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
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
3
Q
Which viral infection can be associated with inclusions in circulating lymphocytes, neutrophils and erythrocytes in dogs?
A
CDV
4
Q
What infections are spread by Ixodes ticks?
A
Borrelia, Anaplasma, Ehrlich, Babes, Bartonella, tick-borne encephalitis
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
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
7
Q
How do Bb and tick-borne relapsing fever infections vary?
A
Bb generally does not circulate in the blood or body fluids
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%
9
Q
What % of dogs seropositive for Bb have Lyme nephritis?
A
<2%
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
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
12
Q
What is the main risk factor for M. microti infection?
A
Hunting rodents
13
Q
What are the routes of infection for tuberculous mycobacteriosis?
A
Skin, GI, respiratory tracts
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
15
Q
What are the most common manifestations of TB in dogs?
A
Non-specific - lethargy, anorexia, weight loss, cough, dyspnoea, v/d, pyrexia
16
Q
How is TB infection confirmed?
A
Demonstrating acid-fast bacteria on histo
Culture
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
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)
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
20
Q
How is saprophytic mycobacteriosis diagnosed?
A
Acid-fast staining, PCR
21
Q
How does treatment of saprophytic mycobacteriosis differ from that of tuberculous disease?
A
Greater resistance to treatment
22
Q
How do leproid syndromes present? Are they reported in cats or dogs?
A
Discrete cutaneous lesions.
Both
23
Q
How is feline leprosy transmitted?
A
Rodent bites
24
Q
When is feline leprosy more common?
A
Colder months
25
Where is canine leprosy reported? When is it more common?
Zimbabwe, Australia, Brazil, Warmer months
26
How is canine leprosy transmitted?
Insect bites
27
How are younger and older cats affected by leprosy?
Young - rapidly progressive, ulcerated
Old - diffuse, non-ulcerated slowly progressing lesions
28
How is leproid infection diagnosed?
Acid fast - impression smears
PCR
29
How are leproid syndromes treated?
May not be needed, spontaneous regression - dogs > cats
Surgical resection and dual AB therapy
30
Where is actinomyces most commonly found?
Mucous membrane commensal
GI and urinary tract
31
What are the common presentations of actinomyces infection?
SC or soft tissue abscess, pleuritic, pneumonia
32
How do actinomyces appear on cytology?
Non-acid fast filamentous organisms
33
Where are nocardia spp commonly found?
Soil
34
How does nocardia infection present?
Cutaneous lesions, pneumonia, pyothorax
Disseminated disease in young/immunocompromised
35
What empirical AB can be chosen in actinomyces infection?
Penicillin
36
What empirical AB can be chosen in nocardia infection?
Sulphonamide ABs
37
How is brucellosis shed?
Urine, vaginal discharges, aborted tissues, milk, saliva, nasal secretions
38
What happens following brucella crossing a mucous membrane?
Phagocytosed by macrophages and moved to LN
39
Following infection with brucella, when is bacteraemia seen and how long does it persist?
7-30 days
Up to 6 months
40
What are the clinical signs of Brucella infection?
Abortion, infertility, acute epididymitis, lethargy, weight loss, back pain, lymphadenopathy, poor vision
41
When can brucella serological testing be performed?
4 weeks after infection
42
How can the specificity of a brucella RSAT be improved?
By the addition of 2-mercaptoethanol
43
Which diseases are associated with clostridial organisms?
Tetanus and botulism
44
How do the susceptibility of dogs and cats to tetanus differ?
Cats 10x more resistant to infection than dogs
45
What exotoxins are associated with tetanus? What do they do?
Tetanolysin - damages otherwise viable tissue
Tetanospasmin - causes clinical syndrome of tetanus
46
What is the structure and function of tetanospasmin?
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
47
What cells are affected by tetanospasmin?
Motor, then sensory and autonomic nerves
Can spread to brainstem via spinal cord
Predominantly affects inhibitory neurons
48
What are the consequences of autonomic inhibition by the tetanus toxin?
Sympathetic overactivity and excess plasma catecholamine levels
49
What is the explanation for the long duration of clinical tetanus?
Neuronal blinding of toxin is irreversible, recovery requires growth of new nerve terminals
50
When do clinical signs of tetanus become apparent?
Normally within 5-12 days of infection, can take up to 3 weeks
51
What is the mortality rate of tetanus?
8-50%
52
What autonomic signs are seen with tetanus?
Bradycardia, t tachycardia, hypertension, vasoconstriction, hyperthermia. Dysuria, urinary retention, constipation
53
What is the tetanus severity classification system?
I - facial signs
II - generalised rigidity/dysphagia
III - I + II + recumbency/seizures
IV - I + II + III + abnormal HR/RR/blood pressure
54
What biochemical abnormality is present in >50% of dogs with tetanus?
Elevated CK
55
How can tetanus be definitely diagnosed?
Measurement of serum antibodies against tetanospasmin
PCR for detecting toxin gene in wounds described but not available
56
What are the aims of treating tetanus?
1 - toxin neutralisation
2 - destruction of organism
3 - minimise effects of toxin
57
What is the preferred route of equine tetanus antitoxin? What is the risk?
IV
Anaphylaxis
58
How should a wound in a tetanus patient be managed?
Radical debridement and 3% hydrogen peroxide
59
Which AB has been shown to be superior for management of clinical tetanus?
Metronidazole
60
Which botulinum toxin has been associated with disease in dogs and cats?
C
61
Where is botulism toxin found?
Rancid food, dead birds
Rarely following colonisation of tissue and coprophagia
62
What is the pathogenesis of botulism?
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
63
What are the clinical signs of botulism?
Afebrile placid paralysis
+/- cholinergic signs - altered HR, pupil changes (mydriasis and reduced PLR), KCS, urinary retention, constipation
64
What is the vector for Bartonella?
Blood sucking arthropods
Mostly cat fleas, also detected in Pulex fleas, Ixodes and Rhipicephalus
65
What are the targets of Bartonella infection?
Erythrocytes, endothelial cells, bone marrow progenitor cells
66
What affects the severity of clinical signs with Bartonella infection?
In primary host may be persistent bacteraemia without clinical signs
When non-adapted host infected, clinical signs more severe
67
What is the life cycle of Bartonella?
Replicate in midgut of arthropod and excreted in faeces
Inoculated through bite or scratching of area
Infect microglial cells, macrophages and CD34+ progenitor cells
68
What is responsible for Bartonellas invasion?
Adhesins - mediate bacterial adherence
Type IV secretion systems - transport DNA into cell
69
What is responsible for Bartonellas virulence?
Bartonella-effector proteins
70
What structure characterised the invasion of Bartonella?
Invasive - well organised bacterial aggregate engulfed and internalised by the targeted cell
71
How is Bartonella acquired by its vector?
Bacterial released from blood-seeding niche, bind to and invade erythrocytes without causing haemolysis
Released into circulation at 5 day intervals
72
What cells are suppressed to cause the immunosuppression seen with Bartonella?
CD8+ lymphocytes
73
How is Bartonella infection distributed in the body?
All tissues can be involved
74
75
What are the common clinical manifestations of Bartonella infection in dogs?
Pyrexia
Lymphadenopathy
Endocarditis
Myocarditis
Arthritis
Disseminated granulomatous disease (skin, LeNs, liver, spleen)
Neuro signs
Pleural, pericardial, peritoneal effusions
76
What proportion of canine endocarditis are caused by Bartonella?
19-28%
77
Which Bartonella species is commonly associated with endocarditis?
B. vinsonii subs. berkhoffi
78
In Bartonella endocarditis in dogs, which valve is most often affected?
Aortic
79
What lab abnormalities are associated with Bartonella infection?
Normally none
Non-specific
Hypoglubulinaemia
80
What clinical pathological finding has been associated with a 4x higher risk of being diagnosed with Bartonella?
Hypoglobulinaemia
81
What samples are best tested for Bartonella culture and PCR?
Tissue and non-blood fluids
82
What limits serology in Bartonella infection?
Over half of dogs have bacteraemia without ABs
83
How should Bartonella be treated in dogs?
Exact protocol not known
Combination of AB with high plasma and intracellular concentrations
84
What is a potential side effect of treating Bartonella in dogs? How can it be avoided. How should it be managed?
Jarisch-Herxheimer reaction - lethargy, fever, vomiting
By starting ABs 5-7 days apart in clinically stable dogs
Avoid interrupting treatment, anti-inflammatory steroids
85
Which species of Bartonella is most common in cats?
B. henslae
86
What are the clinical signs of Bartonella infection in cats?
Uveitis
Aortic valve endocarditis
Myocarditis
Lymphadenopathy
Pyrexia
Mild neuro signs
Usually subclinical
87
How is Bartonella diagnosed in cats?
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
88
What is the recommended treatment for bartonella in cats?
Doxycycline and pradofloxacin
89
What is the main reservoir host of leptospirosis?
Rodents
90
How do leptospires differ from other gram-negative bacteria?
Do not cause fulminant septic disease shortly after onset of infection - low endotoxic potential of leptospiral lipopolysaccharide
91
How do leptospires evade the host immune response?
Binding inhibitors of complement activation on their surface
92
After the host response, where can leptospires persist?
Eye and renal tubules
93
Which organs are commonly involved in lepto infection?
Kidneys (tubules and glomeruli)
Liver
Lung
94
What are the hallmarks of leptospiral pulmonary haemorrhage syndrome?
Intra-alveolar haemorrhage in the absence of a marked inflammatory cell infiltrate or vasculitis
95
In a study of a cohort of dogs with lepto, what were the most common clinical syndromes (in order)?
Renal
Lung
Hepatic
96
What are the typical radiographic lung findings with lepto?
Pulmonary change in the caudodorsal fields, ranging from mild interstitial to severe reticulonodular
+/- mild mediastinal or pleural effusion
97
What diagnostics are available for lepto?
Culture - challenging, can take 6 months
Darkfield microscopy - low sens/spec
Serology
PCR
98
How long to vaccinal antibodies to lepto persist?
Normally up to 15 weeks, can persist up to 12 months
99
How should LPHS be treated?
Limited evidence exists in humans to suggest benefit of immunosuppression
100
What infections are spread by rhipicephalus sanguineus? Where are they found?
E. canis
A. platys?
R. rickttsii
Worldwide
101
What infections are spread by amblyomma americanum? Where are they found?
E chaffeensis
E ewingii
USA
102
What infections are spread by Ixodes scapularis? Where are they found?
A. phagocytophilum
USA
103
What infections are spread by Ixodes pacificus? Where are they found?
A. phagocytophilum
USA
104
What infections are spread by Ixodes persulcatus? Where are they found?
A. phagocytophilum
Eastern Europe and Asia
105
What infections are spread by Ixodes ricinus? Where are they found?
A. phagocytophilum
Europe
106
What infections are spread by Dermacentor variabilis? Where are they found?
R ricketsii
USA
107
What infections are spread by Dermacentor andersoni? Where are they found?
R ricketsii
USA - Rocky Mountain states
108
What disease is caused by E Canis?
CME
109
Where is E Canis distributed?
Worldwide
110
What are the clinical signs of CME
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
111
What are the most common clin path findings in CME?
Panctopenia - BM hypoplasia
Elevated globulins (mono or polyclonal)
PLN
112
How is CME diagnosed?
Morulae within monocytes
Serology - ELISA/IFA
PCR - blood, LN, splenic FNA, BM
113
What is the sensitivity of BM PCR for diagnosis of chronic CME?
25%
114
What tick carries E Canis?
Rhipicephalus sanguineus
115
How should CME be treated?
Doxy x 28 days
116
Where is E. ewingii found? What is the main cause of transmission?
USA, Brazil, Cameroon
Amblyomma americanum
117
What are the clinical signs of E. ewingii?
Lethargy, anorexia, v/d, neuro signs, pyrexia, polyarthritis
118
What are the common Clinical path findings with E ewingii
Anaemia, mild leucopenia or leukocytosis, thrombocytopenia, hyperglobulinaemia, ALP elevation
119
Where is E chaffeensis seen? What spreads it?
USA
Amblyomma americanum
120
What are the clinical signs of E chaffeensis?
Fever, anaemia, leukopenia, thrombocytopenia, lymphadenopathy, epistaxis
121
What causes canine granulocytic ehrlichiosis? What spreads it?
A. phagocytophillum
I. scapularis/pacifinus/ricinus
122
What are the clinical signs of CGE?
Subclinical in many
Nonspecific - pyrexia, lethargy, lameness, stiffness, LN++, splenomegaly
Polyarthritis
Thrombocytopenia in >80%
123
How is CGE diagnosed?
Morula in neutrophils
ELISA serology (rising titre) - cross reactivity with platys
PCR (whole blood)
124
What causes thrombocytic anaplasmosis? What is the vector? Where is it seen?
A. platys
R. sanguineus
USA, South America, Australia, Asia, Europe
125
What are the clinical signs of A. platys infection?
Most subclinical
Transient thrombocytopenia
126
What causes salmon poisoning disease?
Neorickettsia helminthoeca
127
What is the life cycle of Neorickettsia helminthoeca?
Flukes => snails => fish => dogs
128
What happens following infection with N helminthoeca?
Disseminates to Las, spleen, liver, lungs, brain
129
What are the clinical signs of SPD?
Weight loss, LN+++, v/d, thrombocytopenia in 90%
130
What clinical pathology findings are common in SPD?
Thrombocytopenia, v Na, K, alb
^ LEs
131
How is SPD diagnosed?
Trematode eggs in faeces
Neorickettsiae on LN aspirate examination
PCR on lymphoid tissue
132
How is SPD treated?
doxycycline + praziquantel
133
What causes RMSF? What spreads it and where is it found?
R. ricketsii
Dermacentor in USA
R. sanguineus in Arizona
134
What are the clinical signs of RMSF?
Fever, lethargy, anorexia, lymphadenopathy
Oedema and erythema
Stiffness
Ocular signs
Bleeding
Neuro signs
135
What are the clin path changes seen with RMSF?
Leukocytosis, anaemia, thrombocytopenia
136
How is RMSF diagnosed?
Serology - IFA/ELISA
137
What is the most common species of mycoplasma in a) cats and b) dogs?
a) Candidatus M. haemominutum
b) M. haemocanis
138
What is the most pathogenic feline mycoplasma?
M. haemofelis
139
What are the haematological fingers with acute/chronic mycoplasma haemofelis infection>
A - regenerative anaemia - microcytic and hypochromic
C - no significant anaemia
140
What is the sensitivity of cytology for diagnosing mycoplasma infection?
0-37%
141
How is clostridium perfringens typed? How many phenotypes are there based on this method?
Toxins - alpha, beta, epsilon, iota
Phenotypes - A, B, C, D, E
142
What is a known virulence factor for clostridium perfringens>
CPE
143
What is the suspected pathogenesis of clostridium perfringens-associated illness?
Massive sporulation of commensal strains, triggered by diet change, ABs, coinfection => CPE released
144
How does CPE cause clinical signs?
Interacts with epithelial tight junction proteins, forming protein complex. Then interacts with host proteins, forming larger complex. Provides CPE access to occludin.
145
How is clostridium perfringens diagnosed?
Is culture helpful?
CPE detection in faecal samples in combination with PCR detection of cpe gene
NO - isolated from 80% healthy dogs
146
How should clostridium perfringens be treated?
Uncomplicated diarrhoea - no treatment needed
Systemic illness - ampicillin, MNZ, tylosin
147
What toxins are associated with clostridium difficile?
TcdA - enterotoxin
TcdB - cytotoxin
148
What clinical disease is associated with CDI?
Association between TcdA toxin and AHDS in dogs
149
What diagnostic tests are available for CDI?
CTA - detects TcdA - gold standard but £££
Recommended approach is positive culture and/or antigen test AND ELISA detection of TcdA/TcdB
150
How is CDI treated?
MNZ treatment of choice
151
When is campylobacter jejuni shedding most commonly detected?
Dogs <6m
Summer and autumn
152
What toxin is associated with campylobacter?
Cytolethal distending toxin
Proteins CdtA, CdtB, CdtC
153
When should campylobacter infection be treated?
Immunocompromised, febrile, haemorrhagic d+
Erythromycin or fluoroquinolone
154
Describe the pathogenesis of Salmonella
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
How/when should salmonella be treated?
Not necessary in uncomplicated cases.
Fluoroquinolones, chloramphenicol, TMPS, amoxicillin.
156
Is duodenal aspiration and cytology helpful for the diagnosis of Giardia?
Dogs - yes
Cats - no, lives in distal SI
157
How is hepatozoonisis spread?
Ingestion of infected tick
Rhipicephalus
158
Describe the pathogenesis of hepatozoonosis
After ingestion of infected tick sporozoites released - infect mononuclear phagocytes and endothelial cells of spleen, liver, muscle, lungs and bone marrow - form cysts
159
What are the clinical and pathological findings with hepatozoonosis?
Neutrophilic leukocytosis
Periosteal reaction - any bone except skull
160
How should hepatozoonosis be treated?
H. americanum - TMPS, pyrimethamine and clindamycin in acute phase, then decoquinate
H. canis - imidocarb
161
What are the clinical signs of neosporosis in dogs?
Ascending paralysis, polymyositis, multifocal CNS disease, myocarditis, dysphagia, ulcerative dermatitis, pneumonia, hepatitis
162
Describe the pathophysiology of toxo infection
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
What are the common clinical signs of toxo infection
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
Where is trypanosomiasis reported?
North and South America and Caribbean
165
What are the clinical signs of trypanosomiasis?
Cardiomyopathy, ventricular/supraventricular arrhythmia
(Neuro disease)
166
How is trypanosomiasis diagnosed?
Organ demonstration - lymph node aspirates or abdominal effusion
Histo examination of cardiac tissue - amastigotes
167
What are the common Babesia species and how are they transmitted?
B. rossi - Haemaphysalis leachi
B. canis - Dermacentor reticulatus
B. vogeli - Rhipicephalus sanguineus
168
What are the clinical signs of Babesia infection?
Often subclinical
Intracellular replication in RBCs => intravascular haemolysis
Immune reactions worsen
Acute anaemia
169
How is Babesia diagnosed?
Serology - paired titres
Organism demonstration - blood smears
170
How is babesia treated?
Imidocarb - canis
Azithromycin and atovaqone - gibsoni
171
What spreads cytauxzoonosis?
Amblyomma americanum
Dermacentor variabilis - experimentally
172
What is the pathophysiology of cytauxzoonosis?
Infected macrophages line lumen of veins, release merozoites, infect RBCs
Obstruction of blood flow and haemolytic anaemia
173
What species is affected by cytauxzoonosis?
Cats
174
How is cytauxzoonosis diagnosed?
Organism demonstration in RBCs and macrophages on blood smears and bone marrow/splenic/liver/LN cytology
175
Describe the structure of the FIV virus
Enveloped RNA
3 layered structure
Inner genome-nucleocapsid complex
Icosahedral capsid
Envelope with glycoprotein spikes
176
What are the 3 main FIV genes?
gag - vision core proteins (capsid [p24], nucleocapsid and matrix)
pol - reverse transcriptase
env - surface (gp120) and transmembrane virion (gp41) envelope proteins
177
How does FIV invade cells?
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
What happens following FIV invasion of cells?
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
Following cell infection with FIV and integration of viral DNA into the genome, what are the possible consequences?
Latency - no transcription
Activity
180
How can retroviruses cause tumour growth?
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
What are the FIV subtypes? How are they typed?
A-F
Based on env gene
182
How is FIV transmitted?
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
Which cells are targeted by FIV?
Mostly CD4+ T cell
CD8+ T cell, B cells, macrophages, dendritic cells, microglia and astrocytes also affected
184
What are the 3 stages of FIV disease?
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
When does FIV viraemia peak?
8-12 weeks after infection
186
How do cats survive the acute phase of FIV infection?
Strong humeral response, rebound of CD8+
187
What happens to the immune system in the subclinical phase of FIV infection?
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
Draw a graph showing FIV plasma viraemia and CD4 T cell concentration over time, showing the different phases of infection
Sykes pg 212
189
What is the most common neoplasia ins FIV infected cats?
B-cell lymphoma
190
What are the potential neurological signs of FIV?
Increased aggression, tremors, sleep disturbance, anisocoria, abnormal cranial nerve function, seizures
191
Where are FIV inflammatory lesions seen?
Myopathy, enteropathy, ocular
192
How should FIV be diagnosed?
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
What is the target of the point of care FIV ELISA?
p24 antibodies
194
When are a) false positive and b) false negative FIV ELISA results possible
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
FIV PCR sensitivity
80%
196
What topical treatments have been described for FIV stomatitis?
Topical lactoferrin
Chlorhexidine
197
What systemic treatment has been described for cats with FIV? What is the main side effect?
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
What is the prognosis for FIV infected cats?
No significant difference in lifespan of infected/non-infected cats
199
What class of virus is FeLV?
Enveloped, RNA virus
200
What are the possible outcomes after FeLV infection?
Progressive infection
Latent infection
Abortive infection
201
What are the subtypes of FeLV? Describe how they arise
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
Which FeLV subtype is most associated with the development of lymphoma?
FeLV-B
203
Which FeLV subtype is most associated with the development of non-regenerative anaemia?
FeLV-C
204
Which FeLV subtype is most associated with the development of immunodeficiency?
FeLV-T
205
How is FeLV transmitted?
Close contact with salivary secretions
206
What is the median age of infection with FeLV?
3y
207
What is the pathogenesis of FeLV infection following oronasal exposure?
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
What happens in a regressive (latent) FeLV infection?
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
What happens in an abortive FeLV infection?
No viraemia occurs after infection. Antibodies develop
210
What happens in a progressive FeLV infection?
Bone marrow involvement established. Cellular destruction by virus exceeds immune system response.
Persistent viraemia and progressive FeLV-related disease
211
What are the clinical outcomes of progressive FeLV infection?
Neoplasia
Opportunistic infection
PRCA
BM disease
Immune mediated disease
Lymphadenopathy
Neuro disease (anisocoria, urinary incontinence)
Repro failure
GI signs
212
What are the most common types of neoplasia associated with FeLV infection?
Lymphoma
Leukaemia
Fibrosarcoma
213
What type of lymphoma is most associated with FeLV infection?
T-cell
214
Which species are predominantly affected by borna disease virus?
Horses and sheep. Cats also susceptible
215
What are the main clinical signs of borna disease virus?
Motor dysfunction, staggering gait
216
What can help rule out a diagnosis of borna disease virus?
Neurological signs other than motor dysfunction
217
How is borne disease virus diagnosed?
Serology
218
What is the prognosis of borna disease virus?
Generally progressive
219
What are the necropsy findings in borna disease virus?
Nonsuppurative meningoencephalomyelitis of grey matter
220
Where is cowpox virus seen?
Eurasia
221
What is a risk factor for cowpox transmission?
Hunting wild rodents
222
How does cowpox infection present?
Usually primary lesion on head/neck/forelimb
Often widespread secondary skin lesions
Occasionally systemic illness (eg pneumonia)
223
How is cowpox infection diagnosed?
PCR of skin crusts
224
How is cowpox infection treated?
Supportive treatment, BS ABs
225
What is the seroprevalence of feline foamy virus?
Up to 90%
226
What is the significance of feline foamy virus infection?
Unknown, likely asymptomatic
227
What clinical sign is associated with astrovirus infection?
Diarrhoea
228
What is the significance of rotavirus infection in cats?
Clinical disease uncommon - mild diarrhoea
229
What are the two main causes of viral respiratory disease in cats?
FeHV-1
FCV
230
What bacterial pathogens are seen as part of infectious respiratory disease in cats?
Bordatella
Chlamydia felis
Mycoplasma
231
Which clinical signs are associated with FeHV-1 infection?
URT disease - oculonasal discharge, conjunctivitis, sneezing
Occasionally pneumonia, osteolytic change in turbinates and chronic rhinitis
232
What is the most common clinical sign with FCV infection?
Oral ulceration
233
What clinical signs are associated with FCV infection?
Oral ulceration, URT signs, conjunctivitis
Rarely lameness, respiratory/oral disease, interstitial pneumonia
Rarely hypervirulent strains - pyrexia, oedema, anorexia, jaundice - high mortality rate
234
Which feline respiratory disease has a hyper virulent strain?
FCV
235
How does the severity of FeHV-1 and FCV infection compare?
FCV usually milder
236
How is FeHV-1 diagnosed?
PCR
237
How is FCV diagnosed?
Virus isolation
RT-PCR - possibly less sensitive
238
How can cats become infected with H5N1 infection?
Direct contact and consuming infected poultry
239
What are the clinical signs of H5N1 infection in cats?
Severe respiratory disease
240
Where is cryptococcus found?
Worldwide
241
What are the main causes of cryptococcosis?
Cryptococcus neoformans
Cryptococcus gattii
242
Where is cryptococcus neoformans found in the environment?
Associated with pigeon droppings
243
Where is cryptococcus neoformans found in the environment?
Bark and leaf litter of trees in tropics/subtropics
244
What class of fungus is cryptococcus?
Yeast
245
How does infection with cryptococcus occur?
Inhalation
246
What happens after inhalation of cryptococcus yeast?
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
What % of dogs/cats are asympomatic carriers of cryptococcus?
D - 14%
C - 7%
248
What % of dogs/cats develop pulmonary disease with cryptococcus?
10%
249
Which tissues are most often affected by disseminated cryptococcosis?
Skin
CNS
Eyes
250
How do cryptococcus evade the immune system?
Thick capsule inhibits phagocytosis, plasma cell function and leukocyte migration
251
What determines the severity of clinical signs in cryptococcosis?
Immune response
Humoral response not helpful - dependent on cell-mediated immunity
252
What risk factors have been identified in dogs/cats for cryptococcosis infection?
FIV/FeLV
Chronic steroid use
253
What are the clinical signs of cryptococcosis in cats?
URT, nasopharyngeal, cutaneous, ocular, CNS involvement
254
What % of cats with cryptococcosis have eye involvement?
20-25%
255
What are the common ocular signs of cryptococcosis in cats?
Granulomatous chorioretinitis +/- exudative retinal detachment
256
What % of cats with cryptococcosis have neurological involvement?
20%
257
What are the clinical signs of cryptococcosis in dogs?
Depression, anorexia, CNS signs, URT signs
258
What is the sensitivity of CSF cytology for diagnosing cryptococcosis in dogs with CNS involvement?
90%
259
What is the sensitivity of cytology of nasal swabs, FNA of masses and impression smears of exudate in dogs with cryptococcosis?
50-70%
260
What stain can be used to aid a cytological diagnosis of cryptococcosis?
Gram stain
261
What is a limitation of a positive fungal growth from a nasal cavity in a dog suspected to have cryptococcosis?
14% asymptomatic carriers
262
What findings can be seen on thoracic radiographs in dogs with cryptococcosis?
Nodular infiltrates, an interstitial pattern, pleural effusion, tracheobronchial lymphadenopathy
263
If cytology doesn't demonstrate cryptococcal organisms in a suspected case, what test should be performed next?
Histopathology
264
What special stains can aid identification of cryptococcus on histopathology?
PAS, Gridley's fungal, Grocott's Methenamine Silver, Gomori Methenamine Silver
Mucicarmine stains - capsule
265
Is serology useful in diagnosing cryptococcosis?
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
What treatments are available for cryptococcosis?
Amphotericin B
Fluconazole
Itraconazole
267
What is the treatment of choice for animals severely affected with cryptococcosis?
Amphotericin B (+/- flucytosine)
268
What side effects have been reported with flucytosine?
Ulcerative drug eruptions (skin and mucocutaneous junctions), enterocolitis, leukopenia, thrombocytopenia
269
What is the treatment of choice for animals mildly or moderately affected with cryptococcosis?
Fluconazole
270
What are the reported times to cure in cats with cryptococcosis treated with fluconazole and itraconoazole?
F - 4 months
I - 9 months
271
How can treatment of cryptococcosis be monitored? What is a limitation of this approach?
Serial latex agglutination titres
Can remain positive in some
272
What is the prognosis for cryptococcosis in dogs and cats?
Cats without CNS involvement - good
Dogs and cats with CNS involvement - guarded
273
What is the relapse rate for cryptococcosis in cats?
15-20%
274
What forms are coccidioidomycosis found in?
Environment - mycelium (chain of arthroconidia)
Body - spherules
275
What species of coccidiodes are recognised? How are they different?
C. posadasii
C. immitis
Similar clinical signs and drug sensitivity, different geographical distribution
276
What is the pathogenesis of coccidioidomycosis?
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
What are the clinical signs of coccidioidomycosis?
Intermittent fever, lethargy, inappetence and weight loss.
Cough, dyspnoea, exercise intolerance
278
Where are possible sites of dissemination of coccidioidomycosis?
Bone, CNS, skin, peripheral lymph-nodes, pericardium
279
What are common clinicopathological abnormalities in dogs with coccidioidomycosis?
Non-regenerative anaemia, neutrophilia, hypoalbuminaemia, hyperglobulinaemia, proteinuria
280
What is the most common finding on chest radiographs in dogs with coccidioidomycosis?
Hilar lymphadenopathy
281
What infectious disease is associated with pericarditis?
Coccidioidomycosis
282
What diagnostic tests can be used to confirm a diagnosis of coccidioidomycosis?
Serology
283
What is the diagnostic performance of a serologic assay that detects coccidioides antigen in urine?
Unacceptably low (<20%)
284
What treatment is recommended for pulmonary coccidioidomycosis?
Fluconazole or itraconazole
285
What treatment is recommended for coccidioidomycosis with bone involvement?
Itraconazole
286
What treatment can be considered for coccidioidomycosis causing refractory meningoencephalitis?
Voriconazole
287
How can treatment of coccidioidomycosis be monitored?
IgG titres
288
What type of organism is blastomyces?
Thick walled yeast
289
What is a risk factor for blastomycosis infection?
Living within a quarter of a mile of water
290
What is the pathogenesis of blastomycosis?
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
What environmental factors increase blastomycosis infection?
Rain, dew, fog
Activities that disrupt the soil
292
Which organs do blastomycosis commonly disseminate to?
Lymph-nodes, eyes, skin, bones, subcutaneous tissues and prostate
293
What determines the severity of infection with blastomycosis?
The immune response
Recovery dependent on cell mediated immunity
294
What clinical signs are associated with blastomycosis infection?
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
What are the presenting clinical signs of blastomycosis in cats?
Similar to dogs. Large abscesses are more common in cats and neurological involvement often noted
296
What clinicopathological abnormalities are seen with blastomycosis?
Hypoalbuminaemia
Hypocalcaemia in 10%
297
What imaging findings are seen with blastomycosis?
Interstitial lung pattern
Osteolytic bone lesions
Extra-axial CNS lesions on MRI
298
How can blastomycosis be definitely diagnosed?
Organism identification by cytology or histology
Thick walled yeasts
Blastomyces antigen enzyme immunoassay on serum and urine
Serology - low sens/spec
299
What is the treatment of choice for blastomycosis?
Itraconazole unless severe hypoxaemia or CNS infection in which case amphotericin B should be first choice
300
What rate of clinical cure can be expected for blastomycosis?
70 to 75%
301
What is the recurrence rate of blastomycosis?
20%
302
What are considered poor prognostic indicators in dogs with blastomycosis?
Hypoxaemia and involvement of ≥3 body systems
303
Describe the pathophysiology of histoplasmosis?
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
Which organs to histoplasma disseminate to in dogs and cats?
Dogs –lungs, gastrointestinal, lymph nodes, liver, spleen, bone marrow, eyes, adrenal glands
Cats –lungs, liver, lymph-nodes, eyes, bone marrow
305
What determines the severity of clinical disease in histoplasmosis?
The cell-mediated immune response
306
What are the clinical signs of histoplasmosis in cats?
Depression, anorexia, fever, palor, weight loss
Respiratory signs in 50%
Hepatomegaly, splenomegaly, lymphadenomegaly in 1/3
Ocular involvement
Fungal osteomyelitis
Cutaneous lesions
307
What are the clinical signs of histoplasmosis in dogs?
Gastrointestinal signs most common
Fever, anorexia, depression, severe weight loss
Respiratory signs in less than 50%
308
What as a common haematological abnormality and dogs and cats with histoplasmosis?
Thrombocytopenia (50% dogs, 33% cats)
309
What diagnostic imaging abnormalities are commonly seen with histoplasmosis?
Interstitial lung pattern
Lytic bone lesions
310
What are the common cytological findings in histoplasmosis?
Pyogranulomatous lesions with multiple intracellular organisms within macrophages
311
Other than organism identification what tests are available for the diagnosis of histoplasmosis?
Galactomannan antigen EIA
Not specific for histoplasmosis
312
What is the prognosis for histoplasmosis?
Good for dogs with pulmonary signs, guarded for dogs with gastrointestinal disease or severe dissemination. Fair to good for cats
313
What is the most common organism associated with fungal rhinitis and dogs?
Aspergillus fumigatus
314
What is the sensitivity of cytology in detecting aspergillosis when performed on direct smears of nasal discharge and bind end-nasal swabs?
13%
20%
315
What can be done to increase the sensitivity a fungal culture in aspergillosis?
Incubation at 37°
316
What is the sensitivity and specificity of serology in the diagnosis of aspergillosis?
Poorly sensitive highly specific
317
What is the mechanism of action of azole antifungals?
Block synthesis of ergosterol by interaction with the fungal cytochrome p450 system
318
Which organs are commonly associated with systemic aspergillosis?
Intervertebral disc's, bones, lungs, kidneys, eyes, lymph-nodes, brain, gastrointestinal tract
319
Which organism its most commonly associated with systemic aspergillosis?
Aspergillus terreus
Aspergillus deflectus
320
Which breed is associated with systemic aspergillosis?
German Shepherd
321
How is feline aspergillosis classified?
Invasive or non-invasive syndromes
Sinonasal aspergillosis or sino-orbital aspergillosis
322
What is the most common presentation of feline aspergillosis?
Sino-orbital aspergillosis (2/3 of cases)
323
Which organisms are associated with upper respiratory tract aspergillosis in cats?
Aspergillus fumigatus
Aspergillus viridinutans
324
Which breeds are associated with upper respiratory tract aspergillosis?
Brachycephalic pure breed cats of Persian lineage
325
What is a useful screening test for upper respiratory tract aspergillosis in cats?
ELISA serology
326
What species are affected by sporotrichosis?
Dogs - rarely affected
Cats more frequently
327
What is the pathophysiology of sporotrichosis?
Infection usually occurs following trauma and inoculation of infective conidia
Haematogenous dissemination likely
328
What are the three primary forms of sporotrichosis?
1 - cutaneous
2 – cutaneolymphatic
3 –disseminated disease
329
What form of sporotrichosis is most common?
Dogs - cutaneous or cutaneolymphatic
Cats –all forms (dissemination seen in more than 50%)
330
What are the clinical signs of sporotrichosis?
Multiple subcutaneous of dermal nodular lesions
Respiratory signs and weight loss if dissemination
331
What is the treatment of choice for sporotrichosis?
Itraconazole
332
What risk factors are associated with candidiasis?
Prolonged broad spectrum antibiotic use, structural change in tissue, immuno suppression, neutropenia
333
How does disseminated candidiasis present?
Fever with multiple raised microabscesses
334
What is the treatment of choice of urinary tract candidiasis?
Fluconazole
335
What is the treatment of choice of disseminated candidiasis?
Itraconazole and amphotericin B
336
What is a risk factor for pythosis?
Access to warm freshwater habitats
337
What forms of pythosis are recognised?
Cutaneous, gastrointestinal
338
Which regions of the gastrointestinal tract are most commonly affected by pythosis?
Gastric outlow area, duodenum, ileocolic junction
339
What stain should be used to detect pythosis?
Gomori methanemine silver (GMS)
340
What are the histopathological characteristics of pythosis?
Eosinophilic pyogranulomatous inflammation
341
How can pythosis be diagnosed?
Histology
Culture
ELISA serology
342
What is the treatment of choice for pythosis?
Aggressive surgical resection
Itraconazole and terbinafine if 5cm margins not achieved
343
Why does pythosis respond poorly to medical therapy?
Because ergosterol (antifungal drug target) is lacking in the oomycete cell membrane
344
What are the main features of lagenidiosis and paralagenidiosis?
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
What is the structure of parvovirus?
Simple, small, non-enveloped, single-stranded DNA virus
346
What determines the host specificity of parvovirus?
The capsid proteins
347
How does parvovirus enter the host cell?
The transferrin receptor
348
What is the half life of maternally derived parvovirus Ab?
10 days
349
Which cells are affected most by parvovirus?
Rapidly dividing cells
Thymus, bone marrow, spleen, crypt cells
350
What is the pathogenesis of parvovirus infection?
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
What can cause a false positive faecal antigen parvovirus test?
Following vaccination and shedding of the vaccine virus
352
What are recognised negative prognostic indicators in parvovirus infection?
Season, pure breed, body weight, vomiting, hyper coagulability, hypercortisolaemia, hypothyroxinaemia, hypoalbuminaemia, ^CRP, ^TNF, hypocholesterolaemia, hypocitrullinaemia
353
What is the structure of the rabies virus?
354
What is recommended if a vaccinated animal is potentially exposed to rabies?
Booster vaccine and monitor for 45 days
355
What is recommended if a unvaccinated animal is potentially exposed to rabies?
Euthanasia or quarantine for 6 months
356
What is recommended if a healthy animal bites a human and potentially exposes them to to rabies?
The animal should be monitored for 10 days
357
What is the gold standard for rabies diagnosis?
Direct fluorescent antibody test
358
What organisms are associated with CIRD?
CPIV, CAV-2, CHV-1, Bordatella
359
What is the structure of CPIV?
Enveloped, single stranded RNA virus
360
What is the structure of CAV-2?
Non-enveloped, double stranded DNA virus
361
What is the structure of CHV-1?
Enveloped, double stranded DNA virus
362
What are the 2 most prevalent viral causes of CIRD?
CPIV
CRCoV
363
What is bordatella's role in CIRD?
Can be normal inhabitant of URT, primary or secondary pathogen
364
Which mycoplasma is associated with significant disease in association with CIRD?
M. cynos
365
Which pathogen of the CIRD complex can be spread by non-respiratory routes?
CHV-1 (genital secretions)
366
What is the pathogenesis of CIRD?
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
What is the structure of CDV?
Enveloped, single stranded, RNA
368
How is CDV transmitted?
Oronasal exposure to respiratory secretions, vomit, faeces, urine and fomites
369
What is the pathogenesis of CDV?
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
How does the host immune response affect the progression of CDV?
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
What are the clinical signs of CDV?
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
What viral disease is associated with hypereflective retinal lesions?
CDV
373
What neurological sign is strongly suggestive of CDV infection?
Myoclonus
374
What non-neurological clinical signs are related to the likelyhood of developing neurological signs in CDV infection?
Pustular skin lesions - less likely to develop CNS signs
Hyperkeratosis of nasal planum and footpads - increased association with neuro signs
375
What blood smear findings can be seen in CDV?
Intranuclear/intracytopasmic viral inclusions in monocytes, lymphocytes, neutrophils or RBCs
376
What is the most consistent CBC abnormality with CDV?
Lymphopenia
377
How is CDV diagnosed?
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
What is the structure of CHV?
Enveloped, double stranded, DNA
379
What is the pathogenesis of CAV-1?
Tropism for endothelial cells, epithelial cells and hepatocytes
Replicates in tonsils and LNs
Affects liver, eyes, kidneys
380
What are the clinical signs of CAV-1?
Corneal oedema and anterior uveitis
Hepatomegaly, ascites
Respiratory signs
381
What causes pseudorabies?
Ingestion of infected raw pork
