
|
|
Members of which species of bird are particularly susceptible to West Nile virus?
|
Corvid species (crows and blue jays)
|
|
Which mosquitors are carriers of West Nile Virus?
|
Culex (bird)
Aedes (mammal) |
|
What lifestyle change in horses was related to high levels of exposure to West Nile Virus?
|
horses outside year-round
|
|
What was the mean age in the study of horses with West Nile Viruses?
|
9 years
|
|
Which gender of horse is more likely to be infected with West Nile Virus?
|
Geldings 1.4 times more likely than females
Geldings 1.6 times more likely than males |
|
Which breed of horse was at highest risk of West Nile Virus?
|
Standardbreeds
|
|
What are the most common clinical signs of West Nile?
|
Ataxia, weakness, muscle facilculations
Differentiate b/c it is symmetrical |
|
How do you differentiate Rabies from WNV?
|
Rabies has ascending paralysis from rear to front
|
|
How do you differentiate botulism from WNV?
|
botulism shows severe muscle shaking (head, trunk, muzzle)
|
|
How do you distinguis WNV from EPM?
|
EPM is asymmetric incoordination and weakness. WNV is usually symmetrical
|
|
How do you diagnose WNV?
|
CBC and chem will be normal
CSF may show mononuclear pleocytosis Plaque reduction neutralization test- gold standard ELISA for IgM |
|
What is the gold standard for testing for WNV and why is it uncommonly used??
|
the Plaque reduction Neutralization test but it requires a BSL3 lab
|
|
When can IgM for WNV be detected?
|
8 to 10 days post infection and persist for less than 2 months
|
|
How can you diagnose WNV post-mortem?
|
lesions in both gray and white matter
severe lesions in thoracic and lumbar spine moderate to severe spinal cord hemorrhage with horses brainstem lesions changes in cerebral and cerebellar cortices NOT seen (unlike EEE and WEE) |
|
How do you treat West Nile Virus?
|
supportive:
Anti-inflammatories Mannitol for CNS edema Antioxidants (Vit. E) IV fluids and nutrition Slings Feeding Tubes Antivirals |
|
Can a horse pass West Nile to Humans?
|
Precaution is suggested, but we don't really know
use rubber gloves |
|
What is the prognosis for horses with West Nile Virus?
|
unvaccinated: 25-40%
treatment of severe cases is difficult poor prognosis- disease prevention |
|
What are the 2 primary methods of prevention for West Nile Virus?
|
vaccination
Integrated mosquito control |
|
Which vaccine is best for West Nile virus?
|
FDAH vaccine is 5.5% more effective
Chimera vaccine from Intravet is 95% efficacious |
|
What are possible reasons for vaccination failure?
|
overwhelming challenge by the virus
failure of the animal to develop appropriate immune response stress or waning immune response due to age or other |
|
What are vaccine recommendations for WNV?
|
vaccinate in 2 initial doses, 3 to 6 weeks apart
Second dose no later than April 15th if mosquito season starts in mid-May if horses are stressed, booster again in July or first week of August Q3mo in Florida |
|
At what age should you start vaccinating a horse for WNV?
|
foals from vaccinated mares: after 3 mo of age, likely ~6 mo
foals from unvaccinated: 1-2 mo of age start, give 3rd shot at 6 mo, then yearly boosters |
|
What vaccines should you give a horse?
|
EEE, WEE, WNV and Tetanus
VEE if a problem in the area |
|
Which mycobacterium species are obligate pathogenic mycobacteria?
|
M. tuberculosis
M. africanum M. canetti M. bovis M. caprae M. microti M. pinnipedii |
|
What species can be infected by M. avium subspecies avium and hominisuis?
|
birds, pigs, humans
|
|
What species can be infected by M. avium subspecies paratuberculosis?
|
ruminants, european rabbits, humans
|
|
What species can be infected by mycobacterium marinum?
|
aquarium fish, humans
|
|
What are common characteristics of the mycobacterium tuberculosis complex?
|
intracellularly in tissue macrophages
resistant to lethal oxidation in phagosome resistant to killing by antiobiotics, acidic and alkaline impermable to stains small numbers establish infection |
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Where are m. bovis lesions in the cow?
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pulmonary and extrapulmonary
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How did we eradicate (mostly) bovine TB?
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eliminate the disease from the reservoir
pasteurization of milk surveillance in animals and people |
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When was the first treatment for bovine tuberculosis developed and used?
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1940s and 1950s
|
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When was the comparative cervical test for bovine tb developed?
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1973
|
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What are the classifications of a tb test (caudal fold or comparative cervical)?
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Negative
Suspect Reactor |
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What wildlife reservoirs have shown bovine tuberculosis?
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elk, coyotes, raccoons, black bears, bobcats, red foxes, opossums
|
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What are strategies for eradicating tuberculosis in wildlife?
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-reducing deer population densities
-reducing man-made aggregations of deer by restriction or elimination of baiting and recreational feeding |
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How can you mitigate risk of tuberculosis from wildlife?
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feed cattle safely
store feed safely watter cattle safely- approved waterers |
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What are alphaviruses of importance in population medicine?
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EEE
VEE WEE |
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When does EEE incidence peak?
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in late summer and early fall
|
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What are the intermediate hosts of EEE?
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avian or mammalian (in tropics)
|
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When do EEE outbreaks become epizootics?
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When Aedes and Coquilletidia species enter the cycle- bridge vectors
|
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What is the dead-end host of EEE?
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Horses
|
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Enzootic cycling of EEE occurs with what species?
|
mosquito- Culiseta melanura and the IH (bird or mammal)
|
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What is the most important alpha virus?
|
VEE
|
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What species maintain the enzootic cycles of VEE?
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Culex mosquitors and small vertebrates
|
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What species propagate the epizootics of VEE?
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Aedes and Psorophora
|
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Why is VEE more important than EEE or WEE?
|
horses can amplify the disease due to high levels of the virus
very high levels of the virus in the respiratory tract secretions can be spread by direct contact |
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Where has WEE been identified?
|
primarily Argentina and small SA countries
also in Canada, Western US and east of Mississippi |
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What mosquito is responsible for the enzootic cycle of WEE?
|
Culex tarsalis
|
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Epizootics of WEE are attributed to what species?
|
Aedes when there are high numbers of infected domestic birds
|
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What are the clinical signs of EEE?
|
biphasic fever
progresses to severe CNS signs secondary to diffuse cerebrocortical disease signs 5 days after infection Ataxia first leading to somnolence, head-pressing apparent blindness, excitement and aggressive behavoir loss of brainstem function and total laryngeal and tongue paralysis seizures |
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What are the clinical signs of VEE?
|
Fever constantly elevated throughout
epistaxis, pulmonary hemorrhage, oral ulcers and diarrhea related to CNS signs |
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What are the clinical signs of WEE?
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inapparent infections more than VEE or EEE
seizures clinical signs like the others |
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How do you diagnose EEE, VEE and WEE?
|
serologic tests
4 fold rise in titer is diagnostic EEE horses not often alive long enough 8 fold rise in titer diagnostic for EEE IgM ELISA for VEE CSF analysis PCR diagnostics post-mortem |
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What is the pathophysiology of the alpha encephalitis viruses?
|
Initial viral replication in muscle following mosquito bite
low numbers shed after virus reaches lymph nodes replicates in neutrophils and macrophates if cleared, no progression if not cleared- endothelial cells in spleen and liver- high viremia high viremia --> CNS infection and initiation of neurologic signs |
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What will be seen post-mortem on a patient with an alpha encephalitis virus?
|
gross lesions not always seen
brain- discolored or congested histopath- nonseptic suppurative and mononuclear inflammation cerebral cortex, thalamus, hypothalamus most severely effected (different from West Nile) |
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How do you treat alpha encephalitis viruses?
|
supportive care
anti-inflammatories Slings head protection well bedded stalls with foam on walls parenteral nutrition |
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What is the prognosis of the 3 alpha encephalitis viruses?
|
EEE: 75-100%
VEE: 40-80% WEE: 20-50% |
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What is the difference in those that survive EEE vs WEE?
|
2/3 of those with EEE have neuro effects
WEE survivors seldom have residual deficits |
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How do you prevent encephalitides?
|
vaccination
integrated mosquito control |
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How often should you vaccinate for encephalitides?
|
once a year in temperate zones
more frequently when in mosquito areas |
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Why is mosquito control important for encephalitides?
|
no vaccine is 100% effective
|
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How can you control arboviruses?
|
\strain stagnant pools, use larvicides
remove old tires turn over old equipment where water may accumulate turn over old tubs or troughs keep vegetation down on ponds and lagoons keep horses inside during high mosquito activity lights off at night use fanse incadescent lights outside farm property birds away from barn remove potential reservoir mosquito dunks mosquito magnet |
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Where can you find information about mosquito control?
|
Departments of health and agriculture from the state
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