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Foundations of Animal Health 2 > Infectious Diseases > Flashcards

Infectious Diseases Flashcards

1
Q

What are protozoa?

A

Unicellular organisms, parasitic, reproduce asexually by splitting

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2
Q

What are some examples of protozoa?

A

Giardia, Cryptosporidium, Toxoplasma gondii

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3
Q

Giardia

A

Replication in small intestine, faecal-oral transmission, often young animals and humans, often clinical signs (days), acute and chronic infections

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4
Q

Cryptosporidium

A

Gets inside cells and replicates, clinical signs are similar to giardia, causes enteritis, colonization in the small intestine, epithelial cell loss, decreased SA and enzymes, malabsorption, inflammation, increased motility

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5
Q

Toxoplasma gondii

A

Oocyst that sporulates, intermediate host, can replicate in virtually any cell in the body, dormant phase in muscle, brain, or other tissue. Example: toxoplasmosis- under cooked lamb- pregnant women can abort if parasite starts to replicate and gets across into embryo or foetus

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6
Q

Trematodes

A

Flukes or digeneans, flat, unsegmented worms, indirect life cycles, snails as intermediate host, adult and larval stages

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7
Q

Fasciola hepatica

A

Traditional liver fluke, hard to control because indirect life cycle, live in bile ducts, pump eggs out into small intestine. Acute diseases: Black disease & Clostridium. Subacute: atrophy, repair, and regeneration. Chronic: once in the bile duct, no more migration, causes irritation- hyperplasia and hypertrophy, massively enlarge GB

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8
Q

Fascioliasis

A

Acute phase (4-6 weeks) migrate in liver parenchyma and soetimes lung or skin (destruction/ bleeding) & chronic phase (> 6 weeks) hypertrophy of bile duct epithelium

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9
Q

Cestodes

A

Tapeworms, flat, segmented worms, no gut, indirect life cycles, adult worm in intestine, larva in tissues, usually chronic infections

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10
Q

Echinococcus granulosus

A

Hydatid tapeworm.

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11
Q

Nematodes

A

Roundworms, round in cross- section, direct or indirect life cycles, acute and chronic infections, clinical and subclinical

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12
Q

Ascaris sum

A

Direct life cycle (faecal/oral). Round worm. Hepatopulmonary migration.

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13
Q

Dirofilaria immitis

A

Heart worm. Mosquito bites dog or cat and transmits infected larvae, larvae mature into adults in the heart, female adult worms release microfilariae in the blood. Can live up to 5 years inside the dog. Chronic, irritation to the vessel wall leading to thickening of the vessel wall, causes rigidity in the vessels–> decreased laminar blood flow–> turbulence–> thrombus formation–> wet cough and exercise intolerance

Takes years!

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14
Q

Dairy cow common microorganism causing diarrhoea

A

< 1 week: E. coli

1-2 weeks: Salmonellosis

< 4 weeks: Rotavirus (most important viral)

> 3 weeks: Coccidiosis

Rotaviruses, coronaviruses, astroviruses, bredaviruses

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15
Q

Determinants of animal health

A

General factors: housing/ overcrowding, nutrition, age, genetics

Immunity: after infection, previous exposure, vaccination, herd immunity

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16
Q

Source of the organism

A

Environment, other animals, the animal itself

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17
Q

Diseases caused by R. equi

A

Bronchopneumonia, enteric disease, abscess medial thigh (for example).

Huge impact on TB racing industry

Soil saprophyte, loves manure.

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18
Q

What is the biggest indicator of high disease risk in R. equi?

A

high air-borne virulent R. equi associated with high disease prevalence

Air-borne virulent R. equi associated with low soil moisture, poor grass cover, high ambient temperature

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19
Q

Family Picornaviridae, genus aphthovirus: Foot & Mouth Disease

A

Multiple host species, multiple modes of transmission, multiple serotypes, small infective dose, rapid replication, virus shed before clinical signs, highly contagious, carrier state

Could not have a generic vaccination

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20
Q

Equine Herpes Virus (EHV- 1/4 Respiratory Disease)

A

Clinical signs: fever and inappetence, nasal discharge, lymphadenopathy (sub-mandibular)

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21
Q

EHV- 1 caused what?

A

Abortion. Systemic spread from respiratory tract, leukocyte associated viraemia, no premonitory signs, late gestation, epidemic (up to 80% mortality)

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22
Q

Normal flora (the animal itself)

A

Loss of epithelial integrity, immunocompromise, broad spectrum antimicrobial

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23
Q

In the environment, what types of microorganisms are found?

A

Soil saprophyte, viruses (obligate parasites, enveloped), endospores, nosocomial infection

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24
Q

In other animals

A

Species of animal?

Host range (control/ eradication)

Sub-clinical infection (is it spreading while sub-clinical?)

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25
Q

The animal

A

normal flora, loss of epithelial integrity, immunocompromise, antimicrobials

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26
Q

Vertical mode of transmission

A

Mother to offspring transmission in utero or in ovo

Transmission across placenta, in birth canal, in colostrum/ milk

Cause embryonic death, mummification, resporption (time of gestation) or congenital defects

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27
Q

Horizontal mode of transmission

A

Direct contact (licking, rubbing, biting, sexual contact)

Indirect contact (fomites): feed and water containers, bedding, dander, tack, clothes

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28
Q

Iatrogenic transmission

A

vet or doctor becomes contaminated, fails to take biosecurity measures and infects next patient

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29
Q

Nosocomial transmission

A

Hospital or vet hospital; antibiotic resistance

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30
Q

Sites of entry

A

Skin, respiratory tract, GI tract (local to cells lining the intestinal lumen or systemic infections- viruses cross intestinal mucosa and invade underlying tissues and spread within the body), Genitourinary tract, conjunctiva

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31
Q

How can we prevent infectious disease?

A

Prevent exposure: quarantine (local and regional), herd immunity (sufficient immune animals in herd to reduce the spread of infection)

Active protection: vaccination- specific to immunogens in vaccine

Passive protection

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32
Q

Types of vaccines

A

Killed/ inactivated, live/ attenuated, toxoids and anti-toxins, recombinant/ sub-unit, direct DNA

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33
Q

Passive Immunity

A

Sterile intra-uterine (egg) environment

No transplacental immunoglobulin transfer

Functional but naive immune system at birth

Lag between exposure and immune response

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34
Q

Artificial passive immunity

A

Tetanus anti-toxin, snake anti-venom, tick anti- toxin, spider anti-venom

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35
Q

Post exposure rabies

A

Wound management

Human anti-rabies immunoglobulin- infiltrate wound with RIG

Rabies vaccine- induces immunity post exposure 7-10 days

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36
Q

What do I need to know to control the disease?

A
  1. ID the organism
  2. Describe the disease manifestations
  3. Collect samples
  4. Epidemiology
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37
Q

Rhinderpest

A

Single host species, transmission by inhalation, single serotype, labile in environment, virus shedding before clinical signs, highly contagious, no carrier state, high mortality, lasting immunity to vaccine, no wildlife reservoir

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38
Q

Ability of an organism to produce disease

A

Pathogenicity (ability to cause disease in the host)

Virulence (genetic, biochemical, or structural features that enable it to cause disease in the host)

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39
Q

Invasiveness

A

Ability to invade tissues

* colonization, production of extracellular substances which facilitate invasion, ability to bypass or overcome host defence mechanisms

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40
Q

Toxigenesis

A

Ability to produce toxins

* exotoxins, endotoxins

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41
Q

Campylobacter

A

Most common bacterial cause of infectious diarrhoea in developed countries

* Gram negative bacteria, curved rods, motile, fastidious organisms, some species are thermophilic and grow best at 42C

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42
Q

How is campylobacter spread most often in humans?

A

Foodborne. It is zoontic as well.

Poultry- 98% of poultry meat has some level of campylobacter on it

Poultry- mostly C. jejuni (C. coli to a lesser extent)

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43
Q

Diseases caused by Campylobacter

A

Diarrhoea in dogs and cats, enteritis, abortion in sheep and cattle (C. Fetus), veneral disease in cattle as well

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44
Q

Diagnosing Campylobacter

A

Primary isolation (incubation 42C), Colony appearance on plate, gram stain and/or motility performed, NOT gram negative then NOT Campy OR Gram negative rods & motile–> oxidase test (cytochrome c oxidase +/-), if negative then NOT campy, if positive = Campylobacter spp.

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45
Q

Samples for Campylobacter diagnosis

A

Faeces, intestinal contents, foetus from abortion, vaginal mucous from cows

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46
Q

Disease interactions

A

Genetics, scientific method, nutrition, environment (extremes, for example), toxins, welfare, infectious disease

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47
Q

Scours

A

Calf diarrhoea

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48
Q

Examples of diseases that are sub-clinical (for a time)

A

Dogs with early stage heartworm

Cat with calcivirus

Sheep with low nematode burden

Cow with subclinical mastitis

Parainfluenza virus in cattle without any associated bacterial disease (feedlot example)

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49
Q

Group sub-clinical disease

A

* Sheep nematodes, sheep lice (bad for wool), cattle nematodes, cattle mastitis, feedlot pneumonia (shipping fever), Johne’s disease (ruminants), roundworm in puppies, cattery with calcivirus, pound with parainfluenza virus

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50
Q

Mastitis

A

ICCC, BMCC (bulk milk cell count)

$2-3 per test

How frequent should measurement done? BMCC daily, ICCC monthly (varies)

No vaccine

Management strategies: treat spray, hygiene, dry cow therapy

Clinical mastitis (cell count > 250,000)

Cows with cell counts > 800,000 may lose >10% of their milk production per lactation

Milk production losses from cows with cell counts 100,000-500,000 may be far greater (due to proportion of cows in this count range)

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51
Q

Clinical signs of mastitis

A

change in colour of milk

change in consistency of milk

change in volume of milk produced

animal may stop eating

change in size of udder

change in udder tone

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52
Q

Microfilaria

A

Heartworm. Mosquito transferred to dogs. Takes 6 months for adults to go into heart.

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53
Q

Penicillins, cephalosporins (beta-lactam antibiotics) mechanism of action?

A

Inhibition of cell wall synthesis

Cell wall= major difference between bacteria and mammalian cell

Difference in cell wall between gram positive and gram negative (gram + = thicker)

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54
Q

Monensin, imidazoles, polyenes

A

Damage to cell membrane function

Leads to leakage of cellular contents and cell death

Polyenes & imidazoles important in fungal therapy

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55
Q

Sulfonamides, trimethroprim, nitroimidazoles

A

Inhibition of nucleic acid synthesis or function

Most act by binding DNA to inhibit replication or transcription

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56
Q

Tetracyclines, aminoglycosides, macrolides (e.g. Erythromycin)

A

Inhibition of protein synthesis

Selectively inhibit bacterial ribosomes compared to mammalian

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57
Q

Bacteriostatic vs. Bacteriocidal

A

Inhibiting the growth or reproduction vs. killing the bacteria

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58
Q

Choice of antibiotic

A

Location of bacteria, spectrum, cidal vs. static, administration form, duration of treatment, ability to repeat dosage (wild animals), cost, reactions (gut flora, birds and procaine- will kill the bird)

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59
Q

Protozoa drug treatment

A

* amprolium, lasolacid, monensin, toltrazuril

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60
Q

Cestodes drug treatment

A

Praziquantel- wide range of tapeworms

Niclosamide (salicylanilide)- used for tapeworms of sheep, cattle, horses & poultry (also dogs and cats)

Benzimidazoles have moderate activity against tapeworms

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61
Q

Nematodes drug treatment

A

Arsenicals, organophosphates, piperazines, salicylanilides, Benzimidazoles, Imidazothiazoles (levamisole), Avermectins/ milbemycins

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62
Q

Trematodes drug treatment

A

Triclabendazole- good efficacy against adult and immature stage

High dose rates most BZ have moderate kill rates of adult fluke

Salicylanilides- highly effective against adult fluke, moderate to poor against immature

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63
Q

Arthropods drug treatment

A

Organochlorines- generally banned, organophosphates- history of OHS, but used, carbamates, IGRs

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64
Q

Bacteria that causes mastitis

A

Streptococcus agalactiae and Streptococcus dysgalactiae

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65
Q

What would you use to treat an animal for a cestode (tapeworm) infection?

A

Praziquantel

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66
Q

Which of the following would you use to treat a bacterial infection?

A

Tetracycline

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67
Q

What is the key reason why there is a financial penalty for farmers witha moderately elevated bulk milk cell count?

A

The milk has reduced processing attributes for cheesemaking.

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68
Q

How do you treat a herd of cattle if the owners are concerned the cows may have subclinical mastitis?

A

Treat cows based on culturing a number of cows with elevated cell count or clinical mastitis and determining in vitro sensitivity to antibiotics

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69
Q

Sublicincal disease…?

A

Often requires further diagnostic testing

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70
Q

What exists as a commensal organism in the intestinal tract of chickens?

A

Campylobacter jejuni

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71
Q

Herd immunity

A

Can protect susceptible animals in a population of immune animals

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72
Q

Passive immunity in lambs is acquired via

A

Immunoglobulin transfer from colostrum

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73
Q

Active immunity can be achieved by:

A

Immunization and exposure to pathogens

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74
Q

Rinderpest has been eradicated as an animal disease, whereas Foot and Mouth Disease (FMD) is still present in the world. Why?

A

Rinderpest affects cattle only, whereas FMD affects a number of species

Rinderpest does not have carrier animals, whereas animals can be carriers of FMD

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75
Q

What is the technical name for a round worm?

A

Ascaris

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76
Q

Which bacteria and viruses commonly cause diarrhoea in young calves under 6 weeks of age?

A

Rotaviruses, E. coli, Salmonella

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77
Q

Which clinical signs is the most characteristic of diarrhoea in calves caused by Salmonella?

A

Septicaemia with high fever and depression; foul smelling faeces with blood

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78
Q

Which would you use to treat an animal for cestode (tapeworm) infection?

A

Praziquantel

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79
Q

What is the key reason why there is a financial penalty in terms of reduced milk price for farmers with a moderately elevated bulk milk cell count?

A

Milk has reduced processing attributes for cheesemaking

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80
Q

What do you do if an owner is concerned their cows have subclinical mastitis?

A

Treat cows based on culturing a number of cows with elevated cell count or clinical mastitis and determine in vitro sensitivity to antibiotics

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81
Q

What must you do to detect subclinical disease?

A

Further diagnostic testing

82
Q

Campylobacter jejuni exists where? What kind of organism?

A

Commensal organism in the intestinal tract of chickens

83
Q

What can herd immunity do?

A

Protect susceptible animals in a population of immune animals

84
Q

What kind of disease transmission is infection of offspring in utero?

A

Vertical

85
Q

What is a tetanus toxoid injection?

A

Chemically purified subunit vaccine

86
Q

What is a tetanus antitoxin?

A

An example of passive immunity

87
Q

How do lambs acquire passive immunity?

A

Immunoglobulin transfer from colostrum

88
Q

How can active immunity be achieved?

A

Exposure to pathogens and immunization

89
Q

What are two reasons Rinderpest was successfully eradicated as an animal disease?

A

Rinderpest affects only cattle and it does not have carrier animals (FMD is the opposite in both areas)

90
Q

Who does rabies affect?

A

Warm blooded animals. Many strains each predominating on a particular animal species in a particular geographical area.

91
Q

What does rabies cause?

A

Various biotypes but in all affected species- rabies causes progressive inflammation of the brain and spinal cord resulting in death.

92
Q

How is rabies transmitted?

A

Contamination of fresh wounds and mucous membranes with infectious saliva.

93
Q

What are the two cycles of rabies?

A

Urban and wildlife cycles. The urban cycle is maintained by infections in dogs, unvaccinated and stray usually. Most human infections. The wildlife (or sylvatic) cycle occurs in more rural areas where infection is perpetuated by wildlife species such as foxes, racoons, wolves, and insectivorous bats.

94
Q

Who is “free of rabies”?

A

AUS, NZ, UK, japan, singapore, png, pacific islands

95
Q

When do signs develop?

A

Anywhere between 10 days and several months- death usually occurs within 10 days once signs develop

96
Q

What is the general course of infection?

A

Behavioural change, progressive paralysis, coma, and death

97
Q

How does the disease spread?

A

Rabies virus concentrates in the saliva of infected animals. Spreads when it comes into contact with fresh wounds and unprotected mucous membranes (eyes and mouth)

98
Q

What are control measures other than vaccines?

A

Population management of stray and feral dog and cat programs reduces the pool for potential rabies reservoir in urban cycles.

In people:

Avoid contact with stray or unknown animals, prior to traveling to a region with endemic rabies seek vaccination, if bitten or scratched by an animal- clean the wound vigorously, apply disinfectant, and seek medical attention

99
Q

What is used for control in the wildlife?

A

Licensed oral vaccines are used for mass immunisation of wildlife to reduce rabies virus reservoir

100
Q

In people what is the incubation period of rabies?

A

2-8 weeks but can last up to several years.

101
Q

What is post exposure medial treatment?

A

Five doses of rabies vaccine given over 28 days produces antibodies against the rabies virus. A dose of rabies immunoglobulin is also given- ready made antibodies to counteract the rabies virus.

102
Q

What are chemoautotrophs?

A

Use chemical energy- breakdown more complex chemical structures. CO2 building block. These are all pathogenic bacteria.

103
Q

What is the smallest of bacteria?

A

Chlamydia psittaci- psittichosis in people

104
Q

How does Leptospirosis move?

A

Can move through urine by twisting on its own axis- attaches to hooves of sheep with fine appendages

105
Q

What causes strangles in horses?

A

Streptococcus

106
Q

What is rotavirus?

A

Protein with nucleic acid core

107
Q

What is an indirect life cycle?

A

Snails or other intermediate hosts

108
Q

What is influenza virus ?

A

Lipid membrane around the outside- nucleic acid in the inside

109
Q

What is the genome of Viruses? And what are some facts?

A

Nucleic acid wrapped up in some protein, RNA or DNA, infect cell and trick host cell into replicating, have to be inside a host cell to do anything becuase they can’t generate their own energy, start at one micron and get smaller

110
Q

What are obligate parasites?

A

Not able to survive independently

111
Q

What are trematodes?

A

Flukes, flat, unsegmented worms, all have indirect life cycles, snail as intermediate host, adult and larval stages, fasciola hepatica

112
Q

What is Koch’s Postulates?

A

Found in lesions, isolated in pure culture, experimental reproduction, recovered from experimental disease

113
Q

What are some problems with Koch’s postulates?

A

Some have never been grown in pure culture, lameness in sheep has 2 bacteria present to cause, importance of other factors in the environment that contribute to the disease

114
Q

What do tapeworms cause?

A

Cysts in intermediate host

115
Q

What are cestodes?

A

Tapeworms, flat, segmented worms, no gut, all have indirect life cycles, adult worm in intestine; larva in tissues, usually chronic infections, difficult to diagnose in live animals

116
Q

What are arthropods?

A

Ticks

117
Q

What is Giardia and Cryptosporidium?

A

Faecal-oral transmission, often young animals and humans, often clinical signs (days), acute and chronic infections, colonization in the small intestine, epithelial cell loss, inflammation increased motility, diarrhoea, malabsportion

118
Q

Which protozoa are often associated with diarrhoea in young calves?

A

Cryptosporidium, Eimeria, Giardia

119
Q

Which parasite groups are often associated with diarrhoea in young calves?

A

Protozoa (protists) & Roundworms (nematodes)

120
Q

How are viruses, bacteria, and parasites IDed?

A

PCR- DNA is enzymatically amplified using a pair of specific oligonucleotide primers through many cycles of denaturation, annealing, and extension

121
Q

What are the determinants of animal health?

A

Housing/ overcrowding, nutrition, age, genetics

Immunity: after infection, previous exposure, vaccination, herd immunity

122
Q

Why was smallpox irradication successful?

A

Only in the human population- not environmental, not in the animal population

123
Q

Where do organisms come from?

A

Environment, other animals, the animal itself

124
Q

What is R. equi?

A

Soil saprophyte, when aerosolized, foals became sick

125
Q

What is horizontal transmission?

A

Direct contact (licking, rubbing, biting, sexual contact)

Indirect contact (fomites)- feed and water containers, bedding, dander, tack, clothes, etc.

126
Q

What are the sites of entry?

A

Skin, respiratory tract, GI tract, genitourinary tact, conjunctiva

127
Q

How can we prevent infectious disease?

A

Prevent exposure with quaratine and herd immunity, vaccination, passive protection

128
Q

What are killed/inactivated vaccines?

A

Many vaccines in Aus are this; safe and successful; Disadvantages- reduced immunogenicity, boosters required, adjuvants required

129
Q

What are some adverse effects of vaccinations?

A

Teratogenc/abortigenic, immunosupressed animals, local injection site reaction, hypersensitivity, neoplasia, underattenuation

130
Q

What is the innate immune system?

A

Non-specific- barriers- first line of defence- skin, stomach acid, oil on the skin surface

Second line of defence- inflammatory (bring leukocytes to the site), phagocytes (engulfing cell)- WBCs/ leukocytes

131
Q

What tests are available to detect the agent?

A

Culture (bacterial and viral)

PCR

Agglutination

Immunoassay

Immunofluorescence

Immunohistochemistry

FACs

132
Q

What tests are available to detect an antibody?

A

Agglutination, precipitation, complement fixation, neutralization, immunoassay

133
Q

What tests are available to detect Cell Mediated Immunity?

A

Hypersensitivity, blastogenesis assays, cytokine assays

134
Q

What is a ring vaccination?

A

The vaccination of all susceptible individuals in a prescribed area around an outbreak of an infectious disease. Ring vaccination controls an outbreak by vaccinating and monitoring a ring of people around each infected individual. The idea is to form a buffer of immune individuals to prevent the spread of the disease.

135
Q

What do you need to know to control the disease?

A
  1. ID the organism
  2. Describe the disease manifestations
  3. Collect samples
  4. Epidemiology (of bovine mastitis)
136
Q

What is the most common bacterial cause of acute infectious diarrhoea in developed countries? What kind of bacteria is it?

A

Campylobacter.

Gram negative (curved rods, motile (polar flagella), fastidious organisms, some species are thermophilic and grow best at 42C)

137
Q

Where does C. jejuni and C. coli come from before chickens?

A

The environment, carried by wild animals- flies, rats, feed

138
Q

What are the diseases caused by Campylobacter?

A

Diarrhoea, enteritis- calves and sheep, abortion in sheep, veneral disease and sporadic abortions in cattle

139
Q

What causes late term abortions in sheep (and sometimes cattle)?

A

C. fetus (ingested when sheep graze)

140
Q

Cows with cell counts >800,000 may lose what percent of their milk production per lactation?

A

>10%

141
Q

What does a bacteriostatic antibiotic do? Bacteriocidal?

A

Inhibits growth or reproduction.

Killing bacteria.

142
Q

What is the best method for treating subclinical mastitis?

A

Intramammary antibiotic.

143
Q

What’s the best way to treat a sheep for parasite control (esp. nematodes- round worms)?

A

Two summer drenches and long acting capsule or injection. Northern VIC- May before lambing.

144
Q

If a bulk flock FEC count is 250 epg, which class of sheep would be of the biggest concern?

A

4 month old weaned Merinos.

145
Q

What is VPH?

A

The sum of all contributions to the physical, mental and social well-being of humans through an understanding and application of veterinary science.

146
Q

What is One Health?

A

Concept of incorporating interdisciplinary collaborations and communcations in all aspects of health care for humans, animals and the environment. Human health, animal health, and ecosystem health are inextricably linked.

147
Q

What is Tinea?

A

Fungal infection of the skin (ringworm or dermatophytosis). Mycotic diseases in humans. Sources: Anthropophilic (from humans; Geophilic (from soil); Zoophilic (from animals)

148
Q

Why do diseases emerge (and spread)?

A

Ecological changes or disruption (i.e. climate change), introduction of animals to new areas, increasing global movement (people and animals), cultural changes and changes to agricultural practices

149
Q

How is Hendra Virus transmitted?

A

Flying fox (reservoir- contaminating horse feed from urine, saliva, birth products- animals moving into new areas)–> spillover to horse (horse to horse transmission as well- via fomites or direct contact)–> human (respiratory secretions and or blood from horses)

150
Q

What are some ways you can control Hendra Virus?

A

Stabling horses at night to keep them from contact with flying foxes, isolate sick horses, enveloped virus- doesn’t survive lon in the environment, test and cull infected horses (and dogs), vaccines for Hendra virus, disinfectants, hygiene and PPE

151
Q

How is WNV transmitted? Who are the dead end hosts?

A

From mosquito sucking bird’s blood- bird is the reservoir host.

Horses and humans are dead end hosts.

152
Q

How did West Nile virus get to the US from Africa, Europe, Middle East?

A

Migratory birds perhaps?

153
Q

How is WNV controlled and prevented?

A

Eliminate standing water around house, insecticides, vaccines (potentially), for humans- insect repellents, protective clothing, screens, vaccines (potentially), horses- vaccines (potentially)

154
Q

What is Variant Creutzfeldt-Jakob disease?

A

Better known as Mad cow disease (bovine spongiform encephalopathy). Recently emerged food-borne disease. Emerged in the UK in 1996. Fatal human neurodegenerative condition. Infectious prion (protein)

155
Q

How did vCJD emerge?

A

Change in agricultural practices. Feeding of meat and bone meal to cattle as a protein supplement. Facilitated spread of disease to a large number of animals. Modern food processing practices (minced beef) spread infectious material to large number of people (not destroyed by cooking)

156
Q

How do you prevent the spread of vCJD?

A

Ban feeding of meat and bone meal. Cull infected cattle (4.5 million cattle were culled). Avoid beef consumption. There was a ban on British beef at the time.

157
Q

Why do we need National and International organizations?

A

Control of transboundary disease, harmonize disease definitions, harmonize diagnostic, treatment, and vaccination methods, promote exchange of disease intelligence, promote collaboration in agreed eradication campaigns, facilitate trade

158
Q

What did the OIE, WHO, and FAO do with HeV?

A

Disease not on OIE list, Manual of Diagnostic Tests and Vaccines for Terrestrial Animals- HeV is in there. OIE publishes info on HeV (scientific and technical review journal)

WHO- not a human disease- but published a facts sheet

FAO- not directly involved with HeV, website gives access to many non-FAO documents on Hendra virus (not a food security risk)

159
Q

What are some key international organizations?

A

World Organization for Animal Health (OIE), Food and Agriculture Organisation of the United Nations (FAO), World Health Organization (WHO)

160
Q

What does DEPI do?

A
  1. Emergency management
  2. Policy development
  3. Regulation and Compliance
161
Q

What does the DA do?

A

enhance and sustain Aus’ agriculture, food, fisheries, and forestry industries. Safeguard AUS from exotic pests and disease

162
Q

What does the OIE do?

A

Coordinate disease eradication, meetings, official country disease status, health standards, publications and documentation.

163
Q

What does the FAO do?

A

Improve nutrition, increase agricultural productivity, raise the standard of living in rural populations and contribute to global economic growth. Food security focus. “Let there be bread”

164
Q

What does the WHO do?

A

Human health. Arm of UN. Technical support for countries, leadership on global health matters, norms and standards, shaping the health research agenda

165
Q

How did the organizations work together for Hendra Virus DEPI and DA?

A

DEPI- information for horse owners and workers in VIC; case reporting; DEPI field staff provide direction and assistance in virus investigations with private vets collaboration. Report to DA.

DA- information sheets, AUSVETPLAN for HeV, emergency animal disease hotline for reporting suspected cases, manage market access issues that may arise. e.g. export of horses, dogs, and cats, analyze and share technical information for other govt dept., situation updates to all states, manage regulatory measures around the new HeV vaccine, research funding for HeV, Notify OIE of significant developments

166
Q

What is giardia and cryptosporidium?

A

Protozoa. Parasite.

167
Q

What is Toxoplasma gondii?

A

Protozoa. Parasite.

168
Q

What is Fluke?

A

Trematode. Parasite

169
Q

What are tapeworms?

A

Cestodes. Parasites.

170
Q

What do cestodes (tapeworms) cause?

A

Cysts in the intermediate host.

171
Q

What are round worms? Give some examples.

A

Nematodes. Parasites.

Ascaris suum. Hepatopulmonary migration.

Dirofilaria immitis. Heartworm. (Mosquito)

172
Q

What are ticks?

A

Arthropods. Parasites.

173
Q

Pathogenesis

A

The cellular events and reactions and other pathological mechanisms occuring in the development of the disease

174
Q

Virulence

A

The degree of pathogenicity of a microorganism

175
Q

What are the most important microbial toxicoses?

A

Botulism, mycotoxicoses, and toxic algal (actually cyanobacterial) blooms

176
Q

What are exotoxins?

A

Bacterial food-borne toxicoses are caused by exotoxins, which are proteins produced and secreted by bacterial cells. ADP ribosylating toxins are examples (diphtheria, cholera, pertussis toxins, shiga toxins) and zinc endoproeinases (botulinum and tetanus toxins).

177
Q

What is the fimbriae or pili from gram negative an example of?

A

They are how gram negative bacteria adheres to an animal’s tissues. They contain a protein- which is the adhesin.

178
Q

The animal itself as a host of the organism?

A

Previously infected and not completely resolved, reactivation of previously latent infection, opportunistic pathogen

179
Q

What are toxoids (type of vaccination)?

A

Detoxified bacterial exotoxins. Tetanus, diphtheria, botulinum toxin.

180
Q
A
181
Q

How does Campylobacter need to be controlled in poultry?

A

On farm hygiene and biosecurity

At the abattoir- cleaning and disinfection (scalding, chlorine washes, ect) & chilling

Consumption- proper handling and cooking

182
Q

Why would milk production from cows with cell counts of 100,000-500,000 vs. 800,000 be much greater?

A

Subclinical disease perhaps and more cows in this range- you could lose a lot more milk overall from the herd.

183
Q

What are some general preventives?

A

Good diet, good bacteria, environment

184
Q

What are some ways to reduce the speed of parasite resistance to drench?

A

Reducing drenching frequency

drenching when there was a moderate number of parasites on pasture

Using multiple drenches at one time

Not drenching all the sheep in each mob

185
Q

When do you know when to treat (drench)?

What should be done on sheep to decide on efficacy of treatment?

A

FEC

Drench resistance test- where different drenches are tested to determine their efficacy. So treat them then do a FEC about 12 days later.

186
Q

What are the most important parasite in sheep and next?

A

Round worms (nematodes) and then flat worms (flukes- trematodes)

187
Q

What is a blanket vaccination?

A

Mass vaccination to protect large number of animals over a wide area from infection and clinical signs of disease.

188
Q

When would you use ring vaccination?

A

Surrounding an infected area to protect animals from infection– separate infected from uninfected for example. Or to protect a specific high value or rare group in uninfected area (targeted vaccination)

189
Q

What do I need to know to control disease?

A
  1. ID the organism and know what other normal flora might be found
  2. Describe the disease manifestations (acute mastitis vs. sub-clinical mastitis)
  3. Collect appropriate sample (how do I collect an uncontaminated sample?)
  4. Speciate the organism (contagious, environmental, alter treatment, obligate or opportunisitic- underlying disease)
  5. Epidemiology- how is it spread, how do I stop it (Hygiene before and after milking, ascending infection through open teat orifice after milking- treat teat with intramammary antibiotic)
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Foundations of Animal Health 2 (3 decks)

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