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Infectious disease Flashcards

1
Q

How should swabs for bacterial culture be handled if their is a delay expected?

A

> 3 hours - transport medium
4 hours - refridgerarion

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2
Q

How long can most aerobes survive in a) tissue and b) fluid

A

a) 48 hours (refrigeration)
b) 1-2 hours at 20oC, 24 hours at 4oC or 72 hours at 4oC with transport medium

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3
Q

Which viral infection can be associated with inclusions in circulating lymphocytes, neutrophils and erythrocytes in dogs?

A

CDV

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4
Q

What infections are spread by Ixodes ticks?

A

Borrelia, Anaplasma, Ehrlich, Babesia, Bartonella, tick-borne encephalitis

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5
Q

Describe the life cycle of borrelia

A

Transstadial, not transovarial transmission in ticks
Ticks have 2y life cycle
Eggs hatch outdoors, larvae attach to birds/mice/small mammals and become infected
Overwinter, become nymphs, infect birds/mice/small mammals/dogs/deer/people next spring
Nymphs feed, moult and emerge the following autumn and transmit to third host - often larger mammals

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6
Q

How does Bb develop following a tick bite?

A

Migrates interstitially, hides with collagen and fibroblasts
Does not circulate in blood or body fluids

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7
Q

How do Bb and tick-borne relapsing fever infections vary?

A

Bb generally does not circulate in the blood or body fluids

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8
Q

What % of dogs seropositive for Bb have signs of lameness?

A

<5% - although suggested that 40% are false +ves, true number may be nearer <3%

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9
Q

What % of dogs seropositive for Bb have Lyme nephritis?

A

<2%

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10
Q

What are the 5 Lyme antigens?

A

OspA - vaccines, also host
OspC - increased 2-3 weeks after exposure, declined after 3-5 months, some vaccines
OspF - rises 6-8 weeks after exposure, persists
p39 - 88% naturally exposed
SLP

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11
Q

What are the members of the mycobacterium tuberculosis complex? What are their main reservoir hosts? Which affect dogs/cats?

A

M. bovis (C, D) - cattle
M. microti (C) - field voles
M. tuberculosis (C, D) - humans

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12
Q

What is the main risk factor for M. microti infection?

A

Hunting rodents

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13
Q

What are the routes of infection for tuberculous mycobacteriosis?

A

Skin, GI, respiratory tracts

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14
Q

What are the most common manifestations of TB in cats?

A

SC masses with draining tracts and regional lymphadenopathy, with non-specific systemic signs

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15
Q

What are the most common manifestations of TB in dogs?

A

Non-specific - lethargy, anorexia, weight loss, cough, dyspnoea, v/d, pyrexia

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16
Q

How is TB infection confirmed?

A

Demonstrating acid-fast bacteria on histo
Culture

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17
Q

How is TB treated in cats?

A

Surgical debridement
2 months rifampicin, FQ + clarithromycin/azithromycin, followed by 4-6 months of rifampicin and FQ or macrolide

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18
Q

What are the saprophytic mycobacterial species in dogs and cats? How are they classified?

A

Rapid growing - M. fortuitum, M. smegmatis (C)
Slow growing - M. avid (D/C)

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19
Q

How do slow and rapid growing saprophytic mycobacteriosis present?

A

Slow - local/systemic gramulomatous disease - weight loss, vomiting, diarrhoea, dyspnoea. Peripheral lymphadenopathy and pyrexia
Rapid - diffuse infections, panniculitis of ventral abdomen

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20
Q

How is saprophytic mycobacteriosis diagnosed?

A

Acid-fast staining, PCR

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21
Q

How does treatment of saprophytic mycobacteriosis differ from that of tuberculous disease?

A

Greater resistance to treatment

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22
Q

How do leproid syndromes present? Are they reported in cats or dogs?

A

Discrete cutaneous lesions.
Both

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23
Q

How is feline leprosy transmitted?

A

Rodent bites

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24
Q

When is feline leprosy more common?

A

Colder months

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25
Q

Where is canine leprosy reported? When is it more common?

A

Zimbabwe, Australia, Brazil, Warmer months

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26
Q

How is canine leprosy transmitted?

A

Insect bites

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27
Q

How are younger and older cats affected by leprosy?

A

Young - rapidly progressive, ulcerated
Old - diffuse, non-ulcerated slowly progressing lesions

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28
Q

How is leproid infection diagnosed?

A

Acid fast - impression smears
PCR

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29
Q

How are leproid syndromes treated?

A

May not be needed, spontaneous regression - dogs > cats
Surgical resection and dual AB therapy

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30
Q

Where is actinomyces most commonly found?

A

Mucous membrane commensal
GI and urinary tract

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31
Q

What are the common presentations of actinomyces infection?

A

SC or soft tissue abscess, pleuritic, pneumonia

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32
Q

How do actinomyces appear on cytology?

A

Non-acid fast filamentous organisms

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33
Q

Where are nocardia spp commonly found?

A

Soil

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34
Q

How does nocardia infection present?

A

Cutaneous lesions, pneumonia, pyothorax
Disseminated disease in young/immunocompromised

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35
Q

What empirical AB can be chosen in actinomyces infection?

A

Penicillin

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36
Q

What empirical AB can be chosen in nocardia infection?

A

Sulphonamide ABs

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37
Q

How is brucellosis shed?

A

Urine, vaginal discharges, aborted tissues, milk, saliva, nasal secretions

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38
Q

What happens following brucella crossing a mucous membrane?

A

Phagocytosed by macrophages and moved to LN

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39
Q

Following infection with brucella, when is bacteraemia seen and how long does it persist?

A

7-30 days
Up to 6 months

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40
Q

What are the clinical signs of Brucella infection?

A

Abortion, infertility, acute epididymitis, lethargy, weight loss, back pain, lymphadenopathy, poor vision

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41
Q

When can brucella serological testing be performed?

A

4 weeks after infection

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42
Q

How can the specificity of a brucella RSAT be improved?

A

By the addition of 2-mercaptoethanol

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43
Q

Which diseases are associated with clostridial organisms?

A

Tetanus and botulism

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44
Q

How do the susceptibility of dogs and cats to tetanus differ?

A

Cats 10x more resistant to infection than dogs

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45
Q

What exotoxins are associated with tetanus? What do they do?

A

Tetanolysin - damages otherwise viable tissue
Tetanospasmin - causes clinical syndrome of tetanus

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46
Q

What is the structure and function of tetanospasmin?

A

Heavy chain - affinity for ganglioside surface receptors on motor end plates. Responsible for internalisation, cytosolic translocation and retrograde axonal transport of light chain.
Light chain - presents neurotransmitter release by cleaving and inactivating synobrevin - essential or docking of NT vesicles with presynaptic membrane. Can also cross-link synaptic vesicles to cytoskeleton

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47
Q

What cells are affected by tetanospasmin?

A

Motor, then sensory and autonomic nerves
Can spread to brainstem via spinal cord
Predominantly affects inhibitory neurons

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48
Q

What are the consequences of autonomic inhibition by the tetanus toxin?

A

Sympathetic overactivity and excess plasma catecholamine levels

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49
Q

What is the explanation for the long duration of clinical tetanus?

A

Neuronal blinding of toxin is irreversible, recovery requires growth of new nerve terminals

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50
Q

When do clinical signs of tetanus become apparent?

A

Normally within 5-12 days of infection, can take up to 3 weeks

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51
Q

What is the mortality rate of tetanus?

A

8-50%

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52
Q

What autonomic signs are seen with tetanus?

A

Bradycardia, t tachycardia, hypertension, vasoconstriction, hyperthermia. Dysuria, urinary retention, constipation

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53
Q

What is the tetanus severity classification system?

A

I - facial signs
II - generalised rigidity/dysphagia
III - I + II + recumbency/seizures
IV - I + II + III + abnormal HR/RR/blood pressure

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54
Q

What biochemical abnormality is present in >50% of dogs with tetanus?

A

Elevated CK

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55
Q

How can tetanus be definitely diagnosed?

A

Measurement of serum antibodies against tetanospasmin
PCR for detecting toxin gene in wounds described but not available

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56
Q

What are the aims of treating tetanus?

A

1 - toxin neutralisation
2 - destruction of organism
3 - minimise effects of toxin

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57
Q

What is the preferred route of equine tetanus antitoxin? What is the risk?

A

IV
Anaphylaxis

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58
Q

How should a wound in a tetanus patient be managed?

A

Radical debridement and 3% hydrogen peroxide

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59
Q

Which AB has been shown to be superior for management of clinical tetanus?

A

Metronidazole

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60
Q

Which botulinum toxin has been associated with disease in dogs and cats?

A

C

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61
Q

Where is botulism toxin found?

A

Rancid food, dead birds
Rarely following colonisation of tissue and coprophagia

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62
Q

What is the pathogenesis of botulism?

A

Toxin released from spores, binds to protein complexes - forms progenitor toxins
Absorbed from SI => lymphatics => blood stream
Heavy chain binds with presynaptic peripheral nerve terminal
Modifies SNARE proteins needed for exocytosis of ACh

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63
Q

What are the clinical signs of botulism?

A

Afebrile flaccid paralysis
+/- cholinergic signs - altered HR, pupil changes (mydriasis and reduced PLR), KCS, urinary retention, constipation

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64
Q

What is the vector for Bartonella?

A

Blood sucking arthropods
Mostly cat fleas, also detected in Pulex fleas, Ixodes and Rhipicephalus

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65
Q

What are the targets of Bartonella infection?

A

Erythrocytes, endothelial cells, bone marrow progenitor cells

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66
Q

What affects the severity of clinical signs with Bartonella infection?

A

In primary host may be persistent bacteraemia without clinical signs
When non-adapted host infected, clinical signs more severe

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67
Q

What is the life cycle of Bartonella?

A

Replicate in midgut of arthropod and excreted in faeces
Inoculated through bite or scratching of area
Infect microglial cells, macrophages and CD34+ progenitor cells

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68
Q

What is responsible for Bartonellas invasion?

A

Adhesins - mediate bacterial adherence
Type IV secretion systems - transport DNA into cell

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69
Q

What is responsible for Bartonellas virulence?

A

Bartonella-effector proteins

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70
Q

What structure characterised the invasion of Bartonella?

A

Invasive - well organised bacterial aggregate engulfed and internalised by the targeted cell

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71
Q

How is Bartonella acquired by its vector?

A

Bacterial released from blood-seeding niche, bind to and invade erythrocytes without causing haemolysis
Released into circulation at 5 day intervals

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72
Q

What cells are suppressed to cause the immunosuppression seen with Bartonella?

A

CD8+ lymphocytes

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73
Q

How is Bartonella infection distributed in the body?

A

All tissues can be involved

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74
Q
A
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75
Q

What are the common clinical manifestations of Bartonella infection in dogs?

A

Pyrexia
Lymphadenopathy
Endocarditis
Myocarditis
Arthritis
Disseminated granulomatous disease (skin, LeNs, liver, spleen)
Neuro signs
Pleural, pericardial, peritoneal effusions

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76
Q

What proportion of canine endocarditis are caused by Bartonella?

A

19-28%

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77
Q

Which Bartonella species is commonly associated with endocarditis?

A

B. vinsonii subs. berkhoffi

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78
Q

In Bartonella endocarditis in dogs, which valve is most often affected?

A

Aortic

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79
Q

What lab abnormalities are associated with Bartonella infection?

A

Normally none
Non-specific
Hypoglubulinaemia

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80
Q

What clinical pathological finding has been associated with a 4x higher risk of being diagnosed with Bartonella?

A

Hypoglobulinaemia

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81
Q

What samples are best tested for Bartonella culture and PCR?

A

Tissue and non-blood fluids

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82
Q

What limits serology in Bartonella infection?

A

Over half of dogs have bacteraemia without ABs

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83
Q

How should Bartonella be treated in dogs?

A

Exact protocol not known
Combination of AB with high plasma and intracellular concentrations

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84
Q

What is a potential side effect of treating Bartonella in dogs? How can it be avoided. How should it be managed?

A

Jarisch-Herxheimer reaction - lethargy, fever, vomiting
By starting ABs 5-7 days apart in clinically stable dogs
Avoid interrupting treatment, anti-inflammatory steroids

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85
Q

Which species of Bartonella is most common in cats?

A

B. henslae

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86
Q

What are the clinical signs of Bartonella infection in cats?

A

Uveitis
Aortic valve endocarditis
Myocarditis
Lymphadenopathy
Pyrexia
Mild neuro signs
Usually subclinical

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87
Q

How is Bartonella diagnosed in cats?

A

Culture definitive but not sensitive
Serology - limited value, can be useful for assessing exposure but false negatives possible
PCR - no more sensitive than normal blood culture
Combined PCR and culture preferable

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88
Q

What is the recommended treatment for bartonella in cats?

A

Doxycycline and pradofloxacin

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89
Q

What is the main reservoir host of leptospirosis?

A

Rodents

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90
Q

How do leptospires differ from other gram-negative bacteria?

A

Do not cause fulminant septic disease shortly after onset of infection - low endotoxic potential of leptospiral lipopolysaccharide

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91
Q

How do leptospires evade the host immune response?

A

Binding inhibitors of complement activation on their surface

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92
Q

After the host response, where can leptospires persist?

A

Eye and renal tubules

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93
Q

Which organs are commonly involved in lepto infection?

A

Kidneys (tubules and glomeruli)
Liver
Lung

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94
Q

What are the hallmarks of leptospiral pulmonary haemorrhage syndrome?

A

Intra-alveolar haemorrhage in the absence of a marked inflammatory cell infiltrate or vasculitis

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95
Q

In a study of a cohort of dogs with lepto, what were the most common clinical syndromes (in order)?

A

Renal
Lung
Hepatic

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96
Q

What are the typical radiographic lung findings with lepto?

A

Pulmonary change in the caudodorsal fields, ranging from mild interstitial to severe reticulonodular
+/- mild mediastinal or pleural effusion

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97
Q

What diagnostics are available for lepto?

A

Culture - challenging, can take 6 months
Darkfield microscopy - low sens/spec
Serology
PCR

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98
Q

How long to vaccinal antibodies to lepto persist?

A

Normally up to 15 weeks, can persist up to 12 months

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99
Q

How should LPHS be treated?

A

Limited evidence exists in humans to suggest benefit of immunosuppression

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100
Q

What infections are spread by rhipicephalus sanguineus? Where are they found?

A

E. canis
A. platys?
R. rickttsii
Worldwide

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101
Q

What infections are spread by amblyomma americanum? Where are they found?

A

E chaffeensis
E ewingii
USA

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102
Q

What infections are spread by Ixodes scapularis? Where are they found?

A

A. phagocytophilum
USA

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103
Q

What infections are spread by Ixodes pacificus? Where are they found?

A

A. phagocytophilum
USA

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104
Q

What infections are spread by Ixodes persulcatus? Where are they found?

A

A. phagocytophilum
Eastern Europe and Asia

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105
Q

What infections are spread by Ixodes ricinus? Where are they found?

A

A. phagocytophilum
Europe

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106
Q

What infections are spread by Dermacentor variabilis? Where are they found?

A

R ricketsii
USA

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107
Q

What infections are spread by Dermacentor andersoni? Where are they found?

A

R ricketsii
USA - Rocky Mountain states

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108
Q

What disease is caused by E Canis?

A

CME

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109
Q

Where is E Canis distributed?

A

Worldwide

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110
Q

What are the clinical signs of CME

A

Acute - non specific, LN enlargement, splenomegaly
Ocular,nasal discharge, peripheral oedema
Petechiae/ecchymoses
Neuro
Chronic - mild to life threatening
Non specific + weight loss, lymphadenopathy, splenomegaly, anterior uveitis
Bleeding

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111
Q

What are the most common clin path findings in CME?

A

Panctopenia - BM hypoplasia
Elevated globulins (mono or polyclonal)
PLN

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112
Q

How is CME diagnosed?

A

Morulae within monocytes
Serology - ELISA/IFA
PCR - blood, LN, splenic FNA, BM

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113
Q

What is the sensitivity of BM PCR for diagnosis of chronic CME?

A

25%

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114
Q

What tick carries E Canis?

A

Rhipicephalus sanguineus

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115
Q

How should CME be treated?

A

Doxy x 28 days

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116
Q

Where is E. ewingii found? What is the main cause of transmission?

A

USA, Brazil, Cameroon
Amblyomma americanum

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117
Q

What are the clinical signs of E. ewingii?

A

Lethargy, anorexia, v/d, neuro signs, pyrexia, polyarthritis

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118
Q

What are the common Clinical path findings with E ewingii

A

Anaemia, mild leucopenia or leukocytosis, thrombocytopenia, hyperglobulinaemia, ALP elevation

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119
Q

Where is E chaffeensis seen? What spreads it?

A

USA
Amblyomma americanum

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120
Q

What are the clinical signs of E chaffeensis?

A

Fever, anaemia, leukopenia, thrombocytopenia, lymphadenopathy, epistaxis

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121
Q

What causes canine granulocytic ehrlichiosis? What spreads it?

A

A. phagocytophillum
I. scapularis/pacifinus/ricinus

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122
Q

What are the clinical signs of CGE?

A

Subclinical in many
Nonspecific - pyrexia, lethargy, lameness, stiffness, LN++, splenomegaly
Polyarthritis
Thrombocytopenia in >80%

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123
Q

How is CGE diagnosed?

A

Morula in neutrophils
ELISA serology (rising titre) - cross reactivity with platys
PCR (whole blood)

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124
Q

What causes thrombocytic anaplasmosis? What is the vector? Where is it seen?

A

A. platys
R. sanguineus
USA, South America, Australia, Asia, Europe

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125
Q

What are the clinical signs of A. platys infection?

A

Most subclinical
Transient thrombocytopenia

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126
Q

What causes salmon poisoning disease?

A

Neorickettsia helminthoeca

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127
Q

What is the life cycle of Neorickettsia helminthoeca?

A

Flukes => snails => fish => dogs

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128
Q

What happens following infection with N helminthoeca?

A

Disseminates to LNs, spleen, liver, lungs, brain

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129
Q

What are the clinical signs of SPD?

A

Weight loss, LN+++, v/d, thrombocytopenia in 90%

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130
Q

What clinical pathology findings are common in SPD?

A

Thrombocytopenia, v Na, K, alb
^ LEs

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131
Q

How is SPD diagnosed?

A

Trematode eggs in faeces
Neorickettsiae on LN aspirate examination
PCR on lymphoid tissue

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132
Q

How is SPD treated?

A

doxycycline + praziquantel

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133
Q

What causes RMSF? What spreads it and where is it found?

A

R. ricketsii
Dermacentor in USA
R. sanguineus in Arizona

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134
Q

What are the clinical signs of RMSF?

A

Fever, lethargy, anorexia, lymphadenopathy
Oedema and erythema
Stiffness
Ocular signs
Bleeding
Neuro signs

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135
Q

What are the clin path changes seen with RMSF?

A

Leukocytosis, anaemia, thrombocytopenia

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136
Q

How is RMSF diagnosed?

A

Serology - IFA/ELISA

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137
Q

What is the most common species of mycoplasma in a) cats and b) dogs?

A

a) Candidatus M. haemominutum
b) M. haemocanis

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138
Q

What is the most pathogenic feline mycoplasma?

A

M. haemofelis

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139
Q

What are the haematological fingers with acute/chronic mycoplasma haemofelis infection>

A

A - regenerative anaemia - microcytic and hypochromic
C - no significant anaemia

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140
Q

What is the sensitivity of cytology for diagnosing mycoplasma infection?

A

0-37%

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141
Q

How is clostridium perfringens typed? How many phenotypes are there based on this method?

A

Toxins - alpha, beta, epsilon, iota
Phenotypes - A, B, C, D, E

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142
Q

What is a known virulence factor for clostridium perfringens>

A

CPE

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143
Q

What is the suspected pathogenesis of clostridium perfringens-associated illness?

A

Massive sporulation of commensal strains, triggered by diet change, ABs, coinfection => CPE released

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144
Q

How does CPE cause clinical signs?

A

Interacts with epithelial tight junction proteins, forming protein complex. Then interacts with host proteins, forming larger complex. Provides CPE access to occludin.

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145
Q

How is clostridium perfringens diagnosed?
Is culture helpful?

A

CPE detection in faecal samples in combination with PCR detection of cpe gene
NO - isolated from 80% healthy dogs

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146
Q

How should clostridium perfringens be treated?

A

Uncomplicated diarrhoea - no treatment needed
Systemic illness - ampicillin, MNZ, tylosin

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147
Q

What toxins are associated with clostridium difficile?

A

TcdA - enterotoxin
TcdB - cytotoxin

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148
Q

What clinical disease is associated with CDI?

A

Association between TcdA toxin and AHDS in dogs

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149
Q

What diagnostic tests are available for CDI?

A

CTA - detects TcdA - gold standard but £££
Recommended approach is positive culture and/or antigen test AND ELISA detection of TcdA/TcdB

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150
Q

How is CDI treated?

A

MNZ treatment of choice

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151
Q

When is campylobacter jejuni shedding most commonly detected?

A

Dogs <6m
Summer and autumn

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152
Q

What toxin is associated with campylobacter?

A

Cytolethal distending toxin
Proteins CdtA, CdtB, CdtC

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153
Q

When should campylobacter infection be treated?

A

Immunocompromised, febrile, haemorrhagic d+
Erythromycin or fluoroquinolone

154
Q

Describe the pathogenesis of Salmonella

A

Ingestion of organisms => invasion of M-cells in Peyer’s patches. Salmonella express fimbriae - allow adherence to epithelial cells.
Genes necessary for invasion coded by Salmonella pathogenicity islands (SPI-1, SPI-2)
Inject bacterial effector molecules into cytoplasm.
Invasion followed by inflammation, influx of neutrophils, macrophages => secretory diarrhoea

155
Q

How/when should salmonella be treated?

A

Not necessary in uncomplicated cases.
Fluoroquinolones, chloramphenicol, TMPS, amoxicillin.

156
Q

Is duodenal aspiration and cytology helpful for the diagnosis of Giardia?

A

Dogs - yes
Cats - no, lives in distal SI

157
Q

How is hepatozoonisis spread?

A

Ingestion of infected tick
Rhipicephalus

158
Q

Describe the pathogenesis of hepatozoonosis

A

After ingestion of infected tick sporozoites released - infect mononuclear phagocytes and endothelial cells of spleen, liver, muscle, lungs and bone marrow - form cysts

159
Q

What are the clinical and pathological findings with hepatozoonosis?

A

Neutrophilic leukocytosis
Periosteal reaction - any bone except skull

160
Q

How should hepatozoonosis be treated?

A

H. americanum - TMPS, pyrimethamine and clindamycin in acute phase, then decoquinate
H. canis - imidocarb

161
Q

What are the clinical signs of neosporosis in dogs?

A

Ascending paralysis, polymyositis, multifocal CNS disease, myocarditis, dysphagia, ulcerative dermatitis, pneumonia, hepatitis

162
Q

Describe the pathophysiology of toxo infection

A

Tachyzoites - disseminate in blood and lymph during active infection, replicate intracellularly
Bradyzoites - slow dividing, persistent, tissue stage, form in extra intestinal tissue. Form tissue cysts in CNS, muscles, visceral organs

163
Q

What are the common clinical signs of toxo infection

A

Death, hepatic, pulmonary, CNS and pancreatic signs
Depression, anorexia, dever, hypothermia, peritoneal effusion, icterus and dyspnoea if disseminated
Chronic - uveitis, fever, muscle hyperaesthesia, weight loss, ataxia, seizures, icterus, diarrhoea, pancreatitis

164
Q

Where is trypanosomiasis reported?

A

North and South America and Caribbean

165
Q

What are the clinical signs of trypanosomiasis?

A

Cardiomyopathy, ventricular/supraventricular arrhythmia
(Neuro disease)

166
Q

How is trypanosomiasis diagnosed?

A

Organ demonstration - lymph node aspirates or abdominal effusion
Histo examination of cardiac tissue - amastigotes

167
Q

What are the common Babesia species and how are they transmitted?

A

B. rossi - Haemaphysalis leachi
B. canis - Dermacentor reticulatus
B. vogeli - Rhipicephalus sanguineus

168
Q

What are the clinical signs of Babesia infection?

A

Often subclinical
Intracellular replication in RBCs => intravascular haemolysis
Immune reactions worsen
Acute anaemia

169
Q

How is Babesia diagnosed?

A

Serology - paired titres
Organism demonstration - blood smears

170
Q

How is babesia treated?

A

Imidocarb - canis
Azithromycin and atovaqone - gibsoni

171
Q

What spreads cytauxzoonosis?

A

Amblyomma americanum
Dermacentor variabilis - experimentally

172
Q

What is the pathophysiology of cytauxzoonosis?

A

Infected macrophages line lumen of veins, release merozoites, infect RBCs
Obstruction of blood flow and haemolytic anaemia

173
Q

What species is affected by cytauxzoonosis?

174
Q

How is cytauxzoonosis diagnosed?

A

Organism demonstration in RBCs and macrophages on blood smears and bone marrow/splenic/liver/LN cytology

175
Q

Describe the structure of the FIV virus

A

Enveloped RNA
3 layered structure
Inner genome-nucleocapsid complex
Icosahedral capsid
Envelope with glycoprotein spikes

176
Q

What are the 3 main FIV genes?

A

gag - vision core proteins (capsid [p24], nucleocapsid and matrix)
pol - reverse transcriptase
env - surface (gp120) and transmembrane virion (gp41) envelope proteins

177
Q

How does FIV invade cells?

A

Via primary receptor CD134 (expressed on CD4+ T cells, B cells, activated macrophages)
Secondary receptor CXCR4

Viral envelope fuses with cell membrane, capsid enters cytoplasm

178
Q

What happens following FIV invasion of cells?

A

Reverse transcription occurs, double stranded copy of retroviral genome is made
Additional sequences - long terminal repeats added to each end
Virus passes to nucleus, dsDNA integrated into host genome
Transcription of DNA, controlled by LTRs leads to synthesis of new virion components and virus assembly

179
Q

Following cell infection with FIV and integration of viral DNA into the genome, what are the possible consequences?

A

Latency - no transcription
Activity

180
Q

How can retroviruses cause tumour growth?

A

RT prone to error - mutation rate high
Integration of viral DNA can disrupt genes responsible for cell growth
Cellular oncogenes carried by retroviruses develop mutations, then re-inserted

181
Q

What are the FIV subtypes? How are they typed?

A

A-F
Based on env gene

182
Q

How is FIV transmitted?

A

Bites
Transplacental, during parturition, through milk experimentally documented
Venereal not documented, but virus present in semen and can be experimentally cause by inoculation of semen into vagina

183
Q

Which cells are targeted by FIV?

A

Mostly CD4+ T cell
CD8+ T cell, B cells, macrophages, dendritic cells, microglia and astrocytes also affected

184
Q

What are the 3 stages of FIV disease?

A

Acute - virus replicates in lymphoid tissue, decline in CD4+ and CD8+. Transient non-specific signs
Subclinical - CD4+ rebounds, plasma virus declines, progressive immune system dysregulation
Terminal - infection, neoplasia, myelosuppression, neuro disease

185
Q

When does FIV viraemia peak?

A

8-12 weeks after infection

186
Q

How do cats survive the acute phase of FIV infection?

A

Strong humeral response, rebound of CD8+

187
Q

What happens to the immune system in the subclinical phase of FIV infection?

A

Progressive decline in CD4+ T cells => reduction in CD4:CD8 ratio
+/- hyperglobulinaemia (due to B cell hyper activation)
T cells have reduced ability to respond to stimulation
Altered lymphocyte cell surface molecules, altered dendritic/neutrophil function => immunosuppression
Slow influx of immune cells into brain

188
Q

Draw a graph showing FIV plasma viraemia and CD4 T cell concentration over time, showing the different phases of infection

A

Sykes pg 212

189
Q

What is the most common neoplasia in FIV infected cats?

A

B-cell lymphoma

190
Q

What are the potential neurological signs of FIV?

A

Increased aggression, tremors, sleep disturbance, anisocoria, abnormal cranial nerve function, seizures

191
Q

Where are FIV inflammatory lesions seen?

A

Myopathy, enteropathy, ocular

192
Q

How should FIV be diagnosed?

A

Serology has highest sensitivity (unless vaccinated)
- ELISA - if positive confirmation with WB or ELISA from other manufacturer recommended (based on low prevalence of disease)

193
Q

What is the target of the point of care FIV ELISA?

A

p24 antibodies

194
Q

When are a) false positive and b) false negative FIV ELISA results possible

A

a) Vaccination
Maternal AB (is mother exposed/infected)
b) Early in course of disease (<60 days)
In the terminal phase (impaired AB production) - use PCR in this instance

195
Q

FIV PCR sensitivity

196
Q

What topical treatments have been described for FIV stomatitis?

A

Topical lactoferrin
Chlorhexidine

197
Q

What systemic treatment has been described for cats with FIV? What is the main side effect?

A

Zidovudine (AZT)
Myelosuppression

Fozivudine - reduced viraemia, less haematological side effects

Plerixafor - decreased proviral load without adverse effects, no improvement in clinical or immunological variables

198
Q

What is the prognosis for FIV infected cats?

A

No significant difference in lifespan of infected/non-infected cats

199
Q

What class of virus is FeLV?

A

Enveloped, RNA virus

200
Q

What are the possible outcomes after FeLV infection?

A

Progressive infection
Latent infection
Abortive infection

201
Q

What are the subtypes of FeLV? Describe how they arise

A

FeLV-A - least pathogenic, only transmittable subtype
FeLV-B - created by recombination of FeLV-A proviral DNA and endogenous FeLV sequences in host cells
FeLV-C - arises from accumulation of mutations or insertions in env

202
Q

Which FeLV subtype is most associated with the development of lymphoma?

203
Q

Which FeLV subtype is most associated with the development of non-regenerative anaemia?

204
Q

Which FeLV subtype is most associated with the development of immunodeficiency?

205
Q

How is FeLV transmitted?

A

Close contact with salivary secretions

206
Q

What is the median age of infection with FeLV?

207
Q

What is the pathogenesis of FeLV infection following oronasal exposure?

A

Virus replicates in lymphoid tissue then circulates in monocytes/lymphocytes
Some travel to BM - infect precursor cells and subsequently lymphoid and epithelial cells throughout the body
Once epithelial cells of salivary glands infected, viral shedding

208
Q

What happens in a regressive (latent) FeLV infection?

A

Immune system suppresses viral replication, before BM infected.
Proviral DNA present, production and shedding do not occur

May remain in this state, be reactivated with immunosuppression or develop malignancies.

209
Q

What happens in an abortive FeLV infection?

A

No viraemia occurs after infection. Antibodies develop

210
Q

What happens in a progressive FeLV infection?

A

Bone marrow involvement established. Cellular destruction by virus exceeds immune system response.
Persistent viraemia and progressive FeLV-related disease

211
Q

What are the clinical outcomes of progressive FeLV infection?

A

Neoplasia
Opportunistic infection
PRCA
BM disease
Immune mediated disease
Lymphadenopathy
Neuro disease (anisocoria, urinary incontinence)
Repro failure
GI signs

212
Q

What are the most common types of neoplasia associated with FeLV infection?

A

Lymphoma
Leukaemia
Fibrosarcoma

213
Q

What type of lymphoma is most associated with FeLV infection?

214
Q

Which species are predominantly affected by borna disease virus?

A

Horses and sheep. Cats also susceptible

215
Q

What are the main clinical signs of borna disease virus?

A

Motor dysfunction, staggering gait

216
Q

What can help rule out a diagnosis of borna disease virus?

A

Neurological signs other than motor dysfunction

217
Q

How is borne disease virus diagnosed?

218
Q

What is the prognosis of borna disease virus?

A

Generally progressive

219
Q

What are the necropsy findings in borna disease virus?

A

Nonsuppurative meningoencephalomyelitis of grey matter

220
Q

Where is cowpox virus seen?

221
Q

What is a risk factor for cowpox transmission?

A

Hunting wild rodents

222
Q

How does cowpox infection present?

A

Usually primary lesion on head/neck/forelimb
Often widespread secondary skin lesions
Occasionally systemic illness (eg pneumonia)

223
Q

How is cowpox infection diagnosed?

A

PCR of skin crusts

224
Q

How is cowpox infection treated?

A

Supportive treatment, BS ABs

225
Q

What is the seroprevalence of feline foamy virus?

226
Q

What is the significance of feline foamy virus infection?

A

Unknown, likely asymptomatic

227
Q

What clinical sign is associated with astrovirus infection?

228
Q

What is the significance of rotavirus infection in cats?

A

Clinical disease uncommon - mild diarrhoea

229
Q

What are the two main causes of viral respiratory disease in cats?

230
Q

What bacterial pathogens are seen as part of infectious respiratory disease in cats?

A

Bordatella
Chlamydia felis
Mycoplasma

231
Q

Which clinical signs are associated with FeHV-1 infection?

A

URT disease - oculonasal discharge, conjunctivitis, sneezing
Occasionally pneumonia, osteolytic change in turbinates and chronic rhinitis

232
Q

What is the most common clinical sign with FCV infection?

A

Oral ulceration

233
Q

What clinical signs are associated with FCV infection?

A

Oral ulceration, URT signs, conjunctivitis
Rarely lameness, respiratory/oral disease, interstitial pneumonia

Rarely hypervirulent strains - pyrexia, oedema, anorexia, jaundice - high mortality rate

234
Q

Which feline respiratory disease has a hyper virulent strain?

235
Q

How does the severity of FeHV-1 and FCV infection compare?

A

FCV usually milder

236
Q

How is FeHV-1 diagnosed?

237
Q

How is FCV diagnosed?

A

Virus isolation
RT-PCR - possibly less sensitive

238
Q

How can cats become infected with H5N1 infection?

A

Direct contact and consuming infected poultry

239
Q

What are the clinical signs of H5N1 infection in cats?

A

Severe respiratory disease

240
Q

Where is cryptococcus found?

241
Q

What are the main causes of cryptococcosis?

A

Cryptococcus neoformans
Cryptococcus gattii

242
Q

Where is cryptococcus neoformans found in the environment?

A

Associated with pigeon droppings

243
Q

Where is cryptococcus neoformans found in the environment?

A

Bark and leaf litter of trees in tropics/subtropics

244
Q

What class of fungus is cryptococcus?

245
Q

How does infection with cryptococcus occur?

A

Inhalation

246
Q

What happens after inhalation of cryptococcus yeast?

A

Most too large to reach lungs, settle in nasal cavity or nasopharynx - can cause disease or asymptomatic carrier status
Small forms inhaled into lungs => pulmonary diseas
Cell-mediated immune response => granuloma formation
Dissemination by haematogenous route or local extension

247
Q

What % of dogs/cats are asympomatic carriers of cryptococcus?

A

D - 14%
C - 7%

248
Q

What % of dogs/cats develop pulmonary disease with cryptococcus?

249
Q

Which tissues are most often affected by disseminated cryptococcosis?

A

Skin
CNS
Eyes

250
Q

How do cryptococcus evade the immune system?

A

Thick capsule inhibits phagocytosis, plasma cell function and leukocyte migration

251
Q

What determines the severity of clinical signs in cryptococcosis?

A

Immune response
Humoral response not helpful - dependent on cell-mediated immunity

252
Q

What risk factors have been identified in dogs/cats for cryptococcosis infection?

A

FIV/FeLV
Chronic steroid use

253
Q

What are the clinical signs of cryptococcosis in cats?

A

URT, nasopharyngeal, cutaneous, ocular, CNS involvement

254
Q

What % of cats with cryptococcosis have eye involvement?

255
Q

What are the common ocular signs of cryptococcosis in cats?

A

Granulomatous chorioretinitis +/- exudative retinal detachment

256
Q

What % of cats with cryptococcosis have neurological involvement?

257
Q

What are the clinical signs of cryptococcosis in dogs?

A

Depression, anorexia, CNS signs, URT signs

258
Q

What is the sensitivity of CSF cytology for diagnosing cryptococcosis in dogs with CNS involvement?

259
Q

What is the sensitivity of cytology of nasal swabs, FNA of masses and impression smears of exudate in dogs with cryptococcosis?

260
Q

What stain can be used to aid a cytological diagnosis of cryptococcosis?

A

Gram stain

261
Q

What is a limitation of a positive fungal growth from a nasal cavity in a dog suspected to have cryptococcosis?

A

14% asymptomatic carriers

262
Q

What findings can be seen on thoracic radiographs in dogs with cryptococcosis?

A

Nodular infiltrates, an interstitial pattern, pleural effusion, tracheobronchial lymphadenopathy

263
Q

If cytology doesn’t demonstrate cryptococcal organisms in a suspected case, what test should be performed next?

A

Histopathology

264
Q

What special stains can aid identification of cryptococcus on histopathology?

A

PAS, Gridley’s fungal, Grocott’s Methenamine Silver, Gomori Methenamine Silver
Mucicarmine stains - capsule

265
Q

Is serology useful in diagnosing cryptococcosis?

A

Titres not useful - most infected animals do not mount humoral response
Latex agglutination assays for cryptococcal capsular antigen sensitive and specific (serum, urine, CSF)

266
Q

What treatments are available for cryptococcosis?

A

Amphotericin B
Fluconazole
Itraconazole

267
Q

What is the treatment of choice for animals severely affected with cryptococcosis?

A

Amphotericin B (+/- flucytosine)

268
Q

What side effects have been reported with flucytosine?

A

Ulcerative drug eruptions (skin and mucocutaneous junctions), enterocolitis, leukopenia, thrombocytopenia

269
Q

What is the treatment of choice for animals mildly or moderately affected with cryptococcosis?

A

Fluconazole

270
Q

What are the reported times to cure in cats with cryptococcosis treated with fluconazole and itraconoazole?

A

F - 4 months
I - 9 months

271
Q

How can treatment of cryptococcosis be monitored? What is a limitation of this approach?

A

Serial latex agglutination titres
Can remain positive in some

272
Q

What is the prognosis for cryptococcosis in dogs and cats?

A

Cats without CNS involvement - good
Dogs and cats with CNS involvement - guarded

273
Q

What is the relapse rate for cryptococcosis in cats?

274
Q

What forms are coccidioidomycosis found in?

A

Environment - mycelium (chain of arthroconidia)
Body - spherules

275
Q

What species of coccidiodes are recognised? How are they different?

A

C. posadasii
C. immitis
Similar clinical signs and drug sensitivity, different geographical distribution

276
Q

What is the pathogenesis of coccidioidomycosis?

A

Following inhalation, arthroconidia are phagocytoses by alveolar macrophages and then enlarge into a spherule. Endospores released when spherule ruptures => pyogranulomatous inflammation.
Surviving endospores enlarge into spherules. If ineffective host response, migrate to lymph nodes and resp tract

277
Q

What are the clinical signs of coccidioidomycosis?

A

Intermittent fever, lethargy, inappetence and weight loss.
Cough, dyspnoea, exercise intolerance

278
Q

Where are possible sites of dissemination of coccidioidomycosis?

A

Bone, CNS, skin, peripheral lymph-nodes, pericardium

279
Q

What are common clinicopathological abnormalities in dogs with coccidioidomycosis?

A

Non-regenerative anaemia, neutrophilia, hypoalbuminaemia, hyperglobulinaemia, proteinuria

280
Q

What is the most common finding on chest radiographs in dogs with coccidioidomycosis?

A

Hilar lymphadenopathy

281
Q

What infectious disease is associated with pericarditis?

A

Coccidioidomycosis

282
Q

What diagnostic tests can be used to confirm a diagnosis of coccidioidomycosis?

283
Q

What is the diagnostic performance of a serologic assay that detects coccidioides antigen in urine?

A

Unacceptably low (<20%)

284
Q

What treatment is recommended for pulmonary coccidioidomycosis?

A

Fluconazole or itraconazole

285
Q

What treatment is recommended for coccidioidomycosis with bone involvement?

A

Itraconazole

286
Q

What treatment can be considered for coccidioidomycosis causing refractory meningoencephalitis?

A

Voriconazole

287
Q

How can treatment of coccidioidomycosis be monitored?

A

IgG titres

288
Q

What type of organism is blastomyces?

A

Thick walled yeast

289
Q

What is a risk factor for blastomycosis infection?

A

Living within a quarter of a mile of water

290
Q

What is the pathogenesis of blastomycosis?

A

Infection occurs via respiratory route after host inhales conidiophores
5–12 week incubation
Conidia phagocytosed by alveolar macrophages
Pyogranulomatous inflammatory response
In some cases infection controlled
In others phagocytosed yeast are transported into the pulmonary interstitum
From he can gain vascular and lymphatic access

291
Q

What environmental factors increase blastomycosis infection?

A

Rain, dew, fog
Activities that disrupt the soil

292
Q

Which organs do blastomycosis commonly disseminate to?

A

Lymph-nodes, eyes, skin, bones, subcutaneous tissues and prostate

293
Q

What determines the severity of infection with blastomycosis?

A

The immune response
Recovery dependent on cell mediated immunity

294
Q

What clinical signs are associated with blastomycosis infection?

A

Anorexia, depression, weight loss, cachexia and fever
Pulmonary signs in 65 to 85%
Lymphadenopathy in 40 to 60%
Cutaneous signs in 30 to 50%
Paronychia common in dogs
Ocular involvement in 20-50%
Osteomyelitis in 10-15%
Prostatitis or orchitis in 5-10%

295
Q

What are the presenting clinical signs of blastomycosis in cats?

A

Similar to dogs. Large abscesses are more common in cats and neurological involvement often noted

296
Q

What clinicopathological abnormalities are seen with blastomycosis?

A

Hypoalbuminaemia
Hypocalcaemia in 10%

297
Q

What imaging findings are seen with blastomycosis?

A

Interstitial lung pattern
Osteolytic bone lesions
Extra-axial CNS lesions on MRI

298
Q

How can blastomycosis be definitely diagnosed?

A

Organism identification by cytology or histology
Thick walled yeasts
Blastomyces antigen enzyme immunoassay on serum and urine
Serology - low sens/spec

299
Q

What is the treatment of choice for blastomycosis?

A

Itraconazole unless severe hypoxaemia or CNS infection in which case amphotericin B should be first choice

300
Q

What rate of clinical cure can be expected for blastomycosis?

301
Q

What is the recurrence rate of blastomycosis?

302
Q

What are considered poor prognostic indicators in dogs with blastomycosis?

A

Hypoxaemia and involvement of ≥3 body systems

303
Q

Describe the pathophysiology of histoplasmosis?

A

Infection is via inhalation or ingestion of infective conidia
Conidia transform to the yeast phase and are phagocytosed by cells of the macrophage monocyte system
Haematogenous and lymphatic dissemination

304
Q

Which organs to histoplasma disseminate to in dogs and cats?

A

Dogs –lungs, gastrointestinal, lymph nodes, liver, spleen, bone marrow, eyes, adrenal glands
Cats –lungs, liver, lymph-nodes, eyes, bone marrow

305
Q

What determines the severity of clinical disease in histoplasmosis?

A

The cell-mediated immune response

306
Q

What are the clinical signs of histoplasmosis in cats?

A

Depression, anorexia, fever, palor, weight loss
Respiratory signs in 50%
Hepatomegaly, splenomegaly, lymphadenomegaly in 1/3
Ocular involvement
Fungal osteomyelitis
Cutaneous lesions

307
Q

What are the clinical signs of histoplasmosis in dogs?

A

Gastrointestinal signs most common
Fever, anorexia, depression, severe weight loss
Respiratory signs in less than 50%

308
Q

What as a common haematological abnormality and dogs and cats with histoplasmosis?

A

Thrombocytopenia (50% dogs, 33% cats)

309
Q

What diagnostic imaging abnormalities are commonly seen with histoplasmosis?

A

Interstitial lung pattern
Lytic bone lesions

310
Q

What are the common cytological findings in histoplasmosis?

A

Pyogranulomatous lesions with multiple intracellular organisms within macrophages

311
Q

Other than organism identification what tests are available for the diagnosis of histoplasmosis?

A

Galactomannan antigen EIA
Not specific for histoplasmosis

312
Q

What is the prognosis for histoplasmosis?

A

Good for dogs with pulmonary signs, guarded for dogs with gastrointestinal disease or severe dissemination. Fair to good for cats

313
Q

What is the most common organism associated with fungal rhinitis and dogs?

A

Aspergillus fumigatus

314
Q

What is the sensitivity of cytology in detecting aspergillosis when performed on direct smears of nasal discharge and bind end-nasal swabs?

315
Q

What can be done to increase the sensitivity a fungal culture in aspergillosis?

A

Incubation at 37°

316
Q

What is the sensitivity and specificity of serology in the diagnosis of aspergillosis?

A

Poorly sensitive highly specific

317
Q

What is the mechanism of action of azole antifungals?

A

Block synthesis of ergosterol by interaction with the fungal cytochrome p450 system

318
Q

Which organs are commonly associated with systemic aspergillosis?

A

Intervertebral disc’s, bones, lungs, kidneys, eyes, lymph-nodes, brain, gastrointestinal tract

319
Q

Which organism its most commonly associated with systemic aspergillosis?

A

Aspergillus terreus
Aspergillus deflectus

320
Q

Which breed is associated with systemic aspergillosis?

A

German Shepherd

321
Q

How is feline aspergillosis classified?

A

Invasive or non-invasive syndromes
Sinonasal aspergillosis or sino-orbital aspergillosis

322
Q

What is the most common presentation of feline aspergillosis?

A

Sino-orbital aspergillosis (2/3 of cases)

323
Q

Which organisms are associated with upper respiratory tract aspergillosis in cats?

A

Aspergillus fumigatus
Aspergillus viridinutans

324
Q

Which breeds are associated with upper respiratory tract aspergillosis?

A

Brachycephalic pure breed cats of Persian lineage

325
Q

What is a useful screening test for upper respiratory tract aspergillosis in cats?

A

ELISA serology

326
Q

What species are affected by sporotrichosis?

A

Dogs - rarely affected
Cats more frequently

327
Q

What is the pathophysiology of sporotrichosis?

A

Infection usually occurs following trauma and inoculation of infective conidia
Haematogenous dissemination likely

328
Q

What are the three primary forms of sporotrichosis?

A

1 - cutaneous
2 – cutaneolymphatic
3 –disseminated disease

329
Q

What form of sporotrichosis is most common?

A

Dogs - cutaneous or cutaneolymphatic
Cats –all forms (dissemination seen in more than 50%)

330
Q

What are the clinical signs of sporotrichosis?

A

Multiple subcutaneous of dermal nodular lesions
Respiratory signs and weight loss if dissemination

331
Q

What is the treatment of choice for sporotrichosis?

A

Itraconazole

332
Q

What risk factors are associated with candidiasis?

A

Prolonged broad spectrum antibiotic use, structural change in tissue, immuno suppression, neutropenia

333
Q

How does disseminated candidiasis present?

A

Fever with multiple raised microabscesses

334
Q

What is the treatment of choice of urinary tract candidiasis?

A

Fluconazole

335
Q

What is the treatment of choice of disseminated candidiasis?

A

Itraconazole and amphotericin B

336
Q

What is a risk factor for pythosis?

A

Access to warm freshwater habitats

337
Q

What forms of pythosis are recognised?

A

Cutaneous, gastrointestinal

338
Q

Which regions of the gastrointestinal tract are most commonly affected by pythosis?

A

Gastric outlow area, duodenum, ileocolic junction

339
Q

What stain should be used to detect pythosis?

A

Gomori methanemine silver (GMS)

340
Q

What are the histopathological characteristics of pythosis?

A

Eosinophilic pyogranulomatous inflammation

341
Q

How can pythosis be diagnosed?

A

Histology
Culture
ELISA serology

342
Q

What is the treatment of choice for pythosis?

A

Aggressive surgical resection
Itraconazole and terbinafine if 5cm margins not achieved

343
Q

Why does pythosis respond poorly to medical therapy?

A

Because ergosterol (antifungal drug target) is lacking in the oomycete cell membrane

344
Q

What are the main features of lagenidiosis and paralagenidiosis?

A

Progressive solitary or multifocal cutaneous or subcutaneous lesions - locally invasive
Typically occult lesions in the abdomen/thorax
Culture and RNA sequencing needed for definite diagnosis
Lagenidiosis - aggressive surgical resection, prognosis poor
Paralagenidioisis - surgery often curative

345
Q

What is the structure of parvovirus?

A

Simple, small, non-enveloped, single-stranded DNA virus

346
Q

What determines the host specificity of parvovirus?

A

The capsid proteins

347
Q

How does parvovirus enter the host cell?

A

The transferrin receptor

348
Q

What is the half life of maternally derived parvovirus Ab?

349
Q

Which cells are affected most by parvovirus?

A

Rapidly dividing cells
Thymus, bone marrow, spleen, crypt cells

350
Q

What is the pathogenesis of parvovirus infection?

A

Following oral infection virus disseminates to the regional lymph nodes of the pharynx and the tonsils
Cell free viraemia
Thymic atrophy, lymphoid depletion, lymphopenia, immunosuppression
Crypt necrosis, villous collapse, loss of the normal gut barrier function

351
Q

What can cause a false positive faecal antigen parvovirus test?

A

Following vaccination and shedding of the vaccine virus

352
Q

What are recognised negative prognostic indicators in parvovirus infection?

A

Season, pure breed, body weight, vomiting, hyper coagulability, hypercortisolaemia, hypothyroxinaemia, hypoalbuminaemia, ^CRP, ^TNF, hypocholesterolaemia, hypocitrullinaemia

353
Q

What is the structure of the rabies virus?

354
Q

What is recommended if a vaccinated animal is potentially exposed to rabies?

A

Booster vaccine and monitor for 45 days

355
Q

What is recommended if a unvaccinated animal is potentially exposed to rabies?

A

Euthanasia or quarantine for 6 months

356
Q

What is recommended if a healthy animal bites a human and potentially exposes them to to rabies?

A

The animal should be monitored for 10 days

357
Q

What is the gold standard for rabies diagnosis?

A

Direct fluorescent antibody test

358
Q

What organisms are associated with CIRD?

A

CPIV, CAV-2, CHV-1, Bordatella

359
Q

What is the structure of CPIV?

A

Enveloped, single stranded RNA virus

360
Q

What is the structure of CAV-2?

A

Non-enveloped, double stranded DNA virus

361
Q

What is the structure of CHV-1?

A

Enveloped, double stranded DNA virus

362
Q

What are the 2 most prevalent viral causes of CIRD?

363
Q

What is bordatella’s role in CIRD?

A

Can be normal inhabitant of URT, primary or secondary pathogen

364
Q

Which mycoplasma is associated with significant disease in association with CIRD?

365
Q

Which pathogen of the CIRD complex can be spread by non-respiratory routes?

A

CHV-1 (genital secretions)

366
Q

What is the pathogenesis of CIRD?

A

Virus infects ciliated epithelial cells
Replication causes loss of coordinated beating of cilia, ciliostasis and loss of cilia
Ciliated cells often replaced by goblet cells
Mucociliary escalator ineffective - allows secondary infection

367
Q

What is the structure of CDV?

A

Enveloped, single stranded, RNA

368
Q

How is CDV transmitted?

A

Oronasal exposure to respiratory secretions, vomit, faeces, urine and fomites

369
Q

What is the pathogenesis of CDV?

A

Virus replicase in macrophages and monocytes in the tonsils, upper respiratory tract epithelium, and regional lymph nodes
Viraemia and spread to the stomach, small intestine, spleen and hepatic macrophages, bone marrow and other lymphoid tissue
Fever and lymphopenia
Further spread of the virus to epithelial cells in other organs including eyes, skin and CNS

370
Q

How does the host immune response affect the progression of CDV?

A

Poor immune response - severe clinical signs and death or maintain virus in tissue and later develop CNS disease
Intermediate immune response - mild clinical disease, with virus persisting in lungs, skin or CNS - may develop CNS disease or complete recovery
Strong immune response - no signs of systemic disease, but may develop CNS disease

371
Q

What are the clinical signs of CDV?

A

Older dogs - mild/asymptomatic
Puppies - severe disease
Early signs
Lymphopenia - conjunctivitis/respiratory
V/D
Anterior uveitis, optic neuritis
Kidney/bladder dysfunction
Pustular rash/hyperkeratosis

1-3 weeks after recovery from acute signs - neuro signs - seizures, ataxia, paraparesis. Myoclonus

372
Q

What viral disease is associated with hypereflective retinal lesions?

373
Q

What neurological sign is strongly suggestive of CDV infection?

374
Q

What non-neurological clinical signs are related to the likelyhood of developing neurological signs in CDV infection?

A

Pustular skin lesions - less likely to develop CNS signs
Hyperkeratosis of nasal planum and footpads - increased association with neuro signs

375
Q

What blood smear findings can be seen in CDV?

A

Intranuclear/intracytopasmic viral inclusions in monocytes, lymphocytes, neutrophils or RBCs

376
Q

What is the most consistent CBC abnormality with CDV?

A

Lymphopenia

377
Q

How is CDV diagnosed?

A

RT-PCR - most body tissues, sensitive but unable to differentiate field vs vaccine virus
Serology - may be low due to immunosuppression
IgM supportive of infection

378
Q

What is the structure of CHV?

A

Enveloped, double stranded, DNA

379
Q

What is the pathogenesis of CAV-1?

A

Tropism for endothelial cells, epithelial cells and hepatocytes
Replicates in tonsils and LNs
Affects liver, eyes, kidneys

380
Q

What are the clinical signs of CAV-1?

A

Corneal oedema and anterior uveitis
Hepatomegaly, ascites
Respiratory signs

381
Q

What causes pseudorabies?

A

Ingestion of infected raw pork

Ettinger (13 decks)

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