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Animal Health and Diseases > Infectious Diseases 3.0 > Flashcards

Infectious Diseases 3.0 Flashcards

1
Q

what type of virus is caprine arthritis encephalitis (CAE) in terms of speed?

A

a lentivirus, slow

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2
Q

how is CAE typically transmitted?

A
  1. vertical transmission: mom to baby

2. horizontal transmission: goat to goat

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3
Q

how is vertical transmission of CAE accomplished?

A

from mother to kid through the ingestion of colostrium milk

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4
Q

what kind of disease does CAE cause in kids?

A

neurologic, erratice movement observed

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5
Q

what symptoms does CAE cause in adult goats?

A
  1. arthritis
  2. pneumonia
  3. mammary disease (endurant mastitis)
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6
Q

what characteristic position will you often find adult goats with CAE in and why?

A

kneeling due to joint pain

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7
Q

what is the prevalence of CAE in what countries and why?

A

greater than 65% in highly developed countries like US, Canada, France, Norway, due to highly selective practices in goats

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8
Q

where is CAE less prevalent and why?

A

local, low stress breeds of goats in less developed countries due to lower selection pressure and more outbreeding increasing heterosis and resistance

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9
Q

how does horizontal transmission of CAE take place? (4)

A
  1. direct contact
  2. fomites at feed bunks and water troughs
  3. ingestion of contaminated milk (from firs strip) in milking parlors
  4. iatrogenic: re-use of needles or equipment in contact with blood
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10
Q

does CAE have the ability to survive in the environmet outside a host cell?

A

sure does, can live in environment for a while

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11
Q

describe how caprine arthritis encephalitis is a lentivirus

A

can hide inside host cells as a latent provirus

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12
Q

what type of cells does CAE prefer to hide in and what does this explain?

A

it prefers joint cells because there is less access to the immune system that way, this explains the arthritis part

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13
Q

what kind of pathogen is CAE?

A

an opportunistic one because it thrives when the immune system is down

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14
Q

is there any vaccine or specific treatment for caprine arthritis encephalitis? how do you deal with it?

A

nope, can only provide supportive care for opportunistic bacterial infections

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15
Q

describe disease control of CAE (3)

A
  1. appropriate kid and colostrum management (PASTEURIZE)
  2. test and segregate to prevent spread
  3. cull adult infected goats
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16
Q

what must you also do when you encounter a case of CAE on your goat farm other than treat the animal?

A

report to state veterinarian

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17
Q

what kind of bacteria causes caseous lymphadenitis, what kind of bacteria is it, and why is it called that?

A

Cornyebacterium pseudotuberculosis, an anaerobic bacteria that produces similar symptoms to the bacteria that causes tuberculosis

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18
Q

describe Caseuous lymphadenitis

A

a chronic, contagious disease that affect lymphnodes and lymphatic tissue

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19
Q

what is the one health concern about caseous lymphadenitis and what precautions should you take?

A

is zoonotic! so wear gloves and PPE when dealing with cases

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20
Q

how resistant is Cornyebacterium pseudotuberculosis (causes caseous lymphadenitis) to the environment?

A

very resistant, can live on surface for up to 2 months and in soil for up to 8 months

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21
Q

how do the bacteria that causes caseous lymphadenitis enter the host?

A

through mucous membranes or damaged skin

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22
Q

what is the issue with the bacteria that cause caseous lymphadenitis once they are present in the soil?

A

they become endemic to that region and are almost impossible to remove

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23
Q

how long is the incubation period for caseous lymphadenitis?

A

1-3 months

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24
Q

does caseous lymphadenitis affect only internal lymph nodes?

A

no, affects internal and external lymph nodes, can actualy trace back infection point to most s affected lymph node

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25
Q

what is observed in lymph nodes affected by caseous lymphadenitis?

A

layers from where immune system blocks bacteria and the bacteria break through and cycle repeats

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26
Q

when are internal lymph nodes usually affected in caseous lymphadenitis?

A

when transmission occur through ingestion

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27
Q

what are the symptoms (2) of caseous lymphadenitis?

A
  1. chronic weight loss

2. failure to thrive

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28
Q

describe treatment of caseous lymphadenitis (3)

A

1, challenging to eradicate from an individual because recurrence is common

  1. treat individuals by draining or lancing abscesses tho
  2. treatment aimed more at limiting transmission to other animals in the flock
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29
Q

what are the 4 aspects of prevention of caseous lymphadenitis?

A
  1. STRICT BIOSECURITY
  2. awareness of fomites and disinfection of environment
  3. cull affected animals
  4. vaccination
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30
Q

why is chronic weight loss and failure to thrive the symptoms of caseous lymphadenitis?

A

swollen lymph nodes (mediastinal abscesses) push on esophagus and trachea = no food and hard to breathe = weight loss and failure to thrive

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31
Q

are chronic weight loss and failure to thrive the ONLY symptoms of caseous lymphadenitis?

A

no, abscess production everywhere can lead to other symptoms based on what grows near

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32
Q

are goats the only species affected by caseous lymphadenitis?

A

no, can occur in sheep too but is less common in sheep

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33
Q

what is contagious ecthyemia?

A

a disease in small ruminants that causes sore mouth; not many symptoms but hard way to live

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34
Q

what is Johne’s disease (paratuberculosis)?

A

a mycobacteria (bastard) that causes inflammation of the intestinal tract that leads to malabsorption of nutrients and makes growth hard; not mucn to do about this

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35
Q

what is the problem with vaccinating against Johne’s disease?

A

the mycobacteria could cause a cross reaction with tuberculosis tests

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36
Q

what type of virus is rabies?

A

a lyssa virus in that Rhabdovirus family

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37
Q

how many variants of rabies exist?

A

15

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38
Q

what is the important thing to keep in mind about rabies variants?

A

when species’ specific variants infect other species it can produce resorvoirs instead of infections

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39
Q

what mammals is rabies most common in?

A

canivores and bats

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40
Q

is rabies limited to infecting carnivores and bats?

A

nope, can affect ANY mammal

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41
Q

what is rabies?

A

acute viral encephalomyelitis

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42
Q

at what point is rabies fatal?

A

once clinical signs appear

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43
Q

describe the geography of rabies?

A

found throughout the world, global spread

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44
Q

what is the one health concern of rabies?

A

zoonotic

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45
Q

what are the 6 resorvoirs of rabies?

A
  1. dogs
  2. bats
  3. coyotes
  4. skunks
  5. foxes
  6. raccoons (3-6 wildilife)
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46
Q

describe the shift of rabies concern in recent years

A

we were more worried about domestic animals but vaccinations shifted focus to wildlife

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47
Q

why is rabies in wildlife a concern?

A

dogs and wildlife can both serve as resorvoirs, exhibit no symptoms but spread rabies, wildlife has easy access to livestock and dogs = bad news bears

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48
Q

if you are vaccinated against rabies and get exposed what happens?

A

infection is still possible but usually not fatal

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49
Q

describe transmission of rabies and what measures humans need to take

A

through virus-laden saliva into tissues, usually through bites or contact with wounds (so wear PPE!!)

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50
Q

what are the 3 phases of clinical signs of rabies?

A
  1. prodromal phase
  2. furious/acute excititative
  3. paralytic/endstage
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51
Q

describe the prodromal phase of clinical signs of rabies

A

vague, non-specific signs, lasts 1-3 days

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52
Q

describe the furious/acute excititative phase of clinical signs of rabies

A

“mad-dog syndrome” animal has no fear; will attack and use teeth, claws, horns, or hooves; alert posture

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53
Q

explain why fewer rabies infections occur from infected ruminants than infected carnivores

A

ruminants really only have horns to attack, so less ways to spread/cause wounds. carnivores bite and scratch

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54
Q

describe the paralytic form/endstage phase of clinical signs of rabies

A

ataxia and paralysis, coma, death within hours

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55
Q

describe the pathogenesis of rabies

A
  1. virus moves from site of entry to
  2. peripheral nerves to
  3. spinal cord to
  4. brain where replication leads to encephalitis and the salivary glands to continue transmission before
  5. to the rest of the body causing symptoms and host death
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56
Q

what is so scary about rabies and its transmission style?

A

it knows the salivary glands are the best place to go to infect other hosts, so it goes there before causing host death

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57
Q

how do you diagnose rabies?

A

euthanize if see symptoms, then send head off for histopathological analysis

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58
Q

what is the pathognomonic sign of rabies?

A

Negri bodies in the brain tissue

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59
Q

describe what happens governmentally (national and state) in terms of rabies control

A

there is a qualified lab to run histopathology for rabies in each state, and all cases must be reported to ensure that we keep the high public health risk of rabies as low as possible

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60
Q

at what point is rabies fatal?

A

once symptoms start

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61
Q

what organizations control prevention of rabies?

A

WHO and NASPHV (National Association of State Public Health Veteriarians)

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62
Q

list the 5 aspects of rabies prevention in dogs

A
  1. notification of suspected dogs, euthanization of clinical dogs and those bitten by clinical dogs
  2. reduction of contraction rates by leash, controlling dog movement, and quarantine
  3. MASS IMMUNIZATION
  4. stray dog control
  5. dog registration
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63
Q

describe rabies prevention in wildife, old times and now

A

until recently: population reduction of wildife

now: oral vaccines and recombinant virus in feed released into wild

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64
Q

what kind of virus is influenza virus

A

orthomyxovirus

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65
Q

what are the 4 types of influenza virus?

A

Type A
Type B
Type C
Type D

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66
Q

how is influenza virus Type A classified?

A

by hemagglutinin (H 1-18) and neuriminidase (N 1-11), the proteins outside the virus

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67
Q

which of the influenza viruses is constantly changing?

A

influenza A viruses

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68
Q

what is antigenic drift?

A

small changes or mutations n the genes of influenza viruses that can lead to changes in proteins

69
Q

what is the reason why the flue vaccine changes every year?

A

antigenic DRift

70
Q

what is anitgenic shift?

A

abrupt, major chnage resulting in new H and/or new N proteins

71
Q

describe when antigenic SHift occurs

A

when an influenza virus specific for one species (say, a pig) meets say and chicken with another species-specific influenza virus, the two viruses co-mingle in the same cells, use the same machinery to replicate, and make a totally new virus with proteins from both

72
Q

what type of influenza is avian influenza?

A

influenza virus Type A

73
Q

what are the 2 forms of avian influenza?

A
  1. low pathogenic avian influenza

2. high pathogenic avian influenza

74
Q

how many subtypes of avian influenza exist?

A

16

75
Q

which of the avian influenza subtypes result in highly pathogenic avian influenza?

A

5 and 7

76
Q

describe low pathogenic avian influenza in terms of symptoms (2)

A
  1. most birds asympotmatic

2. if bird symptomatic, will be respiratory disease and drop in egg production

77
Q

describe high pathogenic avian influenza in terms of symptoms (3)

A
  1. sudden death
  2. multiple organ failure
  3. high mortality rate
78
Q

is there any antiviral treatment approved for avian influneza?

A

noope

79
Q

what is used to treat avian influenza?

A

antibiotics for secondary bacterial infections

80
Q

how is avian influenza prevented and under what terms?

A

with vaccines that must be used under the direction of the state veterinarian

81
Q

how is avian influenza controlled? (2)

A
  1. strict biosecurity in domestic poultry bc can easily be spread by wild fowl
  2. mass depopulation in affected flocks
82
Q

what type(s) of influenza cause swine influenza?

A

mainly Type A but types B and C have been isolated as well

83
Q

what is an agent of swine respiratory syndrome?

A

swine influenza

84
Q

when is swine influenza more prevalent? why?

A

in cold months, closer contact (for warmth) equals more pig-to-pig transmission and rapid spread

85
Q

is there any treatment for swine influenza? why or why not?

A

no, it’s a virus

86
Q

what do you do for a pig with swine influenza?

A

antibiotics for secondary bacterial infections

87
Q

what is the best prevention of swine influenza?

A

vaccination and control movements of different aged pigs in between farms in production chain

88
Q

what type of influneza is equine influenza?

A

Type A

89
Q

what is the most common respiratory disease in horses?

A

equine influenza

90
Q

when do most cases of equine influenza occur (what age)?

A

1-5 year old horses

91
Q

how long does it take a horse with a mild case of equine influenza to recover?

A

2-3 weeks

92
Q

how long does it take a horse with a severe case of equine influneza to recover?

A

up to 6 months, with long lasting latent symptoms

93
Q

describe treatment for horses with equine influenza

A

based in rest and supportive care

94
Q

what are the best ways to prevent equine influenza? (2)

A
  1. hygienic practices

2. vaccine prevention

95
Q

define mastitis

A

inflammation of mammary gland, predominantly caused by bacterial pathogens

96
Q

is mastitis often caused by viral agents? why or why not?

A

no, viruses don’t really like mammary glands

97
Q

does mastitis affect all mammary glands at once all the time?

A

no, usually affects independent quarters or glands

98
Q

what are the 2 general symptoms of all types of mastitis?

A
  1. decreases milk production

2. decreases weight gain in suckling offspring

99
Q

are mastitis cases more often severe?

A

no, most cases subclinical with local inflammation or mild cases

100
Q

what is agalactia?

A

no milk production

101
Q

what can severe mastitis cases lead to?

A

agalactia, profound systemic involvement, or death

102
Q

when does mastitis occur?

A

when microbes enter through the teat via teat canal

103
Q

what kind of pathogens cause a high percentage of mastitis cases?

A

opportunistic

104
Q

when does contagious mastitis spread occur?

A

during milking by contact with milker’s hands or milking units, and 30 minutes after milking before teat seals

105
Q

what are environmental mastitis infections due to?

A

lack of hygiene

106
Q

what period of life/production is mastitis associated with?

A

periods of high production demands, transition periods in ruminants and swine

107
Q

what are the 2 ways to get mastitis?

A
  1. contagious spread

2. environmental infection

108
Q

why do teat cups have water flow in between lineups?

A

to prevent contagious spread of mastitis

109
Q

what is another way contagious spread of mastitis occurs other than the milking parlor?

A

in nursing animals; if one teat is infected the suckling baby can spread to the rest of the teats

110
Q

what is the main bacteria that causes environmental mastitis and how?

A

E. coli lives in feces, so if sandbeds or stalls are dirty, this bacterium can enter open teat canal post milking

111
Q

how do you control environmental mastitis spread?

A

with good milking protocols and keeping gloves clean

112
Q

why is suckling the period of time when most swine get mastitis?

A

so many piglets means the teat canals are almost always open leading to the high risk for mastitis

113
Q

why does mastitis milk look chunky?

A

bacterial growth makes milk more acidic, causing it to curdle and look like cheese due to coagulated protein

114
Q

what are the 4 main categories of common mastitis causing bacteria?

A
  1. Staphlycoccus aureus
  2. Escherichia coli
  3. many streptococci
  4. Mycoplasma bovis
115
Q

list the 7 types of bacteria that commonly cause mastitis

A
  1. Staphylococcus aureus
  2. coagulase-negative staphylococcus
  3. Streptoccus uberis
  4. Streptococcus dyslactiae
  5. Streptococcus agalactiae
  6. Enterococci and coliform bacteria (E. coli)
  7. Mycoplasma bovis
116
Q

list the 4 less common bacteria that cause mastitis

A
  1. Pseudomonas aeruginosa
  2. Trueperella pyrogenes
  3. Nocardia asteroids
  4. Klebsiella spp.
117
Q

what are the 3 types of mastitis?

A
  1. clinical
  2. gangrenous
  3. subclinical
118
Q

what are the 2 types of clinical mastitis?

A
  1. mild clinical mastitis

2. severe clinical mastitis

119
Q

what kind of pathogens cause clinical mastitis?

A

a broad range

120
Q

what is the most common symptom of clinical mastitis? discuss how skin color affects observation of this

A

mammary gland inflammation, can see redness and heat on white-skinned individuals, but it is harder to see in animals with black skin

121
Q

describe the milk in cases of clinical mastitis

A

physical changes in milk, can range from a few milk clots to appearing like serum with clumps of fibrin

122
Q

?what mostly causes clinical mastitis?

A

environmental pathogens

123
Q

do all clinical mastitis milk cultures yield organisms in culture? do we know why?

A

no, 30-40% don’t yield organisms on culture and we don’t know why

124
Q

what are the 6 signs of clinical mastitis? (milk signs)

A
  1. visual (milk)
  2. pH changes (more acidic)
  3. increased electrical conductivity in milk
  4. Bulk tank SCC increases, or electronic somatic cell counters
  5. culture testing may yield organisms
  6. positive CMT
125
Q

what type of bacteria cause severe clinical mastitis?

A

coliforms (E. coli or Klebsiella)

126
Q

what do the coliforms that cause severe clinical mastitis do? (severity wise)

A

cause higher incidence of death or agalactia-related culling

127
Q

what do the coliform bacteria that cause severe clinical mastitis release?

A

LPS (lipopolysaccharide A) endotoxin into circulation

128
Q

describe treatment for severe clinical mastitis

A

treatment for first endotoxic symptoms and then antimicrobial treatment

129
Q

what bacteria causes gangrenous mastitis?

A

Staphylococcus aureus

130
Q

what do some strains of Staph produce in gangrenous mastitis and what does this do?

A

secrete an alpha toxin that causes vasoconstriction and ischemia to the udder resulting in gangrene

131
Q

what kind of outcomes arise from treatment of gangrenous mastitis?

A

poor treatment results

132
Q

how do we often deal with animals suffering from gangrenous mastitis?

A

isolate the animal, possibly cull

133
Q

what is the problem with severe clinical mastitis caused by E. coli in terms of treatment?

A

E. coli tend to produce antibiotic resistance pretty quickly, so treatment is difficult and you will likely have to cull the animal

134
Q

describe what is happening in terms of bacteria and the mammary gland when agalactia occurs

A

bacteria have infected all of the mammary gland, and even though the paranchema (mammary tissue) regenerates every lactation, if all the epithelium is infected, the gland will never produce milk again

135
Q

will you normally see gangrenous mastitis in all the mammary glands? what does this mean?

A

no, usually only infects one gland that tends to fall off or can be removed and animal might be fine

136
Q

if clinical signs occur in a case of mastitis, what is most likely the kind of mastitis occuring?

A

mild clinical mastitis

137
Q

why is it hard to say what microorganisms cause mild clinical mastitis?

A

because microorganisms are not isolated from 30-40% of bacteriologic cultures of milk samples collected from cows with clinical mastitis

138
Q

do you always have to intervene in cases of mild clinical mastitis?

A

not always, many mild intramammary infections resolve before treatment due to immune system doing its job!

139
Q

what is the main problem we have to deal with with mild clinical mastitis?

A

many of these mild cases develop into chronic infections of mastitis, meaning a constant battle that results in mammary tissue being damaged forever and will still probably have to cull the animal

140
Q

is treatment effectiveness guaranteed if a case of mild clinical mastitis is chronic? why or why not?

A

no, because bacteria can hide in damaged tissue until you “finish” treatment, and the occur again

141
Q

when can you use culture based therapy in mild clinical mastitis?

A

if you can find the specific bacteria causing the infection in a culture, then the best treatment is a specific antibiotic

142
Q

describe the range of subclinical mastitis prevalence

A

5-75% depending on farm hygiene

143
Q

what is the estimated cost of subclinical mastitis to the US dairy industry per year?

A

more than $1 billion

144
Q

describe subclinical mastitis

A

mammary tissue infection so mild that there is no change to milk other than an increase in SCC (immune cells) and bacteria in the milk at levels that do not show so milk passes visual inspection

145
Q

what kind of reduction in milk production does subclinical mastitis cause? how does this compound and buildup

A

only causes a mild reduction in production, like 1/2 lb a day, but adds up between all the cows to cost the dairy industry all that money

146
Q

how do you diagnose subclinical mastitis and why?

A

there is no sign of infection in mammary gland or milk, so diagnose by an increase in somatic cell count beyond normal level

147
Q

what is the ONLY change seen in subclinical mastitis?

A

increase in SCC

148
Q

describe the range of allowed somatic cell counts by states and countries

A

Dairy states allow lower levels of SCCs and Europe, Aus, NZ, and Canada all allow less then the US

149
Q

what is the SCC threshold for an individual cow to be diagnoses with subclinical mastitis?

A

if an individual cow has more than 200,000 somatic cells per mL they are diagnosed with subclinical mastitis

150
Q

how is SCC determined in a cow?

A

CMT: california mastitis test

151
Q

what 2 bacteria is subclinical mastitis most often associated with?

A
  1. S. aureus (non-toxin producing)

2. Streptococcus spp.

152
Q

how is subclinical mastitis prevented?

A

good hygiene

153
Q

describe what you need to consider when treating subclinical mastitis

A

manage expectations and how much you need to treat the cow, cost effectiveness

154
Q

when do you generally avoid treatment of subclinical mastitis?

A

in lactating cows

155
Q

what is the best way to select an antibiotic to treat subclinical mastitis? does this method always provide a clear way forward?

A

culture is a good way to see what antibiotic to use, but is not always effective because infection is so mild that shedding is low

156
Q

why do you try to avoid treatment of subclinical mastitis in lactating cows?

A

because you will have a withold period of wasted milk if you treat with antibiotics

157
Q

what is cobactin (relates to mastitis)

A

an intramammary treatment with a shorter withold period than systemic treatments

158
Q

what is the most effective way to deal with subclinical mastitis?

A

prevention!

159
Q

list 7 methods of prevention of subclinical mastitis

A
  1. proper milking and appropriate milking amchine maintenance
  2. teat dipping pre and post milking
  3. early treatment of clinical cases to prevent spread and start of more subclinical cases
  4. dry cow therapy at end of lactation and teat sealant
  5. cull cows with chornic mastitis
  6. appropriate vaccination with a gram-negative core antigen vaccine to prevent coliform infections
  7. hygiene in bedding and rest areas
160
Q

what does post dip usually contain to protect teats after milking before sealing?

A

iodine

161
Q

describe udder infectious diseases in small ruminants (hella general)

A

similar to those that infect cows

162
Q

what is contagious agalactia?

A

a multi-etiological syndrome affecting small ruminants worldwide

163
Q

what is the most common/main agent causing contagious agalactia in sheep and goats?

A

Mycoplasma agalactiae

164
Q

what are the 3 symptoms of contagious agalactia?

A
  1. mastitis
  2. conjunctivits
  3. arthritis
165
Q

are all three symptoms of contagious agalactia observed together in the same animal?

A

rarely

166
Q

what is an important problem that needs to be addressed in the control of contagious agalactia?

A

the presence of asymptomatic carries

167
Q

what is the effect of antimicrobials and vaccines on contagious agalactia?

A

reduce clinical impact, but are not suitable measures to eliminate or present infection at the individual or herd level

168
Q

what is the only way to guarantee an immediate contagious agalactia-free status?

A

culling animals

Animal Health and Diseases (24 decks)

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