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
What is the stimulus for respiration in mammals, reptiles and birds? How does this affect oxygen therapy?
Mammals: hypercapnia - give 100% oxygen | Reptiles and birds: hypoxia - give 30-50% oxygen
26
What is the maximum blood draw from healthy animals?
1% BW (1ml/100g) | Include anticipated haemorrhage/haematoma
27
Emergency minimum blood tests for exotics?
``` Gluocse Ca2+ PCV TS Lactate ```
28
What is the blood volume of exotic mammals, birds and reptiles?
Mammals: 50-80ml/kg Birds: 60-120ml/kg Reptiles: 40-80ml/kg
29
Venipuncture sites for exotic mammals?
``` – Jugular – Cranial Vena Cava – Saphenous – Cephalic – Lateral tail vein (rats) – Marginal auricular vein (rabbits) ```
30
Venipuncture sites for birds?
– Right jugular – Medial metatarsal vein – Basilic/ulnarvein
31
Venipuncture sites for reptiles:
``` 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 ```
32
How to calculate the basal energy requirement (BER) for exotics?
``` 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 ```
33
What drugs are contraindicated in rabbits, rodents, birds and chelonia?
``` 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 ```
34
Where to administer IM drugs in exotic mammals?
Quadriceps Epaxial muscles Hedgehogs - orbicularis muscle
35
Where to administer IM drugs in birds?
Pectoral muscles - caudal 2/3 to avoid brachial plexus, care with flying birds e.g. racing pigeons Quadriceps
36
Where to administer IM drugs in reptiles?
Chelonia - triceps/biceps/any palpable muscle mass Lizards - triceps/quadriceps, epaxial muscles - care re autotomy Snakes - epaxial muscles (33% itv length)
37
What is refeeding syndrome?
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
38
How to avoid refeeding syndrome?
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
39
CPCR compressions:breaths for mammals and birds?
5 compressions to one breath
40
When to use crystalloids in exotics?
Rescuscitation and maintenance Hypertonic saline works synergistically with colloids in resuscitation 3-5ml/kg over 10 mins
41
When to use colloids in exotics? How much?
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
42
When to use Haemoglobin based oxygen carrier fluids in exotics? How much?
Indicated where increased O2 delivery needed Non antigenic so no cross matching needed Very effective for haemorrhagic shock 2-5ml/kg
43
When to use blood products for exotics? How much?
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
44
What is the most common cause of seizures in an African Grey Parrot? Treatment?
Hypocalcaemia IM or IV calcium salts required for emergency treatment + benzodiazepine for seizures
45
Reasons to spay rabbits? Method - anatomy to be aware of? types of sutures?
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
46
Resons to castrate rabbits? Method? Anatomy to be aware of? Sutures? When non fertile?
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
47
Reasons to spay rodents? Method?
``` 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 ```
48
Reasons to castrate rodents? Method?
``` Reason: reproductive control Prescrotal vs scrotal vs abdominal Infection risk Semi closed or closed technique Splash block (lidocaine/bupivocaine) Intradermal skin sutures ```
49
Reasons to spay ferrets?
Control of musky odour Oestrogen toxicity Consider alternatives due to adrenal disease
50
Method for spaying ferrets? Anatomy to be aware of? Types of sutures?
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
51
Reasons to castrate ferrets? Method?
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
52
Reasons to vasectomise ferrets? When non fertile?
Jills are induced ovulators 75% cessation of oestrus on first mating No risk of adrenal disease Can be fertile ? 7 weeks post vasectomy
53
Examples of rapid absorbable suture materials?
``` Polygactin 910 (Vicryl) Polydioxanone (PDS) ```
54
What types of skin sutures should be used for reptiles and why? When removed?
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
55
How long does it take for transplastron coeliotomy of chelonia to heal?
12-18 weeks | Acrylic/epoxy resin left for 6-12 months
56
What is Carboxymethylcellulose?
'Belly jelly' Use as topical gel/sheet to aid tissue lubrication post-op for mammals Left in coelom/abdomen after surgery
57
Hormonal control of reproduction - options in mammals?
``` Deslorelin implant - licensed in male ferrets hCG Proligestone Leuprolide acetate Aglepristone ```
58
Indications for hormonal control of reproduction in birds? Examples?
``` Reproductive disease Chronic egg laying Behaviour Dystocia Deslorelin Leuprolide ```
59
Indications for hormonal control of reproduction in reptiles? Examples?
Pre and post ovulatory stasis Deslorelin Leuprolide
60
What main licensed vaccinations are available for birds?
Pigeons - PMV, Pox Chickens - IBD, IB, Salmonella, CAV Psittacines (USA/Canada) - Polyoma virus
61
What licensed vaccines are there for rabbits? When given?
RHD1-myxo - from 5 weeks, annual | RHD2/RHD1 - from 30 days, 2 weeks apart from RHD1 vaccination
62
What licensed vaccinations are there for ferrets and rodents?
Ferrets - rabies, distemper (not licensed) | Rodents - guinea pig Bordetella vaccine?
63
Treatment of endoparasites in birds?
Amidostomum/Echinuria (waterfowl) - praziquantel/pyrantel | Roundworms, Syngamus, hairworm, caecal worm (poultry) - flubendazole (0 day egg withdrawal)
64
Drugs for ectoparasite control in exotic mammals?
Ferrets - fipronil and S-methoprene (frontline combo), imidocloprid/moxidectin (advocate) Rabbits - imidacloprid licensed for fleas (advantage), cyromazine (rearguard), ivermectin, selamectin Fipronil toxic in rabbits!
65
Drug used for endoparasites of rabbits?
Fenbendazole Not for routine worming Encephalitozoon cuniculi
66
Drugs for ectoparasite control of reptiles?
Nothing licensed Fibronil spray (wipe) Ivermectin - not chelonia
67
Drug of choice for treatment of endoparasites in reptiles?
Fenbendazole
68
What to do if trimming pet bird wings?
Symmetrical only Primary feathers only Postpone if blood feathers found
69
What is pinioning? How?
``` 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 ```
70
Placement of microchips in birds and reptiles?
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
71
ASA categories for anaeshesia?
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
72
Behavioural and postural responses for pain recognition in exotics?
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
73
Indicative pain behaviours?
``` = behaviours that are rarely seen prior to painful stimulus but often afterwards Twitching Wincing Staggering Flinching Belly pressing Slow postural adjustments Shuffling gait ```
74
Side effects of opioids in exotics?
Respiratory depression Gut motility Nausea Excitation
75
Why are steroids avoided in exotics?
Profound immune suppressive effect - WBC lysis | Lots of exotics may have underlying clinical pathology
76
Which receptors does each opioid work on?
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)
77
Which opioid receptors do birds and reptiles have?
``` Birds = primarily k Reptiles = vary between k and uncategorised receptors which are similar to mammalian mu receptors ```
78
NSAIDs - What must be monitored? Side effects? Dosing frequency? Examples?
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
79
How does tramadol work?
u receptor agonist Seratonin and adrenaline re-uptake inhibition Alpha-2 agonist Appears to be very safe and effective for most exotic species
80
Gabapentin/pregabalin - use in exotics? side effects?
Anti-convulsant that modifies the perception of neuropathic pain Can see ataxia and sedation
81
Which exotic species can paracetamol not be used in?
Ferrets
82
Ketamine and amantadine - how does it work?
At very low doses blocks NMDA receptors | Prevents wind up pain
83
What types of pain are a2 agonists useful for in exotics?
Visceral, musculoskeletal and neuropathic pain
84
Maropitant - how does it work? Use?
Centrally acting anti-nausea drug due to effect on CTZ | Also good anti-inflammatory and show to be anaesthetic sparing in dogs
85
Which drugs can be given as constant rate infusions for pain relief? Benefits? Cons?
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
86
What is EMLA?
Topical local analgesia | Lidocaine with prilocaine
87
What are benzodiazepines, ketamine, a2 agonists and alfaxolone/prpofol good/bad for in anaesthesia?
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
88
Common anaesthetic protocols for exotics?
Triple combination - a2 agonist + opiate + ketamine Ketamine + benzodiazepine Benzodiazepine + opiate + propofol or alfaxolone + volatile agent Opiate/ACP + propofol or alfaxolone + gas Volatile agent alone
89
Antagonism of a2 agonists, benzodiazepines and opioids - Which drug? What to be aware of?
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)
90
Should rodents and rabbits be staved pre-op?
No Risk of hypoglycaemia Can't vomit/low risk Take food out 0.5-1h before and check mouth for food once anaesthetised
91
Limiting factors for endotracheal intubation of exotic mammals?
``` 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) ```
92
Methods of intubating exotic mammals?
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
93
What are supraglottic airway devices?
``` V-gel Quick and easy to insert No risk of tracheal trauma/stricture Expensive Ideally use capnography to ensure correct porition ```
94
When to feed exotic mammals post-op?
Within 1 hour recovery
95
What recumbency should avians be in for recovery? What to be careful of?
``` 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 ```
96
Which animals have complete tracheal rings?
Birds - don't cuff tubes | Rabbits?
97
Positions of birds for anaesthesia - problems?
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
98
What do birds and reptiles rely on for breathing?
Birds - rely on movement of air sacs and ventral chest excursions Reptiles - rely on chest excursions (legs in chelonia)
99
Why is ventilation mandatory for reptile anaesthesia?
May be quite resistant to reduced ventilation/apnoea | May not breathe frequently enough on gas anaesthesia to keep themselves asleep
100
ET intubation in reptiles?
Short ETT Essential for IPPV as apnoea common Rostral glottis in snakes and carnivorous lizards Herbivores glottis at base of fleshy tongue
101
Anaesthetic monitoring in reptiles - reflexes and responses?
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
102
What to do in recovery for reptiles - ventilation? drugs? recovery time?
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
103
Anaesthesia methods for fish?
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
104
Stages of fish anaesthesia?
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
105
Where are rabbit caecotrophs digested?
Stomach
106
Why can't rabbits vomit?
Strong muscular cardiac sphincter
107
Anatomy of the caecum in the rabbit? What happens there?
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
108
Anatomy of the colon in the rabbit? What happens there?
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
109
Problems with gut stasis in rabbits?
Interstitial fluid flows into gut - dehydration Painful Potentially fatal, electrolyte derangement as not secreted/reabsorbed so GA not option
110
Diagnosis of gut stasis in rabbits?
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
111
Possible causes of gut stasis in rabbits?
GI blockage | Dysbiosis
112
In the case of GI obstruction causing gut stasis, what treatment is needed? Which drugs are contraindicated?
Surgical intervention Must stabilise prior to surgery Pro-kinetics are contraindicated pre and post-op
113
What is dysbiosis? Causes? Signs? Treatment?
= 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
114
Why may a rabbit not be eating caecotrophs?
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)
115
Significance of diarrhoea in rabbits? Causes?
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)
116
What is mucoid enteropathy in rabbits? Cause? Treatment?
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
117
What is bloat in rapids? Why does it happen? Treatment?
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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What is caecal impaction in the rabbit? What happens? Treatment?
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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When is Coccidiosis typically seen in rabbits? Risk factors? Which forms cause what?
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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Which are the major gut parasites in rabbits?
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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What is dysautonomia in rabbits? Which age affected? Risk factor? Signs? Cause? Treatment?
= 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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What pro-kinetics can be used in rabbits? When are they contraindicated?
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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When should rabbits and other small furries be support fed?
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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Should fluids be given to a rabbit that is not eating?
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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Are pro-biotics ok for rabbits?
Evidence for and against Worst case is don't work Unlikely to do harm
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What type of teeth do rabbits have? How quick do they grow?
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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Causes of dental disease in rabbits?
Congenital Acquired - anorexia Trauma - fractured teeth/jaw
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Clinical signs of dental disease in rabbits?
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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Treatment for dental disease in rabbits?
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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Why are dental X-rays important in rabbits? How many views?
2/3 of tooth is within jaw | 5 views
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Dental anatomy of rabbits to be aware of when burring?
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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Dental anatomy of guinea pigs?
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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Dental anatomy of chinchillas?
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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Causes of oral/dental abscesses in rabbits? Treatment?
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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Risk factors for pododermatitis in rabbits? Treatment/prevention?
``` 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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Risk factors for barbering in rabbits?
Dominant conspecific | Insufficient dietary fibre
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What ectoparasites do rabbits get?
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)
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Treatment of fly strike in rabbits? Prevention?
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)
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What infectious skin diseases do rabbits get? Signs? Treatment?
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
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What calici viruses do rabbits get? Signs? Diagnosis?
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
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What is agent that causes the respiratory disease 'Snuffles'? Risk factors? Signs?
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
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Treatment of respiratory disease in rabbits?
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
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Causes of head tilts in rabbits? Diagnostics? Treatment?
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)
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Encephalitozoon cuniculi - what is it? Transmission? what can it cause? treatment?
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
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Encephalitozoon cuniculi - When is testing positive?
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
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Renal disease in rabbits - Age? Signs? Key diagnostic? Causes? Treatment?
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)
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How is calcium metabolism different in rabbits?
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
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What is urine sludge in rabbits? Signs? Treatment?
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
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What is urolithiasis in rabbits? Diagnostics? Treatment?
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
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What reproductive diseases are seen in rabbits? Signs etc?
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)
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Which rodents are hystricomorphs? What do they all have in common?
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
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Features of the GIT of hystricomorphs?
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
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What is typhlitis/typhilocolitis in hystricomorphs? Causes? What happens?
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
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Which protozoa affect hystricomorphs? Risk factors? Diagnosis? Treatment?
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
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Bloat in hystricomorphs - significance? Signs? What happens? Treatment?
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
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Bordetella bronchiseptica - which hystricomorph species is affected? Transmission? Risk factors? Diagnosis?
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
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Cavy adenovirus - what does it cause? Treatment?
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
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Cardiac diseases seen in hystricomorphs? Signs?
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
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Cardiac diagnostics for hystricomorphs? Treatment?
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?
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Ectoparasites of guinea pigs? Signs?
(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
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Pododermatitis in hystricomorphs - what is it? Risk factors? What can happen? Treatment?
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
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Risk factors for fur matting and barbering in hystricomorphs?
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
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What do fur slip and tail slip of hystricomorphs mean? Treatment?
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
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What are fur rings of hystricomorphs? Treatment?
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
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Ringworm in hystricomorphs - Which species? Signs? Which animals? Diagnosis? Treatment?
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
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Ovarian cysts in hystricomorphs - Signifcance? Types? Treatment?
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
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Reproductive diseases seen in hystricomorphs?
Ovarian cysts Pyometra Pregnancy toxaemia Uterine torsion
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Pregnancy toxaemia in hystricomorphs - Forms? Signs? Treatment?
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
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Signs of uterine torsion in hystricomorphs?
``` Acute pain Shock Lateral recumbency Dyspnoea Seizures ```
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Hypovitaminosis C (Scurvy) in Guinea Pigs - Why prone? Requirement? What happens? Treatment?
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.
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Urolithiasis in hystricomorphs - When seen? Signs? Treatment?
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
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Crystalluria/pain on urination in hystricomorphs? Signs? Treatment?
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
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Interstitial cystitis in hystricomorphs? Which species? Signs? What happens? Treatment?
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
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Common neoplasias seen in hystricomorphs?
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
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Hyperthyroidism in guinea pifs - Signs? Treatment?
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
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Diabetes mellitus in hystricomorphs - Which species? Signs? Treatment?
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
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Cloacal impaction in guinea pigs? When seen? Signs? Treatment?
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
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Cervical lymphadenitis in guinea pigs - cause?Treatment?
Streptococcus zooepidemicus causes caseous masses in intermandibular space Removal or marsupialisation is necessary
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Which species are myomorphs? What do they all have in common?
Rats, mice, hamsters, gerbils Much less specialised guts (except hamsters!) Omnivorous Incisors grow constantly, cheek teeth don’t
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How common is GI disease in myomorphs? Risk factors? Signs?
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
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What causes antibiotic associated enteritis?
C difficile – use of inappropriate antibiotic (PLACE antibiotics)
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What can cause wet tail in hamsters? Age affected? Treatment?
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
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Cheek pouch disease in hamsters - What is is? Causes? Diagnosis? Treatment?
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
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How do Strep pneumonia and Corynebacterium kutscheri affect myomorphs? Signs? Diagnosis? Treatment?
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
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What is the most common cause of chronic respiratory disease in rats? Risk factors? Signs?
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
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Treatment of chronic respiratory disease of myomorphs?
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
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Cilia associated respiratory bacillus in myomorphs? Significance? Transmission?
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
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What skin diseases/problems are seen in myomorphs?
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
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Skin diseases specific to hamsters?
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
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Which ectoparasites affect myomorphs? Significance?
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
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Which endoparasites affect myomorphs? Significance?
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)
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Reproductive diseases seen in myomorphs?
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
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Cystic ovaries in myomorphs? How common? Signs? Diagnosis? Treatment?
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
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Haematuria in myomorphs - Differentials?
``` 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 ```
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Mammary neoplasia in rats - How many mammary glands? Type of neoplasia? Which rats affected? Hormone involvement? Prevention? Treatment?
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
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Pituitary disease in rats? What is it? What happens? Treatment?
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
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Hanta virus in myomorphs - Type of virus? Significance? What does it cause?
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)
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Lymphocytic choriomeningitis virus (LCMV) in myomorphs - Type of virus? Transmission? Significance?
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
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Leptospirosis in myomorphs - signs? Spread? Significance?
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
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Chromodacryorrhoea in myomorphs - What is it? Diagnosis? Risk factors? Signs? Treatment?
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
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Features of ferrets GIT and diet requirements?
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
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Helicobacter mustelae - which ferrets affected? Transmission? Signs? Diagnosis? Treatment?
<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)
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What do coronaviruses cause in ferrets? Features? Signs? Treatment?
``` 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 ```
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What causes proliferative colitis in ferrets? Treatment?
Lawsonia intracellular Usually younger ferrets, proliferative bowel Chloramphenicol 14-21 days
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What age are ferrets with IBD?
>2yo
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What infectious GI diseases can ferrets get?
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
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When do ferrets normally moult?
Spring/summer
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What skin lesions can be seen with ferrets?
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
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What ectoparasites affect ferrets?
``` Sarcoptes scabiei Lynxacarus mustelae - facial fur mite, kits, immunosuppresion Demodex Otodectes cynotis Ticks, fleas, myiasis ```
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Oestrogen toxicity in jills - explanation? clinical signs? treatment?
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
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Adrenal gland disease in ferrets? Aetiology? What happens?
Aetiology - genetics, indoor housing/photoperiod, neutering On average 3.4 years post neutering Zona reticularis - elevated androgen hormones (hyperandrogegism) - androstenedione, 17ahydroxyprogesterone and oestrodiol
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What is the stimulus for ferret breeding season?
Stimulus is increasing day length Regulated by melatonin produced by pineal gland Longer days -> less melatonin -> GnRH production by hypothalamus
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Pathophysiology of why neutering ferrets can cause adrenal gland disease?
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
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Clinical signs of adrenal disease in ferrets?
Adrenal hyperplasia -> adenoma -> adenocarcinoma ``` Androgen stimulation Bilateral symmetrical alopecia - seasonal, cranially progressive Pruritus (25%) Behaviour change/aggression Vulval swelling - elevated oestradiol Gynaceomastia Prostateomegaly -> dysuria ```
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Diagnosis of adrenal disease in ferrets?
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?
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Treatment for adrenal disease in ferrets?
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
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Prevention of adrenal disease in ferrets?
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
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Options for managing entire males, preventing strong musky odour?
Castration Implant with suprelorin - lasts 4 years Neuter +/- implant at same time (re adrenal disease)
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Aetiology and signalment of inulinomas in ferrets? Clinical signs?
``` 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) ```
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Diagnosis and treatment of insulinomas in ferrets?
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
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Dilated cardiomyopathy in ferrets - what happens? Diagnosis? Treatment?
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
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Left ventricular hypertrophic cardiomyopathy and restrictive cardiomyopathy in ferrets? What happens? Treatment?
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
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Degenerative valvular heart disease in ferrets?
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
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Which endoparasites are significant in ferrets?
``` 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) ```
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Influenza in ferrets - type of virus? Signs? Treatment?
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
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Canine distemper in ferrets -Virus type? Transmission? phases? Clinical signs? Diagnosis? Treatment?
``` 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 ```
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Aleutian disease virus in ferrets - type of virus? age affected? Clinical signs? Diagnosis? Treatment? Vaccination?
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
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What are the most common neoplasia of ferrets?
1. insulinoma 2. adrenal gland disease 3. lymphoma
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Lymphoma in ferrets - forms? Clinical signs? Diagnosis?
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
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Causes of splenomegaly in ferrets?
``` Common finding Extra hepatic haematopoiesis Chronic inflammation Neoplasia Tranient splenomegaly by certain anaesthetic agents ```
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Licensed ectoparasiticides for ferrets? Endoparasite treatment?
Imidacloprid/Moxidectin Fipronil-S-methoprene Rarely get pathogenic burdens of endoparasites and routine treatment not warranted
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Why is dog food not appropriate for ferrets?
Very high in carbohydrates
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Anatomy of birds which differs to mammals?
``` 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 ```
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Hypocalcaemia of birds - Seen in which birds commonly? Signs? Causes? Diagnosis? Treatment?
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
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Hepatic lipidosis in birds - Cause? Risk factors? Clinical signs?
``` 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) ```
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Hepatic lipidosis in birds - Biochemistry findings? Diagnosis? Treatment?
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
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Diabetes mellitus in birds - Cause? Signs? Diagnosis? Treatment?
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.
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In which birds is thyroid disease common in? Association? Sign? Treatment
Budgerigars Associated with iodine deficiency - treat with iodine supplementation May have palpable goitre
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Diabetes insipidus in birds - When diagnosed?
Increased drinking where no other cause is found and where water deprivation testing does not result in concentration of urine
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Testicular tumours in birds - Which birds? Signs?
Budgies | See brown hypertrophy of cere and may see lameness in leg on same side (sciatic nerve impingement)
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Renal anatomy and physiology of birds?
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
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Renal failure in birds - Signs? Diagnosis? Treatment?
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
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Gout in birds - Causes? Why does it happen? Diagnosis? Treatment?
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
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Reproductive anatomy of birds?
Single ovary or testis - usually left Ovary -> infundibulum -> magnum -> isthmus -> uterus -> vagina Intromittant organ - ratites, anseriformes Non-intromittnet phallus - domestic fowl Neither - psittaciformes
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Egg yolk peritonitis/coelomitis in birds - Non infectious cause? Signs?
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
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Egg binding/dystocia in birds - Causes? Diagnosis? Risk factors? Treatment?
``` 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 ```
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How often do most birds lay an egg once laying?
One every 24-48h dependent on species
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Pre-ovulatory follicular stasis in birds - What happens? Signs? Differentials? Associations? Diagnosis? Treatment?
= 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)
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Chronic egg production/over production in birds - Which birds? What happens? Problems? Risk factors? Management?
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)
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Cloacal prolapse in birds - Causes? What must be determined? Treatment?
``` 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 ```
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What cardiac diseases are seen in birds? Signs? Diagnosis?
``` 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 ```
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Bird air sacs?
``` 2 cervical 1 interclavicular 2 cranial thoracic 2 caudal thoracic 2 abdominal ```
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Sinusitis in birds - Signs?
``` Facial/nares deformity Periocular swelling Oculonasal discharge Matted feathers around the face Dyspnoea ```
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Treatment for URT disease in birds? Diagnosis?
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
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LRT diseases in birds?
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
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Aspergillosis in birds? Method of transmission? Species more susceptible? Risk factors? When does it cause a problem? Signs? Diagnosis? Treatment?
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
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Teflon toxicity in birds (Polytetrafluoroethylene, PTFE)? How happens? Signs? Treatment? Prognosis?
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
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Neurological diseases in birds - Signs? Causes? Treatment to stabilise?
``` 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 ```
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What can conjunctivitis be associated with in birds?
``` Psittacosis Mycoplasmosis Irritants Excessive UV exposure Respiratory disease ```
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How can Hypovitaminosis A affect the eyes of birds?
Can cause squamous metaplasia of conjunctival tissue
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What can acute blindness in budgies be related to?
Pituitary neoplasia
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What to do immediately with bird trauma?
``` Control active bleeding Fluid therapy/transfusion Nutritional support Analgesia Care with handling - stress/flapping can worsen ```
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Problems with soft tissue wounds in birds?
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
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Key features of bird skeletons and fractures?
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
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Which diet can lead to hypovitaminosis A? Skin signs?
Seed diet without supplementation Hyperkeratosis Scaling
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Feather destructive behaviour (plucking) in birds? - Aetiology? Differentials?
Medical vs environmental vs psychogenic aetiology DDX Psittacine Beak and Feather Disease (PBFD) - Circovirus, polyoma virus, PDD Flock birds Boredom Sexual frustration Enrichment essential
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Diagnosis and treatment for feather destructive behaviour?
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
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Wing clipping, collars and limping of parrots?
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
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Mites in birds?
``` 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 ```
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Pododermatitis (Bumblefoot) in birds? Which birds? Causes? Treatment?
``` 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 ```
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Wing tip oedema in birds? What is it? When seen/which birds? Signs? Treatment?
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
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Uropygial (preen) gland disease in birds? Where is it? Which birds don't have? What can happen? Signs? Treatment?
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)
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Polyfolliculitis? Xanthomatosis? Feather cysts? Gout tophi?
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
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Disorders of the beak and bill in birds?
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
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Differentials of white plaques in the oral cavity of birds?
``` Trichomoniasis Candidiasis Capillariasis Diphtheritic pox Hypovitaminosis A ```
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What crop conditions of birds are there?
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
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What to do with crop conditions of birds?
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
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Causes of vomiting/regurgitation in birds?
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
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Causes of ileus in birds?
``` Foreign body Parasite burden Torsions Adhesions Strictures Neoplasia Extra-intestinal disease Papillomatous lesions PDD Peritonitis Heavy metal toxicity ```
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Causes of diarrhoea in birds?
``` Campylobacter Chlamydophila E.coli Pseudomonas Salmonella Many viral diseases Heavy metal toxicity Dietary change Stress Anorexia Septicaemia ```
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What does Avian Gastric Yeast cause? Species? Risk factors?
Macrorhabdus ornithogaster, Megabacteriosis Progressive wasting in budgies Difficult to treat Associated with stress and overcrowding
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Heavy metal toxicities in birds - Which metals? How? Organs affected? Signs? Treatment?
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
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Normal bacterial flora of birds?
Lactobacillus Corynebacterium Non-haemolytic Streptococci Staphylococcus epidermidis
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Common bacterial pathogens of birds?
``` 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 ```
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Psittacosis in birds - Agent? Features of agent? Risk factors? Presentation? Clinical signs? Spread? Diagnosis? Treatment?
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
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Mycobacteriosis in birds - Agent? Transmission? Clinical signs? Diagnosis? Treatment?
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
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Mycoplasmosis in birds? Agent? Problems caused? Spread?
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
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Signs of salmonella in birds?
``` Diarrhoea Multisystemic disease Septicaemia Osteomyelitis Dehydration Lethargy Ileus ```
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Botulism in birds - Agent? Which birds? Signs? Treatment?
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
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Features of Avian Influenza?
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
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Proventricular Dilation Disease in birds? Agent? What happens? Differentials? Species? Signs? Diagnosis? Treatment?
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
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Psittacine beak and feather disease virus (PBFD)? - Agent? What does it cause? Spread? Species affected? Signs? Diagnosis? Treatment?
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
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Polyoma virus in birds? Agent? Which birds affected? Signs?
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
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Viscerotropic velogenic Newcastle Disease of birds? Type of virus? Transmission? Signs? Treatment?
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
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Psittacid Herpes Virus 1 in birds? Signs? Appearance? Associations? Diagnosis?
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
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Neoplasia in birds? Factors associated? Diagnosis? Treatment?
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
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Anorexia in birds - consequences?
``` Dehydration Loss of muscle mass Nutritional deficiencies Crop/GI stasis Weakness Anaemia ```
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Factors leading to aggression in birds?
Pain Systemic disease Poor sight Normal hormonal activity Neurological disease Frustration from inappropriate pair-bonding with human Inadvertant positive reinforcement of aggressive behaviours
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What is star gazing in snakes? Cause? Diagnostics needed?
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
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Causes of loss of righting reflexes of snakes (unable to right itself when placed in dorsal recumbency)?
Suggests discontinuity of spinal cord's ability yo transmit neural impulses or an inability of the muscles to respond Trauma, spinal osteoarthropathy, spinal mycobacteriosis
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Signs of weakness on clinical exam of snake?
Unable to raise head | Unable to constrict when stimulated
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Causes of thyroid disease in snakes? Signs?
``` 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 ```
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How often do normal snakes shed?
4-6 times a year (dependent on age)
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Dysecdysis in snakes - What is it? Causes?
``` = 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 ```
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What to do if dysecdysis of snake?
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
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Retained spectacles in snakes - Appearance? Why problem? Treatment?
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
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Thermal burns of snakes - Why happens? How happens? Signs? Treatment?
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
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Blister disease in snakes - What is it? Appearance? Cause? Diagnosis and treatment?
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
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Mites in snakes
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
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Stomatitis in snakes - When seen? Signs? Risk factors? Diagnosis? Treatment?
‘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
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Anorexia in snakes - Causes?
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
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Regurgitation in snakes - Causes? Other associated signs? Treatment?
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
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Cryptosporidia in snakes - Agent? Signs? Transmission? Diagnosis Treatment?
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
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Entamoebiasis in snakes? Species? Risk factors? Signs? Diagnosis? Treatment?
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
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Causes of respiratory disease in snakes?
``` 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 ```
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Signs of respiratory disease in snakes? Diagnosis? Treatment?
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
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Paraphimosis in snakes - What is it? Which animals? Risk factors? Consequences? Treatment?
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
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Inclusion body disease in snakes - Which species? Cause? Signs? Diagnosis? Treatment?
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
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Paramyxovirus in snakes? Common in which snakes? Transmission? Risk factors? Signs? Diagnosis? Treatment?
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
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Sunshine virus in snakes?
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
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Reovirus in snakes?
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
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Proliferative spinal osteoarthropathy in snakes? What is it? Which species? Risk factors? Signs? Cause? Diagnosis? Treatment?
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
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Salmonella in snakes - Type of organism? When infected? Treatment? Prevention?
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
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Unusual anatomy of lizards?
``` No diaphragm No loop of henle Internal gonads Hemipenes No urinary bladder ```
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What glands do lizards have?
Scent glands in vent (squamates) Prefemoral glands/pores (geckos, bearded dragons, iguanas) Temporal glands (Chameleons) Salt glands in nares (marine iguanas, turtles)
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Phases of ecdysis in lizards? What is it regulated by?
Renewal phase - fragile skin, dull skin, behaviour changes Resting phase - between ecdysis Regulated by temperature, humidity and thyroid hormone
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How do reptiles differ in ecdysis?
Snakes - in toto shed | Lizards and chelonia - flakes
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Dysecdysis in lizards? What can happen? Causes? Treatment?
``` 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? ```
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Skin diseases of lizards?
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)
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CAN-V in lizards? What does it cause? Animals affected? Risk factors? Spread? Signs? Diagnosis? Prevention? Treatment? Prognosis?
= 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
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Dentition of chameleons, bearded dragons, water dragons?
Acrodont = non rooted and directly attached to underlying bone Weak attachment, easily lost and not replaced
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Dentition of iguanas, geckos, monitors?
Pleurodont = regularly shed and replaced | Periodontal disease rare
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Risk factors for periodontal disease of acrodont dentition lizards? Clinical signs? Treatment?
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
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Significance of nematodes in lizards?
Some (Oxyurids in particular) thought be beneficial and a natural part of multi biota so low burdens shouldn't be treated
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Licensed treatment for Coccidiosis in bearded dragons?
Sulfatrim
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Metabolic bone disease (nutritional secondary hyperparathyroidism) in lizards? Causes? What happens? Clinical signs? Other metabolic bone disease causes?
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)
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Treatment of hypocalcaemia in the acute and chronic phases of lizards?
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
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Substrate impactions in lizards - aetiology? clinical signs? diagnosis? treatment?
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
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Pre-ovulatory follicular stasis in lizards? What happens? Treatment? Clinical signs? Diagnosis?
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