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Veterinary Technician Complete (3 years) > Microbiology and Immunology (2nd) > Flashcards

Microbiology and Immunology (2nd) Flashcards

All information that was taught to me while attending Vanier College's "Animal Health Technology" Program, located in St-Laurent Montreal.

1
Q

What are the general characteristics of viruses

A

Can have multiple shapes, have a capsule and some have an envelope, no organelles, have either DNA or RNA or, need an electron microscope to view, need a host, lysogenic or lytic cycle

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2
Q

What is a host range

A

Spectrum of what the virus can affect. Only affect certain cells such as hair

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3
Q

What is a bacteriophage

A

A virus that only affects bacteria

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4
Q

What is the structure of a bacteriophage

A

Have s capsid, nucleic acid and sometimes an envelope

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5
Q

What are the five steps of the lytic cycle for a bacteriophage

A

Attachment, penetration, biosynthesis, maturation, release which lyse the cell

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6
Q

Describe the attachment phase of the lytic cycle

A

Specific and based on host range

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7
Q

Describe the penetration phase of the lytic cycle

A

Lysosome makes holes (enzyme)

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8
Q

Describe the biosynthesis phase of the lytic cycle

A

Replication. Uses host cell mechanisms for replication

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9
Q

Describe the release phase of the lytic cycle

A

Lyse the cell to allow virus to infect neighbour cells

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10
Q

What are the 5 stages of the lysogenic cycle

A

AttachmentPenetrationDna integrationHost cell replication Virus dna removes itself from the host cell dna

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11
Q

Describe the DNA integration phase of the lysogenic cycle

A

The virus puts its DNA into host DNA. The virus now becomes a prophage

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12
Q

Describe the host cell replication phase of the lysogenic cycle

A

It also replicates the viruses DNA

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13
Q

Describe the virus DNA removal phase of the lysogenic cycle

A

The virus DNA removes itself from the host cell DNA and can now join the lytic cycle and then go through biosynthesis

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14
Q

What’s the difference between animal and bacterial viruses

A

In animal viruses the full virus goes into the host cell but with bacterial viruses the DNA/rna goes inside

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15
Q

How does virus remove its envelope/capsid after penetration

A

By fusion/endocytosis

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16
Q

Where is Viral replication in bacterial infections

A

In the cytoplasm

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17
Q

In DNA animal viruses the replication occurs where

A

️Nucleus

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18
Q

In rna animal viruses the replication occurs where

A

In the cytoplasm

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19
Q

What does a lysogenic cycle mean for an animal

A

Chronic infections, latent infection, slow viral infection and cancer

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20
Q

What happens to a cell if a virus has an envelope

A

It won’t lyse the cell

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21
Q

What happens to a cell if a virus doesn’t have an envelope

A

It will lyse the cell and steal part of the plasma membrane

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22
Q

What are the 4 things a virus needs to cause disease

A

A route of infection Disemmenation (to get where it needs to be - generalized or local)Cause disease (has an incubation period)Shed and transmit itself

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23
Q

Describe an acute disease

A

Short term, clinical signs, persistant

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24
Q

Describe a latent disease

A

Virus is inside of host cell but doesn’t have symptoms

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25
Q

Describe a chronic disease

A

Virus is present and can be shed

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26
Q

Describe a slow infection

A

Virus load increase over years and eventually kills you

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27
Q

What is vertical transmission

A

Mother to child

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28
Q

What is horizontal transmission

A

Via fomites/vectors from person to person

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29
Q

What are the seven feline viral diseases

A

Panleukopenia, rhinotracheitis, calici virus, feline Corona virus/FIP, feline leukemia virus, feline immunodeficiency virus, rabies

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30
Q

What family is Panleukopenia in

A

Parvoviridae

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31
Q

Describe the structure of the Panleukopenia virus

A

Non-envelope DNA virus

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32
Q

How long can panleukopenia survive in the environment

A

For years on contaminated surfaces. Extremely stable virus

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33
Q

What can Panleukopenia cause in kittens

A

Severe acute gastroenteritis and leukopenia

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34
Q

Who are the most susceptible for panleukopenia

A

2 to 6 months of age cats

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35
Q

Describe the mortality rate for panleukopenia in kittens

A

Very high mortality rate. Can also kill susceptible older cats

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36
Q

Describe the incubation period for Panleukopenia

A

Five days

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37
Q

What is the route of infection for panleukopenia

A

Oral route

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38
Q

What happens if a mother is infected with panleukopenia in utero infection in first trimester

A

Abortion and fetal death

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39
Q

Describe what happens if a mother is affected with panleukopenia in second and third trimester

A

Cerebellar hypoplasia. Versus myocarditis for puppies

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40
Q

How is Panleukopenia transmitted

A

Virus is shed on all body secretions but primarily feces and can be transmitted in utero

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41
Q

What are the clinical signs of panleukopenia

A

Lethargy, dehydration, vomiting, diarrhea, abdominal pain, turgid intestines, fever, hypothermia

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42
Q

What are the clinical signs if a kitten is infected in utero or neonatally

A

Ataxia, hypermetria, incoordination. The signs persist for life but are not progressive

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43
Q

What is the treatment for Panleukopenia

A

Hospitalization with aggressive supportive treatment. IV fluids, antibiotics, antiemetics antacids

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44
Q

How do you prevent Panleukopenia

A

Disinfection of cages, floors, food and water dishes with bleach. Vaccination

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45
Q

What causes feline upper respiratory infection

A

A complex of viral and bacterial agents. Sneezing nasal congestion and nasal discharge. Herpes virus, calici virus, Bordetella bronchiseptica, chlamydia Felis, mycoplasma

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46
Q

What family is rhino in

A

Herpesviridae

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47
Q

Describe the structure of the rhinovirus

A

Envelope dna virus. Latent infection possible

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48
Q

Which cats do rhinotracheitis infect

A

Cats of all ages but mostly kittens. Can also in fact many exotic cats.

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49
Q

What does rhinotracheitis cause

A

Acute upper respiratory tract infection. Very widespread in the cat population

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50
Q

What Is the incubation period for rhinotracheitis

A

2 to 6 days

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51
Q

What is the route of infection for the rhinotracheitis virus

A

Oral, intranasal or conjunctival exposure

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52
Q

What is the pathogenesis of the rhinotracheitis virus

A

Attacks epithelial cells and causes necrosis of the upper respiratory tract and ocular epithelia. Pulmonary involvement is rare. All cats infected become chronic carriers

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53
Q

What are the clinical signs of the rhinotracheitis virus

A

Sneezing, Serous to micro purulent nasal discharge. Turbinate distruction might be permanent and lead to chronic sinusitis. Possible ulcerative keratitis, occasional oral ulcers. Possible anorexia

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54
Q

What can happen if kittens under four weeks of age get rhinotracheitis

A

Can be fatal.

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55
Q

What happens if pregnant queens get rhinotracheitis

A

Can abort or have severe infections in neonates

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56
Q

What is the treatment for rhinotracheitis

A

Frequent cleaning of eyes a nose. IV fluid antibiotics antivirals appetite stimulants nebulization reducing stress

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57
Q

What family is the calici virus in

A

Caliciviridae

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58
Q

Describe the structure of the calici virus

A

Non-envelopes are in a virus. Many different strains of variable degrees of Virulence

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59
Q

What is calici virus cause

A

Common viral respiratory disease of domestic and exotic cats. Highly contagious. Common in multi-cat household and breeding catteries

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60
Q

Who’s susceptible to the calici virus

A

Cats of any age but young kittens more susceptible. High morbidity and mortality can reach 30% in young kittens. Prognosis is excellent in older kittens unless severe pneumonia develops

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61
Q

What is the incubation period for calici virus

A

2-6 days

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62
Q

What are the three forms of calici virus

A

PneumotropicRheumaticVirulent systemic

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63
Q

Describe the pneumotropic form of calici virus

A

Affect the upper respiratory tract and rarely of the lower respiratory tract

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64
Q

Describe the rheumatic form of the calici virus

A

Joint pain and lameness in kittens

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65
Q

Describe the Virulent systemic form of calici virus

A

Severe clinical signs in adults

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66
Q

Describe the route of infection for calici virus

A

Ingestion

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67
Q

What is the dessemination of the calici virus

A

Replication and oropharyngeal tissues. Spreads primarily to epithelium of conjunctiva, nose and oral cavity. Causes rapid cytolysis of infected cells.

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68
Q

What are the clinical signs of calicivirus

A

Anorexia, dehydration, fever, conjunctivitis, oral discharge, blepharospasms, chemosis, ulcers on tongue, dyspnea

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69
Q

What is the treatment for calici virus

A

Clean eyes and nose, supportive treatment if anorexic, antibiotics, ophthalmic antibiotics

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70
Q

Describe the transmission for calici virus

A

Cat to cat contact, virus shed and high amounts and affected cats. Recovered cats can be persistently infected and shed smaller quantities of virus in their saliva

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71
Q

How do you prevent calici virus

A

Isolation, disinfection, vaccination

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72
Q

What family does the corona virus belong to

A

Corona Viridae

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73
Q

Describe the structure of the coronavirus

A

Enveloped RNA virus

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74
Q

What can the coronavirus cause

A

Feeling Coronaviral enteritis, feline infectious peritonitis

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75
Q

Describe feline coronal viral enteritis

A

Mild, self-limiting diarrhea. Transmitted mainly by fecal oral route or through saliva. Can also be transmitted intraplacental. No vaccinations

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76
Q

Describe feline infectious peritonitis

A

Occur sporadically. Chronic debilitating disease. Usually fatal with mortality near hundred percent. In vivo mutation transforms the low Verelint introduced into the aggressive lethal virus. More common in cats six months to two years of age and more common in males

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77
Q

Describe the pathogenesis for FIP

A

FIP virus replicates in the upper respiratory tract. Viruses taken up by the micro fighters and transported throughout the body. Replication of perivascular sites cause nodules and liver spleen lungs etc. lesions also appear in Pericarditis

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78
Q

What are the two forms of FIP

A

Wet form (effusive) and dry form (non effusive). Host immune status determines the pathogenesis and clinical outcome

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79
Q

What are the clinical signs for the wet form of FIP

A

Abdominal distention with ascites, pleural effusion, muffled heart sounds, abdominal masses

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80
Q

What are the clinical signs for the dry form of FIP

A

Uveitis, ataxia, personality changes, seizures, abdominal masses

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81
Q

What is the treatment for FIP

A

Incurable. Wet form will die within two months. Dry form have chronic disease but fatal

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82
Q

What family is the feline leukemia virus and feline immunodeficiency virus part of

A

Retrovirudae

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83
Q

Describe the structure of the retroviruses

A

Enveloped RNA virus

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84
Q

What does leukemia result in

A

Immunosuppression myelosuppression and neoplasia. Cats under one year more susceptible. Outdoor cats are more at risk. And males are more at risk than females

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85
Q

What’s the route of infection for feline leukemia

A

Oral and nasal cavities

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86
Q

Describe the dissemination for feline leukemia

A

Virus replicates an oral pharyngeal lymphoid tissues. Cats can moat a few full immune response on the limited the infection or have an ineffective at me and response and become very manic. Once premier occurs the virus replicates and other lymphoid tissues and bone marrow. Latent infection may be reactivated after stress

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87
Q

What are the clinical signs of feline leukemia virus

A

Anemia, weight loss, anorexia, diarrhea, respiratory distress, liver and kidney disease, lymphoma

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88
Q

What’s the treatment for feline leukemia cats

A

No treatment if no clinical signs. Antibiotics, blood transfusion, chemotherapy. Leukemia positive cats can live for several years

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89
Q

How is the feline leukemia virus transmitted

A

Through saliva, can also be transmitted through blood and transplacentally. Mutual grooming, same food and water bowls

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90
Q

Who is at risk for the feline immunodeficiency virus

A

All feelings. Male cats are two times more likely than females. Stray intact adult male cats are at higher risk.

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91
Q

Describe the acute phase of the feline immunodeficiency virus

A

Viral replication and salivary gland, lymph nodes, Simons. Last days to a few weeks. May cause fever and lethargic

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92
Q

Describe the clinically latent phase of feeling immunodeficiency virus

A

Immune system contains but does not eliminate the virus, no clinical signs, cats are transmitting virus through bite and blood, lasts months to several years

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93
Q

Describe the terminal phase of feeling immunodeficiency virus

A

Viral replication overwhelms the immune system. Immune deficiency causes opportunistic infections and neoplasia

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94
Q

How is feline immunodeficiency virus transmitted

A

Cat bites. Through bite wounds and blood contamination. Also transmitted through colostrum

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95
Q

What are the seven canine viral diseases

A

Distemper, adenovirus, para influenza, parvovirus, coronavirus, papilloma virus, rabies

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96
Q

What is the family name for canine distemper

A

Paramyxoviridae

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97
Q

Describe the structure of the canine distemper virus

A

Enveloped RNA virus

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98
Q

What symptom manifestations does distemper cause

A

Respiratory, gastrointestinal, central nervous system

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99
Q

What is the host range for distemper

A

Dogs, wolves, foxes, ferrets, raccoons, skunks, lion

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100
Q

How is the morbidity and mortality in dogs

A

High morbidity and mortality . 50% mortality and unvaccinated dogs

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101
Q

Which age range is more susceptible to distemper

A

3 to 6 months more susceptible

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102
Q

What is the incubation period for distemper

A

3 to 8 days

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103
Q

Describe the route of infection for distemper

A

Inhaled droplets of infected secretions

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104
Q

Describe the dissemination of distemper

A

Macrophages carry the virus to local lymph nodes and then the virus spreads via viremia to respiratory, gastrointestinal, urogenital tract and central nervous system

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105
Q

What are the non-neurological signs of distemper

A

Fever, anorexia, nasal and ocular thick discharge, coughing, vomiting, diarrhea

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106
Q

What are the neurological signs of distemper

A

Seizures, circling, ataxia, paralysis

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107
Q

What happens to dogs that survive distemper

A

They often have lifelong nervous system complications

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108
Q

How do you treat distemper

A

Supportive care, IV fluid, antibiotics, anticonvulsive, analgesic

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109
Q

How long do infected dogs with distemper shed the virus for

A

Several months

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110
Q

How do you prevent canine distemper

A

Vaccination, prevent contact with wildlife, disinfection, isolation of infected puppies

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111
Q

What is the family of the canine adenovirus

A

Adenoviridae

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112
Q

Describe the structure of the canine adenovirus

A

Non-envelope DNA virus

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113
Q

What is type one canine adenovirus

A

Infectious hepatitis

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114
Q

What is type two canine adenovirus

A

Respiratory infection

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115
Q

What can canine adenovirus one infect

A

Foxes, wolves, coyotes, skunks, bears

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116
Q

What can canine adenovirus one cause

A

Acute or chronic hepatitis

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117
Q

In which age range is the at T9 adenovirus most common

A

Dogs less than one year of age

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118
Q

What is the incubation period for the acute disease version of K9 adenovirus one

A

4 to 9 days

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119
Q

What is the route of infection for canine adenovirus one

A

Oro nasal

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120
Q

What is the dissemination for canine adenovirus one

A

Virus replicates in tonsils then the following viremia there is viral replication in the liver, kidney, spleen, lungs

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121
Q

What are the clinical signs for canine adenovirus one

A

Most cases are asymptomatic. Can have peracute, acute or mild disease

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122
Q

Describe the clinical signs for the acute disease

A

Fever, anorexia, Lethargy, vomiting, diarrhea, hepatomegaly, abdominal pain

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123
Q

What will 20% of dogs get when they get infected with canine adenovirus one

A

Anterior uveitis and corneal edema. hepatitis Blueeye

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124
Q

How do you treat canine adenovirus one

A

Fluid therapy, antibiotics, antiemetics, antiacids

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125
Q

How is canine adenovirus one transmitted

A

Through feces and saliva. Once were covered dogs we should the virus in their urine for several months

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126
Q

How do you prevent canine adenovirus one

A

Vaccination

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127
Q

Describe canine adenovirus two

A

Mild respiratory disease. Causes tonsillitis, pharyngitis, bronchitis, bronchopneumonia. Involved in the tracheobronchitis infection kennel cough

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128
Q

What is the family for para influenza

A

Paramyxoviridae

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129
Q

Describe para influenza

A

Highly contagious upper respiratory tract infection which is an important cause of tracheobronchitis. Usually does not cause a severe disease but to make the dog more susceptible to secondary bacterial and viral infections

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130
Q

What is infectious tracheobronchitis

A

Highly contagious, acute disease that is localized in the airways. Can be caused by one or more infectious agents such as canine adenovirus two, para influenza virus, Bordetella bronchiseptica

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131
Q

What are the clinical signs of infection is tracheobronchitis

A

Sudden onset of severe productive or nonproductive cough. Cough is worse worse with exercise, excitement, pressure on the neck from collar. Trachea palpation induces cough on GPE. Can also have gagging, retching or nasal discharge

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132
Q

What is the treatment for infectious tracheal bronchitis

A

In most dogs the diseases self-limiting with resolution of clinical signs into weeks. Rest for 7 to 14 days to limit constant irritation of airways caused by coughing. Cough suppressant’s or antibiotics may be prescribed if the condition persists

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133
Q

How do you prevent infections tracheobronchitis

A

Isolate sick animals. If it’s at a kennel evacuate the kennel for 1 to 2 weeks and disinfect

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134
Q

What is the family for parvovirus

A

Parvoviridae

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135
Q

Describe the structure of the parvovirus

A

Non-envelope DNA virus

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136
Q

Describe canine parvovirus type two

A

Has two strains type a and type B.

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137
Q

What can canine parvovirus type two infect

A

Dogs, wolves, coyotes

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138
Q

What are the risk factors for canine parvovirus type two

A

Season. More likely in the summer months. If a Rottweiler, Doberman, pitbull, Labrador retriever. If six weeks to six months old. If not vaccinated

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139
Q

What is the route of infection for parvovirus

A

Fecal to oral

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140
Q

What is the initial replication cycle of parvovirus

A

The laryngeal tissues, virus is spread to other tissues and organs by the bloodstream. Infects and destroys rapidly dividing cells

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141
Q

What happens if parvovirus destroys the precursor cells of white blood cells

A

Leukopenia

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142
Q

What happens if parvovirus destroys the intestinal crypt cells

A

Shortened villi, malabsorption, diarrhea

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143
Q

What happens if a neonatal puppy is infected with parvovirus

A

Results in myocarditis and death. Some puppies may survive but with a lifelong cardiac condition

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144
Q

What is the incubation period for parvovirus

A

4 to 14 days

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145
Q

What are the clinical signs of parvovirus

A

Anorexia, vomiting, hemorrhagic diarrhea, weight loss, Lethargy. Severe disease results in sepsis. Can be fatal

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146
Q

What is the treatment for parvovirus

A

Hospitalization with aggressive supportive treatment, IV fluids, antibiotics, anti-vomiting, anti-acid, analgesic

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147
Q

What happens if an animal survives parvovirus

A

Lifelong immunity after natural infection

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148
Q

Describe the transmission of parvovirus

A

Virus is shed and high amounts in feces one clinical signs are present. Virus may also be shed after late into incubation period for a limited time after recovery. 2 to 3 weeks. Direct contact with contaminated stool surfaces bulls collars and leashes. Flies can carry contaminated fecal matter to food bowls. Spread by Hans and clothing of people in contact with affected dogs

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149
Q

How long can parvovirus stay in the soil

A

Months

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150
Q

How do you prevent and control parvovirus

A

Isolation of sick animals, gloves and protective clothing, disinfection, vaccination

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151
Q

What is the family of the coronavirus

A

Coronaviridae

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152
Q

Describe the structure of a coronavirus

A

Envelope RNA virus

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153
Q

What is the root of infection for the coronavirus

A

Fecal to oral

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154
Q

What is the pathogenesis of the coronavirus

A

Affects the epithelial cells of the intestinal villi but not the crypt cells

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155
Q

What are the clinical signs of the coronavirus

A

Mild gastroenteritis, anorexia, Lethargy

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156
Q

What is the transmission for the coronavirus

A

Virus is shed in feces for two weeks

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157
Q

What is the incubation period for the coronavirus

A

1 to 3 days

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158
Q

What is the treatment for coronavirus

A

Most dogs recover without treatment. Some patients may need supportive care

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159
Q

How do you prevent and control coronavirus

A

Strict sanitation and isolation protocols, vaccine is available but controversial

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160
Q

What family is the papilloma virus in

A

Papillomaviridae

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161
Q

Describe the structure of a papilloma virus

A

Non-envelope DNA virus

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162
Q

Describe the thing that special about the Papilloma virus

A

Highly host specific and tissue restricted. Virus can only affect terminally differentiated cells like skin cells. Stimulates cell hyperplasia. Infected tissue forms benign tumors. Canine papillomas occurred on the lips and in the mouth of young dogs

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163
Q

How do you transmit the Papilloma virus

A

Close contact

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164
Q

What is an antiviral

A

An agent that kills a virus or that suppresses its ability to replicate and hence inhibits its capacity to multiply and reproduce

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165
Q

Why is it difficult to make antivirals

A

Since viruses use the hosts cells to replicate which makes this difficult to find targets for the drug that would interferes with the virus without also harming the host cells. And virus variation.

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166
Q

How do most antivirals work

A

Interfere with viral nucleic acid synthesis or regulation. Or interfere with viral cell binding or interruption of virus coating or release. Some antivirals also enhance the immune system of the host

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167
Q

What is a prion

A

Proteinaceous infectious particles that resist inactivation by procedures that degrade or damage nucleic acids. Prions are normal cellular proteins that undergo confirmational changes and become pathogenic. Very resistant to environmental effects. Do not invoke inflammatory or immune response. Can be transmitted horizontally and perhaps vertically

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168
Q

Describe prion diseases

A

Transmissible spongiform and cephalopod to use. 9 neurodegenerative diseases with long incubation period for months to years. Cause large vacuoles to form in the brain. Fatal diseases

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169
Q

Name all of the transmissible spongiform encephalopathies of animals

A

Scrapies, bovine spongiform encephalopathies, feline spongiform encephalopathies, chronic wasting disease, transmissible mink encephalopathies

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170
Q

What are the human transmissible spongiform encephalopathies

A

Creutzfeld-Jakob disease, fatal familial insomnia, kuru, gersttman-straussler-scheinker disease

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171
Q

What is scrapies

A

Does occur in Canada and United States. Has been known since 1732 but infectious agent remain unknown until 1982. Affects sheep and goats between 3 to 5 years of age. Incubation. 2 to 5 years. Does not appear to be transmittable to humans

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172
Q

What are the clinical signs of scrapie’s

A

Behavior changes, may become excitable. Tremors of the head and neck. Intense pruritis, weakness, ataxia, fatal

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173
Q

What is the diagnosis for scrapie

A

Based on clinical signs, flock history and, microscopic evaluation of the brain

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174
Q

How do you prevent scrapie

A

Infectious and could be transmitted to other sheep. Slaughter infected sheep and those sheep that were in contact with infected sheep

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175
Q

What is bovine spongiform encephalopathy

A

mad cow disease

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176
Q

What are the clinical signs of bovine spongiform encephalopathic

A

Change in behavior, incoordination, milk production disease, weight loss, fatal. Most cattle affected or 3 to 5 years of age

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177
Q

How do you diagnose bovine spongiform encephalopathy

A

Based on clinical signs, third history, microscopic a valuation of the brain

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178
Q

How did mad cow disease first start

A

From feeding cattle meat and bone meal that contains infected products from a spontaneously occur in case of bovine spongiform encephalopathy

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179
Q

How does bovine spongiform start

A

Spread to cats and certain zoo animals by a protein supplements Added from the rendered cattle products added to animal feed including commercial cat food

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180
Q

How do you prevent mad cow disease

A

Slaughter of infected animals, bans on meat imported from bse infected countries

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181
Q

How are enhanced animal protection from bse

A

In infected cattle, bse concentrates on certain tissues known as specified risk material (srm). These tissues are removed from all cattle slaughtered for human consumption.

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182
Q

What are srm

A

Brain, skull, eyes, ganglia, spinal cord, vertebral column, tonsils

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183
Q

Are bse and scrapies reportable

A

Yes

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184
Q

What is mycology

A

Study of fungi

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185
Q

What does the fungi group involve

A

Microorganisms, molds, mushrooms

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186
Q

What are the characteristics of fungi

A

Eukaryotes, cell wall contains chitin, closely related to animals, no mechanisms of locomotion, range in size of microscopic to very large.

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187
Q

What are heterotrophs

A

No chloroplasts for photosynthesis Uses organic material for growth.

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188
Q

What is an autotroph

A

An organism that uses inorganic material for growth and produce organic material

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189
Q

How do fungi get nutrients

A

Acquired by absorption.. Usually from decaying material

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190
Q

are fungi aerobic ?

A

Aerobic or facultative anaerobic, only a few anaerobic fungi are known

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191
Q

How do fungi reproduce

A

Asexually or sexually

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192
Q

What are the three fungi categories

A

Saprophytic, parasitic, mycorrhizal (symbiotic)

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193
Q

What is a saprophytic categories

A

Largest group of fungi, they grow on dead organic matter and work to rot or digest that organic matter. Good with fallen trees, dead leaves etc

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194
Q

What is the parasitic fungi categories

A

Second largest group, prefer a living host.. Can cause damage to a host

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195
Q

What is a mycorrhizal fungi

A

Form a partnership mainly with trees and plants. Mutually beneficial

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196
Q

Describe yeast

A

Non filamentous, microscopic, unicellular fungi. Oval or spherical. Larger than bacteria. Widely distributed. Reproduces by budding or fission

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197
Q

Describe the yeasts budding

A

Budding yeast divide unevenly. Parent cell forms a protuberance on its outer surface. Bud elongates and parents cells nucleus divides, makes a cell wall division, bud breaks away

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198
Q

How many yeasts cell can produce

A

24 daughter cells by budding

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199
Q

What is a fission yeast

A

Divide evenly to produce two new cells. Parent cell elongates, parent cell nucleus divides, two daughter cells are produced

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200
Q

What is a yeast capable of

A

Facultative anaerobic growth.

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201
Q

What happens if oxygen is present for yeast

A

Performs aerobic respiration to metabolize carbohydrates to carbon dioxide and water

202
Q

What happens with yeast if no oxygen is present

A

They ferment carbohydrates and produce ethanol and carbon dioxide

203
Q

What is yeast used for in the food industry

A

Bakers yeast, bubbles, beer yeast, wine yeast

204
Q

What is a hyphae

A

Thallus (body) of a mild or fleshy fungus consists of long filaments of cells joined together.

205
Q

What are septa

A

Molds that have hyphae that contain cross walls

206
Q

What is a vegetative hyphae

A

Portion of hypha that obtains nutrients and forms mycelium

207
Q

What are Aerial hyphae

A

Portion of hypha concerned with reproduction and projects from surface of medium

208
Q

What are most molds

A

Aerobic

209
Q

Why is the life cycle of fungi

A

Filamentous fungi can reproduce asexually by fragmentation of their hyphae. Both sexual and asexual reproduction occurs by the formation of spores. Fungi is identified by spore type

210
Q

What are the molds in the industry used for

A

Food, pharmaceutics.

211
Q

What is a dimorphic fungi

A

Some fungi, especially the pathogenic species exhibit dimorphism. Can grow as a mold or a yeast. Non pathogenic fungi dimorphism can be co2 dependant.

212
Q

What is the structure of rabies virus

A

Enveloped RNA virus

213
Q

What is rabies

A

A viral disease that affects the central nervous system of all mammals including humans. Almost always fatal

214
Q

Who is at risk for rabies

A

Mammals of all ages. Endemic in wild animals with periodic outbreaks.

215
Q

In Canada and usa who are the most common transmitters of the disease

A

Bats, foxes, skunks and raccoons.

216
Q

In Asia and Africa what are the most common transmitters of rabies

A

Dogs are the main carriers

217
Q

Describe the pathogenesis of rabies

A

Virus enters through wound or mucus membrane, virus replicates in local tissues, virus is protected once it enters the CNS or peripheral nervous system. Replicates in CNS, moves to salivary glands.

218
Q

What is the incubation period for rabies

A

2 weeks to 6 months dependant on innervation at bite site, distance of bite from cns, virus variant, amount of virus at exposure

219
Q

Once clinical signs are present with rabies, how long until death

A

7-10 days

220
Q

Describe what 10% of dogs get when they get rabies

A

Vicious form of rabies with foaming mouth.

221
Q

What are the majority of dogs with rabies like

A

Lethargic and poorly responsive

222
Q

Describe the prodormal form of rabies

A

Change in behaviour, fever, pruritis…. Lasts 2-3 days. Followed by paralytic or furious form

223
Q

Describe the paralytic form

A

Majority of canine cases, lethargy, difficulty swallowing, drooling, voice change, paralysis in wounded limb.

224
Q

How long does the paralytic form of rabies last from onset of overt signs

A

1-7 days

225
Q

Describe the furious form of rabies

A

Majority of feline cases, aggression, biting, hydrophobia, possible hyperesthesia, hyperreponsiveness, ataxia, paralysis

226
Q

How long does the furious form of rabies last from overt signs of the disease until death

A

2-4 days

227
Q

Describe the transmission of rabies

A

Through saliva. Also aerosolized virus from exposure to bats, ingestion of infected tissues is also possible. Organ transplant too.

228
Q

What happens when rabies in saliva is dried

A

When exposed to open air

229
Q

What is the risk of human infection following a rabid animal bite

A

5-80%

230
Q

What is the risk of human infection following a scratch

A

0.1-1%

231
Q

How do you diagnose rabies

A

Ifa of brain or nervous tissue. Submit the brain to a state approved laboratory.

232
Q

How do you treat rabies

A

Fatal, dies within 7-10 days of clinical signs.

233
Q

What do you do if you suspect rabies

A

Report disease under health of animals act

234
Q

How do you recommend monitoring

A

10 days confined period after human exposure from a suspected dog or cat. Monitor for behavioural/neurological signs

235
Q

What happens if a healthy dog or cat bites a human

A

Quarantined for 10 days

236
Q

What happens if an unvaccinated cat/dog bites a human

A

Quarantined for 6 months. Monitored for onset of clinical signs. Vaccinate 1 month prior to release

237
Q

What happens if a vaccinate dog or cat bites a human

A

Immediate revaccination for rabies. Owner monitors for 45 days

238
Q

What happens if exposure is suspected

A

Immediately wash wound for 15mins. Remove contaminated clothing. Seek medical advice

239
Q

What is the publics responsibility with rabies

A

Vaccination, keep pets on leash, stay away from wild animals

240
Q

Describe the vaccination schedule for rabies

A

Vaccinated after 12 weeks, again 1 year later and then every year or 3 years depending on regulation. Ferrets are vaccinated yearly against rabies.

241
Q

What’s special about rabies vaccination and traveling

A

Dependant on where you are going

242
Q

What do wildlife departments do to help control rabies

A

Oral vaccines in bait.

243
Q

What are most fungi considered

A

Opportunistic pathogen’s

244
Q

What causes a fungal proliferation

A

Treatment with antibiotics which wipes out normal bacteria microflora, decreased immune system secondary to neoplasia, corticosteroids, diabetes mellitus

245
Q

Describe the characteristics of fungal infections

A

Chronic and slow progressing. Inflammatory response is granulomatous, immunity is cell mediated

246
Q

What is Dermatophytosis a.k.a. ringworm

A

Contagious infection of keratinized skin, hair, claws. Caused by one of several species of superficial fungi, the dermatophytes

247
Q

Describe the host range for ringworm

A

Species are host adapted, but can cross host barriers. Any animal species may contact her dermatophytosis. Particularly important in cats and is zoonotic.

248
Q

What is the general age range infected with ringworm

A

Most commonly a disease of young animals do to immaturity of immune system

249
Q

What are the risk factors for dermatophytosis

A

Immune deficiency. Inadequate husbandry conditions, high population density, stress, poor nutrition

250
Q

Which are the breeds of cats that are predisposed to dermatophytosis

A

Persians and Himalayan’s

251
Q

What are the most common dermatophytes of cats and dogs

A

Microsporum canisMicrosporum gypseumTrichophyton mentagrophytes

252
Q

Describe the dermatophytosis lesions

A

Circular areas of alopecia and scaling patches with central hair regrowth and inflamed edges. Often multiple lesions. Not all lesions are classic

253
Q

Describe where the dermatophytosis lesions are on dogs

A

Face or paws

254
Q

Describer where the dermatophytosis lesions are on cats

A

Ear pinnea and face

255
Q

Why is dermatophytosis underdiagnosed in cats

A

Due to the variation in lesion presentation

256
Q

How do you diagnose dermatophytosis

A

Woods lamp. Look for Applegreen florescence. Not all dermatophytes fluoresce. Fungal culture to confirm diagnosis and monitor treatment

257
Q

What percentage of microsporum canis strains will flouresce a bright green color upon exposure to a uv light

A

50%

258
Q

What materials can cause a false positive when diagnosing ringworm

A

Scales or dandruff and topical products which can florescence

259
Q

How do you confirm that it’s a true positive when diagnosing ringworm

A

Bright green in hairs only. Allow the lamp five minutes to warm up

260
Q

What do you do when you have fluorescing hairs in diagnosing ringworm

A

Sent for fungal culture. Pluck hair from edges of lesions using a sterile hemostat and submit. Or a toothbrush is vigorously combed over the lesions for 2 to 3 minutes. Wrap in plastic to submit to laboratory

261
Q

Name the in clinic fungal culture method

A

DTM. Dermatophyte testing medium. Place hair on culture medium or inbed toothbrush. Cover plates and incubate at room temperature. Watch daily for growth.

262
Q

How do you know that you have ringworm based on a culture

A

Look for off-white, fluffy to powdery colony with the red color change in the medium at the same time that the colony first appears. Examine them under the microscope for confirmation

263
Q

How quickly does ringworm grow on culture medium

A

Growth happens within 7 to 14 days though plates are kept for 21 days before being deemed negative for growth

264
Q

How do you perform the microscopic confirmation of ringworm

A

Brush a strip of clear tape over the colony. Mount tape sticky side down onto a drop of methyl blue on a microscope slide. Examine it 10 X to 40 X for typical appearance of dermatophyte macroconidia

265
Q

Describe the appearance of microsporum canis generally speaking

A

Canoe shaped, thick walled macroconidia with terminal knobs

266
Q

Describe how you would microscopically identify microsporum gypseum

A

Numerous thin walked macroconidia with slightly rounded proximal ends

267
Q

Describe how you would microscopically identify trichiphyton mentagrophytes

A

Cigar shaped microconidia which may be few in number. Numerous globose microconidia . Spiral hypae might be present

268
Q

How do you treat ringworm

A

Usually self limiting. Treatment strongly advised to accelerate recovery and minimize spread l

269
Q

What does the best treatment for ringworm include

A

Topical, systemic and environmental treatment

270
Q

How long do you do a treatment for ringworm

A

Continued until clinical and ideally mycologic cure is achieved, usually 8-16weeks

271
Q

At what time in treatment do you repeat fungal culture for ringworm

A

After 2 months of treatment then once per month until 2 negative culture

272
Q

Give an example of a ringworm topical treatment

A

Imaverol dilution with e collar.

273
Q

Describe a systemic treatment for ringworm for dogs as well as cats

A

Itrafunol for cats. Ketoconazole in dogs.

274
Q

Describe an environmental treatment for ringworm

A

Disinfect environment with diluted bleach

275
Q

How is ringworm transmitted

A

Direct contact or fomites.

276
Q

What is the protocol you should follow with ringworm

A

Handle infected patients with gloves and wash your hands. Disinfect cages and consultation tables with diluted bleach. Remind owners of the zoonotic nature of disease

277
Q

Describe malassezia pachydermatis

A

Pear shape yeast. Part of normal flora of ear in small quantities. Can cause otitis externa in dogs, uncommon in cats and can also cause dermatitis

278
Q

What are the predisposing factors of otitis externa

A

Conformation, lifestyle, obstructive lesions

279
Q

Describe which conformations are most susceptible to otitis externa

A

Cocker spaniels, basset hounds, beagles, sharpeis, english Bulldogs, chow chows, poodles

280
Q

What life style factors can predispose you to otitis externa

A

Swimming, grooming, excessive ear care

281
Q

What types of obstructive lesions can cause otitis externa

A

Polyps, neoplasia

282
Q

How do you treat otitis externa

A

Topical antibacterial, Antifungal, glucocorticoid combination therapy

283
Q

What is malassezia dermatitis caused by

A

Secondary to allergies and excessive licking.

284
Q

How do you treat malassezia dermatitis

A

Treated topically (surolan) or systemically (itraconazole)

285
Q

Describe Candida albicans

A

Part of the normal flora of the mouth, intestine, lower urogenital tract of animals and humans

286
Q

Describe the virulence of Candida albicans

A

Opportunistic, can invade locally and usually causes superficial infections of skin and mucosa. Can cause systemic infections in severely immunocompromised patients

287
Q

What are different examples of candida

A

Whitish hyperkeratitis on tongue, mouth, stomach. Diaper rash in babies. Mastitis in cows. Vaginitis in women

288
Q

What is a blastomyces dermatitidis

A

Slow growing dimorphic fungus. Mold form in the environment and very large yeast in the body. Most common systemic mycotic infection

289
Q

Describe blastomycosis

A

Can affect many mammalian species but occurs most often in people and dogs. Outdoor roaming dogs near waterway have increased risk. Majorly August-October

290
Q

Describe the dissemination of blastomycosis

A

Young male hunting dog inhales spores. Spores germinate in lung to large budding yeast form, most individual resist infection. Predisposition/heavy load leads to development of chronic granulomatous pneumonia. Usually then disseminates to skin, bone, prostate, testes, eyes. Blocks capillaries and forms ulcerations.

291
Q

What are the clinical signs of blastomycosis

A

Fever, cough, weight loss, lameness, skin ulcers, uveitis

292
Q

Describe histoplasma capsulatum

A

Dimorphic fungus, small yeast in tissue.

293
Q

Where is histoplasmosis found

A

Mostly in soil, especially contaminated with bird or bat droppings

294
Q

How do you get histoplasmosis

A

Inhalation of small microconidia. Oral exposure can also result in disease. Disease may remain confined to lungs, gi tract or may become disseminated.

295
Q

What does histoplasmosis cause

A

Granulomatous pneumonia, lymphadenopathy, colitis, emaciation

296
Q

What is cryptococcosis

A

Dimorphic fungus with the yeast phase Being infective. The yeast is fast growing and slimy.

297
Q

What does c. Neoformans var. neoformans affect

A

Immunocompromised individuals. Frequent in bird manure

298
Q

What does c. Neoformans var. Gatti affect

A

More virulent, can affect healthy individuals, associated with plant debris

299
Q

What are the forms of cryptococcosis

A

Respiratory, cutaneous, cns, ocular forms

300
Q

Describe cryptococcosis in cats

A

Unilateral or bilateral nasal discharge, sneezing, firm swelling over bridge of nose, submandibular lymphadenopathy

301
Q

What can cryptococcosis cause in cats or dogs

A

Multifocal neurologic signs, ocular abnormalities, cutaneous lesions

302
Q

What is aspergillosis

A

Mold. Causes regional or disseminated infection. Dogs more commonly affect than cats.

303
Q

What breeds does systemic aspergillosis affect

A

Middle aged German shepherd

304
Q

What breeds are affected with nasal aspergillosis

A

Medium to large breed dogs

305
Q

Describe the appearance of aspergillus fumigatus

A

Common grey green mold found on moldy bread, cheese and oranges.

306
Q

Describe aspergillus fumigatus

A

Causes a wide variety of disease depending on host predisposition. Can cause chronic sinusitis in dogs, cats, horses.

307
Q

What are the limitations of zone of inhibition experiment

A

Designed for rapid growing bacteria. Ph and moisture etc can affect it

308
Q

What are the factors that can affect efficiency of antibiotics in clinical cases

A

Site of infection, concentration of antibiotic in tissues, drug pharmacodynamics, host response

309
Q

How do you do a gram stain

A

Crystal violetGrams iodineDecolorizerSafranin

310
Q

Describe bacterial conjugation

A

Transmit info through sex pili between pos/Neg bacteria

311
Q

What is bacterial transduction

A

Virus takes a portion of bacteria and gives it to another bacteria

312
Q

What is bacterial transformation

A

Bacteria dies and DNa free floats and other bacteria pick it up

313
Q

Do different strains of the Same bacteria look the same ?

A

Yes

314
Q

How do you know if conjugation as transfer of dna has occurred ?

A

If two bacteria are individually resistant to different antibiotics as once mates they grew on plates with the presence of both antibiotics

315
Q

What is a plaque

A

Clear areas in agar medium that was previously Seeded with bacteria. Represents the lysis of a phage infected bacterial cell

316
Q

What are plaque forming units

A

Used to quantitate the number of infective phage particles in the culture

317
Q

What stain do you use for yeast

A

Methylene blue

318
Q

What is malassezia pachydermatis

A

The infections of ear and skin of dogs

319
Q

What does malassezia pachydermatis look like in gram stain

A

Gram stain: purple and round

320
Q

What does microsporum canis

A

Canoe with compartments

321
Q

What does a microsporum gypseum

A

Thin cigars with a million of them

322
Q

What does trichiphyton m look like microconidia

A

Small circles

323
Q

What does tricophyton m macroconidium look lik

A

Cigars

324
Q

What indicator is in dtm

A

Phenol red

325
Q

What is resistance

A

Ability to ward off disease through our defenses

326
Q

What is susceptibility

A

Vulnerability or lack of resistance

327
Q

What are the two different types of the body’s defenses

A

Non specific defences (innate)Specific defences: immune response (acquired)

328
Q

What is the first line of defence

A

Skin and mucous membranes, normal microbial flora

329
Q

What is the second line of defence

A

Phagocytes, inflammation, fever, and antimicrobial substances

330
Q

What is the third line of defence

A

Acquired immunity: lymphocytes and antibodies

331
Q

What defences are considered non specific

A

1 and 2nd

332
Q

What defences are considered specific

A

3rd line

333
Q

What do non specific defences do

A

Protect us against any pathogenActs in the same way regardless of the pathogen

334
Q

What is the mechanical process of the first line of defence

A

Physical barriers to entry or processes that remove microbes from body’s surface

335
Q

What is the chemical form of the first line of defence

A

Substances made by the body that inhibit microbial growth and destroy them

336
Q

Describe general characteristics of skin

A

Largest organ 3 layers: epidermis DermisHypodermis

337
Q

Describe the epidermis

A

Top layer, consisting of dead cells rich in keratin

338
Q

Describe the hypodermis

A

Sub cutaneous tissues

339
Q

List some of the skin defences

A

Dryness and acidity of skin inhibit growth. Skin shedding removes microbes on skin surface Sebum creates a protective film that inhibits certain bacteriaPerspiration flushes the skin and has lysozymes to break down gram + bacteria cell walls

340
Q

Which bacteria is usually involved in a dermatitis

A

Staphylococci bacteria since it is the normal inhabitant of the skin

341
Q

Describe mucus membranes

A

Cover respiratory, gastrointestinal and urogenital tract. Less protective than skin. Epithelial layer secretes mucus which is a slightly viscous glycoprotein. Mucus traps microbes and dust which prevents tracts from drying

342
Q

Describe the ciliary escalator

A

Mucus membrane cells are covered with cilia that move in a wave- like motion to propel microbes and dust that become trapped in mucus upward toward the throat where it is coughed, sneezed or swallowed.

343
Q

Describe saliva

A

Helps dilute the numbers of Microorganisms and wash them from the surface of teeth and mucus membranes in the mouth. Contains lysozymes that break down bacteria

344
Q

Describe the characteristics of the stomach

A

Gastric secretions are a mixture of hydrochloric acid, enzymes, mucus. High acidity destroys most bacteria and toxins Some Microorganisms enter intestines by being protected in food particles.

345
Q

Describe the characteristics of urogenital tract

A

Flow of urine cleanses the urethra Vaginal secretions move Microorganisms outside the body. Also slightly acidic to inhibit bacterial growth

346
Q

Describe the lacrimal apparatus

A

Lacrimal glands produce tears, blinking spreads the tears over the eye, tears evaporate and drain into the nasolacrimal duct

347
Q

What happens in the lacrimal apparatus if irritating substances or Microorganisms done in contact with the eye

A

Lacrimal glands produce more tears to wash away the irritating factor. Tears contain lysozyme.

348
Q

What is commensalism

A

One organism benefits from a larger organisms which is unaffected

349
Q

Where are normal microbiota found

A

Skin and GI tract.

350
Q

What are normal microbiota good for

A

Reduces area available for pathogens to attach establish. Competes with pathogens for nutrients. Produces substances harmful to pathogens.alters conditions that affect the survival of pathogens. Usually harmless but can cause disease if conditions change

351
Q

Describe the second line of defense

A

Phagocytosis, inflammation, fever, complement system, interferons

352
Q

What is Phagocytosis

A

Ingestion of micro organisms or particles such as debris by phagocytic cells.

353
Q

What white blood cells are Phagocytic

A

Neutrophils, eosinoPhils, macrophages

354
Q

Phagocytosis is part of what process

A

Inflammation

355
Q

Describe neutrophils

A

Highly phagocytic and motile. Active in initial stages of infection. Can leave the blood and enter infected tissue to destroy microbes and foreign particles

356
Q

Describe eosinophils

A

Somewhat phagocytic Active in initial stages of infection. Ability to leave the bloodProduce toxic proteins against parasites such as helminthsDischarge peroxide ions to destroy helminths.

357
Q

What does having a high number of eosinophils mean

A

Parasitic infections and allergic (hypersensitivity reactions)

358
Q

Describe macrophages

A

Matured monocytes Active as infection progresses Dispose of bacteria, worn out blood cells as infection subsides. Involved in cell mediated immunity.

359
Q

What are the two types of macrophages

A

Fixed and wandering

360
Q

What is the other name for fixed macrophages

A

Histiocytes

361
Q

What do wandering macrophages do

A

Roam the tissues and gather at sites or inflammation or infection.

362
Q

What is chemotaxis

A

Chemical attraction of phagocytes to Microorganisms.

363
Q

What are the chemotactic chemicals

A

Microbial products, wbc components, damaged tissue cells

364
Q

Describe adherence

A

Attachment of phagocytes plasma membrane to the surface of the Microorganisms or other foreign material.

365
Q

What is opsonization

A

The coating process with certain serum proteins that promote attachment of micro organism to the phagocyte

366
Q

What is ingestion

A

Plasma membrane extends pseudopods that engulf the micro organism. The pseudopods join and fuse to create phagosomes.

367
Q

Describe digestion in phagocytes

A

Phagosome in cytoplasm contacts lysosomes containing digestive enzymes and bacteriocidal substances. The two fuse membranes to form a phagolysosome.

368
Q

What are the four mechanisms of phagocytosis

A

Chemotaxis, adherence, ingestion, digestion.

369
Q

How do bacteria avoid distruction by phagocytosis

A

Have structures that inhibit adherence, some microbes can escape the phagosome before fuses with Lysozomes. so microbes can survive inside the phagocyte and require the low pH inside the phagolysosomes to replicate.

370
Q

What is inflammation

A

Defense mechanism following tissue damage caused by microbial infection, physical agents such as heat electricity or sharp objects, or chemical agents such as acids or bases.

371
Q

What are the four signs of information

A

Redness or Erythema, heat, swelling or edema, pain

372
Q

What is acute inflammation

A

If the cause of inflammation is removed in a short period of time. Intense response

373
Q

What is chronic inflammation

A

If the cause of information is difficult or cannot be removed. Longer-lasting and less intense response. Overall more destructive

374
Q

What are the functions of inflammation

A

Destroy and remove the injurious agent if possible. If destruction is not possible, to limit the effects on the body if I can finding or walling off the injurious agent. Repair or replace damaged tissue.

375
Q

What are the three stages of inflammation

A

Vasodilation and increased permeability of blood vessels, phagocytose migration and phagocytosis, tissue repair

376
Q

Why is vasodilation part of the information process

A

Increased permeability permits defensive substances to pass through the walls of blood vessels and enter the injured area. Help deliver clotting elements to form a clot

377
Q

What is vasodilation responsible for

A

The erythema and heat of inflammation.

378
Q

What is increased permeability responsible for

A

The Edema of inflammation.

379
Q

What is a localized accumulation of pus

A

Absess

380
Q

What is vasodilation and increased permeability of blood vessels caused by

A

Chemicals released by damage cells in response to injury. Histamines, kinins, prostaglandins, leukotrienes.

381
Q

What do histamines, kinins, prostaglandins, leukotrienes do

A

Attract phagocytic cells and T cells from the immune system

382
Q

What is margination

A

When neutrophils and monocytes stick to lining of blood vessels

383
Q

What is diapedesis

A

Phagocytes squeeze between the endothelial cells of blood vessels to reach the damaged area

384
Q

What do monocytes mature into

A

Macrophages

385
Q

What do macrophages do

A

Phagocytize destroyed tissues, dead neutrophils, invading Microorganisms

386
Q

What do dead neutrophils and macrophages form

A

Pus

387
Q

What happens to pus

A

Fistulates or is gradually destroyed and absorbed by the body

388
Q

When does tissue repair start

A

During active phase of inflammation but is not completed until harmful substances have been removed.

389
Q

When is a tissue repaired

A

When it’s stroma or parenchyma produces new cells

390
Q

What is a stroma

A

Supportive connective tissue

391
Q

What is a parenchyma

A

Functioning part of the tissue

392
Q

What is fever

A

Abnormally high body temperature produced in response to a bacterial or viral infection.

393
Q

What part of the brain controls body temperature

A

Hypothalamus

394
Q

What does a chill in a fever mean

A

The body responses to cold temperature with increased blood vessel constriction, increased rate of metabolism and shivering

395
Q

What is the crisis point in a fever

A

Where the infection subsides the body temperature lowers and he losing mechanisms such as vasodilation and sweating occur

396
Q

What are two antimicrobial substances

A

Proteins of the complement system, interferons

397
Q

What is the complement system

A

Complement system consists of a group of serum proteins produced by the liver that activate one another in the cascade to destroy invading microorganisms. Complement proteins are in active until they are split into products

398
Q

What happens when the three complement system pathways end in the activation of C3

A

Inflammation,opsonization or phagocytosis, cytolysis

399
Q

What are interferons

A

Antiviral proteins produced in response to a viral infection. Host cell specific but not virus specific

400
Q

What do alpha and beta IFN interferons do

A

Induce uninfected cells to produce antiviral proteins that prevent viral replication

401
Q

What does the gamma IFN interferon do

A

Activates neutrophils and microphones is to kill bacteria by phagocytolysis

402
Q

What Do the specific defenses of the immune system do

A

Recognizes foreign substances is not belonging to the body develops a specific immune response against them

403
Q

What are antigens

A

Substances that provoked a specific response

404
Q

What are anti-bodies

A

Proteins produced by the body in response to an antigen

405
Q

What is acquired immunity

A

Protection and animal develops again certain types of microbes or foreign substances. Developed during an individual’s life time. Can be acquired actively or passively

406
Q

What is active immunity

A

Immune system response following exposition to microorganisms or foreign substances

407
Q

What is passive immunity

A

Antibodies are preformed by some other animal. Lasts only as long as the antibodies are present which is weeks to months

408
Q

What is humoral immunity. Antibody mediated

A

Production of antibodies against foreign organisms and substances.

409
Q

Where are anti-bodies found

A

In extracellular fluid’s such as blood plasma, lymphatic fluid, mucus secretions

410
Q

Which cells are responsible for production of antibodies

A

The B lymphocytes

411
Q

What does a Humoral immunity protect against

A

Bacteria, bacterial toxins and viruses

412
Q

What is cell mediated immunity

A

Involve specialized T cells that acts against foreign organisms or tissues. Regulate the activation and proliferation of other immune system cells like macrophages

413
Q

What is cell mediated immunity the most effective against

A

Bacteria and viruses within phagocytic or infected host cells, fungi, protozoa, Helminthes.

414
Q

What is cell mediated immunity important for

A

Primary responder to transplanted tissue an important defense against cancer

415
Q

What are antigens

A

Substance that the body recognizes as being foreign against which enemy in response will be mounted. Most are proteins are large polysaccharides. Lipids nucleic acid’s are usually only anti-genic if combined with proteins are polysaccharides.

416
Q

What are non-microbial agents that have antigens

A

Pollen, egg white, blood cell surface molecules, serum proteins from other individuals

417
Q

What are antigenic determinant’s or epitopes

A

Specific region on the surface of an antigen against which anti-bodies are formed. An antigen usually has several antigenic determinant sites that cause the production of different anti-bodies

418
Q

What is a Hapten

A

Substance of low molecule wait that does not cause the formation of antibodies by itself but does when combined with the carrier molecule

419
Q

What are antibodies

A

Highly specific proteins that are made in response to an antigen. Recognize unbind antigens. Hope to neutralize or destroy antigens

420
Q

Describe the structure of an anti-body

A

Each anybody has at least two identical binding sites that bind antigenic determinant.

421
Q

What is a valance

A

Number of antigen binding sites. Most anti-bodies are bivalent and are monomers

422
Q

Describe the shape of an antibody monomer

A

It is a Y shape with 2 antigen binding sites

423
Q

What does the variable region of the antibody monomer do

A

Has 2 binding sites that are antigen specific.

424
Q

What are the constant regions for

A

For the 5 classes of immunoglobulins

425
Q

What is the FC region of the antibody monomer

A

Fragment that crystallized in cold storage. If exposed after both arms Jim binding sites attached to an antigen the FC regions of adjacent antibodies combined complement and destroy the pathogen. Can bind to a cell and leave the antigen binding sites of adjacent antibodies free to react with antigens.

426
Q

Describe the immunoglobulin classes

A

Five classes, determined by the constant regions. Each class please a different role in the immune response.

427
Q

Describe immunoglobulin G

A

Bivalent monomer. Accounts for 80% of all antibodies in zero. Readily crosses walls of blood vessels and enters tissue fluids. Protect against circulating bacteria and viruses, neutralize bacterial toxins, trigger complement system, enhances phagocytosis when bound to an antigen. Maternal IgG can cross the placenta and confirm passive immunity to a fetus also present in the colostrum. 

428
Q

Describe immunoglobulin M

A

It is a pentamer. 5 to 10% of antibodies in serum. It’s large-size prevents RGM from moving freely and it generally remains in blood vessels. First antibodies to appear in response to initial exposure to an antigen in and relatively short-lived, a second exposure results mostly in increased IgG production. Valuable in the diagnosis of the disease since it is first to appear in primary infection and is very short-lived. Effective in aggregating antigens and then reactions were involving complement. Can enhance ingestion of target cells by phagocytic cells

429
Q

Describe immunoglobulin a

A

10 to 15% of antibodies in serum, but common in most mucous membranes and body secretions. Most abundant immunoglobulin in the body. Has two Forms

430
Q

What are the two forms of immunoglobulin a

A

Serum IGA, secretory IGA

431
Q

Describe the serum IGA

A

Circulates mostly as a monomer

432
Q

Describe the secretory IGA

A

Diameter, produced by plasma cells and mucous membranes, enters and passes through a mucosal so word acquires a secretary component that protect against enzymatic Tegra Dacian. Prevents attachment of pathogens to mucosal surfaces. Present in colostrum

433
Q

What is immunoglobulin D

A

0.2% of serum antibodies. Bivalent monomer. Found in blood and lymph and on surfaces of B cells. No known function in serum. Act as antigens receptors on B cells.

434
Q

What is immunoglobulin E

A

0.002% of total serum antibodies. They’re specialized cells that participate in allergic reactions. Once binded to an antigen, it triggers release of histamine which causes an allergic reaction.

435
Q

Describe the B cell cycle

A

B cells exposed to antigens.Activate B cells Divide and differentiate into plasma cells Antibody production

436
Q

Where are B cells created

A

From stem cells in red bone marrow in adults and liver in fetuses

437
Q

Where do mature B cells migrate to

A

Lymphoid organs such as lymph nodes or spleen

438
Q

How do B cells recognize antigens

A

By means of antigen receptors on their cell surfaces. Once stimulated they immediately make antibodies associated with the assistance of T cells and cell mediated immune system.

439
Q

How many antigens can b cells recognize

A

An infinite number of antigens

440
Q

Each B cell can produce antibodies against how many antigens

A

Only one specific antigen

441
Q

What does a B cell coming in contact with an antigen trigger

A

Proliferation of a cell that is specific for that antigen into a clone of cells with the same specificity.

442
Q

What are the two series of self tolerance for B cells

A

Self and nonself. B and T cells that interact with self antigens are destroyed during fetal development. The body discriminates between dangerous and non dangerous cells

443
Q

DeScribe the antigen-antibody complex

A

When an antibody encounters an antigen for which it is specific. Tags foreign cells and molecules for distraction by phagocytes and complements.

444
Q

What components are part of the antigen-antibody complex

A

Agglutination, opsonization, neutralization, ab-dependent cell mediated cytotoxicity an action of complement

445
Q

What is an antibody titer

A

Amounts of antibody and serum. Reflects the intensity of your humoral response.

446
Q

What is the primary immune system response

A

Initial contact with the antigen, slow rise in antibody tighter. First IGM then IgG. Gradual decline in antibody tighter and takes a few days.

447
Q

What is the secondary immune system response or memory response

A

Immune response after second exposure to an antigen. Memory cells rapidly differentiate into an anti-body producing plasma cells. Mostly IgG antibodies.

448
Q

What cells are involved in cell mediated immunity

A

Involve specialized lymphocytes. T cells. Response to intracellular pathogens and non-transferred to the fetus via placenta

449
Q

What is a cytokine

A

Chemical messengers within the immune system.

450
Q

What is a interleukin

A

Messenger between leukocytes

451
Q

What is a chemokine

A

induce the migration of leukocytes into infected areas

452
Q

What are interferons

A

Help protect against viral infection of cells

453
Q

What is the tumor necrosis factor

A

Very important and inflammatory reactions

454
Q

What is the colony stimulating factor

A

Stimulate formation of various blood cells

455
Q

Where do T cells develop

A

In stem cells of bone marrow

456
Q

Where do the T cells migrate to

A

Migrate from bone marrow and mature in thymus then migrate to lymphoid organs

457
Q

What are the types of T cells

A

Helper T cells, cytotoxic T cells, delayed hypersensitivity T cells, suppressor T cells, CD4 cells, CD8 cells

458
Q

What must happen for a T cell to interact with an antigen

A

Antigen must be displayed on the cell surface called and antigen presenting cell.

459
Q

What are the primary antigen presenting cells

A

Macrophages and dendritic cells.

460
Q

What do antigen presenting cells do

A

Ingest and process the antigen, then displays fragments of antigen on the cell surface

461
Q

What is necessary for a T-cell to recognize the antigenic fragment on the antigen presenting cell

A

Must be a close association with cell surface self molecules which are components of major histocompatibility complexes.

462
Q

How is IL -1 created

A

Binding of helper T cells to antigen MHC complex on antigen presenting cell stimulates the secretion of IL-1

463
Q

What does IL-1 do

A

Activates helper T cell which secretes IL-2

464
Q

What does IL-2 do to the helper T cell

A

Stimulates receptor on that helper T cell which will proliferate and differentiate into mature helper T cells.

465
Q

Which T cells are affected by IL-2

A

It is non specific but only Helper T cells that were stimulated by an antigen have IL-2 receptors

466
Q

What do cytotoxic T cells do

A

Destroy target cells on contact.

467
Q

How does a cytotoxic T cell lyse a cell

A

Cytotoxic T cell binds with MHC antigen complex on the cell surface of a viral infected cell. Releases a protein called perforin which Lyses the infected cell by forming pores in the cell membrane.

468
Q

How long do cytotoxic T cells work for

A

Continue their activity as long as Antigen persists then undergo apoptosis

469
Q

Describe delayed hypersensitivity T cells

A

Probably not separate population but mostly helper T cells and cytotoxic T cells. Associated with certain allergic reactions and rejection of organ transplant

470
Q

What are suppressor T cells

A

Regulate the immune system by turning it off with an antigen is no longer present. May be helper T cells and cytotoxic T cells.

471
Q

What activates the macrophages

A

Increased phagocytic capacities, larger and ruffled. Stimulation is primarily by ingestion of antigenic Material. Cytokines released by helper T cells. Ability to attack and destroy cancer cells. Antigen presenting cells.

472
Q

Describe natural killer cells

A

Attack and destroy virus infected cells and tumor cells. Can undergo large parasites. doesnt need to be stimulated by an antigen. not phagocytic. participates in antibody dependant cell mediated cytotoxicity.

473
Q

describe the production of antibodies

A

T independent antigens directly stimulate B cells to produce antibodies

474
Q

describe antibody dependent cell mediated cytotoxicity

A

The parasite becomes coated with antibodies leaving their FC region extended. Immune system cells attached to the parasite and secrete lytic enzymes and other factors that destroy the parasite.

475
Q

What is an auto immune disorder

A

Sometimes the immune system identifies parts of its own body as foreign and attacks them.

476
Q

What is a hyper sensitivity or allergic reaction

A

The immune system over reacts to foreign invaders by producing too many antibiotics or other chemicals

477
Q

What is immuno suppression

A

When the immune system does not react or cannot generate an appropriate immune response

478
Q

What are the three types of immune disorders

A

Hypersensitivity, immune deficiencies, immunoproliferative disorders

479
Q

What are the two types of hypersensitivity reaction

A

Allergic reaction, auto immune disease

480
Q

What is hypersensitivity

A

Antigenic response beyond what is considered normal. Animal is sensitized to an antigen if exposed to that antigen again the immune system reacts in a damaging manner.

481
Q

What are the four types of hypersensitivity

A

Type one, type two, type III, type 4

482
Q

What is a type one hypersensitivity reaction

A

Anaphylactic shock

483
Q

What is a type 2 hypersensitivity reaction

A

Cytotoxic

484
Q

What is a type III hypersensitivity reaction

A

Immune complex

485
Q

What is a type 4 hypersensitivity reaction

A

Cell mediated or delayed hypersensitivity

486
Q

Describe an anaphylactic reaction

A

Allergic reaction provoked by reexposure to a specific Allergan. Exposure may be by ingestion, inhalation, injection, direct contact.

487
Q

What is the treatment for an anaphylactic reaction

A

Epinephrine, antihistamines, corticosteroids

488
Q

Describe the sensitization form of an anaphylactic reaction

A

An antigen is presented to helper T cells that stimulate the B cell production of ige antibodies specific to the antigen. Ige antibodies bind to the FC receptors on the surface of mast cells and basophils. Mast cells and basophils coated with ige become sensitized

489
Q

Describe the. Second exposure form of an anaphylactic reaction

A

He antigen combines with two IGE antibodies on sensitized cells. Degranulation and secretion of histamines, prostaglandins and some other chemicals. Vasodilation of blood vessels and smooth muscle contraction

490
Q

What is a systemic anaphylactic reaction

A

If antigen appears in blood, the result can be either anaphylactic shock or more localized reaction

491
Q

What is a localized anaphylactic reaction

A

If Antigen enters to the skin, is ingested or inhaled the localized reaction is typical.

492
Q

What is anaphylactic shock

A

Rare, life-threatening, immediate allergic reaction to food, and injection, and insect sting. Signs include severe respiratory distress and the sudden onset of diarrhea, vomiting, excessive drooling, shock, seizures, coma, death. Animals gums are very pale and the limbs are cold. Heart rate is fast but post is weak.

493
Q

How do you counteract an anaphylactic reaction

A

IV injections of epinephrine is administered to counteract the reaction. Treatment for other associated problems such as difficulty breathing may be needed.

494
Q

What is hives or urticaria

A

Allergic reaction to drugs, chemicals, something eaten, insect bites, sunlight. Develops within 20 minutes of exposure to allergens

495
Q

Describe hives

A

These severe type of anaphylactic reaction. Small bumps occur on the skin. Often the hair stands up over the swellings and sometimes they itch

496
Q

Describe facial swelling

A

Most often noticed on the face especially on the lips, the muzzle, around the eyes. Usually not life-threatening. Give antihistamines and corticosteroids

497
Q

What is allergic asthma

A

Most often in cats. Occurs more frequently in summer and after going outdoors. Asthma attacks can be moderate or lengthy and severe

498
Q

Describe the signs of allergic asthma

A

Coughing, shortness of breath, mouth breathing, breathing with abdominal efforts. This conviction occurs as a result of construction of the breathing passages triggered by the release of compounds such as histamines that combat allergens

499
Q

What is the treatment for allergic asthma

A

Oral or inhaled corticosteroids but they do not treat the underlying cause of the asthma. Determining allergic trigger can be difficult

500
Q

What’s one warning about cats with asthma attacks

A

Decompensation and stress can be fatal to them, may need sedation before procedures like radiographs

Veterinary Technician Complete (3 years) (26 decks)

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