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Dealing with threats final exam review > Exam 1 Material > Flashcards

Exam 1 Material Flashcards

Review material covered in week 1-2 from exam 1

1
Q

What does VINDICATE mean for diagnosis differential?

A

V-Vascular
I-Infectious
N-Neoplastic
D-Degenerative
I-Inflammation
C-Congenital
A-Autoimmune
T-traumatic
E-Endocrine/metabolic

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2
Q

Gram positive cocci

A

Cluster or chains

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3
Q

Gram positive cocci clusters

A

Staphlyococcus

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4
Q

Gram positive cocci chains

A

Streptoccous

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5
Q

Gram positive rods

A

no spores
or spores

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6
Q

Gram positive rods with spores

A

Bacillus

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7
Q

Gram positive rods without spores
Filamentous

A

Erysipelothrix

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8
Q

Gram positive rods without spores
Nonfilamentous

A

Coryenbacterium or listeria

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9
Q

flagella

A

important for motility

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10
Q

pilli

A

important for adherence

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11
Q

Spores

A

Important for long survival and physical resistance

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12
Q

biofilms

A

a bacterial population becomes adherent to each other

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13
Q

quorum sensing

A

when a biofilm act as one organism

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14
Q

how do biofilms help in the pathogenesis of bacterial infections

A

avoiding colonization
avoiding phagocytosis
avoiding antibiotics

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15
Q

How do bacteria increase in number

A

binary fission

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16
Q

generation time of bacteria

A

length of time required for a single bacterium to yield two daughter cells

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17
Q

what are three factors that influence growth of bacteria

A

genetics
nutritional factors
chemical, physical, and environmental factors, microbiome

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18
Q

Small colonies=

A

Small growing bacteria

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19
Q

Big colonies=

A

fast growing

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20
Q

optimal pH for bacterial growth?

A

neutral of alkaline (7-14)

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21
Q

optimal tonicity for bacterial growth

A

isotonic to hypotonic

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22
Q

Require O2 for growth

A

obligate aerobes

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23
Q

Are killed by O2

A

obligate anaerobes

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24
Q

can grow aerobically or anaerobically

A

facultative anaerobes

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25
Q

Require reduced O2 and increase CO2

A

microaerophiles

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26
Q

Characteristics of bacteria genomes

A

Haploid circular chromosomes
Double stranded DNA

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27
Q

What are plasmids?

A

Small circular DNA which can replicate on their own

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28
Q

What do plasmids hold?

A

virulence (toxin) and antibiotic resistant genes

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29
Q

host

A

any organism that supports the survival and growth of a microorganisms

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30
Q

Saphrophytes

A

Organisms that live on dead or decaying organic matter
Usually not parasites of animals

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31
Q

Commensal relationship

A

an organism lives in/on the host without causing disease

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32
Q

Pathogenic relationship

A

parasitic and saprophytic bacteria that have the potential to cause disease

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33
Q

Carriers

A

animals that have a pathogen present while they do not show signs of clinical disease they still shed the pathogen

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34
Q

endogenous infections

A

arise from bacteria that live on skin

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35
Q

exogenous infections

A

arise from environmental bacteria

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36
Q

Pathogenicity

A

the capability of a bacteria to produce disease in the host

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37
Q

First line of defense against bacteria

A

Skin, GIT, physical barrier and chemical barrier—–(innate immunity)

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38
Q

Second line of defense against bacteria

A

Non-specific cellular barrier also innate immunity

Examples=neutrophils, macrophages, dendritic cells

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39
Q

Third line of defense against bacteria

A

Specific cellular barrier, aka adaptive immunity

examples= B cells, T cells, and antibodies

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40
Q

How does antibody-mediated immunity (AMI) work

A

the adaptive immune response destroys extracellular bacteria-lysis, phagocytosis, neutralization of toxin

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41
Q

How does cell mediated immunity (CMI) work

A

Destruction of intracellular bacteria by cytotoxic T cells

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42
Q

Plasma appearance, lipidemia

A

Looks like butter

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43
Q

Plasma appearance, Hemoglobinemia

A

Plasma looks bloody

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44
Q

Plasma appearance, Bilirubinemia

A

Yellow plasma

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45
Q

How is a PCV measured?

A

Microhematocrit tube

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46
Q

How is Hematocrit measured?

A

(RBC M x MCVfL)/10
Should equal PCV

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47
Q

Hct on bloodwork

A

Hematocrit

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48
Q

Hgb on bloodwork

A

Hemaglobin concentration

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49
Q

How is the hemoglobin concentration measured?

A

Sprectrophotometric method
should be 1/3 of PCV

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50
Q

RBC on bloodwork

A

red blood cell concentration

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51
Q

How is RBC measured?

A

Impedance count

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52
Q

MCV on bloodwork?

A

Mean cell volume

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53
Q

how is the MCV measured?

A

Impedance

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54
Q

What is MCHC on bloodwork?

A

Mean cell hemoglobin concentration

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55
Q

Normal PCV for a dog?

A

~45%

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56
Q

Normal PCV for a cat?

A

~35%

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57
Q

erythocytosis

A

dehydration

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58
Q

polycythemia

A

dehydration

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59
Q

Mild anemia markers?

A

Dogs >33%, cats>26%

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60
Q

Moderate anemia markers?

A

Dogs >24%, cats>23%

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61
Q

Marked anemia markers?

A

Dogs<23%, cats<23%

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62
Q

What is epidemiology?

A

the study of the distribution and determinants of health and disease in populations

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63
Q

Epidemiologic triad

A

host, environment, agent

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64
Q

type of tempral pattern on epidemic curves

A

Sporadic-small peaks over time
endemic-steady amount of cases over time
Epidemic-point source-One large peak over time
epidemic-propagating- steady amount of cases over time then a large increase of cases

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65
Q

Prevalence

A

How many animals are sick right now?

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66
Q

Incidence

A

What is the rate of occurrence of new cases

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67
Q

primary prevention

A

action that prevents the development of disease in an animal who is healthy

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68
Q

secondary prevention

A

identifies animals with disease at a point early enough to prevent symptoms

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69
Q

tertiary prevention

A

prevention of complications in animals who have disease

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70
Q

What is an outbreak?

A

The occurrence of disease in an area at a level exceeding the normally expected number of cases

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71
Q

P value

A

the probability that a difference of this size or larger would be observed if there really was no difference between the groups

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72
Q

P value is statistically significant

A

P value<0.05

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73
Q

Outbreak investigation process

A

-establish that an outbreak exists
-determine the key questions
define the cases and noncases
-record all events
collect data on epidemiologic factors
-look for patterns and associations between risk factors and disease
-form and test hypotheses about disease control
-Plan and implement control methods

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74
Q

Examples of innate immunity

A

-physical barriers
-Cellular components (neutrophils, macrophages)
-immediate response to infections

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75
Q

Examples of adaptive immunity

A

-B cells and antibody-mediated immunity
-T cells and cell-mediated immunity
-Memory cells and long-term protection

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76
Q

Primary immune response

A

the initial reaction of the immune system when it encounters a specific antigen for the first time

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77
Q

Latency

A

The primary immune response takes time to develop because the immune system needs to recognize the new antigen

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78
Q

Which immune response is slower and weaker?

A

The primary

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79
Q

What memory cells are generated during the primary immune response?

A

Memory B cells and memory T cells

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80
Q

How do memory B cells and memory T cells work?

A

the cells “remember” the antigen to have faster reaction if organism is re-exposed to pathogen

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81
Q

Secondary immune response

A

Occurs upon re-exposure to the same antigen

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82
Q

Why is the secondary immune response work more quickly?

A

Memory B cells and memory T cells are able to quickly recognize the antigen and trigger an immune response

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83
Q

The production of antibodies during the secondary immune response

A

There is a higher production of antibodies compare to the primary response so the antibodies can eliminate the pathogen more efficiently

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84
Q

Is the secondary immune response long-lasting or short-lasting?

A

Long-lasting due to the presence of memory cells

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85
Q

Specificity of the secondary immune response

A

The secondary immune response is highly specific to the encountered antigen

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86
Q

What immune systems are involved in response against bacterial infections?

A

The innate immune system and the adaptive immunity

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87
Q

How does the innate immune response work against bacterial infections?

A

The system assists in bacterial destruction through opsonization and lysis

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88
Q

What are key components of the innate immune system?

A

Neutrophils and macrophages

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89
Q

How does the adaptive immune system respond to bacterial infections?

A

The antigens of the bacteria present stimulate B cells to produce antibodies

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90
Q

How do T cells play a roll against bacterial infections?

A

T cells help activate macrophages and cytotoxic T cells–which kills infected cells

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91
Q

What immunity fights against extracellular bacteria?

A

humoral immunity

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92
Q

How does the humoral immune system attack extracellular bacteria?

A

-neutralize toxin
-opsonization by antibodies
-killing by classical complement pathway
-phagocytosis activated by macrophages

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93
Q

What type of immunity is used against intracellular bacteria?

A

Cell mediated immunity

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94
Q

What does cell mediated immunity do?

A

-Macrophage activation and killling
-Destruction by cytotoxic T cells

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95
Q

What bacteria causes Canine Pyoderma infection in dogs?

A

Staphylococcus spp.

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96
Q

How does the innate immune system respond to viral infections?

A

IFNs are released
-antiviral proteins called interferons

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97
Q

How does the adaptive immune system respond to viral infections?

A

-B cells produce antibodies that neutralize viruses
-long-lived plasma cells and memory B cells contribute to long term immunity
-T cells destroy virus infected cells
-Helper T cells coordinate the immune response by activating other immune cells
-Memory T cells contribute to long-lasting immunity

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98
Q

What recognizes viral patterns in the cell?

A

PRRs

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99
Q

IFNs

A

interferons, glycoproteins that regulate gene expression

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100
Q

How do antibody binding prevent viral infections?

A

-blocking viral invasion
-stimulating phagocytosis
-triggering complement-mediated virolysis
-promoting viral clumping
-NOT by direct virus destruction

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101
Q

What cells target infected cells for destruction? (relating to viruses)

A

NK cells and cytotoxic T cells

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102
Q

How do cytotoxic T cells play a role in cell-mediated immunity to viruses?

A

-Induce apoptosis
-Recognize peptide-MHC-I complexes and kill cells
-sensitized by type I interferons

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103
Q

How do helper T cells provide support to other immune cells?

A

-Cytotoxic T cells (killing)
-Macrophages (phagocytosis)
-B cells (antibody production)

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104
Q

How do RNA viruses evade the immune system?

A

Antigenic variation

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105
Q

Anatomy

A

Shape and structure of organisms

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106
Q

Anatomic Pathology

A

Morphologic alteration

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107
Q

Pathogenesis

A

Mechanism of disease

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108
Q

Diagnosis

A

Medical ability of recognizing lesions in a live or dead animal, understanding the etiology and pathogenesis, establishing recommendation for treatment/control and prevention of a disease

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109
Q

Necropsy

A

Post mortem examination

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110
Q

Lesion

A

Abnormal tissue change

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111
Q

Etiology

A

Cause of disease

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112
Q

The different factors that cause disease

A

Predisposing-cold, overcrowding
determinant-infectious agents, deficiencies

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113
Q

Where does fat become removed in the body?

A

First the skin, then abdomen, then kidneys, then heart, then bone marrow

114
Q

Abrasion

A

Skin damage with loss of epidermis and a portion of the dermis

115
Q

Lacerations

A

Deep cut or tear in skin or flesh

116
Q

puncture

A

penetrating wound caused by a sharp object

117
Q

Incision

A

Wound created by a sharp tool

118
Q

Perforations

A

A hole that develops through the wall of a body organ

119
Q

Rupture

A

A break or tear in any organ or soft tissue

120
Q

Presumptive diagnosis

A

Fast determination of potential problems

121
Q

Cell/tissue response to injury

A

-Adaptation
-Degeneration
-Death (by apoptosis or necrosis)

122
Q

What is hypertrophy

A

Increase in cell size

123
Q

Where is hypertrophy most common?

A

In striated muscle due to increased workload

124
Q

Is hypertrophy reversible or irreversible?

A

Reversible

125
Q

Primary disease of the myocardium; common in cats

A

Hypertrophic Cardiomyopathy

126
Q

Hyperplasia

A

Increase in cell number

127
Q

Cells that are unable to undergo hyperplasia?

A

Epidermis, intestinal, epithelium, bone marrow, neurons, cardiac/skeletal muscle

128
Q

Physiological causes of hyperplasia?

A

-Hormonal
-Compensatory

129
Q

Difference between hyperplasia and neoplasia

A

Hyperplasia is the increase in cell number due to a stimulus. Once stimulus stops, the hyperplasia stops. In neoplasia cell replication is uncontrolled and does not respond to external stimuli

130
Q

What is metaplasia?

A

One differentiated cell type replaced by another

131
Q

What causes metaplasia?

A

It is an adaptive change to withstand adverse environmental conditions

132
Q

Is metaplasia reversible or irreversible?

A

Potentially reversible

133
Q

What is atrophy?

A

The decrease in size of a cell, tissue, or organ after normal growth has been reached

134
Q

Reduction of cell numbers uses what mechanism

A

Apoptosis

135
Q

What are the physiological causes of atrophy?

A

Involution

136
Q

What are the pathological causes of atrophy?

A

Inadequate nutritive supply, decreased workload, denervation, pressure, loss of endocrine stimulation

137
Q

What are characteristics of a virus?

A

-Consist of DNA or RNA, NOT both
-Lack independent metabolic system
-Require host cells for replication
-Consists of an intracellular reproductive cycle and an extracellular transmissive cycle

138
Q

Where do viroids replicate?

A

Nucleus

139
Q

Where do virusoids replicate?

A

Cytoplasm

140
Q

What are prions?

A

Proteins only, a small proteinaceous infectious particle

141
Q

Why are prions hard to destroy?

A

They have a high resistance to heat, UV, irradiation, and chemicals

142
Q

What are non-enveloped viruses made of?

A

-Protein subunit
-Structure Unit
-Capsomer
-Capsid
-Nucleocapsid

143
Q

What are envelope viruses made out of?

A

-Protein subunit
-Structure unit
-Capsomer
-Capsid
-Nucleocapsid
-Envelope (peplomer/spike, matrix, proteins, and lipids)

144
Q

Do enveloped or non-enveloped viruses survive better in the environment? Why?

A

Non-enveloped viruses survive better in the environment. Enveloped viruses are easier to inactivate and destroy

145
Q

Pathogenesis of enveloped viruses

A

Budding through infected cells, chronic/persistent infections

146
Q

Immunology of enveloped viruses

A

Grlycoprotein antigens: VN, CMI, vaccine immunity

147
Q

Pathogenesis of non-enveloped viruses

A

Lytic cell infection, associated with acute disease

148
Q

What is the role of the capsid?

A

Protecting the genome

149
Q

What are the non-structured components of the virus?

A

Enzymes, replication, regulatory proteins

150
Q

Endemic/Enzootic

A

multiple, continuous transmissions, disease presence in a defined population/region/time

151
Q

Epidemic/epizootic

A

Peaks in incidence exceeding the endemic baseline

152
Q

Pandemic/panzootic

A

Worldwide epidemic

153
Q

Case/infection ratio

A

Proportion of infections resulting in clinical disease

154
Q

Case/fatality ratio

A

proportion of infections resulting in lethal disease

155
Q

New biotypes

A

Changed characteristic

156
Q

Direct contact

A

Licking, rubbing, biting, sexual contact

157
Q

Indirect contact

A

Fomites, eating, bedding, vehicles, surgical instruments, needles

158
Q

Vertical transmission

A

Movement of virus from parents to their offspring during gestation via placenta, perinatally, colostrum, milk

159
Q

Germline transmission

A

Virus integrated into genome of ovum, transcription and replication in offspring

160
Q

Biological vector

A

Virus replicate and magnify in vector

161
Q

Mechanical vecctor

A

No virus replication in vectors, not efficient for transmission

162
Q

Zoonotic transmission

A

Viral diseases transmissible under natural conditions from animal to humans

163
Q

Latrogenic transmission

A

Patient to patient transmission under veterinary care during the interactions between the vets and the animals

164
Q

Nosocomial transmission

A

Occurs while animals are in hospital or clinic under care of veterinarians

165
Q

Syncytia

A

A characteristic CPE, the membrane fusion of neighboring cells

166
Q

How does Herpes viruses enter cells?

A

By fusing with the cell membrane

167
Q

Where does the herpes virus replicate?

A

In the nucleus of the host cells

168
Q

How is the herpes virus spread?

A

Close contact

169
Q

Bovine herpesvirus 1

A

Alphaherpesvirinae

BHV1.1 Respiratory and reproductive (abortion)
BHV1.2 Genital
1.2a:abortions, 1.2:no abortions

170
Q

How is infectious bovine rhinotracheitis (IBR) spread?

A

Through aerosol transmission

171
Q

Where does IBR replicate?

A

The mucous membranes of the upper respiratory system

172
Q

Where does the IBR shed?

A

In nasal secretions

173
Q

IBR can lead to what respiratory diseases?

A

Rhinitis, trachelitis, secondary bacterial pneumonia (bovine respiratory disease complex)

174
Q

IBR can cause what in pregnant cows?

A

Viremia, resulting in abortion

Multifocal hepatic necrosis in the fetus with intranurclear inclusions

175
Q

What are clinical signs of IBR?

A

Necrotizing tracheitis and ulcerative dermatitis

176
Q

Multifocal necrosis in the liver is indicative of what?

A

Herpesvirus abortion

177
Q

Describe the lesion that would be found in a cow infected with IBR with secondary bacterial bronchopneumonia

A

Consolidated cranial lobes of the lungs

178
Q

Equine Herpes Virus 1 two strains:

A

EHV1 D752, N752

179
Q

What are the effects of EHV1 D752

A

Respiratory-rhinopneumonitis
Reproductive- abortion
Neurological

180
Q

What are the effects of EHV2 N752

A

Respiratory, reproductive, non-neurologic

181
Q

How is equine rhinopneumonitis spread?

A

Through aerosol trasmission

182
Q

Where does the virus EHV-1 and EHV-4 replicate

A

The mucous membranes of the upper respiratory tract and regional lymph nodes

183
Q

Respiratory diseases due to equine rhinopneumonitis

A

-Respiratory disease: rhinitis, tracheitis, extend to lungs in young animals

184
Q

Reproductive disease as a result of equine rhinopneumonitis

A

-Viremia in pregnant mare=abortion
-EHV-1 can result in placental vasculitis and thrombosis
-Multifocal hepatic necrosis in the fetus with intranuclear inclusions

185
Q

What strain of equine herpesvirus is associated with equine herpes myeloencephalopathy

A

The D752 strain

186
Q

What are the neurological effects?

A

Vasculitis, necrosis, and hemorrhage in the spinal cord and brain

187
Q

Are you required to report EHV1 D752?

A

If it is the neurological form, yes

188
Q

How is Canine herpesvirus 1 contracted?

A

Through aerosol or in utero

189
Q

Where does the canine herpesvirus 1 replicate?

A

In the mucous membranes of the upper respiratory tract, pharynx, and tonsils

190
Q

Where does the Canine herpesvirus 1 shed?

A

From nasal and vaginal secretions

191
Q

When is the most efficient time for the canine herpesvirus 1 to replicate?

A

Replication is most efficient in temperatures below body temperature

192
Q

What age of dogs are most susceptible to canine herpesvirus 1?

A

Neonatal pups, during first 3 weeks of life

193
Q

Will pups get canine herpesvirus 1 from their mother?

A

If the mom is infected within 3 weeks prior to giving birth yes

194
Q

If a mother is infected with canine herpesvirus 1 will following litters be affected?

A

No, the mom has immunity and the pups won’t have any problems

195
Q

How is feline herpesvirus 1 spread?

A

Through aerosol contact

196
Q

Where does feline herpesvirus 1 replicated?

A

In the mucous membranes of the upper respiratory tract and conjunctivia

197
Q

How does feline herpesvirus 1 shed?

A

Through nasal secretions

198
Q

Is feline viral rhinotracheitis common?

A

About 40% of respiratory disease in cats is from viral rhinotracheitis

199
Q

What are the clinical signs of feline herpesvirus 1?

A

Upper respiratory tract infection: sneezing, hypersalivation, conjunctivitis

200
Q

What can result from feline herpesvirus 1?

A

Ulcerative keratitis

201
Q

Is porcine herpesvirus 1 host specific?

A

No, this is the only alphaherpesviruses that can infect other species but NOT humans

202
Q

Is porcine herpesvirus 1 eradicated?

A

In US swine hers but wild pigs may still be infected

203
Q

Another name for porcine herpesvirus 1

A

Aujeszky’s disease
Pseudorabies in other animals

204
Q

How is Aujeszky’s disease transmitted?

A

Through aerosol

205
Q

Where does the porcine herpesvirus 1 replicate?

A

In the epithelium of the oropharynx and tonsils

206
Q

What secretions are large amount of porcine herpesvirus 1 shed?

A

Nasal secretions, milk, and semen

207
Q

What is the mortality rate of Aujeszky’s disease?

A

Almost 100% in suckling pigs

208
Q

How does psuedorabies present in animals other than pigs?

A

Manifests as severe neurological disease and pruitis and death

Some young pigs show neurological signs

209
Q

How does Aujesky’s disease affect a pregnant sow?

A

Usually results in abortion with hepatic necrosis and intranuclear inclusions in the fetus

210
Q

What type of cells do gammaherpes viruses infect?

A

Lymphocytes

211
Q

Where do parvoviruses replicate?

A

In the nucleus of rapidly dividing cells
Examples: crypt epithelial cells, leukocytes, and the developing fetus

212
Q

True or false
Parvoviruses form intranuclear inclusion bodies

A

True

213
Q

Why do parvoviruses spread so easily from organism to organism?

A

Parvoviruses are able to survive in the environment for a long time. They are resistant to heat, solvents, disinfectants, pH changes

214
Q

What type of genome does parvovirus have?

A

Linear, single stranded DNA genome

214
Q

What are examples of viruses that are host-range mutants of feline paleukopenia virus?

A

Canine parvovirus, mink enteritis virus, and raccoon parvovirus

214
Q

How does feline panleukopenia shed in the environment?

A

Through the feces of infected cats, lives in environments

214
Q

When does feline panleukopenia disease occur in cats?

A

Typically in weaned kittens after maternal antibody wanes

215
Q

What does the seasonal pattern of feline panleukopenia relate to?

A

The pattern of birth of kittens

215
Q

What occurs if a pregnant mother contracts feline panleukopenia?

A

Abortion or cerebellar hypoplasia

215
Q

How does feline panleukopenia spread?

A

It’s transmitted through inhalation or ingestion

216
Q

Where does feline panleukopenia replicate?

A

In the oropharynx and regional lymph nodes

217
Q

How soon does viremia develop in cats infected with feline panleukopenia?

A

Within 24 hours

218
Q

What cells does feline panleukopenia infect?

A

Intestinal crypts, bone marrow, thymus, lymph nodes, and spleen

219
Q

What are clinical signs of feline panleukopenia?

A

Depression, vomiting, diarrhea, fetal death, intention tremors (cerebellar ataxia)

220
Q

Why does death occur in cats with feline panleukopenia?

A

It typically occurs due to secondary infections or dehydration

221
Q

What do pups die from in utero when the adult contracts canine parvovirus?

A

Myocarditis and heart failure

222
Q

What age do dogs typically become infected with canine parvovirus?

A

Pups between weaning and 6 months of age

223
Q

Why do some dogs who are suspected to have canine parvovirus not test positive on a snap test?

A

Due to the virus mutating and new variants emerging

224
Q

How is canine parvovirus spread?

A

Through ingestion

225
Q

Where does replication of canine parvovirus occur?

A

Oropharynx and Peyer’s patches (found in the intestine)

226
Q

How soon does viremia develop after canine parvovirus infects dogs?

A

24 hours

227
Q

Where does canine parvovirus replicate?

A

In the intestinal crypts, bone marrow, thymus, lymph nodes, and spleen

228
Q

What are clinical signs of canine parvovirus?

A

Depression
Vomiting
Bloody diarrhea
Fetal death through myocardial necrosis

229
Q

Why does death often occur in dogs with canine parvovirus?

A

Death occurs secondary to dehydration and endotoxemia

230
Q

What kinds of pigs are immune to porcine parvovirus?

A

Sows are typically immune in endemic farms

231
Q

How could gilts be susceptible to infection from porcine parvovirus?

A

Through mating and pregnancy

232
Q

What cells does porcine parvovirus target

A

Mitotically active cells in the fetus

233
Q

How soon does transplacental infection of porcine parvovirus occur after infection of the mother?

A

10-14 days

234
Q

When does damage occur to the fetus as a result of porcine parvovirus?

A

Usually before 70 days gestation due to the fetus’ poor immunity

235
Q

What occurs when embryos contract porcine parvovirus?

A

Resorption and infertility

236
Q

What occurs when a fetus before day 70 of gestation contracts porcine parvovirus?

A

Still birth or mummification of the fetus

237
Q

What occurs to a fetus that contracts porcine parvovirus after day 70 of gestation?

A

Pigs are born alive and healthy

238
Q

What are the possibilities that can occur when an embryo or fetus contracts porcine parvovirus?

A

SMEDI syndrome
Stillbirth Mummification Early embryonic Death Infertility

239
Q

What are characteristics that all parvoviruses have?

A

-They replicate in rapidly dividing cells
-They are extremely stable in the environment (live in the environment for a while)

240
Q

What are similarities between feline parvovirus and canine parvovirus?

A

-Primarily enteric
-Fetal death/abortion is possible

241
Q

What is different about poxviruses compared to other DNA viruses?

A

Poxviruses replicate in the cytoplasm

242
Q

What is the largest virus that causes disease in domestic animals?

A

Poxviruses

243
Q

How are poxviruses in the environment

A

They are stable in the environment while there are dry conditions

244
Q

How are poxviruses spread?

A

Aerosol
Direct contact
Mechanical (insects)

245
Q

What causes the raised skin lesions that occur due to infection of poxviruses?

A

Viral proteins are released resulting in epidermal proliferation

246
Q

Capripox viruses occur in what area of the United States?

A

NONE, they’ve been eradicated in the US–if it is found in the US due to foreign animals and is a reportable disease

247
Q

What is capripox viruses called when sheep or goats are infected?

A

Sheep pox
Goat pox

248
Q

What is the capripox virus called when cattle are infected?

A

Lumpy skin disease

249
Q

What are three different types of avipox viruses?

A

Fowl pox
Pigeon pox
Turkey pox

250
Q

What animals are affected by fowl pox?

A

Chickens and turkeys

251
Q

How does fowl pox present?

A

Lesions on the head and oral mucous membranes

252
Q

How is fowl pox transmitted?

A

By biting arthropods

253
Q

What does suipoxvirus cause?

A

Mild skin disease

254
Q

How is suipoxvirus spread?

A

By the pig louse (looks like a tick)

255
Q

What type of parapoxviruses are zoontoic and able to spread to humans?

A

All of parapoxviruses are transmissible to humans

256
Q

What causes the orf virus?

A

Parapoxvirus

257
Q

What animal is typically affected by orf virus?

A

Young sheep

258
Q

Where are the lesions that occur as a result or orf virus?

A

The muzzle and lips

259
Q

What parapoxvirus affects young calves?

A

Bovine papular stomatitis

260
Q

Where are the lesions when a calf has bovine papular stomatitis?

A

On the muzzle, tongue, and esophagus

261
Q

What paravirus causes milker’s nodules in people?

A

Pseudocowpox

262
Q

Where are lesions common as a result of pseudocowpox?

A

The teat

263
Q

What type of virus is rabbit myxoma virus?

A

Leporipoxviruses

264
Q

What are the natural hosts of rabbit myxoma virus?

A

Cottontail rabbits—they only develop mild disease

265
Q

What clinical signs do European rabbits develop as a result of Rabbit myxoma virus?

A

Severe disease with swelling of the facial and periocular tissues

266
Q

Why was rabbit myxoma virus introduced to Europe, Australia, and Chile?

A

As a biological control measure

267
Q

What does squirrel fibroma virus cause?

A

Fibromas in squirrels

268
Q

What’s another word for Red Blood cells?

A

Erythrocytes

269
Q

What are the hierarchy of controls for workplace hazards?

A

-Elimination
-Substitution
-Engineering controls
-Administrative Controls
-PPE

270
Q

What three elements of infectious agents are required for transmission?

A

A source/reservoir
A susceptible host
A mode of transmission

271
Q

What are the three levels of biosecurity?

A

-Conceptual
-Structural
-Procedural

272
Q

What is cleaning?

A

Remove the dirt, organic matter, debris from surface (decreases the number of microbes)

273
Q

What is disinfection?

A

Using a disinfecting agent to remove most microbes

274
Q

What is sterilization?

A

Destroying all forms of microbial life

275
Q

Proper way to handle boots/footwear after using

A
  1. Remove gross organic matter
  2. Apply detergent+water
  3. Rinse water
  4. Apply disinfectant
  5. May rinse with water
  6. Dry
276
Q
A

Dealing with threats final exam review (1 decks)

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