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VMS 4001 > Camelid Medicine > Flashcards

Camelid Medicine Flashcards

1
Q

How do we BCS a camelid?

A
  • Hands-on!!
  • Ribs -> fat coverage
  • Lumbar area - coverage
  • Rear end -> cover over top of leg and abdo contour of animal from behind
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2
Q

Where do we place catheters in them?

A

Jugular and carotid very close!!
Always check jugular blood before injecting
Right hand side the two vessels are slightly further apart
ALWAYS place needle downards

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3
Q

Where do we sample blood ?

A
  • Jugular- right upper/lower
  • Cephalic in young animals
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4
Q

Details on blood sampling ?

A
  • Challenging as the jugular cannot
    usually be seen or palpated
  • Palpated vertebrae 6/7 laterally
    and palpate the trachea medially=
    insert needle ‘blind’
  • RHS- vein is further from artery
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5
Q

IM injectiion?

A

not much muscle!
* Quadreceps
* Semitendonous- risk of damage to
siatic nerve

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6
Q

SC injection?

A
  • in front of shoulder
  • Dorsal surface of scapula
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7
Q

Describe stomach tubing camelids?

A
  • Gag required to stop chewing the food
  • Wooden gag
  • Tube put over the back of dorsal
    tongue and get alpaca to swallow
  • Nasopharyngeal tubing=high risk of
    epistaxis
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8
Q

Microchipping ?

A
  • Commonly performed by the vet
  • Not food producing animals in UK so can be microchipped for identity
  • Left dorsal neck- 3-4
    th vertebrae
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9
Q

Teeth trimming?

A
  • Common procedure
  • May be required secondary to
    malocculsion
  • Embryotomy wire
  • Very good restraint
  • Annual basis in problem animals
  • No anaesthesia
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10
Q

Claw Clipping ?

A
  • Over grown feet common
  • Used to being worn down but hard rocky
    surfaces V’s soft footing in UK
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11
Q

Abdominocentesis in camelids?

A
  • Ventral midline approach
  • A lot of intraperitoneal fat
  • 90 degrees into abdomen to avoid going into fat
  • Right body wall approach
  • Unlikely to yield fluid sample unless significant abdominal
    fluid present
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12
Q

Liver biospy ?

A
  • Right side approach
  • 9
    th intercostal space
  • 15-20cm from dorsal midline
  • Aim needle ventro-medially (opposite elbow)
  • Tru-cut biospy
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13
Q

How much do camelids eat?

A
  • Adults consume 1.5% of body weight as dry matter daily.
  • Adults approx. 70Kg weight = 1kg dry matter!
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14
Q

How much dry matter in grass vs hay?

A

Grass = 20% dry matter = 5kg of grass to eat enough dry
matter/day
* Hay = 90% dry matter = 1.2 kg/day

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15
Q

Pasture for nutrition?

A
  • Pasture will supply more energy, protein and fibre needs for
    maintenance
  • Additional: growth, pregnancy, lactation may need
    supplementation
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16
Q

WHAT SUPPLEMENTATION IS KEY?

A

VIT D

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17
Q

Are any drugs licensed in camelids?

A

nop

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18
Q

NSAID?

A

Equine dose- Meloxicam/Flunixin/Ketaprofen

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19
Q

POUR -ONs?

A
  • Not well absorbed. Avermectins do not get absorbed in sufficient quantities. Injectable avermectins at 1/5x times dose
    for cattle
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20
Q

Oral anthelmintics ?

A

Unreliable
* Avermectins unreliable absorption but suggests using 1.5x times
cattle dose
* Oral Levamisoles are recommended against due to small
therapeutic doses- could be toxic

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21
Q

IV fluids?

A

Care with overloading. Accurate weights and rates important!

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22
Q

How many offsprings / year and how long is pregnancy?

A
  • 1 Cria/year
  • Pregnancy is 345 days. 11.5 months
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23
Q

When are females mated?

A

3 weeks post-calving

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24
Q

Cria weaning?

A

6months

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25
Q

What horn do 90% of pregnancies happen in ?

A

LEFT horn

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26
Q

MAting length?

A
  • Prolonged mating period 20-25 minutes
  • Male orgling
  • Cush position
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27
Q

What kind of ovulators are they?

A
  • Induced ovulators
  • Ovulation occurs 24 hours post mating
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28
Q

What reproductive problems are common in camelids?

A
  • Unable to conceive following multiple
    mating’s
  • Continuously rejecting the male
  • Abortions
  • Visible abnormalities of the external genitalia
  • Lots of congenital/inherited genetic problems
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29
Q

How can we induce ovulation ?

A
  • Mating but no pregnancy- possibly repeat
    breeder- no spit off even day 7
  • hCG
  • GnRH
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30
Q

What to do for Persistent CL/induction of abortion?

A
  • Constant spitting off despite negative U/S
  • 2 doses Cloprostensol 24 hour interval
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31
Q

Inducing parturition?

A

Prostaglandin + glucocorticoids

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32
Q

Dilation of cervix?

A

Oestrodoil - dilation 24 hrs later

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33
Q

Pregnancy diagnosis?

A
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34
Q

Describe parturition?

A
  • Anterior presentation
  • Cria can hang from mother for 10-15minutesnormal stage of partuirition
  • Dam wont lick cria or remove membranes
  • Cria sat up Kush withing 10-15 minutes of birth
  • Suckle within 1 hour
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35
Q

Timings of each stage of parturition?

A
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36
Q

Describe Dystocia in CamelidS?

A
  • Hygiene
  • Same approaches as ruminants
  • Gentle
  • Less room available in pelvis
  • Manipulation generally easy and successful
  • Caesarean section can be indicated
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37
Q

What postpartum issues?

A
  • Mastitis is rare
  • Retained membranes are rare but can be serious if untreated.
  • Hypocalcaemia rare
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38
Q

What basic neonatal knowledge?

A
  • 6-8 Kg at birth
  • Dress naval with iodine after
    birth
  • Hypothermia and Hypoglycaemia
    soon after birth common
  • Born May/June/July
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39
Q

What neonatal issues can we see?

A

Prematurity
Teeth not erupted
Floppy ears
Unable to stand or hold head up
Low birth weight
Down on pasterns

40
Q

What immunity at birth?

A

Cria born with no immunity!

41
Q

Failure of passive transfer?

A

Routine monitoring
* Or sample some at risk cria
* Total Protein (TP) used to obtain a crude way to assess passive transfer

42
Q

Failur eof passive tansfer - what values of TP?

A
43
Q

How much colostrum in first 12hrs ?

A

10%

44
Q

Tx for failure fo passive transfer?

A

Plasma transfusion 300ml IV
Plasma provided by another adult from the herd
Can be given IV, Stomach tube ?? or Intraperitoneal

45
Q

Plasma transfusion - how to do it?

A
  • Take whole blood
  • Centrifuge blood
  • Decant plasma- syringes or into fluid
    giving bag
  • Can freeze and thaw with care@
46
Q

What donors for plasma transfusion?

A
  • Donor animals- well condition
    animals doing no ‘work’ usually
    wethers
47
Q

HOW MUCH BLOOD?

A

t 0.5-1 L blood

48
Q

What common neonatal conditions?

A
  • Congenital defects
    Choanal atresia
    Umbilical hernias
    Cleft palate
    Atresia ani
    Musculoskeletal defects
    Wry face
  • Umbilical infections
  • Joint ill
  • Septicaemia/meningitis (secondary to FPT)
  • Hypothermia/hypoglycaemia
  • Diarrhoea
49
Q

What common medical problems in camelids?

A
  • Vitamin D deficiency
  • Ectoparasites/parasitic skin disease
  • Endoparasites
  • Tooth root abscesses/Osteomyelitis of the jaw
  • Mycoplasma
  • Bovine TB
50
Q

Who is more suceptibel to Vit D/ Hyophosphspatemic Rickets

A
  • Cria born in late summer/early autumn
  • But all cria are susceptible
  • Dark coated animals
51
Q

CLS of Vit D def?

A
  • Shifting leg lameness
  • swollen joints
  • angular limb deformities
  • reluctance to move
  • ill thrift
  • poor weight gain
52
Q

Diagnosis of Vit D def?

A
  • History and presentation
  • Low blood phosphorus/Vitamin D
  • Xray- bone density/growth plates
53
Q

Tx/Prevention Vit D def?

A
  • Vitamin D supplementation
  • CARE: toxicity
  • Routine administration of Vitamin D
    done regularly now
  • Every 3 months for growing Cria
  • Twice annually for breeding
    females
  • Surgical correction?
54
Q

What Parasitic skin dx can they get?

A
  • Sarcoptic mange
  • Chorioptic mange
  • Psoroptic mange
55
Q

What do we often see?

A
  • Often see a combination of one or more of these mites in one infestation
  • Seen on head, nose, ears, feet and legs and under armpits, perineum and inguinal areas
  • Secondary bacterial infection with significant crusting of skin seen.
56
Q

What signs of parasitic skin dx?

A

Hair loss, erythema, pruritis, scaling and
crusting

57
Q

Diagnosis of Parasitc skin dx?

A
  • Different areas affected/patterns of disease with each mite
  • Difficult to diagnose from this alone
  • Deep skin scrapes
58
Q

Tx of parasitic skin dx?

A

First line:
* Injectable avermectins q7-14 days
* Repeated injections
* Topical therapies
* Pour-on?
* Pasture management
* Fipronil?!!
* Treat whole herd?

59
Q

What other skin conditions fo they get?

A
  • Zinc-responsive dermatitis
  • ‘Munge”
  • Orf
60
Q

Zinc-responsive dermatitis - describe?

A
  • Alopecia, scales, thick crusts, hyperkeratosis
  • DDx Parasitic skin disease
  • Improves with Zn treatment
  • Suspect over-diagnosed?
61
Q

describe ‘munge’

A
  • Idiopathic nasal/perioral hyperkeratotic dermatosis
  • Secondary infection
  • Painful
  • DDx parasitic skin disease
62
Q

What endoparasites are they prone to?

A

Susceptible to nematodes, cestodes, trematodes of sheep, cattle and goats including live
fluke.
* Remain susceptible throughout lifetime
* Routine FEC

63
Q

What effect of communal dung?

A

limits larvae spread onto pasture if no co-grazing
* Increased larvae when co-grazing with other species

64
Q

CLS of endoPs?

A

Weight loss, diarrhoea, poor growth, ill thrift

65
Q

Dx of endoPs?

A

Faecal float

66
Q

what can haemonchus cause?

A

severe anaemia in alpacas
* Usually not causing diarrhoea
* PCV <10%

67
Q

what faecal egg test ?

A

McMasters may not be
sensitive enough for camelids
Modified Stolls Test= sensitive
to 5 epg

68
Q

Control of endoparasites?

A
  • Oral ivermectin anthelmintics ineffective.
  • Injectable ivermectins are effective and first line.
  • Levamisoles low toxic dose in camelids
  • Fenbendazole largely ineffective due to resistance
  • Pasture rotation/management
  • Avoid co-grazing with other ruminants
  • Regular FECs
69
Q

Which coccidia are camelids prone to?

A

Small coccidia
E Punoensis
E alpacae
A lamae
* Large coccidia
E macusaniensis (tear shaped oocyst)
“E.mac”
E ivitaensis

70
Q

Disease from small coccidia?

A
  • Small coccidia causes disease in younger
    alpacas with higher counts seen
  • Counts > 200epg unusual/clinically relevant
71
Q

What do we see with ‘EMac’

A
  • Any age affected
  • Cause of death within 2-3 weeks
  • COlicn WL, ill thirft, tenesmus, D+
  • All ages affected
72
Q

Dx & Tx of ‘EMac’?

A

Dx- clinical signs/ faecal float?
TMPS
Toltrazil (Baycox)

73
Q

Describe tooth rot abscess?

A
  • Common in camelids
  • Mostly cheek teeth affected
  • Food particles penetrating into the periodontal ligament
  • Usually associated with eruption of the permanent molars (age 4)
  • Actinomyces spp- gram positive, facultative anaerobe
  • Ecoli- gram negative facultative anaerobe
  • Bone involvement
74
Q

CLS tooth rot abscess?

A
  • Swelling along mandible
  • Salivation
  • Weight loss
  • Pain on Palpation
  • Ocular discharge
75
Q

Medical dx of rooth abscess?

A
  • Long term antibiotics
  • 6-8 weeks
  • 50% success??
  • Most tolerated drugs?
  • Analgesia- NSAIDs
76
Q

Surgical tx of tooth rot abscess?

A
  • Tooth extraction
  • Tooth splitting
  • Tooth root resection
  • Referral surgery options
  • Lateral alveolar plate resection
77
Q

What strain of Mycoplasma causes dx?

A

Mycoplasma haemolamae

78
Q

Describe Mycoplasma haemolamae?

A
  • Parasite in erythrocytes
  • Transmitted through arthropod vectors/lice/ticks
  • Opportunistic pathogen? Comorbities?
79
Q

CLS of Mycoplasma?

A
  • Lethargy, anaemia, recumbent, weight loss, death, all ages affected
  • Subclinical
80
Q

Diagnosis of Mycoplasma?

A
  • Clinical suspicion
  • Blood smear & stain- evidence of parasite
  • Blood smears made on farm- organisms drop off
  • Small numbers found in clinically normal animals
81
Q

Tx fo mycoplasma?

A
  • Oxytetracyclines + supportive therapy- blood transfusion?
  • Chronic carriers after resolution of clinical signs?
82
Q

What signs on smear?

A

Mild- severe regen or non regen anaemia

83
Q

Which stomach gets gastric ulcers? why?

A

C3-> * Stress- hospitalisation, kept alone, weather, otherwise unwell

84
Q

CLS of Gastric ulcer?

A

Teeth grinding
Salivation
Inappetence
colic/laying down a lot
Melena
Full thickness= rupture, acute abdominal pain peritoneal contamination,
peritonitis and death

85
Q

Dx Gastric ulcer?

A

Ultrasound shows thickening and oedema of C3 mucosa

86
Q

Tx of Gastric ulcer?

A

Drugs in other species don’t work well- oral omeprazole doesn’t alter pH so
not effective
Sulcrafate
Pantoprazole (proton pump inhibitor)
Ranitidine (H2-receptor antagonists

87
Q

Describe Hepatic lipidosis?

A
  • Fatty Liver
  • Mostly associated with negative energy
    balance
  • Fat deposits mobilised and transported
    to liver
  • Excessive accumulation of triglycerides
    in hepatocytes
88
Q

Who does hepatic lipidosis affect?

A
  • Males and females
  • May be pregnant or lactating
  • Not always in fat animals
89
Q

Diagnosis of Fatty liver?

A
  • Biochemistry, liver biopsy
  • Liver insufficiency
  • Coagulopathy
  • Elevated liver enzymes-AST and bile
    acids
90
Q

Tx & Pg?

A
  • Heptatic support- fluids, glucose
  • B vitamins
  • Increased energy diet- pregnancy

poor pg

91
Q

CLS of fatty liver?

A

Lethargy
Depression
Ataxia
Recumbency
Abortion
Anorexia

92
Q

Which clostridial diseases are they prone to?

A

Susceptible to Clostridium
perfringens C & D
* Well recognised in camelids

93
Q

Vaccination against clostridial dx?

A
  • Early vaccination from 6 weeks+
  • Twice annual vaccine
  • Poorer immune response
    compared to other species so
    need repeat dose more regularly
94
Q

What do each strain of clostridia cause?

A

Clostridum perfringens type Centeritis and enterotoxaemia

Clostridium Perfringens type DEnterotoxaemia/neurological
disease

95
Q

Describe TB in Camelids?

A

Bovine TB
* Lungs, lymph nodes, udder etc
* High incidence of TB in cattle= more likely in alpacas

96
Q

CLS of TB?

A
  • Often subclinical
  • Exercise intolerance, chronic persistent coughing, respiratory signs, anorexia, weight loss,
    weakness, lethargy
97
Q

Dx TB?

A
  • Intradermal test
  • Blood test- Enferplex
  • Not routinely done in UK like cattle
  • Need to be an OV for this and get prior authorisation from APHA
  • Like cattle: Tests aren’t 100 sensitive: False negatives

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