SA Exotics Flashcards

1
Q

How to tell the gender of a reptile: Lizards? Snakes? Chelonia?

A

Lizards - hemipenile bulge, femoral pores, sexual dimorphism
Snakes - popping, probing, pinging
Chelonia - tail length, plastron concavity, width of anal scutes, carapacial shape, palpation of intromittent organ on ventral wall of cloaca

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2
Q

How to tell the gender of a bird?

A
Behaviour/egg laying - song/voice
Sexual dimorphism - plumage, feather shape, eye colour
Vent sexing
DNA sexing - blood feather, blood
Endoscopy
Radiography?
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3
Q

How to tell the gender of a ferret?

A

Size
Genito-anal distance - further in males
Extrude penis/palpate testicles
Presence of os penis

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4
Q

How to tell the gender of a rabbit?

A

Buck - wider genitoanal distance, circular shaped penis with rounded tip
Doe = very short genitoanal distance, vulva has slit and pointed shape
Teat differences

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5
Q

How to tell the gender of a rodent?

A

Testicles
Males - longer genito-anal distance
Hamster - scent gland of males

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6
Q

What is UV light needed for in birds and reptiles?

A

Calcium metabolism
Vision in birds
UVA - affects behaviour
UVB - vitamin D production

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7
Q

Where is the heart positioned in ferrets?

A

Caudally - 6-9/10th rib spaces

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8
Q

Where is the heart found in snakes?

A

20-33% STV length

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9
Q

Normal temperature ranges for birds, small furries and hedgehogs?

A

Birds: 40-42C
Small furries: 36.5-40C
Hedgehog: 35-37C

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10
Q

Assessing hydration of birds and reptiles?

A
Weight loss
Skin tenting less reliable in birds and difficult to assess in reptiles as less elastic (lateral body wall for squamates)
Mucous membranes
Saliva viscosity
PCV
Total solids
Birds only:
- glazed or sunken eyes
- thick pasty urates
- cold extremities
- basilic vein refill time < 1-2s
- albumin
Reptiles only:
- constipation/impaction
- CRT (palatine vessel)
- sodium/chloride
- plasma osmolarity elevations
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11
Q

Maintenance fluid requirements for exotic mammals, birds and reptiles? Over how long should you replace fluid deficits?

A

Mammals: 75-100ml/kg/day
Birds: 50ml/kg/day
Reptiles: 10-30ml/kg/day
Replace deficits over 24-48 hours for mammals and birds, 48-96 hours for reptiles

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12
Q

What is hyaluronidase?

A

Enzyme that breaks down collagens in subcutaneous space - improves rate of s/c absorption of fluids

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13
Q

Limitations for giving oral fluids to exotics?

A
Respiratory distress - don't give
Seizures
Recumbency
Aspiration risk
GI stasis/ileus/obstruction
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14
Q

Limitations of S/C fluids for exotics?

A
Mild dehydration only 
Hypoalbuminaemia
Dehydration
Absorption time
Limited S/C space e.g. reptiles
Reptiles - skin sloughing with some drugs, skin pigment changes, inelastic skin so leakage possible
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15
Q

Where to administer SC fluids to exotics?

A

Mammals - inter scapular, lateral body wall
Birds - pre-crural fold, inter scapular, lateral body wall
Reptiles - lateral body wall (squamates), inguinal/axillary folds in chelonia

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16
Q

Limitations of IV fluids in exotic mammals and birds?

A

IV access challenging/impossible in small/collapsed patients
Appropriate sized catheters
Stress of restraint (GA/sedation?)
Mammals - Thick skin
Birds - tolerance of drip line, maintenance/self removal of IV catheter

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17
Q

Where to administer IV fluids in rabbits and rodents?

A

Rabbits - cephalic, lateral saphenous, marginal auricular (challenging in dwarf breeds)
Rodents - cephalic, lateral saphenous, jugular, lateral tail)

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18
Q

Where to administer IV fluids in birds?

A

Medial tarsal vein
Basilic vein
Right jugular vein
Consider prior IO volume resuscitation in collapsed patients

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19
Q

Limitations of IV fluids in reptiles?

A

IV access challenging/impossible in small/collapsed patients
Accessibility of veins - larger chelonia
Surgical cut down technique usually required for catheter placement (analgesia, anaesthesia)

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20
Q

Where to administer IV fluids in reptiles?

A

Lizards - ventral tail/caudal vein, cephalic, jugular, ventral abdominal vein
Snakes - ventral tail vein, jugular
Chelonia - jugular, dorsal tail vein

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21
Q

In which animals are intraperitoneal, intracoelomic and epicoelomic fluids used? How much?

A

Intraperitoneal in mammals: 20-50ml/kg (care re caecum in hindgut fermenters ie avoid in rabbits)
Intracoelomic in reptiles: 20-30ml/kg/day maximum (care air sacs and carapacial fractures (chelonia) - not really recommended
Epicoelomic in chelonia: 10-20ml/kg (between plastron – add from slides

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22
Q

How to do fluid administration via bathing for chelonia and lizards? How does it work?

A

20 minutes twice daily

Absorption into bladder

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23
Q

Limitations of intraosseous fluids?

A

Analgesia/anaesthesia for placement
Positive pressure required
Knowledge of anatomy
Species variation - e.g. hedgehogs curling, birds bipedal, snakes stylette/cortical plugs

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24
Q

Where to administer intrasseous fluids in birds, mammals and reptiles?

A

Birds - distal ulna (dorsal condyle), proximal tibiotarsus (tibial crest)
Mammals - proximal tibia (tibial crest), proximal femur (trochanteric fossa)
Reptiles - proximal tibia (tibial crest), proximal humerus, distal femur, plastrocarapacial bridge (chelonia)

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25
Q

What is the stimulus for respiration in mammals, reptiles and birds? How does this affect oxygen therapy?

A

Mammals: hypercapnia - give 100% oxygen

Reptiles and birds: hypoxia - give 30-50% oxygen

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26
Q

What is the maximum blood draw from healthy animals?

A

1% BW (1ml/100g)

Include anticipated haemorrhage/haematoma

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27
Q

Emergency minimum blood tests for exotics?

A
Gluocse
Ca2+
PCV
TS
Lactate
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28
Q

What is the blood volume of exotic mammals, birds and reptiles?

A

Mammals: 50-80ml/kg
Birds: 60-120ml/kg
Reptiles: 40-80ml/kg

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29
Q

Venipuncture sites for exotic mammals?

A
– Jugular
– Cranial Vena Cava
– Saphenous
– Cephalic
– Lateral tail vein (rats)
– Marginal auricular vein (rabbits)
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30
Q

Venipuncture sites for birds?

A

– Right jugular
– Medial metatarsal vein
– Basilic/ulnarvein

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31
Q

Venipuncture sites for reptiles:

A
Lizards:
– Ventral coccygeal vein (avoid hemipenes), care autotomy
– Ventral abdominal vein
Snakes:
– Cardiocentesis
– Ventral coccygeal vein (avoid hemipenes)
Chelonia:
– Jugular
– Sub-carapacial sinus (lymph)
– Dorsal tail vein
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32
Q

How to calculate the basal energy requirement (BER) for exotics?

A
kcal/day = K x BW(kg)^0.75
Placental mammals: K=70
Marsupial mammals: K=49
Passerines: K=129
Non passerines: K=78
Reptiles: K=10
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33
Q

What drugs are contraindicated in rabbits, rodents, birds and chelonia?

A
Rabbits: 
- PLACE antibiotics
- Fipronil
- Corticosteroids
Rodents: 
- PLACE antibiotics
- Corticosteroids - more tolerant than rabbits but still avoid
Birds:
- Itraconazole - care in grey parrots (lower dose to avoid hepatotoxicity)
- Fenbendazole when in moult
- Corticosteroids
Chelonia:
- Ivermectin
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34
Q

Where to administer IM drugs in exotic mammals?

A

Quadriceps
Epaxial muscles
Hedgehogs - orbicularis muscle

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35
Q

Where to administer IM drugs in birds?

A

Pectoral muscles - caudal 2/3 to avoid brachial plexus, care with flying birds e.g. racing pigeons
Quadriceps

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36
Q

Where to administer IM drugs in reptiles?

A

Chelonia - triceps/biceps/any palpable muscle mass
Lizards - triceps/quadriceps, epaxial muscles - care re autotomy
Snakes - epaxial muscles (33% itv length)

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37
Q

What is refeeding syndrome?

A

Prolonged anorexia
Blood sugar stabilises but glycogen stores are depleted
Feeding -> blood sugar peaks -> insulin release -> glucose shunted intracellularly in order to replenish glycogen stores, K+ and phosphorous
Leads to hypokalaemia and hypophosphataemia
Clinical signs particularly cardiac signs e.g. bradycardia, as well as neurological signs
Potentially fatal

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38
Q

How to avoid refeeding syndrome?

A

Feed 1/3 of caloric requirement on first day
Feed 2/3 of caloric requirement on second day
Feed 3/3 of caloric requirement on third day
Slower in reptiles

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39
Q

CPCR compressions:breaths for mammals and birds?

A

5 compressions to one breath

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40
Q

When to use crystalloids in exotics?

A

Rescuscitation and maintenance
Hypertonic saline works synergistically with colloids in resuscitation
3-5ml/kg over 10 mins

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41
Q

When to use colloids in exotics? How much?

A

IV volume expanders - can expand blood volume by 1.4x
Rescuscitation
Reduced crystalloid requirements (40-60%)
Administer with crystalloids to avoid interstitial volume depletion
20ml/kg for hetastarch

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42
Q

When to use Haemoglobin based oxygen carrier fluids in exotics? How much?

A

Indicated where increased O2 delivery needed
Non antigenic so no cross matching needed
Very effective for haemorrhagic shock
2-5ml/kg

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43
Q

When to use blood products for exotics? How much?

A

Not usually for emergency resuscitation
Indicated if loss or depletion of albumin, coagulation factors, platelets or RBCs
>20% blood volume lost
Aim to get a PCV > 25%
10-20ml/kg plus other resuscitation fluids

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44
Q

What is the most common cause of seizures in an African Grey Parrot? Treatment?

A

Hypocalcaemia
IM or IV calcium salts required for emergency treatment
+ benzodiazepine for seizures

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45
Q

Reasons to spay rabbits? Method - anatomy to be aware of? types of sutures?

A

Reasons: high rate of uterine adenocarcinoma, social animals - prevents unwanted litters
Midline approach
Bicornuate uterus, two cervices, no true uterine body
Prone to adhesions - careful tissue handling
Fat around ovaries and in mesometrium
Cranial vagina
Synthetic monofilament suture material as prone to reactions
Intradermal skin sutures following routine closure of muscle

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46
Q

Resons to castrate rabbits? Method? Anatomy to be aware of? Sutures? When non fertile?

A

Reasons: behaviour/integration, social animals - prevent unwanted litters
Testes cranial to penis
Able to retract testes into abdomen
Prescrotal or scrotal approach
Semi closed or closed technique
Open inguinal ring - must close tunic to prevent herniation
Intradermal sutures or tissue glue
Can be fertile up to 6 weeks post neutering

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47
Q

Reasons to spay rodents? Method?

A
Prevention of disease:
- cystic ovarian disease (guinea pigs)
- mammary tumours and pituitary tumours (rats)
- pyometra
- neoplasia
Ovariohysterectomy vs ovariectomy
Midline vs flank
Intradermal skin sutures
Local anaesthesia
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48
Q

Reasons to castrate rodents? Method?

A
Reason: reproductive control
Prescrotal vs scrotal vs abdominal
Infection risk
Semi closed or closed technique 
Splash block (lidocaine/bupivocaine)
Intradermal skin sutures
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49
Q

Reasons to spay ferrets?

A

Control of musky odour
Oestrogen toxicity
Consider alternatives due to adrenal disease

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50
Q

Method for spaying ferrets? Anatomy to be aware of? Types of sutures?

A

Ventral midline approach
Similar procedure to cat ovariohysterectomy
Ovary small and embedded in fat
Intradermal suture pattern
Synthetic absorbable suture material
Consider deslorelin implant post neutering

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51
Q

Reasons to castrate ferrets? Method?

A

Control of musky odour
Reproductive control (social groups)
Aggression
Risk of drenal gland disease

Open, scrotal approach - similar to cat
Tend to bleed more in breeding season (vessels larger)
Consider deslorelin implant post neutering or as alternative

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52
Q

Reasons to vasectomise ferrets? When non fertile?

A

Jills are induced ovulators
75% cessation of oestrus on first mating
No risk of adrenal disease
Can be fertile ? 7 weeks post vasectomy

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53
Q

Examples of rapid absorbable suture materials?

A
Polygactin 910 (Vicryl)
Polydioxanone (PDS)
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54
Q

What types of skin sutures should be used for reptiles and why? When removed?

A

Everting skin sutures as reptile skin naturally inverts when healing
Strong suture material
Delayed suture removal - 6 weeks (prolonged healing), ecdysis may lead to premature loss

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55
Q

How long does it take for transplastron coeliotomy of chelonia to heal?

A

12-18 weeks

Acrylic/epoxy resin left for 6-12 months

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56
Q

What is Carboxymethylcellulose?

A

‘Belly jelly’
Use as topical gel/sheet to aid tissue lubrication post-op for mammals
Left in coelom/abdomen after surgery

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57
Q

Hormonal control of reproduction - options in mammals?

A
Deslorelin implant - licensed in male ferrets
hCG
Proligestone
Leuprolide acetate
Aglepristone
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58
Q

Indications for hormonal control of reproduction in birds? Examples?

A
Reproductive disease
Chronic egg laying
Behaviour
Dystocia
Deslorelin
Leuprolide
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59
Q

Indications for hormonal control of reproduction in reptiles? Examples?

A

Pre and post ovulatory stasis
Deslorelin
Leuprolide

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60
Q

What main licensed vaccinations are available for birds?

A

Pigeons - PMV, Pox
Chickens - IBD, IB, Salmonella, CAV
Psittacines (USA/Canada) - Polyoma virus

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61
Q

What licensed vaccines are there for rabbits? When given?

A

RHD1-myxo - from 5 weeks, annual

RHD2/RHD1 - from 30 days, 2 weeks apart from RHD1 vaccination

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62
Q

What licensed vaccinations are there for ferrets and rodents?

A

Ferrets - rabies, distemper (not licensed)

Rodents - guinea pig Bordetella vaccine?

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63
Q

Treatment of endoparasites in birds?

A

Amidostomum/Echinuria (waterfowl) - praziquantel/pyrantel

Roundworms, Syngamus, hairworm, caecal worm (poultry) - flubendazole (0 day egg withdrawal)

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64
Q

Drugs for ectoparasite control in exotic mammals?

A

Ferrets - fipronil and S-methoprene (frontline combo), imidocloprid/moxidectin (advocate)
Rabbits - imidacloprid licensed for fleas (advantage), cyromazine (rearguard), ivermectin, selamectin
Fipronil toxic in rabbits!

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65
Q

Drug used for endoparasites of rabbits?

A

Fenbendazole
Not for routine worming
Encephalitozoon cuniculi

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66
Q

Drugs for ectoparasite control of reptiles?

A

Nothing licensed
Fibronil spray (wipe)
Ivermectin - not chelonia

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67
Q

Drug of choice for treatment of endoparasites in reptiles?

A

Fenbendazole

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68
Q

What to do if trimming pet bird wings?

A

Symmetrical only
Primary feathers only
Postpone if blood feathers found

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69
Q

What is pinioning? How?

A
Permanent flight prevention
Waterfowl downies
< 10 days old only
Unilateral amputation of distal wing tip, distal
to alula
Act of veterinary surgery
3-4 days old, cartilage, skin, down
Alula must be preserved
Metacarpals should be as short as possible
Silver nitrate for haemostasis
Consider myiasis
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70
Q

Placement of microchips in birds and reptiles?

A

Birds - most LHS pectoral, ratites LHS pipping muscle, penguins SQ base of neck
Reptiles - L hindlimb (SQ) in chelonia and lizards, LHS body 3 head spaces back from head in snakes (BVZS) or LHS cloaca

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71
Q

ASA categories for anaeshesia?

A

Class 1 = fit and healthy, no systemic disease
Class 2 = mild to moderate systemic disease only e.g. skin tumour, chronic arthritis, fracture without shock
Class 3 = severe systemic disease, causing mild symptoms/limiting activity but not incapacitating e.g moderate hypovolaemia, anaemia or pyrexia, mild to moderate heart failure
Class 4 = severe systemic disease that is a constant threat to life e.g. severe uraemia, toxaemia, hypovolaemia, heart failure
Class 5 = moribund patient that is not expected to survive 24h with or without operation e.g. extreme sepsis/shock

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72
Q

Behavioural and postural responses for pain recognition in exotics?

A

Lack of alertness/reduced mentation/lack of interest in surroundings
Hiding
Shifting/throwing themselves around/unable to get comfortable
Sitting in hunched position
Failure to use/move certain parts of the body
Head pressing
Increased/unusual aggression

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73
Q

Indicative pain behaviours?

A
= behaviours that are rarely seen prior to painful stimulus but often afterwards
Twitching
Wincing
Staggering
Flinching
Belly pressing
Slow postural adjustments
Shuffling gait
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74
Q

Side effects of opioids in exotics?

A

Respiratory depression
Gut motility
Nausea
Excitation

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75
Q

Why are steroids avoided in exotics?

A

Profound immune suppressive effect - WBC lysis

Lots of exotics may have underlying clinical pathology

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76
Q

Which receptors does each opioid work on?

A

Morphine: pure u agonist (rarely used in rabbits)
Methadone: synthetic pure u agonist
Fentanyl: pure u agonist (can be used alone or in combo with fluanisone)
Buprenorphine: partial u agonist (slow onset but safe)
Butorphanol: mixed u agonist/antagonist (ceiling effect = dose above which no additional effect)

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77
Q

Which opioid receptors do birds and reptiles have?

A
Birds = primarily k
Reptiles = vary between k and uncategorised receptors which are similar to mammalian mu receptors
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78
Q

NSAIDs - What must be monitored? Side effects? Dosing frequency? Examples?

A

Monitor carefully: hydration status and renal function
GI side effects
May affect caecotrophy/coprophagy
Increased dosing frequency in rabbits/rodents e.g. BID
Decreased dosing frequency in reptiles e.g. q 2 days
Meloxicam - COX 2 selective, few side effects, good safety, palatable liquid
Carprofen
Ketofen

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79
Q

How does tramadol work?

A

u receptor agonist
Seratonin and adrenaline re-uptake inhibition
Alpha-2 agonist
Appears to be very safe and effective for most exotic species

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80
Q

Gabapentin/pregabalin - use in exotics? side effects?

A

Anti-convulsant that modifies the perception of neuropathic pain
Can see ataxia and sedation

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81
Q

Which exotic species can paracetamol not be used in?

A

Ferrets

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82
Q

Ketamine and amantadine - how does it work?

A

At very low doses blocks NMDA receptors

Prevents wind up pain

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83
Q

What types of pain are a2 agonists useful for in exotics?

A

Visceral, musculoskeletal and neuropathic pain

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84
Q

Maropitant - how does it work? Use?

A

Centrally acting anti-nausea drug due to effect on CTZ

Also good anti-inflammatory and show to be anaesthetic sparing in dogs

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85
Q

Which drugs can be given as constant rate infusions for pain relief? Benefits? Cons?

A

Generally ketamine with other medications e.g. morphine and lidocaine
Constant delivery of analgesia
Requires very good patient monitoring
Requires accurate fluid delivery ie infusion pump or syringe driver
Really useful to prevent wind up pain and where planned interventions are likely to be painful

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86
Q

What is EMLA?

A

Topical local analgesia

Lidocaine with prilocaine

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87
Q

What are benzodiazepines, ketamine, a2 agonists and alfaxolone/prpofol good/bad for in anaesthesia?

A

Benzodiazepines - good muscle relaxation and anxiolysis, midazolam - amnesia
Ketamine - poor muscle relaxation but good analgesia, supports BP
A2 agonists - good muscle relaxation and some analgesia but haemodynamic issues
(reduced by combining with other drugs)
Alfaxolone/propofol - good muscle relaxation and promotes unconsciousness but no analgesia

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88
Q

Common anaesthetic protocols for exotics?

A

Triple combination - a2 agonist + opiate + ketamine
Ketamine + benzodiazepine
Benzodiazepine + opiate + propofol or alfaxolone + volatile agent
Opiate/ACP + propofol or alfaxolone + gas
Volatile agent alone

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89
Q

Antagonism of a2 agonists, benzodiazepines and opioids - Which drug? What to be aware of?

A

A2 agonists: atipamezole
Benzodiazepines: flumazenil (NB anxiety, restlessness and lowered seizure threshold can occur)
Opioids: naloxone (repeat doses may be needed, also reverse analgesia so can leave patient in acute pain)

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90
Q

Should rodents and rabbits be staved pre-op?

A

No
Risk of hypoglycaemia
Can’t vomit/low risk
Take food out 0.5-1h before and check mouth for food once anaesthetised

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91
Q

Limiting factors for endotracheal intubation of exotic mammals?

A
Palatial ostia in rodents - v difficult
Long oral cavities with limited gape
Fleshy tongue
Size of patient
Risk of tracheal trauma/hypoxia
Risk of tube blockage (check mouth)
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92
Q

Methods of intubating exotic mammals?

A

Direct visualisation - laryngoscope, endoscope, pull tongue forwards, topical anaesthetic, stylette
Blind technique - ventral recumbency, hyperextend head and neck, listen/feel, advance on inspiration with twist, confirm placement with IPPV or condensation, risk of pushing food into trachea and of traumatising larynx

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93
Q

What are supraglottic airway devices?

A
V-gel
Quick and easy to insert
No risk of tracheal trauma/stricture
Expensive
Ideally use capnography to ensure correct porition
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94
Q

When to feed exotic mammals post-op?

A

Within 1 hour recovery

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95
Q

What recumbency should avians be in for recovery? What to be careful of?

A
Lateral recumbency
Care with disorientation, wing flapping
Ensure awake prior to extubation
Muscle twitching common
Hold until able to perch
Crop tube if not eating soon post GA
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96
Q

Which animals have complete tracheal rings?

A

Birds - don’t cuff tubes

Rabbits?

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97
Q

Positions of birds for anaesthesia - problems?

A

Induce in vertical posistion
Maintain in lateral - only compromises 50% of air sacs, care to not restrict wind movement (pneumatised humeri/femurs)
Dorsal recembency - viscera puts pressure on caudal airsick, reduces effective ventilatory volume
Ventral recumbency - limits ventral chest excursions and abdominal viscera press on air sacs

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98
Q

What do birds and reptiles rely on for breathing?

A

Birds - rely on movement of air sacs and ventral chest excursions
Reptiles - rely on chest excursions (legs in chelonia)

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99
Q

Why is ventilation mandatory for reptile anaesthesia?

A

May be quite resistant to reduced ventilation/apnoea

May not breathe frequently enough on gas anaesthesia to keep themselves asleep

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100
Q

ET intubation in reptiles?

A

Short ETT
Essential for IPPV as apnoea common
Rostral glottis in snakes and carnivorous lizards
Herbivores glottis at base of fleshy tongue

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101
Q

Anaesthetic monitoring in reptiles - reflexes and responses?

A

Righting reflex
Toe and tail pinch
Head withdrawal - toe is pinched and head is slightly withdrawn
Palpebral response
Vent response
Tongue withdrawal in snakes – remains present at sx plane
Corneal reflex – remains present at sx plane (except
snakes)
Jaw tone
Reflexes lost cranial to caudal and return caudal to cranial
Cardiovascular and respiratory systems monitoring

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102
Q

What to do in recovery for reptiles - ventilation? drugs? recovery time?

A

Ventilate with room air in recovery - Ambu-bag, spontaneous breathing will return more quickly
Doxapram hydrochloride = effective respiratory stimulant used in apnoeic snakes
Fluids
POTZ
Recovery can take 10-30 mins
Full recovery may take up to 24 hours

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103
Q

Anaesthesia methods for fish?

A

MS222 - make up buffered solution, add to known volume of tank water, volume of drug added correlates to anaesthetic depth
2-Phenoxyethanol - can be used at increased dose for euthanasia, once level of anaesthesia reached remove from water, place on wet surface and can maintain with anaesthetic solution pumped over the gills
Recovery - fresh tank water, until fish remains normally upright

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104
Q

Stages of fish anaesthesia?

A

Stage 1: light - reduced reactivity
Stage 2: deep sedation - loss of reactivity other than strong pressure, normal equilibrium
Stage 3: Light anaesthesia - partial loss of equilibrium, erratic swimming and increased gill movements
Stage 4: Deep anaesthesia - total loss of equilibrium, reacts only to strong pressure, reduced opercular movements
Stage 5: Loss of reflex activity, shallow opercular movements, no reaction to pressure
Stage 6: Medullary depression - gasping followed by gill movements stopping
Monitoring - initially visually and use of reflexes, can use doppler probe for auditory heart monitoring

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105
Q

Where are rabbit caecotrophs digested?

A

Stomach

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106
Q

Why can’t rabbits vomit?

A

Strong muscular cardiac sphincter

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107
Q

Anatomy of the caecum in the rabbit? What happens there?

A

Very large
Folded around 3 times = gyri
Vermiform appendix secretes HCl to control pH
Sacculus rotundus
Where most digestion occurs
Digestible fibre sent back from colon to caecum for further digestion

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108
Q

Anatomy of the colon in the rabbit? What happens there?

A

Separates the large indigestible fibre particles from smaller digestible particles
Haustra act as as an elevator moving digestible particles towards caecum
Proximal colon - 3 hausfrau, 3 taenia
Fusus coli - controlled by aldostereone and prostaglandins, pacemaker of the gut, no taenia?
Distal colon - strong muscular contractions for hard faeces phase, rapid more gentle contraction for soft faeces phase

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109
Q

Problems with gut stasis in rabbits?

A

Interstitial fluid flows into gut - dehydration
Painful
Potentially fatal, electrolyte derangement as not secreted/reabsorbed so GA not option

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110
Q

Diagnosis of gut stasis in rabbits?

A

History - reduced/absent appetite and faecal production
Often lethargic
Lack of gut sounds or abnormally loud borborygmi on abdominal auscultation
Abdominal palpation - ‘empty’ abdomen, or dilated/fluid filled gut loops, or may be painful, or impactions of viscera felt
Blood glucose levels (>18mmol/L suspicious of GI blockage but poor se and sp)
Abdominal ultrasonography
Radiography
Contrast studies
CT/MRI?
Exploratory surgery

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111
Q

Possible causes of gut stasis in rabbits?

A

GI blockage

Dysbiosis

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112
Q

In the case of GI obstruction causing gut stasis, what treatment is needed? Which drugs are contraindicated?

A

Surgical intervention
Must stabilise prior to surgery
Pro-kinetics are contraindicated pre and post-op

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113
Q

What is dysbiosis? Causes? Signs? Treatment?

A

= A challenge to or alteration of the gut bacteria
Causes: antibiotic usage, alteration in body temperature, change in gut motility, drastic alteration in diet
Signs: change in faecal consistency, alteration of appetite
Possibly production of endotoxins if pathogenic bacteria such as Clostridia prevail
Treatment: adsorbents (cholestyramine, activated charcoal) may help in addition to aggressive treatment for the underlying cause

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114
Q

Why may a rabbit not be eating caecotrophs?

A

Change in taste of caecotrophs (diet change, medications, infection)
Change in caecotroph consistency e.g. more runny (infection/inflammation/mural lesion in caecum)
Inability/unwillingness to turn around and eat them (pain-dental disease, spondylosis, osteoarthritis, poor balance-head tilt due to inner ear disease/E.cuniculi)

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115
Q

Significance of diarrhoea in rabbits? Causes?

A

True emergency
Gut motility is seriously disordered
Rapid fluid loss and significant electrolyte imbalance
May be due to protozoan parasites e.g. coccidia, or bacterial infection and endotoxin production e.g. Clostridium piriformis (Tyzzers disease)

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116
Q

What is mucoid enteropathy in rabbits? Cause? Treatment?

A

Distinct diarrhoea complex usually of juvenile rabbits
Often related to very low fibre diets
Small and large intestines are dilated with mucoid diarrhoea
Few/no histological changes found
Causative agent unknown - thought to be a contagious infection
Treatment is often unrewarding

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117
Q

What is bloat in rapids? Why does it happen? Treatment?

A

Defined as gut loops filled with gas
Intensely painful
Bacteria within gut produce gas either when multi biome changes, or diet changes
Can cause functional obstruction of pyloric outflow - gastric dilatation
Rabbit stomachs do not usually progress to torsion
May require surgery in order to allow the gas to pass out of the stomach

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118
Q

What is caecal impaction in the rabbit? What happens? Treatment?

A

Fills with ingesta and fails to empty
Often will continue to produce normal hard faeces but no normal caecotrophs passed
Caecum gets progressively more and more full
Painful
Weight loss as caectrophs that would be absorbed as calories or nutrients are sequestered in the caecum
No really helpful treatment - PGF2a suggested

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119
Q

When is Coccidiosis typically seen in rabbits? Risk factors? Which forms cause what?

A

Weanlings (immune prior to weaning)
Risk factors: poor hygiene, overstocking, stress
Disease rare in adults
Infection common, disease rarer - species vary in pathogenicity
Enteric forms: diarrhoea (+/- mucus/blood), stunting, weight loss, lethargy, anorexia, death
Hepatic forms: subclinical or weight loss, stunting, ascites, jaundice, hepatomegaly

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120
Q

Which are the major gut parasites in rabbits?

A

Coccidia
Passalurus ambiguus - common pinworm, part of multi biome and potentially helps in caecal contents mixing/digestion
Obeliscoides cuniculi - stomach worm, not reported in pet rabbits in UK
Trichostrongylus retortaeformis - intestinal worm in Europe and Australia
Taenia - intermediate host
Routine worming not indicated for most rabbits in UK

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121
Q

What is dysautonomia in rabbits? Which age affected? Risk factor? Signs? Cause? Treatment?

A

= dysfunction of the ANS (degenerative changes in autonomic neurones)
Sometimes called megacolon
Often weanlings but adults can be affected
Risk factor = low fibre diet
Palpable large bowel impaction, pain, reduced gut function - stomach and caecum also don’t empty
Swallowing difficulties and urinary incontinence may also be notes
Cause unknown (C botulinum suspected for grass sickness)
No effective treatment - don’t use oral meds as risk of inhalation pneumonia

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122
Q

What pro-kinetics can be used in rabbits? When are they contraindicated?

A

Metaclopramide, cisapride, ranitidine, domperidone
Contraindicated if GI obstruction and after gut surgery where lumen of gut has been opened
Acts to promote stomach emptying or general persistalsis but many clinicians feel not needed if diagnose and treat underlying issue

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123
Q

When should rabbits and other small furries be support fed?

A

When not eating and not obstructed
Until voluntary eating returns
To ensure gut function is maintained and gut motility is promoted

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124
Q

Should fluids be given to a rabbit that is not eating?

A

Any animal that is not eating voluntarily should be assumed to be at least 5% dehydrated
2-4ml/kg/hr or 100ml/kg/24hr

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125
Q

Are pro-biotics ok for rabbits?

A

Evidence for and against
Worst case is don’t work
Unlikely to do harm

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126
Q

What type of teeth do rabbits have? How quick do they grow?

A

Hypsodont = no true root
Elodont = open rooted, constantly growing
Diphyodont = 2 sets of teeth, first lost at/around birth so should never be seen clinically
Grow 1-3mm/week

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127
Q

Causes of dental disease in rabbits?

A

Congenital
Acquired - anorexia
Trauma - fractured teeth/jaw

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128
Q

Clinical signs of dental disease in rabbits?

A

Anorexia
Drooling
Tooth grinding
Wet below chin/on front paws
Change in dietary preference - stops eating either hay/vegetables or pellets where previously ate them
May be no clinical signs until things are fairly advanced

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129
Q

Treatment for dental disease in rabbits?

A

Make certain gut is working
Correct fluid and electrolyte imbalances
Provide analgesia
Once stable, consider GA, dental X-rays, burring teeth

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130
Q

Why are dental X-rays important in rabbits? How many views?

A

2/3 of tooth is within jaw

5 views

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131
Q

Dental anatomy of rabbits to be aware of when burring?

A

Maxillary arcades are wider than mandibular
Occlusal surface of teeth approximately horizontal to 10 degrees off with mandibular arcades higher on lingual than buccal edge - slope is slightly down away from tongue
Only one side of the dental arcades can be occluding at any one time
Check for specific spurs, loose teeth, areas that appear abnormal
Check ROM

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132
Q

Dental anatomy of guinea pigs?

A

Mandibular arcades are wider than maxillary arcades
Occlusal surface is approximately 30 degrees off horizontal with the mandibular arcades being lower on the lingual than buccal sides
The caudal portion of the dental arcades are closer together than the rostral portions - distance between the arcades becomes very narrow at the back of the mouth

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133
Q

Dental anatomy of chinchillas?

A

Mandibular arcades slightly wider than maxillary - not as pronounced as in guinea pigs
Occlusal surface is between horizontal and 10- 15 degrees off with the slope being down towards the lingual side of the mandibular teeth
Jaw ROM is similar to guinea pigs
Degus are very similar to chinchillas

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134
Q

Causes of oral/dental abscesses in rabbits? Treatment?

A

Secondary to trauma/bite wounds, post-op or dental disease
Best treatment method is radical/complete surgical excision and primary closure of a clean wound - not always possible
Remove affected teeth if dental abscess
Long course of antibiotics
Antibiotic Impregnated Poly Methyl Methacrylate beads (AIPMMA beads)

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135
Q

Risk factors for pododermatitis in rabbits? Treatment/prevention?

A
Risk factors:
- (No foot pads)
- obesity
- soiled bedding
- wire floors
- rex rabbits
Treatment:
- deep bedding
- analgesia, antibiotics
- surgical intervention in severe cases
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136
Q

Risk factors for barbering in rabbits?

A

Dominant conspecific

Insufficient dietary fibre

137
Q

What ectoparasites do rabbits get?

A

Psoroptes cuniculi (ear mites)
Cheyletiella parasitovorax (walking Dandruff)
Sarcoptes scabiei
Leporacarus gibbus
Haemodipsus ventricosus (rabbit sucking louse - uncommon)
Ctenocephalides felis, C. canis, Spilopsyllus cuniculi (fleas)
Lucilia (flystrike)

138
Q

Treatment of fly strike in rabbits? Prevention?

A

Sedation for through exam and exploration
Analgesia
Clip and clean lesions
Insecticidal e.g. F10 and Cypermethrin
Ivermectin
Surgical intervention/debridement in severe cases
Prevention - cyromazine (rearguard)

139
Q

What infectious skin diseases do rabbits get? Signs? Treatment?

A

Treponema cuniculi (rabbit syphilis):
- genital lesions
- auto-innoculation - facial lesions, lips, eyelids
- sexually transmitted disease
- treat with parenteral penicillin
Myxomatosis
- poxvirus - insect vectors
- systemic form - facial and genital oedema
- cutaneous form
Trichophyton metagrophytes/Microsporum
canis
- crusty, erythematous alopecia +/- pruritus
- young animals (pet shops with high stocking
densities)
- zoonotic

140
Q

What calici viruses do rabbits get? Signs? Diagnosis?

A

RHD1:
- european brown hare is reservoir
- high mortality: acute death or within hours of becoming ill
- febrile, severely lethargic, may bleed from nose/mouth
- reverse age susceptibility (young are immune until 5-6 weeks)
RHD2:
- lower mortality rates
- longer incubation
- similar clinical signs
Diagnosis by PM often and PCR of tissue e.g. liver

141
Q

What is agent that causes the respiratory disease ‘Snuffles’? Risk factors? Signs?

A

Pasteurella multocida
± other pathogens e.g. Bordetella bronchiseptica
Related to stress, husbandry, strain of bacteria present
Signs may be related to URT - nasal discharge, sneezing
LRT - coughing rare, rapid deep breathing is good clue
Also abscesses, balanoposthitis, pyometra

142
Q

Treatment of respiratory disease in rabbits?

A

Get a good diagnosis
Deep nasal swabs
Radiographs
Antibiosis is warranted
NSAIDs, decongestants, fluids, supplemental oxygen
Correct husbandry and address potential stressors
May never completely clear but immune system should be able to cope as long as the factors surrounding are addressed

143
Q

Causes of head tilts in rabbits? Diagnostics? Treatment?

A

Can be consequence of respiratory infection - tracking up into middle/inner ear via Eustachian tube
Can be secondary to Encephalitozoon cuniculi infection
May be peripheral or central nervous system at fault
Central disease can mimic peripheral disease, but peripheral disease can never mimic central disease
Horizontal vs vertical/rotatory nystagmus
Diagnostics - EC titres (not diagnostic), radiographs, CT
Often surgical treatment required
NSAIDs, antibiosis, anti- vertigo drugs (Meclizine, prochloperazine etc)

144
Q

Encephalitozoon cuniculi - what is it? Transmission? what can it cause? treatment?

A

Microsporidian parasite
Up to 75% of rabbit populations have been exposed
May result in neurological disease or renal disease
Oral infection from spores shed in urine of infected animals (NB paratenic hosts)
Treatment - fenbendazole is effective in removing organisms but clinical signs are caused by the host reaction to the organism and may be years after infection
May be related to ‘Floppy Rabbit Syndrome’ and posterior paralysis

145
Q

Encephalitozoon cuniculi - When is testing positive?

A

Day 1: spores ingested, inhaled or transplacentally transferred
Day 7: intradermal testing positive
Day 14: IgM titres positive
Day 14-28: IgG titres positive
Day 31: Infection can be detected in organs with high blood flow
Day 38: IgM titres now negative
Day 42: Urinary shedding of spores detectable
Day 56: Urinary shedding at its peak
Day 63: Antibody response is maximal
Day 63-70: Lesions are visible in the brain and kidney
Day 90: Urinary spore shedding stops
Day 98: Organisms histologically visible in organs of predilection

146
Q

Renal disease in rabbits - Age? Signs? Key diagnostic? Causes? Treatment?

A

Common in older rabbits
Poor appetite/ weight loss
May not see polydipsia consistently
Phosphorus levels are key
Can be related to encephalitozoonosis
Aging results in reduced GFR, reduced renal blood flow and reduced ability to maintain acid-base balance and fluid homeostasis
Affects appetite and therefore gut motility as a secondary issue
Treatment - fluids, dietary correction if needed (often isn’t in rabbits), ACE-I or angiotensin receptor blockers, oral phosphate binders (that do not contain calcium)

147
Q

How is calcium metabolism different in rabbits?

A

Uptake from gut is related directly to dietary content
Not reliant on vitamin D, PTH or calcitonin until dietary levels become very low
Most calcium is excreted via kidneys into urine - suspended, not dissolve

148
Q

What is urine sludge in rabbits? Signs? Treatment?

A

Calcium settles onto ventral bladder wall if mobility restricted - thick paste that is hard to void
Calcium crystals are irritant to urethra in high concentrations - reluctant to void/adopt correct stance
May see haematuria
Likely to see urine scalding
May be coincidental finding on radiography
Treatment - treat underlying cause, consider flushing out bladder, consider medications that will alter solubility of the calcium salts (cannot acidify herbivore urine), fluids, dietary modification

149
Q

What is urolithiasis in rabbits? Diagnostics? Treatment?

A

History - reluctance/inability to void
Progression from urine sludging
Solidification of urine calcium salts into a discrete stone/s
May be in bladder, renal pelvis, ureters or urethra
Blood work essential - need to know renal function not compromised and the degree of hypercalcaemia/hyperphosphataemia present
May have calcification of other soft tissues eg the aorta
Surgical treatment required
Post-op - fluids, analgesia, correction of underlying causes, dietary manipulation and treatment of co-morbidities such as renal disease

150
Q

What reproductive diseases are seen in rabbits? Signs etc?

A

Phantom pregnancy - nesting, fur pulling, lactation without production of kits
Abortion - Pasturella, Treponema
Uterine varices - severe episodes of bleeding (blood can pool in vagina so may only be voided at urination)
Uterine adenocarcinoma - repeated empty cycles predisposes to neoplasia: hyperplasia -> adenoma -> adenocarcinoma
Mastitis - hot swollen mammary glands during milk production, doe may be very unwell, kits may need hand-rearing, mammary glands need to be milked out
Mammary neoplasia - result of long term hormonal stimulation on mammary glands (intact females or result of ovarian remnants post-spay)
Adrenal disease - pituitary production of gonadotrophic hormones is usually shut down after neutering but doesn’t always happen -> LH and FSH remain at stimulatory levels in the blood without gonads to act on -> induces receptor formation on adrenal surface -> LH and FSH bind to the receptors and stimulate adrenal gland to produce active reproductive hormones (very similar to ferrets)

151
Q

Which rodents are hystricomorphs? What do they all have in common?

A

Guinea pigs, Chinchillas, Degus
Reliant on a high fibre/low succulent diet
Hind gut fermenters
Susceptible to high levels of sugar in the diet
Social species

152
Q

Features of the GIT of hystricomorphs?

A

Hind gut fermenters
Poorly adapted to processing simple sugars
Very basic ability to produce caecal faeces - not proper caecotrophs as in rabbits
Coprophagic - from others and their own

153
Q

What is typhlitis/typhilocolitis in hystricomorphs? Causes? What happens?

A

Caecal diarrhoea
Causes: infectious agents or mural lesions, sudden dietary change
Causes similar metabolic and fluid balance issues to those seen in other species
Severe cases will develop endotoxaemia, septicaemia and eventually shock resulting in death

154
Q

Which protozoa affect hystricomorphs? Risk factors? Diagnosis? Treatment?

A

Eimeria caviae, Eimeria chinchillae, Giardia duodenalis
Ris factors: stress, overcrowding, poor hygiene
Diagnosis: faecal flotation, wet mount
Treatment: TMPS, metronidazole, toltrazuril, aggressive supportive care, address environmental issues

155
Q

Bloat in hystricomorphs - significance? Signs? What happens? Treatment?

A

Gastric tympany in chinchillas - doesn’t usually twist
Gastric dilation/volvulus in guinea pigs
Hunched posture, metabolic/electrolyte/fluid balance issues due to gut not moving
Pain
Dilation impedes blood supply -> haemodynamic changes
Size of dilated gut impedes breathing
Treatment of GDV is surgical
Bloat without torsion can potentially be managed medically
Simethicone - surfactant to make gas bubbles smaller and allow them to pass
Analgesia, fluids, pro-kinetics
Care needs to be aggressive

156
Q

Bordetella bronchiseptica - which hystricomorph species is affected? Transmission? Risk factors? Diagnosis?

A

Severe pneumonia in guinea pigs - especially juveniles
Rabbits can carry in nasopharynx without clinical signs (ie risk for guinea pigs housed with rabbits)
Risk factors: stress, overcrowding, poor ventilation, hypovitaminosis C
Diagnosis: culture, radiography, possibly clinical suspicion
NB Streptococcus pneumoniae is a DDx
NB respiratory disease can extend into the middle/inner ear

157
Q

Cavy adenovirus - what does it cause? Treatment?

A

Viral infection in newly purchased guinea pigs
May be low level infection - inapparent clinical signs
Or may be severe signs - pneumonia and even death
May be age related differences in susceptibility and stressors may impact clinical manifestation
Supportive care only: oxygen, NSAIDs, decongestants, mucolytics, antibiotics?, nebulisation?
Can be hard to differentiate from bacterial respiratory pathogens without testing

158
Q

Cardiac diseases seen in hystricomorphs? Signs?

A

Guinea pigs: dilated and hypertrophic cardiomyopathies, pericardial effusions
Chinchillas: hypertrophic cardiomyopathy, VSDs and right ventricular outflow tract obstruction
All species can suffer from valvular disease
Clinical signs may be subtle - exercise intolerance, open mouth breathing, weight loss
May hear adventitious sounds over lung fields and potentially a heart murmur if heart rate low enough

159
Q

Cardiac diagnostics for hystricomorphs? Treatment?

A

ECG, radiography, echocardiography, pro-BNP markers?
Animals with HCM cannot improve cardiac contractility so pimobendan is contra-indicated
DCM can benefit from pimobendan.
Reduce the pre- and afterload - diuretics, ACE-I, oxygen supplementation in the acute phase
Analgesia
Nitroglycerine?

160
Q

Ectoparasites of guinea pigs? Signs?

A

(Ectoparasites are rare in degus and chinchillas)
Trixacarus caviae - symptomless carrier state can occur, although infection can occur
Chirodiscoides caviae - guinea pig fur mite/fur clasping mites
Cheyletiella parasitovorax - scaling and pruritis along dorsum, rabbits implicated
Demodex caviae - life cycle unknown but mite numbers directly related to hosts level of immunity
Lice: Gliricola porcelli and Gyropus ovalis - common but clinical signs related more to debilitation or poor mobility

161
Q

Pododermatitis in hystricomorphs - what is it? Risk factors? What can happen? Treatment?

A

Chronic inflammation or swelling of palmar or plantar pads
Risk factors: obesity, substrate/floor surface, lack of ability to move properly
Can become infected and affect underlying tendons/bone
Pressure related ischaemia causes the lesions.
Analgesia, correct husbandry problems, surgery/dressings may be indicated
Consider use of drugs that will improve blood flow to the area - pentoxyfylline

162
Q

Risk factors for fur matting and barbering in hystricomorphs?

A

Fur matting - lack of grooming/lack of ability to dust bathe in chinchillas, length/type of fur in guinea pigs
Barbering - overcrowding/stress related behaviours

163
Q

What do fur slip and tail slip of hystricomorphs mean? Treatment?

A

Fur-slip = predator avoidance mechanism in chinchillas: large patches of fur can be released during handling to leave a smooth clear area of skin, may require several months to regrow, no treatment required
Tail slip = predator avoidance mechanism in degus: degloving injury to distal end of tail during rough handling, tail will require amputation

164
Q

What are fur rings of hystricomorphs? Treatment?

A

Often around base of penis leading to paraphimosis - sedation and removal of the ring of fur is required
Can also occur around digits - may be human hair or hair from another pet, not just from that animal - the hair constricts around the appendage, affecting blood flow and venous return causing swelling and pain - will often resolve once the ring is removed, although severe cases may require amputation

165
Q

Ringworm in hystricomorphs - Which species? Signs? Which animals? Diagnosis? Treatment?

A

Primarily Trichophyton mentagraphytes
Less commonly Microsporum canis or Microsporum gypseum
Zoonotic
Often see focal alopecia with scaling but subclinical carriers are common
Fomites can remain infective
Young or immune compromised animals more likely to develop clinical signs - generally not pruritic unless concurrent bacterial skin disease
Culture required for specific diagnosis
Topical or parenteral treatment with itraconazole, terbinafine, enilconazole
Clipping and using lime-sulphur dips
NB environmental decontamination - bleach

166
Q

Ovarian cysts in hystricomorphs - Signifcance? Types? Treatment?

A

Common in guinea pigs (>1/3 of adult females) and other rodents
May not cause clinical signs
Can cause bilateral symmetrical alopecia - non-pruritic, underlying skin appears normal, hairs easily epilated
Can be large enough to impact breathing and gut function - anorexia may be the presenting signs
3 types - follicular, luteal (commonest) or parovarian (rare)
hCG is a common treatment but often fails
Percutaneous drainage is reported
Surgery likely to be required to resolve the condition

167
Q

Reproductive diseases seen in hystricomorphs?

A

Ovarian cysts
Pyometra
Pregnancy toxaemia
Uterine torsion

168
Q

Pregnancy toxaemia in hystricomorphs - Forms? Signs? Treatment?

A

2 forms: metabolic and circulatory
Metabolic form:
- obese females
- foetal growth demands put them into negative energy balance so fat is mobilised for use as energy source
- fluid therapy, glucose, nutritional supplementation may help
Circulatory form:
- due to uteroplacental ischaemia
- size of uterus compresses blood vessels
- rapidly fatal - emergency
- c-section/OVH may be only option

169
Q

Signs of uterine torsion in hystricomorphs?

A
Acute pain
Shock
Lateral recumbency
Dyspnoea
Seizures
170
Q

Hypovitaminosis C (Scurvy) in Guinea Pigs - Why prone? Requirement? What happens? Treatment?

A

Guinea pigs lack L-gulonolactone oxidase so cannot synthesise vitamin C -> depend on dietary intake
Require 10mg/kg/day for maintenance and 30mg/kg/day during pregnancy or if unwell
Hypovitaminosis C reduces resistance to disease and can cause dental disease, swollen joints, lameness, poor fur condition, delayed wound healing
Oral supplementation may be required - avoid supplementation in water as rapidly decomposes and can reduce water intake.

171
Q

Urolithiasis in hystricomorphs - When seen? Signs? Treatment?

A

Most calculi in guinea pigs are calcium based (so are radiopaque)
Common in older guinea pigs and especially in guinea pigs kept indoors - correlation to FLUTD in cats? Also correlated with bacterial cystitis - perhaps more of a management issue?
Pain on urination, haematuria, palpable stones, urine scalding, anorexia
Depending on location and size, either surgical or medical treatment
Recurrence is common and environmental issues need to be addressed

172
Q

Crystalluria/pain on urination in hystricomorphs? Signs? Treatment?

A

Very common
Can be very frustrating to treat
Often related to crystalluria but not always - see also interstitial cystitis
Animals generally well but vocalise when voiding urine, then immediately go back to normal
Herbivores have high calcium load in alkaline urine, and this urine cannot be acidified but oral medications can affect how soluble the calcium salts are
Analgesia alongside potassium citrate and hydrochlorothiazide - to keep animal passing dilute urine can help

173
Q

Interstitial cystitis in hystricomorphs? Which species? Signs? What happens? Treatment?

A

Very common in guinea pigs - related to unwillingness to void urine
Haematuria, abdominal discomfort, anorexia, generally unwell
Bladder lining is so inflamed that when the bladder fills the lining becomes discontinuous and urine can contact the underlying smooth muscle causing even more inflammation
Very painful condition and difficult to resolve
Antibiotics, NSAIDs, glucosamine, pentosan polysulphate, type A proanthocyanidins (cranberry extract) and correction of environmental factors

174
Q

Common neoplasias seen in hystricomorphs?

A

Lymphoma in guinea pigs:
- relatively common
- generalised lymphadenopathy, weight loss
- often in younger guinea pigs
- chemotherapy reported but generally not well tolerated
Liposarcoma in guinea pigs:
- multiple masses under the skin
- differentiate from lipomas and abcesses-
- local recurrence after removal, not malignant
Fibrosarcoma in degus:
- often on/around hindlimbs and can become large rapidly, making removal challenging
- local recurrence and invasion a feature and confounding factor
- thought to be from a related group of animals originally

175
Q

Hyperthyroidism in guinea pifs - Signs? Treatment?

A

Weight loss
Poor hair coat
PU/PD
Soft faeces
Appetite may not be increased and may even be reduced
Thyroid gland may be palpable
Transdermal and oral liquid methimazole are both good options for treatment
Thyroidectomy possible but risk of calcium metabolism issues post-op if parathyroid glands are damaged
Eventually thyroid tumours may become malignant

176
Q

Diabetes mellitus in hystricomorphs - Which species? Signs? Treatment?

A

Guinea pigs, chinchillas and degus
PU/PD
Good appetite but weight loss
Glucosuria (may only be seen in acute stages, may normalise in chronic disease)
Hyperglycaemia
May see cataracts
Related to their relative inability to deal with simple carbohydrates in the diet
Treatment: dietary correction, oral hypoglycaemics, potentially insulin therapy - will need ongoing monitoring and may not result in stabilisation
NB hystricomorph insulin is less biologically active than other mammalian insulin but they have more insulin receptors so insulin therapy can be very unpredictable

177
Q

Cloacal impaction in guinea pigs? When seen? Signs? Treatment?

A

Older guinea pig boars
Cloacal area becomes filled with normal faecal pellets
May be related to reduction in testosterone
Lining of cloaca produces white, strongly smelling discharge which increases with age
Boars on a high carbohydrate/low fibre diet may be predisposed
Manual removal advocated

178
Q

Cervical lymphadenitis in guinea pigs - cause?Treatment?

A

Streptococcus zooepidemicus causes caseous masses in intermandibular space
Removal or marsupialisation is necessary

179
Q

Which species are myomorphs? What do they all have in common?

A

Rats, mice, hamsters, gerbils
Much less specialised guts (except hamsters!)
Omnivorous
Incisors grow constantly, cheek teeth don’t

180
Q

How common is GI disease in myomorphs? Risk factors? Signs?

A

Relatively rare in rats/mice due to more simple gut physiology
Hamsters more prone - tend to cache food and this can become spoiled, have a more complex gut physiology
Increased frequency of defaecation, production of liquid faeces/diarrhoea
Risk factors: stress and overcrowding
Lethargic, perineal soiling (wet tail), anorexia, weight loss, hunched posture

181
Q

What causes antibiotic associated enteritis?

A

C difficile – use of inappropriate antibiotic (PLACE antibiotics)

182
Q

What can cause wet tail in hamsters? Age affected? Treatment?

A

Most commonly Lawsonia intracellularis:
- obligate gram negative intracellular bacterium
- causes proliferative ileitis
- hamsters <5wo are most prone, appear to develop immunity after 12wo
- fluids, supported feeding, analgesics (opiates)
- risk of intussusception, rectal prolapse if gut motility severely affected
Ddx: Clostridium piliforme, Clostridium difficile, E.coli, Campylobacter, Salmonella

183
Q

Cheek pouch disease in hamsters - What is is? Causes? Diagnosis? Treatment?

A

Usually used to store food in evaginations of lateral buccal mucosa
Can become impacted or everted
Diagnosis by examination (GA may be needed) - NB cheek pouches can be massive in comparison to body size
May be related to overfeeding, feeding incorrectly, dental disease
Manual removal of impacted material and flushing if impacted
Change feeding practices
Manual reduction of pouch eversions (if tissue viable) with stay sutures placed to keep pouch in correct position

184
Q

How do Strep pneumonia and Corynebacterium kutscheri affect myomorphs? Signs? Diagnosis? Treatment?

A

Acute bacterial pneumonia
Can be commensals of nasopharynx
Usually secondary to immunosuppression/concurrent infection e.g. Mycoplasmosis
Laboured breathing, sneezing, oculonasal discharge, head tilt, lethargy, cyanosis, porphyrin staining
Chest radiography indicates lung consolidation
Serology available for C.Kutscheri
Often require oxygen therapy and supportive care, antibiotics are indicated
Improve husbandry and reduce stress

185
Q

What is the most common cause of chronic respiratory disease in rats? Risk factors? Signs?

A

Mycoplasma pulmonis
Certain strains of rat are genetically predisposed
Risk factors: ventilation, hygiene, stress, nutrition
Respiratory signs - similar to COPD
May also see otitis media, torticollis and reproductive disease
Primary lesion is subacute chronic bronchitis
Chronic inflammation and hypersecretion of mucus, poor mucociliary clearance contribute to clinical signs
Biofilm is produced protecting the mycoplasms from host defences and most antibiotics

186
Q

Treatment of chronic respiratory disease of myomorphs?

A

Oxygen therapy if very dyspnoeic - will often also need fluids/support feeding
NB antibiotics will NOT eliminate infection
Doxycycline - immunomodulatory properties and is secreted by respiratory epithelium
Enrofloxacin, tylosin, azithromycin all suitable
Decongestants/mucolytics are helpful to break down mucus hypersecretion and overcome biofilm
Corticosteroids
Nebulisation with hypertonic saline +/- other agents

187
Q

Cilia associated respiratory bacillus in myomorphs? Significance? Transmission?

A

Gram negative organism that is hard to culture
Implicated in chronic respiratory disease of rats where mycoplasmas have been ruled out
Horizontal and vertical transmission
Mucopurulent bronchopneumonia progressing to bronchiolectasis
Can be either a sole, or a contributory pathogen

188
Q

What skin diseases/problems are seen in myomorphs?

A

Dermatophytosis - Trichophyton spp and Microsporum spp
Ectoparasitosis - lice, mites and fleas
Bacterial dermatitis
Abscesses -bite wounds, trauma, immunosuppression
Neoplasia - tends to be benign in rats and malignant in mice
Ring tail in rats/mice/gerbils - due to low humidity
Tail slip in gerbils/rats - improper handling
Nasal dermatitis in gerbils and hamsters
Barbering - dominant animal usually, but removing the individual only helps for a while

189
Q

Skin diseases specific to hamsters?

A

Scent glands - can become infected, hyperplastic and neoplastic
Hamster polyomavirus (HaPV) - transmitted via urine, juveniles get mesenteric lymphoma that metastasises, older animals develop epitheliomas (epitheliotrophic lymphoma)
Hormonal skin disease related to HAC:
- thin skin, hyperpigmentation, bilateral symmetrical alopecia
- lesions often in adrenal cortex so overproduction of mineralocorticoids
- PU/PD and change in shape of abdomen
- treatment can be difficult due to size of animal and risks of side effects with trilostane
- use of the injectable medication may be promising if dose can be accurately titrated

190
Q

Which ectoparasites affect myomorphs? Significance?

A

Lice - Polyplax spinulosa, P.serrata
Fleas - Ctenocephalides felis, Xenopsyllus spp
Mites - Demodex merone, D.criceti, D.musculi, D.ratticola, Notoedres notoedres, Notoedres muris, Notoedres cati, Sarcoptes scabiei (var cuniculi) Trixacarus caviae, Liponyssoides sanguineus, Ornithonyssus bacoti, Dermanyssus gallinae

In most cases, host and parasite should be in balance
Parasitic infestations generally a reflection of stress (physical and psychological), environmental inadequacies and potentially nutritional deficiency

191
Q

Which endoparasites affect myomorphs? Significance?

A

Endoparasites rarely cause problems in rodents
Protozoa: Giardia muris, Tritrichomonas muris, Spironucleus muris Cryptosporidium spp
Nematodes:
- rarely if ever cause clinical disease
- various species of pinworms may be noted: Sylphacia obvelata can cause tail base pruritis and mutilation in many species of rodents
Cestodes
- clinical disease is rare
- Hymenolepsis diminuta (rat tapeworm) and R.nana (dwarf tapeworm)

192
Q

Reproductive diseases seen in myomorphs?

A

Pyometra - hamsters, see vulval discharge, usually open, abdominal distension and may have more systemic signs of illness, treatment is ovariohysterectomy
Hydrometra and mucometra recognised in mice
Dystocia - not uncommon in many rodent species, c- sections are possible but NB interference may lead to cannibalism
Cannibalism - seen in many rodent species, associated with post birth stress/disturbance
Infertility - may be noted in breeding colonies, can be associated with cystic ovaries

193
Q

Cystic ovaries in myomorphs? How common? Signs? Diagnosis? Treatment?

A

High incidence in females >2 years
12-20 months of age- incidence is 47% in gerbils
Abdominal distension, bilateral symmetrical alopecia, weight loss and anorexia, infertility
Diagnosis presumptive on palpation (NB cannot rule out neoplasia)
Ideal treatment = ovariohysterectomy
HCG can be effective in some cases
Percutaneous decompression can be tried but cysts usually refill fairly rapidly

194
Q

Haematuria in myomorphs - Differentials?

A
Common presentation in many rodents
Urine can pool in the vaginal vault, so production of blood stained urine will occur if the blood is of uterine or urinary origin
Differentials: 
- cystitis (bacterial less common, interstitial)
- urolithiasis (hamsters and rats)
- uterine varices
- uterine neoplasia
- renal neoplasia
195
Q

Mammary neoplasia in rats - How many mammary glands? Type of neoplasia? Which rats affected? Hormone involvement? Prevention? Treatment?

A

12 mammary glands within mammary chain
Commonest tumours in rats
Fibroadenoma or adenocarcinoma
Females >1yo
Can also occur in males, rats on high fat diets, associated with pituitary tumours
All rats with mammary tumours have elevated levels of prolactin regardless of whether the pituitary involved - oestrogen stimulates prolactin secretion, prolactin levels are also elevated in older rats of both genders
Early neutering of females can reduce risk, and neutering at time of mass removal reduces risk/rate of recurrence due to reduced oestrogen stimulation
Cabergoline, deslorelin and leuprolide are suggested treatments, tamoxifen only with diagnosis of oestrogen receptor exhibiting adenocarcinoma

196
Q

Pituitary disease in rats? What is it? What happens? Treatment?

A

Pituitary adenomas
Also known as chromophobe tumours
Hypersecrete prolactin so often associated with
mammary neoplasia or abnormal lactation
Tamoxifen suppresses prolactin secretion and cabergoline is a prolactin inhibitor
May also be bilateral exophthalmus and neurological signs as disease progresses
Tumours can be induced by oestrogen
NB not all mammary tumours in rats are associated with pituitary tumours, but in these cases prolactin levels will still be elevated

197
Q

Hanta virus in myomorphs - Type of virus? Significance? What does it cause?

A

Bunyaviridae
Zoonotic - direct contact with rodents or contact with urine/droppings
Do not cause disease in rodents
Primarily carried by wild rodents but infection/exposure has been proven in UK pet rat population
Can lead to Hantavirus Pulmonary Syndrome (HPS) (Sin Nombre virus- New World)
Old World (Seoul) hantavirus can cause Haemorrhagic Fever with Renal Syndrome (HFRS)

198
Q

Lymphocytic choriomeningitis virus (LCMV) in myomorphs - Type of virus? Transmission? Significance?

A

Arenavirus
Zoonotic - exposure to urine, droppings, saliva or fomites from infected rodents can lead to infection
Owners of pet mice or hamsters from infected colonies at risk of infection, otherwise wild rodents are more of a risk
Can be asymptomatic in humans or mild febrile illness
Severe forms result in a febrile illness 8-13 days after exposure, followed by a short recovery period then a relapse into fever associated with neurological signs
Most humans recover

199
Q

Leptospirosis in myomorphs - signs? Spread? Significance?

A

Rodents, esp. rats, are reservoir for Leptospirosis
Weils disease can cause renal damage, meningitis, liver failure, respiratory distress and death
Spread via urine from infected rats
Can survive for long periods in soil or water courses
Pets can be asymptomatic and shed bacteria in urine intermittently
Pets are usually infected by contact with wild rodents - directly or indirectly but are not a major source of disease

200
Q

Chromodacryorrhoea in myomorphs - What is it? Diagnosis? Risk factors? Signs? Treatment?

A

Porphyrin pigmented tears secreted by Harderian gland
Fluoresce under Woods Lamp
Risk factors: stress, overcrowding, poor husbandry, underlying disease (mycoplasmosis, SDAV)
May also see laboured breathing or anorexia, poor hair coat due to reduced grooming - all result of underlying disease not the condition itself
Symptom rather than a specific disease - needs investigation
Improve husbandry and minimise stress whilst treatments/diagnostics are ongoing

201
Q

Features of ferrets GIT and diet requirements?

A

Obligate carnivore
Rapid gut transit time (2.5-3h)
Fat main energy source >20% (Arachidonic acid)
Protein 35-40% (Taurine)
Poor utilisation of CHO and fibre not digested well
Good quality dry ferret food (dry cat food in emergency)
Food intake increases 30% in winter
Some owners feed fresh carcass

202
Q

Helicobacter mustelae - which ferrets affected? Transmission? Signs? Diagnosis? Treatment?

A

<2yo or stressed/sick/diet change
Faecal-oral infection to kits from older ferrets
D+, V+, abdo pain, chronic gastritis, duodenitis, melaena, mesenteric lymphadenopathy, anaemia
Stress may precipitate ulcer formation
Chronic infection may result in development of gastric adenocarcinoma or gastric mucosa - associated lymphoid tissue lymphoma
Diagnosis
– Silver staining to visualise organism
– Serologic assay
– PCR on gastric swab PLUS gastric biopsies
Treatment
– Ranitidine, Omeprazole
– ABs (Metronidazole, Amoxicillin)

203
Q

What do coronaviruses cause in ferrets? Features? Signs? Treatment?

A
Epizootic Cattarhal Enteritis
– Green slime disaese
– 48-72 hour incubation period
– V+, green/mucoid d+, weight loss 
– More severe in older ferrets
– Supportive care, broad spectrum ABs, GI protectant, quarantine
Ferret Systemic Coronavirus (FIP)
– mutated form of Coronavirus
– Granulomatous form
– Diarrhoea, weight loss, lethargy, anorexia and hindlimb weakness
– Splenomegaly, Mesenteric lymphadenopathy, pyrexia
– Ddx Lymphoma
– Hypergammaglobulinaemia
– Young Ferrets (c. 11 mo)
– Survival 2 mo
204
Q

What causes proliferative colitis in ferrets? Treatment?

A

Lawsonia intracellular
Usually younger ferrets, proliferative bowel
Chloramphenicol 14-21 days

205
Q

What age are ferrets with IBD?

A

> 2yo

206
Q

What infectious GI diseases can ferrets get?

A

Salmonellosis - profuse diarrhoea
Campylobacteriosis - mucoid bloody diarrhoea, weanlings, asymptomatic carriers can occur, erythromycin?
Colibacillosis - food borne diarrhoea
Giardiasis - potentially zoonotic
Cryptosporidium parvum
Coccidiosis - Eimeria, lethargy, diarrhoea and wasting
GI nematodes - Toxascaris leonina, Dipylidium cancinum, Ancylostoma spp

207
Q

When do ferrets normally moult?

A

Spring/summer

208
Q

What skin lesions can be seen with ferrets?

A

Bite wounds - secondary to mating or territorial disputes
Alopecia - endocrinopathy, neoplasia, barbering, parasites
Wounds
Allergy
Contact dermatitis
Dermatophytosis - Microsporum canis (Trichophyton mentagrophytes)
Bacterial pyoderma
Distemper

209
Q

What ectoparasites affect ferrets?

A
Sarcoptes scabiei
Lynxacarus mustelae - facial fur mite, kits, immunosuppresion
Demodex
Otodectes cynotis
Ticks, fleas, myiasis
210
Q

Oestrogen toxicity in jills - explanation? clinical signs? treatment?

A

Jills are seasonal polyoestrus
Come into season in Spring (Feb-March)
Induced ovulatory - ovulate 30-40h post mating
Unmated jills remain in oestrus for prolonged period (up to 6 months) - 50% develop aplastic anaemia
Signs: swollen vulva, pale mucous membranes
Prevented by neutering
Treatment - ‘jill jab’ proligestone or hCG, blood transfusion

211
Q

Adrenal gland disease in ferrets? Aetiology? What happens?

A

Aetiology - genetics, indoor housing/photoperiod, neutering
On average 3.4 years post neutering
Zona reticularis - elevated androgen hormones (hyperandrogegism) - androstenedione, 17ahydroxyprogesterone and oestrodiol

212
Q

What is the stimulus for ferret breeding season?

A

Stimulus is increasing day length
Regulated by melatonin produced by pineal gland
Longer days -> less melatonin -> GnRH production by hypothalamus

213
Q

Pathophysiology of why neutering ferrets can cause adrenal gland disease?

A

Normally: hypothalamus produces GnRH -> pituitary gland produces FSH and LH -> Gonads produce testosterone/oestrogen with negative feedback on pituitary
Removal of gonads stops the negative feedback
More FSH and LH produced by pituitary gland -> hyperplasia/neoplasia of adrenal gland -> production of androgens from ZR of adrenal gland -> clinical signs of adrenal disease

214
Q

Clinical signs of adrenal disease in ferrets?

A

Adrenal hyperplasia -> adenoma -> adenocarcinoma

Androgen stimulation
Bilateral symmetrical alopecia - seasonal, cranially progressive
Pruritus (25%)
Behaviour change/aggression
Vulval swelling - elevated oestradiol
Gynaceomastia
Prostateomegaly -> dysuria
215
Q

Diagnosis of adrenal disease in ferrets?

A

History and clinical signs
Serum adrenal panel:
- oestradiol, androstenedione, 17 hydroxyprogesterone
- doesn’t distinguish between ovarian remnant as hormones identical
- can have false negatives
Radiography usually unremarkable
- prostatomegaly
- useful preoperative information and for
concurrent conditions eg heart disease
Abdominal ultrasound
- adrenomegaly
- 85% unilateral: 15% bilateral
- can identify ovarian remnant as primary DDX
- abdominal palpation if adrenal gland very large
ACTH stim/L/HDDS not diagnostic
Treatment Trial?

216
Q

Treatment for adrenal disease in ferrets?

A

Exploratory surgery:
- Gold standard
- Concurrent insulinomas common so measure glucose esp perioperatively
- Rule out ovarian remnant
- Remove left adrenal gland if affected
- Debulk right adrenal gland if affected (attached to caudal vena cava)
GnRH analogue:
- Leuprolide Acetate (Lupron) monthly (GnRH superagonist)
- Deslorelin (Suprelorin) implant
- In early stages of disease
- Less effective once disease advanced/neoplastic
- Following left side adrenalectomy to prevent contralateral disease
- Surge of hormones for 2 weeks
- NB Don’t inhibit tumour growth
Melatonin

217
Q

Prevention of adrenal disease in ferrets?

A

Outdoors
Alternatives to neutering:
- Deslorelin in spring: GnRH agonist implant every 12-24 months, licensed, surge of hormones 14d following implant
- Proligestone (‘Jill jab’): when comes into season in spring, single dose, pyometra risk nay require more doses if early season or warm autumn - owner observation important
- Buserelin: GnRH agonist, induces ovulation and pseudopregnancy and return to season after 1-2mo
- Vasectomised hob: mating is violent and goblets smell like entire hobs, care re sharing teaser hobs

218
Q

Options for managing entire males, preventing strong musky odour?

A

Castration
Implant with suprelorin - lasts 4 years
Neuter +/- implant at same time (re adrenal disease)

219
Q

Aetiology and signalment of inulinomas in ferrets? Clinical signs?

A
B cell tumours - adenoma or adenocarcinoma
Dietary and genetic factors
Often males, 4-6yo
Clinical signs:
- hindlimb weakness/ataxia
- stargazing
- dull
- seizures
- may resolve following meal
- collapse
- salivation/pawing at mouth (nausea)
220
Q

Diagnosis and treatment of insulinomas in ferrets?

A

Diagnosis:
- Persistent hypoglycaemia (BG<3.4) after withholding food for 4 hours
- Combined with appropriate clinical signs
- Can assay insulin
- ALT elevated
Treatment:
- Emergency stabilisation: glucose
- Surgical: nodulectomy and/or partial pancreatectomy
- Medical: prednisolone for gluconeogenesis, diazoxide to inhibit insulin release
- Dietary adjunctive: meals high in fat and protein, no simple sugars

221
Q

Dilated cardiomyopathy in ferrets - what happens? Diagnosis? Treatment?

A

Dilated, spherical left ventricular chamber with thin walls, depressed wall motion and variable degrees of left atrial enlargement
Right atrium and ventricle may also be affected
NOT related to taurine deficiency in ferrets
Diagnosis: echocardiography
Treatment: pimobendan could be considered even when asymptomatic

222
Q

Left ventricular hypertrophic cardiomyopathy and restrictive cardiomyopathy in ferrets? What happens? Treatment?

A

Left ventricular hypertrophic cardiomyopathy
- Small or normal left ventricular chamber size
- Normal or hyperdynamic left ventricular wall
motion
Restrictive cardiomyopathy
- Significant left or bilateral atrial enlargement
- Normal left ventricle thickness and contractility
Treatment
- Neither are amenable to treatment with positive inotropes
- No additional capacity to increase force of cardiac contraction
- Symptomatic treatment of CHF

223
Q

Degenerative valvular heart disease in ferrets?

A

Thickening of heart valves and regurgitation at one or more valves
Commonest echocardiographic finding in ferrets
Aortic valve > mitral
Aortic insufficiency may not be clinically significant but -> CHF, particularly if mitral valve is affected concurrently
Diagnosis - heart murmur, arrhythmias, gallop rhythms and adventitious lung sounds, echocardiography

224
Q

Which endoparasites are significant in ferrets?

A
Dirofilaria immitis (Heart Worm)
- Vector borne intravascular parasite that sits in the pulmonary arteries, right hand side of the heart and the vena cava
- Often decompensate rapidly: dyspnoea, pallor, severe lethargy and exercise intolerance, heart murmur audible
Angiostrongylus vasorum (Lungworm)
225
Q

Influenza in ferrets - type of virus? Signs? Treatment?

A

Orthomyxoviridae -strains of human flu virus A and B are infectious to ferrets
Anthroponotic and zoonotic
Causes mainly URT signs - lethargy, sneezing, pyrexia, nasal discharge, conjunctivitis
In neonates can cause bronchiolitis and pneumonia
7-14 day clinical course
Supportive care will be required (fluids, feeding), antibiosis only if secondary bacterial infection

226
Q

Canine distemper in ferrets -Virus type? Transmission? phases? Clinical signs? Diagnosis? Treatment?

A
Canine distemper virus Paramyxovirus (morbillivirus)
Most canids and mustelids are susceptible - up to 100% mortality
Airborne/droplet exposure, contact with urine/faeces
Catarrhal phase (may not always occur) followed by neurological phase
Clinical signs:
- Photosensitivity
- Anorexia
- Pyrexia
- Serous -> mucopurulent oculonasal discharge
- Ataxia, tremors and paralysis
- Hyperkeratosis of foot pads
- Erythema/chin lesion
- Death can occur in as little as 12 hours 
Diagnosis:
- IFA testing available
- clinical signs
- panleucopenia
- PM
- serum Ab titres
Treatment
- No specific treatment
- Supportive care
- 100% mortality rate
- Vaccination
227
Q

Aleutian disease virus in ferrets - type of virus? age affected? Clinical signs? Diagnosis? Treatment? Vaccination?

A

Highly infectious parvovirus (wild mink possible reservoir)
2-4yo
Immune complex mediated disorder
Clinical signs:
- Multiple organ failure
- Progressive weight loss, weakness, hepatomegaly, and splenomegaly, renal failure, posterior ataxia, mild incoordination, ascending paresis, tremors, paraplegia
- NB Asymptmatic carriers shed virus in faeces
Diagnosis:
- Severe hypergammaglobulinemia most consistent finding
- Positive antibody titre
- Serology: ELISA
- NB posiive titres in some clinically normal ferrets
- PCR
Treatment
- No specific treatment
- Anti-inflammatories and immunosuppresants e.g. prednisolone and cyclophosphamide
- Melatonin: immune modulation & anti-oxidant
Vaccination? - Immune mediated disease so contraindicated

228
Q

What are the most common neoplasia of ferrets?

A
  1. insulinoma
  2. adrenal gland disease
  3. lymphoma
229
Q

Lymphoma in ferrets - forms? Clinical signs? Diagnosis?

A

Juvenile form more aggressive (<2yo) - lymphoblastic form: often initial focus thymus, respiratroy signs (mediastinal mass)
Non specific clinical signs in adults (5-7 yo) - Lymphocytic form
- Insidious onset
- Malaise, inappetance, weight loss
- Enlarged peripheral or internal lymph nodes
- Multicentric or gastrointestinal
Diagnosis:
- Infectious agent? (Clusters) FeLV/ADV
- Immunophenotyping (T Vs B)
- Staging (1-5), A (no clinical signs) or B (Clinical signs)
- Helicobacter assoc with gastric lymphoma
- Haematology
- Diagnostic imaging
- FNA/excisional biopsy of lymph node
- Bone marrow biopsy
- Chemotherapy protocols
- Palliative treatment - poor long term prognosis but some good results possible in early stage disease with chemotherapy

230
Q

Causes of splenomegaly in ferrets?

A
Common finding
Extra hepatic haematopoiesis
Chronic inflammation
Neoplasia
Tranient splenomegaly by certain anaesthetic agents
231
Q

Licensed ectoparasiticides for ferrets? Endoparasite treatment?

A

Imidacloprid/Moxidectin
Fipronil-S-methoprene
Rarely get pathogenic burdens of endoparasites and routine treatment not warranted

232
Q

Why is dog food not appropriate for ferrets?

A

Very high in carbohydrates

233
Q

Anatomy of birds which differs to mammals?

A
Air sacs
Rigid lungs
Internal gonads
Single ovary (usually left)
No urinary bladder
Fused vertebrae
No teeth
Proventriculus - secretory portion of stomach
Ventriculus - muscular, grinding portion of stomach
234
Q

Hypocalcaemia of birds - Seen in which birds commonly? Signs? Causes? Diagnosis? Treatment?

A

Common in captive birds (grey parrots), wildlife during rehabilitation (wood pigeons, collared doves) or cockatiels that are chronic layers
Signs:
- muscle fasciculations and weakness
- tremors
- seizures
- pathological fractures
- bone growth deformities
Causes:
- dietary (lack of calcium, excess phosphorus, hypovitaminosis D, hypervitaminosis A and E)
- secondary to lack of UV light
- related to chronic egg laying
Diagnosis: bloods to check total and ionised Ca
Treatment:
- oral (calcium gubionate) or parenteral (calcium gluconate) supplementation
- correct underlying cause
- UVB supplementation (MUST be a specific bird light)
- dietary changes may take a significant amount of time and can be frustrating

235
Q

Hepatic lipidosis in birds - Cause? Risk factors? Clinical signs?

A
Caused by metabolic changes -> excessive accumulation of triglycerides in liver -> cholestasis and hepatic dysfunction
Risk factors:
- high fat
- high protein diet
- overfeeding of neonates
- multinutrient deficient diet
- reduced exercise
- hereditary factors
- active egg-laying
- diabetes mellitus
stress (catecholamine release)
- thyroid disease
obesity
Clinical signs: often non-specific related to:
- liver size (eg dyspnoea)
- poor liver function (hepatic encephalopathy, poor feather production)
- general sick bird (anorexia, weakness)
236
Q

Hepatic lipidosis in birds - Biochemistry findings? Diagnosis? Treatment?

A

Biochemistry:
- hepatocellular damage
- reduced hepatic function
- cholestasis
- serum will often be lipaemic
Diagnosis: radiography or endoscopy will confirm and refine diagnosis
Treatment:
- improve nutritional status of patient
- develop plan for weight loss
- improve liver function (SAMe, ursodeoxycholate)
- treat any secondary conditions identified
- nutritional supplements eg vitamin B complex, E and K, choline and methionine (lipotrophic factors), L- carnitine

237
Q

Diabetes mellitus in birds - Cause? Signs? Diagnosis? Treatment?

A

Pancreas no longer produces insulin or peripheral tissues become resistant - hyperglycaemia in raptors
Psittacines - elevated blood glucose is related to overproduction of glucagon
Signs:
- glucosuria
- hyperglycaemia
- polydipsia/polyuria
- weight loss despite good appetite
- increased susceptibility to infections
Diagnosis:
- persistent hyperglycaemia
- glucosuria
- glucagon levels can be tested but challenging
- ?fructosamine levels
Treatment:
- low carbohydrate diet
- provide enough exogenous insulin to override the effects of the glucagon over-production (serious risk of hypoglycaemia however)
- oral insulin dosing has been suggested
- oral hypoglycaemics such as glipizide or metformin can be tried, and may be safer
There are reports of spontaneous recovery.

238
Q

In which birds is thyroid disease common in? Association? Sign? Treatment

A

Budgerigars
Associated with iodine deficiency - treat with iodine supplementation
May have palpable goitre

239
Q

Diabetes insipidus in birds - When diagnosed?

A

Increased drinking where no other cause is found and where water deprivation testing does not result in concentration of urine

240
Q

Testicular tumours in birds - Which birds? Signs?

A

Budgies

See brown hypertrophy of cere and may see lameness in leg on same side (sciatic nerve impingement)

241
Q

Renal anatomy and physiology of birds?

A

Paired kidneys
Uric acid is excretory product - not osmotically active so requires little fluid loss of excretion
Poor ability to concentrate urine
Partially reptilian and partially mammalian
2 types of nephron: with/without loop of Henle
Water retention in tubules, colon and cecae
Reflux of urine into colon
No urinary bladder
Salt glands: extra renal pathway for salt excretion when a bird consumes more NaCl than able to remove via kidneys

242
Q

Renal failure in birds - Signs? Diagnosis? Treatment?

A

PD
Increased fluid portion within droppings where there is normal formed faeces - owners may struggle to differentiate from diarrhoea
Appetite often affected
Weight loss
Acute renal failure: suddenly very unwell
Chronic renal failure: non specific lower level signs, although articular gout may be noted
Diagnosis on clinical chemistries:
- less reliable than in mammals: uric acid elevated when glomerular filtration reduced by >80% so uric acid may be normal
- urea/creatinine not useful
- NB uric acid maybe elevated post-prandially in carnivorous birds
- imaging/endoscopy helpful
- biopsy for definitive diagnosis
Treatment:
- fluid therapy
- consider ACE-I or angiotensin receptor blockers
- dietary modification in species that have a high protein intake
- treatment for gout
- antibiosis if bacterial infection implicated in acute renal failure

243
Q

Gout in birds - Causes? Why does it happen? Diagnosis? Treatment?

A

Causes:
- period of acute dehydration
- high protein diet
- renal insufficiency
Level of uric acid in blood exceeds solubility threshold -> uric acid crystals deposited on surface and within internal organs (visceral gout) or within joints (articular gout)
Blood uric acid levels not always elevated at time of presentation, but with articular gout the lesions are fairly pathognomic
Treatment:
- initially aggressive fluid therapy and diuresis
- dietary modification if necessary
- treatment is aimed at slowing down uric acid deposits in articular gout (allopurinol, colchicine, vitamin A, omega 3&6 fatty acids) and treating organ compromise for visceral gout
- anti-inflammatories (care with dehydration and renal compromise) and pain management

244
Q

Reproductive anatomy of birds?

A

Single ovary or testis - usually left
Ovary -> infundibulum -> magnum -> isthmus -> uterus -> vagina
Intromittant organ - ratites, anseriformes
Non-intromittnet phallus - domestic fowl
Neither - psittaciformes

245
Q

Egg yolk peritonitis/coelomitis in birds - Non infectious cause? Signs?

A

Secondary to ectopic ovulation (doesn’t always result in coelomitis) - infundibulum of salpinx is not anatomically attached to ovary so ovulated follicles can go astray
Ectopic eggs without surrounding clinical signs may resolve without treatment
Can become depressed, lethargic with coelomic distension
Cystic ovarian disease (follicles are not normally ovulated and remain within the ovary) can also be associated with coelomitis

246
Q

Egg binding/dystocia in birds - Causes? Diagnosis? Risk factors? Treatment?

A
Obstructive dystocia:
- egg/maternal disproportion
- misshapen eggs
- uterine torsion
Non-obstructive dystocia:
- uterine inertia
- hypocalcaemia
Often able to diagnose on examination but radiography needed to determine whether size and position of egg will allow oviposition
Risk factors:
- stress
- environmental temperature
- nutritional and endocrine abnormalities
- disease external to reproductive tract
Treatment:
- consider manual delivery
- ovocentesis
- surgical delivery
- medical treatment with calcium and oxytocin
247
Q

How often do most birds lay an egg once laying?

A

One every 24-48h dependent on species

248
Q

Pre-ovulatory follicular stasis in birds - What happens? Signs? Differentials? Associations? Diagnosis? Treatment?

A

= Failure of ovulation
Often non-specific presentation - anorexia, depression, perhaps nesting behaviour, caudal coelomic distension
Differentials include ovarian neoplasia
May be associated with hepatic lipidosis due to constant mobilisation of fat
Often see polyostotic hyperostosis radiographically due to continual mobilisation of calcium
Diagnosis often endoscopic
Treatment:
- deslorelin
- leuprolide
- tamoxifen
- HCG
- aspiration of follicles, and partial ovariectomy (advanced and complex surgery)

249
Q

Chronic egg production/over production in birds - Which birds? What happens? Problems? Risk factors? Management?

A

Often pet budgies and cockatiels (also chickens, waterfowl, finches, canaries, lovebirds)
Hens lay repeated clutches or more than normal clutch size
-> Calcium and energy requirements are high - may be more than hen can cope with
Predisposes to egg yolk peritonitis, egg bonding/dystocia, nutritional depletion and osteoporosis/pathological fractures
Risk factors:
- high levels of nutrition
- nesting boxes (areas where hens are comfortable laying eggs)
- early removal of eggs (encourages ‘double clutching’)
Management:
- reduce nutritional levels
- remove nesting areas
- do not remove eggs once laid (use dummy eggs or cook the eggs)
- reduce the day length
- remove the ‘mate’
- deslorelin implant
- leuprolide
- tamoxifen (NB side effects)
- HCG
- salpingohysterectomy (very difficult surgery)

250
Q

Cloacal prolapse in birds - Causes? What must be determined? Treatment?

A
Common sequel to repro disease
Causes:
- hypocalcaemia
- egg production
- dystocia
- testicular enlargement
- constipation
- enteritis
- cloacal masses
- intussusception
Need to determine underlying cause, what structures have prolapsed, and whether the tissue is viable
May prolapse oviduct, phallus, ureter, intestines, cloacal tissue or abnormal masses
Treatment:
- viable tissue replaced and anchored in place - bird must be prevented from interfering with the area
- underlying causes must be addressed
- antibiotics and analegsia/anti-inflammatories often indicated
251
Q

What cardiac diseases are seen in birds? Signs? Diagnosis?

A
Atherosclerosis in Amazon parrots
Valvular disease in older birds
Congenital defects in juveniles
Vegetative endocarditis
Pericarditis, pericardial effusion
CHF
Signs:
- respiratory distress
- oedema/ascites
- syncope
- reduced exercise tolerance
- may have audible murmur, variable heart rates, pulse deficits, cyanosis
Diagnosis:
- ECG and chest radiography useful
- echocardiography limited by airsacs
252
Q

Bird air sacs?

A
2 cervical
1 interclavicular
2 cranial thoracic
2 caudal thoracic
2 abdominal
253
Q

Sinusitis in birds - Signs?

A
Facial/nares deformity
Periocular swelling
Oculonasal discharge
Matted feathers around the face
Dyspnoea
254
Q

Treatment for URT disease in birds? Diagnosis?

A

Often chronic and poorly responsive to treatment
Nutritional deficiency (hypovitaminosis A), immunosuppression, poor environmental hygiene, chronic mucosal irritation and organisms that are poorly responsive to treatment are common factors
Diagnosis on clinical signs, +/- imaging, culture, cytology
Treatment can be challenging and long term medications are often required
If purulent or granulomatous material present physical removal may be necessary
Nebulisation may be helpful in addition to oral medication/flushing

255
Q

LRT diseases in birds?

A

Viral tracheitis
Tracheal stenosis - iatrogenic
Syringeal damage - leading to alterations in voice
Pneumonia affecting lung parenchyma
Asthma in macaws
Air sacculitis related to fungal disease or irritant inhalation

256
Q

Aspergillosis in birds? Method of transmission? Species more susceptible? Risk factors? When does it cause a problem? Signs? Diagnosis? Treatment?

A

Inhalation of spores
More susceptible: gyr falcons, grey parrots, Pionus parrots, goshawks, red tailed hawks, golden eagles, swans and penguins
Risk factors:
- stress
- immunosuppression
- long term corticosteroid use
- recent capture from the wild
Often carry spores in lungs for prolonged periods - only cause problem when becomes immunosuppressed
Often dyspnoea but may be non-specific inappetence, lethargy, reluctance to fly/perch
Diagnosis
- haematology: monocytosis with heterophilic leukocytosis, occasionally anaemia
- biochemistry: usually increased AST, LDH, hypoalbuminaemia, hypergammaglobulinaemia
- radiology: may indicate lesions in lungs and airsacs but not very se or sp - endoscopy much better option
- serology confirms exposure to spores
Treatment:
- approx 50% will survive
- most require intensive initial stabilisation (O2, fluids, nebulisation, supported feeding)
- euthanasia should be discussed early on due to severity of disease and cost/length of treatment required
- look for underlying causes and correct these
- itraconazole, voriconazole, terbinafine
- antibiosis for secondary bacterial infections

257
Q

Teflon toxicity in birds (Polytetrafluoroethylene, PTFE)? How happens? Signs? Treatment? Prognosis?

A

Inhalation of fluorinated gas produced when PTFE heated above 240C - cooking, ironing, heat lamps
Sudden death a potential
Usually present as weak and dyspnoeic
Neurological signs are also possible
Pulmonary oedema, haemorrhage and necrosis
Treatment:
- oxygenate and prevent secondary infection
- consider diuretics (furosamide)
- consider bronchodilators (terbutaline, theophylline)
- NSAIDs may be helpful
Prognosis depends on level of exposure, but generally poor

258
Q

Neurological diseases in birds - Signs? Causes? Treatment to stabilise?

A
Signs: seizures, ataxia, paresis, paralysis, tremors, circling, torticollis, head tilt, nystagmus
Causes:
- hepatic disease
- renal disease
- hypoglycaemia
- trauma
- toxicity
- nutritional deficiencies
- neoplasia
- parasitic infection
- viral infection
- bacterial infection
- fungal infection
- cardiac disease
Stabilisation:
- benzodiazepines
- levetiracetam
- gabapentin
- phenobarbital sodium
259
Q

What can conjunctivitis be associated with in birds?

A
Psittacosis
Mycoplasmosis
Irritants
Excessive UV exposure
Respiratory disease
260
Q

How can Hypovitaminosis A affect the eyes of birds?

A

Can cause squamous metaplasia of conjunctival tissue

261
Q

What can acute blindness in budgies be related to?

A

Pituitary neoplasia

262
Q

What to do immediately with bird trauma?

A
Control active bleeding
Fluid therapy/transfusion
Nutritional support
Analgesia 
Care with handling - stress/flapping can worsen
263
Q

Problems with soft tissue wounds in birds?

A

Very thin skin and easily torn - care with tension of sutures
Poor ability to produce granulation tissue to heal by secondary intention
Distal appendages have poor soft tissue coverage and blood supply is easily compromised

264
Q

Key features of bird skeletons and fractures?

A

Light and brittle bones - can make orthopaedics challenging
Nutritional deficiency can predispose to pathological fracture
Pneumatised bones - fractures of femur/humerus can leave air sacs open/compromised
Long term dressings can compromise joint function

265
Q

Which diet can lead to hypovitaminosis A? Skin signs?

A

Seed diet without supplementation
Hyperkeratosis
Scaling

266
Q

Feather destructive behaviour (plucking) in birds? - Aetiology? Differentials?

A

Medical vs environmental vs psychogenic aetiology
DDX Psittacine Beak and Feather Disease (PBFD) - Circovirus, polyoma virus, PDD
Flock birds
Boredom
Sexual frustration
Enrichment essential

267
Q

Diagnosis and treatment for feather destructive behaviour?

A

Full husbandry and dietary review
Full clinical examination
Dermatological: mapping skin lesions if present and categorise into primary and secondary lesions, map areas of feather loss
Skin cytology/feather plucks
Blood sampling- haematology/biochemistries, serology, PCR, heavy metal levels
Radiography/endoscopy
Decide on both medical and behavioural plans
- identify and remove conflict causing the destructive behaviour
- modify environment and alter the birds time budgets by providing enrichment
- consider desensitisation and behaviour modification
- drug therapy is last resort: dopamine antagonsists (haloperidol), opiate receptor blockers (naloxone), tricyclic antidepressants (doxepin, clomipramine), benzodiazepines, anxiolytics, hormone therapy (if associated with breeding birds)
Prognosis for full recovery without future intervention is very poor

268
Q

Wing clipping, collars and limping of parrots?

A

Wing clipping is psychologically cruel - option of last resort for aggression, NEVER in juvenile psittacines that can’t yet fly properly
Collars can be part of a long term care plan for feather plucking
Imping = replacing lost/damaged feathers with sterilised feathers moulted from another bird - designed to allow flight and more normal behaviour

269
Q

Mites in birds?

A
Knemidocoptes mutans, K. pilae, K. gallinae
- scaly leg: poultry, passerines
- scaly face: budgies
Treatment:
- Ivermectin
- Topical Petroleum Jelly, Fipronil
- Analgesia
Dermanyssus gallinae (Red mite)
Ornithonyssus spp (Northern fowl mite)
Quill mites
270
Q

Pododermatitis (Bumblefoot) in birds? Which birds? Causes? Treatment?

A
Commonly raptors
Also Anseriforms, Psittacines, Galliformes
Causes:
- often husbandry related
- inappropriate perch material/shape
- overgrown talons
- obesity/inactivity
- ontralateral lameness
- hypovitaminosis A
Grading systems
Treatment:
- management changes
- analgesia/anti-inflammatories/antibiosis
- surgery/bandaging
271
Q

Wing tip oedema in birds? What is it? When seen/which birds? Signs? Treatment?

A

Dry gangrene syndrome
Affects metacarpus of raptors
Typically birds normally found in warmer climates
Occurs during winter - triggered by period of cold weather - husbandry related disease
Typically birds in their first year - not fully trained and potentially less good blood supply to distal wing
Wing - dropped and swollen, cold tip (pitting oedema)
Can attempt gentle warming, encouraging wing exercise on the fist, fly bird if able
After 1 week, swelling becomes hard and dry
Eventually will be areas that slough -> loss of primary feathers and so loss of flight capability
Treatment - medication causing vasodilation: isoxuprine, benazepril, topical preparation H - only effective if started BEFORE dry gangrene has set in

272
Q

Uropygial (preen) gland disease in birds? Where is it? Which birds don’t have? What can happen? Signs? Treatment?

A

Gland present in many but not all species (Hyacinth macaws and Amazon parrots do NOT have preen glands)
Usually dorsal pelvis area (pygostyle)
Can become impacted with secretions, infected, neoplastic change in the ducts or glands
Will usually present as a mass or an area of clumped feathers
Bird may peck/pluck the area if there is pain
Gland can be removed but has impact on feather and skin health subsequently (particularly waterfowl)

273
Q

Polyfolliculitis? Xanthomatosis? Feather cysts? Gout tophi?

A

Polyfolliculitis - love birds, follicle resection
Xanthomatosis - small Psittaciformes, variable yellow masses on wing & keel, high fat diet, trauma, lipid metabolism derangements, surgical resection
Feather cysts - removal of feather follicle
Gout tophi - not integumentary but may be confused

274
Q

Disorders of the beak and bill in birds?

A

Scissor beak = abnormal beak occlusion - congenital or secondary to trauma/disease
Traumatic damage/avascular necrosis where germinal tissue suffers direct damage and subsequent keratin production is abnormal
Interlamellar necrosis in cockatiels - cause unknown
PBFD - virus damages the germinal tissue leading to necrosis and abnormal production of keratin
Hepatic disease - implicated in budgies and cockatiels but no pathophysiologic cause determined
Brown hypertrophy of the cere - related to excess oestrogen production/reduced testosterone production in male budgies with testicular tumours

275
Q

Differentials of white plaques in the oral cavity of birds?

A
Trichomoniasis
Candidiasis
Capillariasis
Diphtheritic pox
Hypovitaminosis A
276
Q

What crop conditions of birds are there?

A

Crop stasis/sour crop - contents ferment -> toxaemia
Crop impaction - crop content is inappropriate and cannot be emptied e.g. crop feeding formula made too thick, ingestion of grass/fibres etc
Crop foreign bodies - can prevent emptying or cause pain and crop stasis
Crop wounds - from self trauma to the area, if there is underlying disease or secondary to trauma
Thermal burns - chicks being hand-reared where the formula is too hot

277
Q

What to do with crop conditions of birds?

A

Evaluate causes and crop function
Often crop requires emptying - often needs sedation and endotracheal intubation to prevent aspiration
Surgical debridement of wounds/burns
2 layer closure - inverting suture pattern
Fluid therapy, easily digestible feeds whilst function is returning
Prokinetics in some cases
Proventricular feeding

278
Q

Causes of vomiting/regurgitation in birds?

A

Very non-specific sign
Can be behavioural/sexual in nature (mirrors!)
In unweaned psittacines can be related to poor feeding practices
Birds that regurgitate often shake their heads -> food matter sprays onto their faces/heads

279
Q

Causes of ileus in birds?

A
Foreign body
Parasite burden
Torsions
Adhesions
Strictures
Neoplasia
Extra-intestinal disease
Papillomatous lesions
PDD
Peritonitis
Heavy metal toxicity
280
Q

Causes of diarrhoea in birds?

A
Campylobacter
Chlamydophila
E.coli
Pseudomonas
Salmonella
Many viral diseases
Heavy metal toxicity
Dietary change
Stress
Anorexia
Septicaemia
281
Q

What does Avian Gastric Yeast cause? Species? Risk factors?

A

Macrorhabdus ornithogaster, Megabacteriosis
Progressive wasting in budgies
Difficult to treat
Associated with stress and overcrowding

282
Q

Heavy metal toxicities in birds - Which metals? How? Organs affected? Signs? Treatment?

A

Zinc
- new cage disease
- galvanised metal
- absorbed in gut
- primary organ that is damaged is pancreas, but can be found in liver, kidney and repro tract
Lead
- environmental in wildlife
- cage toys/furniture in pets
- absorbed in gut and retained in soft tissues
- causes anaemia, bone marrow suppression, liver damage and CNS oedema
Occasionally copper
Heavy metal must be in gut to be biologically active (lead shot in muscle doesn’t cause toxicity)
Birds are depressed, weak, may see vomiting/diarrhoea, PU/PD, anorexia, ataxia, seizures, haemoglobinuria (lead)
Treatment:
- chelation: Calcium EDTA, D-penicillamine (not if heavy metal still in gut)
- supportive care
- physical removal of particles - either surgically, by flushing or by use of bulk laxatives

283
Q

Normal bacterial flora of birds?

A

Lactobacillus
Corynebacterium
Non-haemolytic Streptococci
Staphylococcus epidermidis

284
Q

Common bacterial pathogens of birds?

A
Gram negative pathogens
- Klebsiella
- Pseudomonas
- Enterobacter
- Proteus
- E.coli
- Pasturella
- Salmonella
Gram positive: 
- Staph aureus
- S.intermedius
- Clostridium
- Enterococcus
- Streptococcus
Mycoplasma, Mycobacteriosis and Chlamydophila also important
285
Q

Psittacosis in birds - Agent? Features of agent? Risk factors? Presentation? Clinical signs? Spread? Diagnosis? Treatment?

A

Chlamydophila (Chlamydia) psittaci - obligate intracellular gram positive bacterium
Zoonotic (ornithosis in humans)
Risk factors:
- stress
- improper environmental conditions/husbandry
- high reproductive activity
- exposure to new birds
- immunosuppression
3 potential scenarios:
- subclinical carriers
- clinical disease
- chronically infected birds showing neurological signs
Often non-specific clinical signs - combo of resp signs with diarrhoea can be a clue
Conjunctivitis and choanal slit inflammation may be present
Spread by direct contact, respiratory secretions, faeces
Enlarged spleen on radiography very suggestive
Can attempt culture (3 days pooled faecal sample) but PCR on conjunctival/choanal/cloacal swabs more useful
Serology available - only indicates exposure
General supportive care will be required
Doxycycline - long treatment length
Azithromycin, fluroquinolones somewhat effective but may induce carrier state rather than clearing the organism

286
Q

Mycobacteriosis in birds - Agent? Transmission? Clinical signs? Diagnosis? Treatment?

A

Mostly M.avium or M.genevense
Oral or airborne transmission
Clinical signs non-specific:
- chronic illness
- weight loss
- diarrhoea
- lameness
- poor feathering
- on examination may find hepatomegaly, intestinal thickening, subcutaneous or coelomic masses (granulomas)
Diagnostics:
- inflammatory leukogram,
- acid-fast organisms seen within cytology or tissue samples - birds do not form classical tubercle.
- PCR is available
- culture can be challenging and time consuming
Treatment controversial because of zoonotic risk but psittacines shown to pose low risk to humans
Combined antibiotic therapy for 6-12 months is required (rifabutin, clarithromycin, ethambutamol, enrofloxacin)
Birds with advanced disease have a poor prognosis

287
Q

Mycoplasmosis in birds? Agent? Problems caused? Spread?

A

M.gallisepticum is economically important disease of poultry
Emerging disease in finch populations
Respiratory disease and septic arthritis in poultry, waterfowl and pet birds that have come into contact with wild birds/poultry
Direct aerosol spread, or fomite spread are both possible
Potential cause of chronic sinusitis in psittacines and conjunctivitis in passerines

288
Q

Signs of salmonella in birds?

A
Diarrhoea
Multisystemic disease
Septicaemia
Osteomyelitis
Dehydration
Lethargy
Ileus
289
Q

Botulism in birds - Agent? Which birds? Signs? Treatment?

A

Clostridium botulinum type C toxins
7 serotypes
Primarily seen in waterfowl
Causes progressive flaccid paralysis - loss of flight, loss of use of limbs, limberneck/respiratory muscle paralysis
Death due to eventual respiratory failure or drowning
Triage, removal of source of toxin, supportive care, adsorbents

290
Q

Features of Avian Influenza?

A

Orthomyxovirus
Most viruses cause subclinical infection with subtle signs such as reduced fertility or respiratory disease
H5N1 form causes severe signs or death in wild bird populations
Notilifiable

291
Q

Proventricular Dilation Disease in birds? Agent? What happens? Differentials? Species? Signs? Diagnosis? Treatment?

A

Progressive, often fatal disease affecting ANS relating to gut-myenteric plexus
Avian Borna Virus - pathophysiology unclear
Incubation 3 weeks to 3 months
Many differentials for proventriculus dilatation - lead toxicity, GI foreign bodies, inflammation of gut
Can be seen in any species - common in macaws, grey parrots, cockatoos, eclectus - budgies appear resistant
Clinical signs:
- dilation of proventriculus, generalised ileus, and non-specific neurological signs
- undigested seed in faeces, regurgitationand
- feather plucking particularly over flanks
- may be very thin/cachectic
Diagnosis:
- PCR on cloacal/pharyngeal swabs
- radiographic confirmation of proventricular dilatation (contrast helpful)
- histopathology
Treatment often unsuccessful
- celecoxib
- prokinetics (metoclopramide, ranitidine, erythromycin)
- amantidine
- recombinant interferon
Prognosis guarded to poor
NB husbandry if a flock, cage/bowl hygiene and biosecurity including proper quarantine procedures

292
Q

Psittacine beak and feather disease virus (PBFD)? - Agent? What does it cause? Spread? Species affected? Signs? Diagnosis? Treatment?

A

Circovirus
Most Psittacine species, passerines and columbiformes
Immune suppressive virus - grey parrots get a pancytopenia from bone marrow suppression
Virus shed in feathers, dander, faeces and saliva
Transmission by ingestion or inhalation
Australian psittacines seem to have severe beak and feather lesions
Other species from different geographical areas show less severe feather signs (African greys)
South American psittacines appear to be more resistant
Classic PBFD - lack of powder/feather dander, beak becomes very shiny, abnormal feather formation- clubbed or constricted at the base, feathers easily epilated and grow back slowly or not at all
Diagnosis from PCR on faeces, feather pulp, blood
Treatment is supportive only, and many birds survive many years with this disease

293
Q

Polyoma virus in birds? Agent? Which birds affected? Signs?

A

Papovavirus, budgerigar fledgling disease
7-14d incubation
Primarily affects young birds- often acute death of unweaned or recently weaned birds
Seen more commonly in UK than USA
Adult birds appear resistant but infected adults may seroconvert and shed virus for up to 90 days
Chicks presented alive may have crop stasis, ecchymotic haemorrhages subcutaneously, coelomic distention and abnormal feather production
Chicks that survive often have chronic feathering abnormalities/dystrophic feathers

294
Q

Viscerotropic velogenic Newcastle Disease of birds? Type of virus? Transmission? Signs? Treatment?

A

Paramyxovirus group 1 (VVND or exotic Newcastle disease)
Transmission by
Clinical signs:
- asymptomaiv -> acute death
- non specific - depression, anorexia, weight loss, bright green diarrhoea
- resp - sneezing, conjuncitivis, oculonasal discharge
- neurological -
Add from slides

295
Q

Psittacid Herpes Virus 1 in birds? Signs? Appearance? Associations? Diagnosis?

A

Systemic Pachecos disease - peracute signs, high mortality
Papillomas in birds that survive
Epithelial hyperplasia
Can arise from skin, mucous membranes and glandular ducts (liver, pancreas, intestines)
Appearance is typical and MM papillomas will blanch if acetic acid is applied
May be associated with development of squamous cell carcinomas as well as biliary, hepatic, intestinal and pancreatic carcinomas
Diagnosis by histopathology, and lesions that are related e.g. to cloaca prolapse or affect normal function should be removed
Birds with internal lesions have a poorer prognosis and a reduced life expectancy

296
Q

Neoplasia in birds? Factors associated? Diagnosis? Treatment?

A

Environmental factors - UV light exposure and melanoma, SCC
Viruses - papillomatosis
Diagnosis - clinical exam, imaging, cytology, histopathology of biopsy
Treatment:
- NSAIDs palliatively
- intralesional chemotherapy
- radiotherapy can be hard to access
- radical excisions surgery most likely treatment to give good results

297
Q

Anorexia in birds - consequences?

A
Dehydration
Loss of muscle mass
Nutritional deficiencies
Crop/GI stasis
Weakness
Anaemia
298
Q

Factors leading to aggression in birds?

A

Pain
Systemic disease
Poor sight
Normal hormonal activity
Neurological disease
Frustration from inappropriate pair-bonding with human
Inadvertant positive reinforcement of aggressive behaviours

299
Q

What is star gazing in snakes? Cause? Diagnostics needed?

A

Abnormal body/head position
Suggests normal CNS function inhibited
A symptom not a disease- e.g. Inclusion body disease, organophosphate toxicity, trauma, excessively high or low body temperature, bacterial meningitis
May be associated with difficulty moving, disorientation, depression, tremors, seizures and lack of adequate righting reflex
Diagnostics: bloods, and potentially advanced imaging

300
Q

Causes of loss of righting reflexes of snakes (unable to right itself when placed in dorsal recumbency)?

A

Suggests discontinuity of spinal cord’s ability yo transmit neural impulses or an inability of the muscles to respond
Trauma, spinal osteoarthropathy, spinal mycobacteriosis

301
Q

Signs of weakness on clinical exam of snake?

A

Unable to raise head

Unable to constrict when stimulated

302
Q

Causes of thyroid disease in snakes? Signs?

A
Improper light cycles
Improper hibernation
Improper temperature gradients
Iodine toxicity/deficiency
Intrinsic thyroid disease
Signs of hyperthyroidism:
- abnormally frequent sheds
Signs of hypothyroidism:
- weight ain
- lethargy
- poor appetite
- depression
- dysecdesis
- goitre
- myxoedema
303
Q

How often do normal snakes shed?

A

4-6 times a year (dependent on age)

304
Q

Dysecdysis in snakes - What is it? Causes?

A
= Failure to shed full skin normally
Poor humidity
Low ambient temperatures
Incorrect periodicity
Hypovitaminosis A,
Mites
Thyroid disease
Dermatitis
Trauma
Incorrect handling (especially when snake is about to shed) resulting in damage to fracture plane 
Bacterial, fungal and viral disease - systemic or dermal
305
Q

What to do if dysecdysis of snake?

A

Correct underlying problems
Place snake in warm damp environment with something that is gently abrasive - warm/damp towel
Apply topical antimicrobials to any areas of skin damage
Parenteral treatment if deeper structures involved

306
Q

Retained spectacles in snakes - Appearance? Why problem? Treatment?

A

Specialised scales over eyes often not fully shed even if rest of shed appears normal
Eyes appear wrinkled and opaque
Requires careful treatment as sensitive secondary spectacles/cornea underneath can easily become damaged
Damage to spectacle can lead to infection and subspectacular abscesses, and this may be associated with bacterial stomatitis
Use wetting solution (hypromellose/lacrilube) for few days to increase local humidity around these scales, then can usually gently encourage off by grasping edge with fine forceps

307
Q

Thermal burns of snakes - Why happens? How happens? Signs? Treatment?

A

Poor dermal perception of heat - often don’t recognise they are at risk of burning until burns have occurred
Often secondary to inadequate ambient temperatures - so th snake is generally cold, with provision of focal heat sources such as ‘Hot Rocks’ or unguarded lamps
Animal is cold so its heat perception will be very poor, and it will also actively seek to increase its body temperature
Burns may not become evident immediately and are often identified after a shed - areas are open, ooze serum and and can easily become infected
Analgesia, potentially debridement of area, topical and systemic antibiosis
Cling film, condoms and proprietary clear dressings can all be used to protect the areas while they heal

308
Q

Blister disease in snakes - What is it? Appearance? Cause? Diagnosis and treatment?

A

Dermatitis/bacterial skin infection - leads to blisters under scales
NB fungal skin disease can also cause blisters
Areas are discoloured and fluid filled - may rupture leaving ulceration
Associated with poor environmental hygiene and immunosuppression
Culture fluid from blisters, correct environment and provide appropriate antibiosis - often Pseudomonas, Aeromonas, Citrobacter
Look for other causes of immunosuppression - underlying systemic disease or management related
Topical treatment (eg silversulphadiazine) and systemic antibiotics

309
Q

Mites in snakes

A

Ophionyssus natricis parasitic mites
Blood feeders - puncture skin and engorge with blood
Skin damage can lead to irritation/pain
Can spread bacterial or viral infection- e.g. Pseudomonas or Inclusion body disease
Environmental treatment - remove anything porous (e.g. wood, bark etc) and deep clean everything else, use newspaper for substrate until mites are controlled
Bathing/submerging in water will kill mites, or Fipronil
Predatory mites - Hypoapsis mites will eat the parasitic mites - much less potentially toxic
Treatment needs to be prolonged due to length of mite life cycle - 40 days minimum

310
Q

Stomatitis in snakes - When seen? Signs? Risk factors? Diagnosis? Treatment?

A

‘Mouth Rot’
Usually a symptom of systemic infection and immunosuppression
Animal becomes unable to keep the bacteria normally present in mouth under control
signs: loss of appetite, red, swollen oral tissues, pus within mouth, discharge from mouth and nose
Infection often spreads to the GIT or lungs
Risk factors: poor husbandry (hygiene/temperatures), oral injury
Diagnosis on examination
Physical cleaning/debridement of damaged tissues and parenteral antibiotics
Correct underlying husbandry concerns

311
Q

Anorexia in snakes - Causes?

A

Can be behavioural:
- preparing to hibernate
- preparing to breed
Can be secondary to improper environment:
- lack of hide boxes
- temperatures too high or too low
- food presented poorly
- wrong food presented
Can be due to systemic disease
Animals that are anorexic because of breeding or brumation will not lose very much weight (<7% BW) during expected time course of behavioural change
Once the anorexia exceeds the expected timeline or the weight loss becomes significant then intervention is required

312
Q

Regurgitation in snakes - Causes? Other associated signs? Treatment?

A

Secondary to handling/upset soon after feeding
Inappropriate environmental temperatures
Reaction to inappropriate food intake/spoiled food
GI blockage - most likely rostral portions of gut
Common sign of cryptosporidiosis
Also associated with Chlamydophila, IBD, amoebiasis, metabolic disease such as renal or hepatic insufficiency
May be associated with weight loss, but fluid balance and electrolyte abnormalities are less likely
Correct husbandry, rehydration therapy if needed, diagnose and treat specific cause

313
Q

Cryptosporidia in snakes - Agent? Signs? Transmission? Diagnosis
Treatment?

A

Cryptosporidium serpentis
Causes gastric hypertrophy -> visible abdominal swelling and regurgitation of typically mucus covered prey - may be sporadic
Weight loss
Oro-faecal transmission
Can get subclinical shedders and non-ophidian reptiles can be carriers
Oocysts very resistant in environment - 5% ammonia and formol saline are effective
Diagnosis:
- can visualise oocysts in faeces (acid fast) but shedding is intermittent
- stomach washes may be more likely to demonstrate organisms
- serology available but not specific for C.serpentis
- histopathology is the gold standard
Treatment and prevention of spread:
- supportive care may be helpful in short term but few helpful medications
- hyperimmune bovine serum (to C parvum) may help
- euthanasia should be considered
- good hygiene is key to stop spread within collection
- euthanase positive snakes
- maintain a closed collection
- test food and water courses for presence of Cryptosporidia
- quarantine and test any snakes being brought into collection

314
Q

Entamoebiasis in snakes? Species? Risk factors? Signs? Diagnosis? Treatment?

A

Entamoeba invadens – commensal in herbivorous reptiles but can invade intestinal mucosa and cause disease in carnivorous reptiles
High morbidity/mortality
Mixed collections are risk factor - especially if poor
husbandry and inadequate quarantine
Direct lifecycle
Poor body condition/muscle tone, anorexia, regurgitation, constipation/diarrhoea
Can see neurological signs
Diagnosis on cloacal wash cytology - but more usually histopathology
Treatment - metronidazole every 2-3 days if clinically ill, every 10-14 days if just exposed

315
Q

Causes of respiratory disease in snakes?

A
Commonly cultured bacteria:
- Pseudomonas
- Klebsiella
- Proteus
- E.coli
- Aeromonas
- Morganella morganii
- Citrobacter freundii
- Pasturella spp
Chlamydophila, Mycobacteria, Mycoplasma, Salmonella IBD, paramyxovirus, Reovirus also cause pneumonia
316
Q

Signs of respiratory disease in snakes? Diagnosis? Treatment?

A

Oral discharge, gaping, gular excursion and orthopnoea position, anorexia, weight loss
Diagnosis:
- culture and sensitivity of lung wash
- culture of organisms from mouth is not diagnostic
- endoscopic evaluation to visualise, clear discharge and biopsy lesions
Oxygen therapy, warm towards POTZ, fluids, appropriate antibiosis, suction of excess secretions from oral cavity

317
Q

Paraphimosis in snakes - What is it? Which animals? Risk factors? Consequences? Treatment?

A

Inability to retract phallus or hemipenes
Seen commonly in ball pythons and boa constrictors, as
well as many chelonians
Risk factors:
- spinal trauma
- nutritional secondary hyperparathyroidism
- excessive breeding (snakes)
- hypovitaminosis A
Trauma to protruded organ and abscessation are possible consequences - must confirm that protruding tissue is in fact phallus/hemipene and not cloacal tissue or gut
Goal is to repair/replace the organs and allow to heal whilst kept in correct position - wound gels, hypertonic sugar solutions, local anaesthesia and replace and suture back into position as for cloacal prolapses

318
Q

Inclusion body disease in snakes - Which species? Cause? Signs? Diagnosis? Treatment?

A

Primarily boas, pythons and related species (Henophidia)
Increased risk in mixed species collections
Often associated with mite infestations
Retrovirus
Characteristically signs of neurological disease
Often fatal
Inclusion bodies found in most tissues on histology
Secondary infections due to immunosuppression - stomatitis, pneumonia, gastritis may be misleading
Neurological signs - opisthotonus (star-gazing), poor righting reflex, reduced mentation
Tissue biopsy (oesophageal tonsils, liver and pancreas are good sites)
Eradication from collection is goal
Eradication of mites - biosecurity and appropriate quarantine prior to introduction of a new specimen into the collection
Avoid keeping geographically separate species in mixed species displays eg boas and pythons

319
Q

Paramyxovirus in snakes? Common in which snakes? Transmission? Risk factors? Signs? Diagnosis? Treatment?

A

Common in viperid snakes
Highly contagious
Infection is from
respiratory secretions
Risk factors: age, stress and immunosuppression
Primarily causes respiratory signs:
- pneumonia
- potentially encephalitis
Secondary infections are common
Mortality rates can be high
PCR on respiratory wash/choanal or pharyngeal swabs confirm diagnosis
Treatment - supportive care only, provide an increased thermal gradient to allow animal to exhibit behavioural fever
Biosecurity important for groups of snakes

320
Q

Sunshine virus in snakes?

A

New paramyxovirus identified in 2016
Discovered in Australian pythons
Snakes display neurorespiratory disease - signs are non specific e.g regurgitation, lethargy, inappetance
Mortality is variable and snakes may not show severe pathology

321
Q

Reovirus in snakes?

A

Non- enveloped RNA Orthoreovirus
Many species other than snakes can also be affected (lizards,
tortoises)
Risk factors not well understood - virus very stable in environment- so hard to disinfect
Presenting signs include pneumonia and encephalitis
High death rates
PCR available - pulmonary washes are sample of choice
Supportive care is only option and prognosis for survival and recovery is guarded

322
Q

Proliferative spinal osteoarthropathy in snakes? What is it? Which species? Risk factors? Signs? Cause? Diagnosis? Treatment?

A

Anomalous displacement or distortion of spinal column characterised by segmented fusion of affected vertebrae by foci of irregular proliferative bone (spinal osteodystrophy)
Any reptile can be affected - snakes and green iguanas most commonly
Risk factors: poor diet, inappropriate husbandry, chronic bacterial infection and trauma
Affects spinal mobility and righting ability
May be swellings noted on the spine
Constipation, faecal/urinary incontinence, inability to strike
Exact cause unknown - potentially hypovitaminosis A, hypervitaminosis D, septicaemia, immune mediated, neoplastic?
Radiography or CT are diagnostic
Euthanasia should be considered in severe cases
Alternatively analgesia, attention to husbandry and diet, antimicrobials if bacterial infection suspected

323
Q

Salmonella in snakes - Type of organism? When infected? Treatment? Prevention?

A

Gram negative facultative anaerobes
Reptiles are likely exposed soon after hatching
Animals raised in high stocking densities are more likely to be infected
Reptile associated salmonellosis is a major public health concern due to zoonotic potential
Reptiles that are clinically normal should not be treated for Salmonellosis as part of normal microflora
Animals presenting with signs of clinical disease should be treated with antibiotics
Successful treatment confirmed by repeat faecal cultures - NB false negative cultures
Salmonella can invade extra-intestinal tissues so treatment may not eliminate all organisms - chronic carriers
Hygiene measures - hand washing, handling behaviour of owners

324
Q

Unusual anatomy of lizards?

A
No diaphragm
No loop of henle
Internal gonads
Hemipenes
No urinary bladder
325
Q

What glands do lizards have?

A

Scent glands in vent (squamates)
Prefemoral glands/pores (geckos, bearded dragons, iguanas)
Temporal glands (Chameleons)
Salt glands in nares (marine iguanas, turtles)

326
Q

Phases of ecdysis in lizards? What is it regulated by?

A

Renewal phase - fragile skin, dull skin, behaviour changes
Resting phase - between ecdysis
Regulated by temperature, humidity and thyroid hormone

327
Q

How do reptiles differ in ecdysis?

A

Snakes - in toto shed

Lizards and chelonia - flakes

328
Q

Dysecdysis in lizards? What can happen? Causes? Treatment?

A
Retained shed
- rings of retained shed may act as
tourniquets
- digit loss
- hemipene prolapse
Causes:
- husbandry (temperature, humidity, surfaces diet)
- dermatitis, parasites, trauma, surgery, hormone imbalances
Soak squamates to facilitate removal of
retained shed
Lubrication
Antibiosis for secondary infection
Injection of vitamin A to induce shed?
Thyroxine supplementation in lizards?
329
Q

Skin diseases of lizards?

A

Blister disease (ulcerative dermatitis)
Bacterial - stomatitis, abscesses, septicaemia
Viral - herpes, pox, papilloma
Fungal - CAN-V
Thermal burns
Ticks - Ixodes, Ambylomma
Mites - Trombicuild mites (Hirstiella spp)

330
Q

CAN-V in lizards? What does it cause? Animals affected? Risk factors? Spread? Signs? Diagnosis? Prevention?
Treatment? Prognosis?

A

= Yellow fungus disease (Chryosporium anamorphic of Nanniziopsis vriesii)
Can be skin or systemic infection
Risk factors unknown - skin damage, stress, poor husbandry, immunosuppression suggested
Direct contact and airborne spread
Skin disease - blisters, progresses to yellowish crusting, hyperkeratosis, epidermal necrosis
Diagnosis - cytology (fungal hyphae) and culture
Biosecurity to prevent spread - isolate cases
Treatment:
- debride skin lesions
- topical and oral treatment required: terbinafine, voriconazole, itraconazole
Guarded prognosis - often fatal

331
Q

Dentition of chameleons, bearded dragons, water dragons?

A

Acrodont = non rooted and directly attached to underlying bone
Weak attachment, easily lost and not replaced

332
Q

Dentition of iguanas, geckos, monitors?

A

Pleurodont = regularly shed and replaced

Periodontal disease rare

333
Q

Risk factors for periodontal disease of acrodont dentition lizards? Clinical signs? Treatment?

A

Diet (food items that are too soft-bodied)
Inappropriate lighting/heating
Trauma
Clinical signs: deformity of lips/mouth, anorexia, discharge from mouth, tooth loss
Treatment: debride abnormal tissues, dental scaling/gels, provide appropriate antibiosis and analgesia, improve diet and address husbandry

334
Q

Significance of nematodes in lizards?

A

Some (Oxyurids in particular) thought be beneficial and a natural part of multi biota so low burdens shouldn’t be treated

335
Q

Licensed treatment for Coccidiosis in bearded dragons?

A

Sulfatrim

336
Q

Metabolic bone disease (nutritional secondary hyperparathyroidism) in lizards? Causes? What happens? Clinical signs? Other metabolic bone disease causes?

A

Nutritional secondary hyperparathyroidism:
- deficiency of calcium or vitamin D
- imbalance of Ca:P
- inadequate UV light provision for fit D activation
Persistent hypocalcaemia increases activity of parathyroid gland -> increased PTH production -> resorption of calcium from bones -> clinical signs
Juvenile or reproductively active females are most likely to show clinical sgns
Clinical signs:
- rubber jaw
- pathological fractures
– swollen fibrous osteodystrophy of long bones
- bloating/constipation
- cloacal prolapse
- follicular stasis/dystocia
- paresis/paralysis if spinal damage
Diagnosis
- radiography
- blood ionised calcium assay?
Other metabolic bone disease causes:
- renal secondary hyperparathyroidism
- hypovitaminosis C (affects collagen production and bone growth)

337
Q

Treatment of hypocalcaemia in the acute and chronic phases of lizards?

A

Acute:
- Stabilise fractures and treat seizures if occurring
- Manage secondary ileus
- Warm animal to POTZ
- Fluid therapy if required
Calcium gluconate IV/SQ if muscle fasciculations
Chronic:
- Correct husbandry/nutritional issues and client education
- Consider underlying reproductive disease
- Nutritional support
- Oral calcium supplementation with calcium glubionate
- Can give vitamin D injections
- Can use calcitonin once normocalcaemic to shut off the parathyroid: improves rapidity of bone repair
Prognosis:
- Dependent on severity
- Spinal lesions/carapace deformity has more guarded prognosis particularly if neurological involvement

338
Q

Substrate impactions in lizards - aetiology? clinical signs? diagnosis? treatment?

A

Aetiology
- inappropriate substrate/food presentation/inappropriate diet
- pica?- renal disease or mineral deficiency, NSHP
Clinical Signs:
- acute anorexia
- some have palpable mass in coelomic cavity
- may also feel recognisably like substrate
Diagnosis: radiography essential
Treatment
- bulk laxatives and fluids
- calcium supplementation
- prokinetics (as long as not obstructed)
- surgical intervention may be necessary

339
Q

Pre-ovulatory follicular stasis in lizards? What happens? Treatment? Clinical signs? Diagnosis?

A

Follicles are not stimulated to ovulate or do not respond to stimulation to ovulate
Remain unovulated on the ovary -> resorption (a factor in hepatic lipidosis) -> necrosis -> systemic illness
May be successfully stimulated to ovulate:
- environmental: heat, humidity, provide nest sites, sight/access to male
- medical interventions (hCG)
Clinical Signs:
- lethargy
- inappetence
- HL weakness
- weight usually stable
or increased
Bloodwork may indicate reproductive activity
Imaging required for diagnosis and comorbidities
If follicles static then ovariectomy indicated before the lizard becomes too unwell