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Small ruminants II > Camelids > Flashcards

Camelids Flashcards

1
Q

Species of camelids

A

Llama, Alpaca, Guano, Vicuna

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2
Q

Differences between llamas and alpacas

A

Size: alpacas smaller

Ears: alpacas have spear shaped ears, curved on both borders; llamas have banana shaped ears, curved inwards

Fleece distribution: alpacas covering body and legs, llama legs have short hair

Teeth: alpaca teeth grow continuously, llama teeth do not grow continuously

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3
Q

Breeds of alpaca

A

Huacaya (commonest, fluffy)

Suri (dread lock fleece)

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4
Q

Breeds of llama

A

Two main categories:
- Ccara (larger, very common in UK)
- Tampuli (smaller and more heavily wooled)

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5
Q

Useful terminology of camelids
- Intact male
- Intact female
- Castrated male
- Young/unweaned
- Weaned
- Act of giving birth
- Haircoat
- Sternal recumbency
- To force sitting

A

Intact male = male, stud, macho

Intact female = female, hembra

Castrated male = gelding

Young/unweaned = Cria

Weaned = juvenile

Act of giving birth = unpacking/creating

Haircoat = fibre, hair, fleece (not wool)

Sternal recumbency = cush

To force sitting = chukkering

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6
Q

Nutrition of camelids

A

Forages main part of diet

Concentrates/beet pulps during periods of high energy demand

Forestomach fermenters

Most in Northern Hemisphere are over conditioned

Ideal BCS: straight lumbar line dorsal to transverse process, can feel ribs with slight pressure, can just see belly through thighs

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7
Q

Routine husbandry of camelids

A

BCS

Teeth

Eyes: FAMACHA

Timings of: shearing, foot trimming, vaccination, deworming, mating

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8
Q

Peculiarities of camelid head

A

Thin lips, used for prehension and sorting

Normally split at upper lip (cleft)

Have an upper dental pad, with no incisors, but lower incisors

Fighting teeth in both genders

Tongue does not protrude (do not lick, even their crias!)

Short nasal bone

Long nasal cartilage (this has some handling consequences: need to place the halter as close as possible to the eyes to avoid compression of this cartilage and suffocation)

Obligated nasal breathers

Choanae = opening between nasal cavity and nasopharynx; congenital atresia occurs leading to dyspnoea

Blue eye colour in white animal often linked to deafness

Late eruption of PM and M teeth has some disease consequences: tooth root abscesses quite common in camelids between 3-5 year of age

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9
Q

Peculiarities of cervical area in camelids

A

Long neck

Bilateral jugulars and carotid

Carotid very close to jugular in distal end of neck

Left sided oesophagus and long laryngeal recurrent nerve

Blood sampling should be (except exceptions) performed from right hand side of the neck

Higher location (C2-C3): for administration of injections and catheterisation

Lower location (C5-C6): only sampling (higher risk of intracarotid injections).

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10
Q

Peculiarities of thoracic area in camelids

A

Twelve pairs of ribs; complete mediastinum (watch fast fluid therapy)

Camelid cud like other ruminants utilising a “figure-of-8” arc during chewing, lasting approx. 15 secs (25-30 fast chews) which may repeat

Oesophagus: mostly skeletal muscle with an opposite distribution compared to ruminants (likely due to the force needed to bring up cud in a long neck): inner longitudinal and an outer circular muscle layer

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11
Q

Peculiarities of abdominal area in camelids

A

Stomachs
-Three stomachs = Compartments 1, 2 and 3;
-C1: largest (15-25 litres in llama, pH 6.6), similar to rumen but more secretory (bicarbonate) and higher efficiency of absorption of volatile fatty acids
-C2: (1-2 litres)
-C3: true stomach
- Oesophageal groove - cardia to C3 in Crias
- C1 and 2 have folds of simple columnar epithelial cells with secretory granules in saccular region and stratified squamous epithelium in non-saccular areas
- C3 mostly covered by glandular epithelium organised in logitudinal folds
- Ulcers occur more frequently in the gastric area of the C3 (mostly) as well as the saccular mucosa and septal area
- Cellular morphology suggests both absorptive and secretory capacity.

Small and large intestines
- Small and large intestine similar to ruminants
- Duodenal ampulla convoluted and small diameter (this area can be place of obstructions)
- Double-helix spiral colon, very narrow allows passage of single pellets (this area can be place of obstructions)
- Spleen smooth like sheep
- Liver:
○ No gall bladder like horses
○ Dorsal hepatic fringes- normal!-

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12
Q

Musculoskeletal system in camelids

A
  • Metatarsal glands on inside of hind legs
    • Interdigital glands on all four feet
    • Walk on leathery pads (P2/P3); non-weightbearing ‘toe-nail’ with continuous growth
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13
Q

Male reproductive system in male camelids

A

Puberty in males: sperm present from 11 months-old, but usually not used for breeding until 2-3 years old.

Cria born with Cameliutial adhesion, which need testosterone for release: full release occurs at 3 years.

Testicles: non pendulous scrotum, located in the cauda perineum Normal scrotal size:. Llama - 4 cm long x 3.5 cm wide; alpaca - 3.5 cm long x 2.5 cm wide

Penis: fibroelastic, small hooklike curve at the tip, sigmoid flexure present and prescrotally

Prepuce 15 cm caudal to navel and oriented caudally (male camelid pee with stream of urine directed caudally

Camelids don’t store semen, i.e. avoid more than 2 serves/ day

Semen has nerve growth factor which stimulates ovulation

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14
Q

Castration of camelids

A

Do not castrate before 18 months old - risk of poor musculo-skeletal development.

Either standing under local infiltration +/- sedation depending on temperament (like piglet/calf), or under sedation in dorsal recumbency (like dog) or lateral recumbency (like colt).

Ligation recommended; some vets twist and pull

Prophylactic antibiotics not always necessary, consider tetanus risk, consider NSAIDs.

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15
Q

Reproductive system in female camelids

A

Puberty in females: 6 months of age, but do not breed until 12 months old; weighing at least 40 kg for alpacas / 60 kg for llamas (60-65% of adult weight)

As in the cow but not the mare, ovarian follicles are arranged in a peripheral cortex, and ovulation can take place at any spot on the surface of the ovary

Pregnancy rate about 70% in yearlings.

Ovulation is induced by penile introduction leading to LH surge and activity of Nerve growth factor contained in semen, no oestrus cycle

Non-seasonal, but breeding usually occurs in spring/summer time for parturitions the following spring

Repetitive follicular waves occur in absence of copulation with recruitment of a cohort of follicles, one of which will become dominant followed by regression if not ovulated

Prior to the final regression of the dominant follicle another overlapping follicular wave occurs producing the coexistence of regressing and growing follicles over several days

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16
Q

Mating and gestation in camelids

A

Average mating time 25 minutes, female usually in sternal recumbency

95% of pregnancies in left horn

Gestation length 345 +/- 30 days;

Diffuse epithelio-chorial placenta (like mare; retained membranes uncommon – but they are an emergency!-treat like mare)

No passage of antibodies through placenta so colostrum fundamental

Entire gestation corpus-luteum dependent

Twin conception occurs (8-10%), but twins are very rarely carried to term

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17
Q

Pregnancy diagnosis in camelids

A

Several methods: female ‘spitting off’ male at 12-14 days after service (about 70% accurate)

rectal ultrasound (with introducer) from 30 day (need a max size 6 glove size!, risk of rectal tears)

rectal palpation from 45 days (need a max size 6 glove size!)

trans-abdominal ultrasound from 35-40 days

high progesterone 15-20 days post-mating suggestive

Some reabsorption occurs between 30- 60 days so better to repeat after day 60

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18
Q

Birth of camelids (unpacking)

A

Usually occurs in daylight, before 2pm

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19
Q

Udders of camelids

A

4 quarter with 4 teats

each quarter has two glands and to openings in teat

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20
Q

Crias

A

Reasonable survival in cria >320 days with intensive care; <310 days = survival unlikely

Births weights: Llama 10-15 kg; Alpaca 5.5-9.5 kg

Colostrum: 8-10% of BW within 6 hours, total of 20% of BW over 24 hours

Colostrum substitutes: goat first then cow

Plasma transfusion common at 48hrs of life if no or incomplete passive transfer suspected

Weight gain:200-400 gr/day

Neonatal growth: Alpaca cria should double birth-weight in first month of life, then gain about 5 kg per month in months 2-4

Milk substitute: Special camelid colostrum and milk replacer now available. Otherwise, goat’s milk best, followed by ewe’s milk then cow. Beware risk of disease transmission (e.g. Johne’s). 10-15% of BW daily.

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21
Q

Vital signs of camelids

A

C1 contractions: 1.5-3x/minute, irregular intervals, left dorsal and lower ventral abdominal area

HR: 60-90 bpm
§ Second degree AV block frequent, resolves with increased heart rate

RR: 10-30 bpm

T: 37.5 – 39.2 C

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22
Q

Locations of drug administrations in camelids

A

IV: jugular and see above. Ideally first third of neck (level of C2-C3)

I/M: like horse, Triangle in front of shoulder; quadriceps or semitendinosus/membranosus

S/C: triangle just caudal to axilla, behind elbow; in front of shoulder - dorsal to cervical spine, about 3 cm from ridge of neck; thoracic area. Do not have a lot of skin ‘give’

Microchip: LEFT DORSAL NECK (3rd-4th vertebra), angle no steeper than 45° to minimise risk of traumatising spine (also do not insert needle fully in youngsters) or left ear cartilage

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23
Q

Common diseases of digestive system in camelids

A

Facial masses

Regurgitation

Diarrhoea

Colic

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24
Q

Common diseases causing weight loss in camelids

A

Parasites

Nutrition

Overgrown teeth (poor prehension)

Lymphoma/lymphosarcoma

Chronic disease, peritonitis, ulcers

TB

Johne’s

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25
Q

Diseases of the integumentary system in camelids

A

Mange

Munge

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26
Q

Common diseases of the musculoskeletal system of camelids

A

Rickets (hypovitaminosis D)

Osteomyelitis

Septic arthritis

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27
Q

Common diseases of the immune system of camelids

A

Anaemia

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28
Q

Common neurological diseases in camelids

A

Polioencephalomalacia

Bacterial meningitis

Listeriosis

Otitis

Cervical luxation/fracture

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29
Q

Common reproductive diseases of camelids

A

Dystocia

Prolapses

Torsion

Retained placenta

Congential abnormalities

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30
Q

Common neonatal diseases in camelids

A

Congenital abnormalities

Umbilical hernias

FPT

Neonatal septicaemia

Metabolic disturbances

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31
Q

Causes of facial masses in camelids (most to least common)

A

§ Jaw/tooth root abscesses
§ Food impaction
§ Lymphoma
§ Sialocele/mucocele
§ Cysts
§ Bone tumours
§ Facial fractures
§ Submandibular oedema (not common)

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32
Q

Jaw/tooth root abscesses in camelids

A

Common around 5 years

Likely secondary to food particles embedding in alveoli in association with exposed pulp cavities/ changing dentition.

More common in mandible> maxilla and molars>premolars>incisors.

Molars and premolars are changed between 3-5 years.

Most common anaerobic bacteria spp like Actinobacillus, Fusobacterium, Bacterioides, Trueperella.

Osteomyelitis (lumpy jaw) usually present around tooth affected; can also be isolated and only on jaw without teeth involvement (2% cases) but suspected to have haematogenous origin.

Facial bones palpation is fundamental to perceive swellings. In some cases tooth root/jaw osteomyelitis presents with draining abscesses on the facial surface.

X-rays or CT scan recommended for further diagnostics.

Treatment:
§ Surgical lump incision and drainage
§ Frequent lavage of area with diluted iodine
§ Aggressive antibiosis (daily for 3 weeks, Penicillin or florfenicol necessary and effective ONLY in early stages.
§ Chronic cases may need surgical curettage of osteomyelitic bone as well as tooth removal. Early detection is key to allow for improved outcome.
§ Severe cases
§ Surgery: Tooth extraction plus bone curettage

33
Q

Food impaction in camelids

A

Lateral masses (accumulation of food fibre) that disappear when palpated.

Usually derived from poor mastication (need to look at dentition, incisors and molars/premolars) and gaps in dentition (lost teeth).

Molar and premolar very rarely need rasping, but if a decision is made to do so this needs to be done carefully because of very thin dentin layer (2-3 mm).

34
Q

Lymphoma and lymphosarcoma in camelids

A

Affects relatively young animals (~3YO alpacas/8YO llamas).

The main locations are respiratory tract (50% cases); Cardiac (25-40%); Intestinal; Gastric; Spinal.

Malignant round cell tumours or B cell lymph more common.

Alpacas more common than llamas

Non-specific clinical signs of
1) lymphadenopathy
2) weight loss altered- frequent. Accompanied by change in behaviour, dyspnoea/diarrhoea, increased recumbency and anorexia.

Note: Lymphnodes usually not readily palpable in older camelids!!

DDX:
§ Other causes of generalized lymphadenopathy: infectious lymphadenitis, TB, CLA
§ Submandibular swelling: mandibular osteomyelitis, actinobacillosis, tooth root abscesses, or right heart failure.
§ Persistent weight loss include poor nutrition, poor dentition, parasitism, Johne’s disease, and chronic inflammatory bowel disease.

Treatment is usually palliative (steroids) until euthanasia is performed. Limited chemotherapy has been attempted in research but poor outcome.

Prognosis is poor, 100 days survival when severe signs are present

35
Q

Fatty liver in camelids

A
  • Treat primary cause
    • Animals can be very sick
    • Appetite stimulant (vit B12/vit B1)
    • Propylene glycol or glycerol
      ○ 60ml once a day
    • IV fluids (added of GLUCOSE)
    • Improving feed intake, more concentrates
    • Referral should be considered
    • Insulin
36
Q

TB in camelids

A
  • Incidental spill over hosts to M. Bovis
    • Contamination from cattle and badgers
    • Human risks due to spitting behaviour
    • Difficult to diagnose based on examination only
      ○ Consider it if chronic loss of condition and debilitating disease
      ○ With or without obvious respiratory signs
      ○ In areas of high bovine TB incidence
    • TB testing
      ○ Skin and serology
37
Q

Regurgitation in camelids

A

Camelids chew cud regularly(8-10 hours daily).

Regurgitation is a clinical sign that could derive from
a. Primary causes: The hungry camelid! Overzealous eating or impaction of fibre/concentrates (choking); toxic plant ingestion (rhododendron, azaleas, laurel)
b. Secondary: Obstruction: C2-C3; pylorus, spiral colon; Megaoesophagus; Neuromuscular dysfunction of oesophagusor vascular ring anomaly; foreign body (compartment, pyloric, spiral colon)

38
Q

Clinical signs of regurgitation in camelids

A

○ Coughing
○ lowering neck
○ palpable left sided mass in neck
○ increased salivation
○ dropping of ingesta
○ depression (especially with toxicities)
○ may have acidosis and dehydration.

39
Q

Treatment of regurgitation in camelids

A

Choke: treat like a horse, monitor, buscopan, oro-gastric intubation

Toxicities: fluids, stomach tubing strong tea or charcoal, compartment lavage, surgical lavage, euthanasia

Megaoesophagus/oesophageal dysfunction: work out cause, elevated feed troughs, surgery

NM dysfunction: nutritional management (vit E/Se)

Vascular ring: surgery

40
Q

Diarrhoea in camelids

A

Sign of prolonged, severe, underlying disease, should be considered as an emergency

Weakness, dehydration, anorexia, death

Acute causes: bacterial, viral, parasitic, endotoxaemia, intussusception, torsion, diet, acidosis, toxicosis, trace element deficiency

Chronic causes: granulomatous, IBD, parasitic, neoplasia, trace element deficiency

Treatment: fluids, antibiosis, anti-inflammatories, anthelmintics

41
Q

Grain overload in camelids

A

Colic, severe depression, may be recumbent

Excessive intake of rapidly fermentable carbohydrates, large production of VFA, production of lactic acid

Signs: obtundation, weakness, ataxia, tachycardia, compartment distension

Treatment: stop access to grain, compartment lavage, bicarbonate, magnesium hydroxide, NSAIDs, antimicrobials etc.

42
Q

Endoparasites that affect C3-glandular region of camelids

A

Haemonchus (anaemia)

Telasodorsagia

Trichostrongylus

Camelostrongylus

43
Q

Endoparasites of camelids affecting small intestine

A

Cooperia

Nematodirus

Trichostrongylus

Strongyloides

Monezia (tape worms

Eimeria (ileum)

Capillaria

Trichuris (whipworms- straining and diarrhoea)

Haemonchus (anaemia)

44
Q

Endoparasites of the colon of camelids

A

Trichuris (caecocolic area) - anaemia

45
Q

Endoparasites of camelids (other)

A

Liver fluke

Small eimeria
- E. punoensis
- E. alpacae
- E. lamae

Large eimeria
- E. macusanensis
- E. ivitaensis

46
Q

Treatment of endoparasites in camelids

A

Avermectins: usually first line:
- Ivermectine
- doramectine
- moxidectine

A lot of resistance reported for Haemonchus for macrolactones, moxidectinne still ok but needs to be used carefully to avoid establishment of resistance

Pour-on does NOT get absorbed in sufficient quantities through fleece for treating endoparasites-only used for ectoparasites

All macrocytic lactones dewormers are given at 2x the sheep dose unless indicated- alpacas metabolise faster

Benzimidazoles:
- Fenbendazole: depending on parasite species (usually capillaria and trichuris) and burden;
- albendazole (NB: avoid in pregnant animals: abortions, teratogen).

Levamisole (careful with overdosing, as narrow safety margins neurological signs); Only use in herd with resistance problem to break build-up of resistant worms.

Monepantel - still no resistance, reserve for needs

Fluke:
○ chlorsulon for affected animals
○ triclabendazole for control
○ albendazole 10 mg/kg for adult flukes

47
Q

Coccidiosis in camelids

A

Small Coccidia: Eimeria llamae, E. alpacae, E.punoensis
- Disease at weaning age more frequent
- Jejunum/ileum
- Haemorrhagic, watery diarrhea progressing to weakness, lethargy, weight loss or poor weight gain, feed refusal, dehydration, and eventually shock, coma, and death

Large Coccidia: E. macusianiensis, E. ivitaensis (long prepatent periods-32-43 days)
- Cobblestone like appearance of intestines may be present leading to hypoproteinaemia
- Diarrhoea not always a feature, but more weight loss or poor weight gain, ill-thrift, and increasing lethargy, weakness, and loss of appetite.
- Colic may be seen
- Hypoproteinaemia may be very severe leading to hydrothorax, ascites, oedemas, sudden death

Treatment
- Baycox (most commonly used).
- Deccox
- Sulfonamides
- Diclazuril (Vecoxan)

48
Q

Giardia in camelids

A

Not frequent but could be seen if animals drink from contaminated water

Fenbendazole

49
Q

Cryptosporidium

A

○ Not frequent
○ Crias <20 days
○ Zoonosis
○ Palliative care until resolved

50
Q

Control of endoparasites

A

○ Dung pile management
○ Haemonchus/trichuris
§ FAMACHA control on top of FEC
§ Every 2 weeks
§ FEC every 2-3 months in spring-autumn, then once in winter
§ BCS

51
Q

Main causes of colic in camelids

A
  • Compartment ulcers
    • Parasitosis
    • Impaction/ foreign bodies/ bezoars
      ○ Pylorus
      ○ Duodenal papillae
      ○ Spiral colon
    • Uterine torsion (last trimester of pregnancy)
    • Intussusception
    • Mesenteric torsion/volvulus
    • GI neoplasia
    • Toxicosis
52
Q

Signs of colic in camelids

A

Prolonged cushing

Laying in lateral recumbency

Swinging rear legs to the side to decrease abdominal pressure

flank watching

rolling

53
Q

Ulcers in camelids

A

More common at glandular C3

Predisposed by rich diet (too much concentrates); stressful event

Clinical presentation
- vague colic signs, depression, anorexia, anaemia (mild usually); melena may or may not be present
- pain at right abdominal palpation, death

Treatment
- Pantoprazole
- Omeprazole
- Antibiotics (amoxacillin clavulanic acid)
- NSAIDs contraindicated
- Suspend grains

Prognosis:
- Good if early treatment. In chronic cases can lead to perforated ulcers and secondary peritonitis

Complications
- May become perforated
- Peritonitis
- Could become chronic
- Late treatment not successful

54
Q

Vaccinations for clostridial diseases in camelids

A
  • Routine yearly vaccination (after full course)
  • Off label
  • Sheep/cattle vaccines
  • Hembras 4-6 weeks pre-unpacking
  • Cria
  • From 3 month of age if from correctly vaccinated dam
  • From 3 days from unvaccinated dam
55
Q

Mange in camelids

A
  • Fairly common.
  • Lightly fleeced areas: mites
  • All types of mites described:
    ○ Chorioptic (more common)
    ○ Sarcoptic (zoonotic)
    ○ Psoroptes (ear canker)
    ○ Demodex
  • Location: ear (especially Psoroptes), nose, axillas, perineal area, legs and toes.
  • Pruritic extensive crusting, hyperkeratosis
  • Perform Skin scrapes, detection and differentiation of mite
    ○ Sarcoptes: Burrowing
    ○ Psoroptes, Chorioptes: Non burrowing
  • Taking a blood for Zinc may help differentiate other diseases
56
Q

Treatment for burrowing mites (sarcoptes)

A

Systemic MLs (Ivermectin)

Treat all animals

57
Q

Treatment of non-burrowing mites (chorioptes/psoroptes)

A

Topical treatment e.g. frontline, fipronil, eprinomectin

58
Q

Munge in camelids

A

Perioral, paranasal crusts sometimes periaural or periocular with variable degrees of hyperkeratosis (heavy, adhered crusts).

Treatment aimed at resolving secondary bacterial infection
○ Topical iodine
○ Antimicrobials
○ Topical glucocorticoids

59
Q

Rickets in camelids

A

Common in the UK due to poor sunlight, especially in the winter period, leading to lack of activated Vitamin D.

Inhibits mineral absorption and promotes parathyroid hormone activity. Parathyroid hormone mobilizes bone to maintain calcium and phosphorous homeostasis. Calcium is allowed to be conserved from urine, however together with a weakened bone, phosphorus is lost.

Clinical signs are more common in young camelids, up to 2 years of age and dark fleeces animals are more prone to the deficiency due to decreased absorption of sunlight through the darker fleece.

Osteoporosis and osteomalacia can occur in the older camelid with the same pathogenesis. These can lead to pathological fractures.

Treatment:
○ Mild cases
§ Vit D supplementation
§ Oral or injectable vitamin
§ Dietary
○ Severe cases
§ Injectable vit D - once
§ Inorganic phosphorus until within limits
§ Consider TLC, pain relief, rest

Prevention is better than cure:
- Vitamin ADE injection (every 8 weeks) or oral paste once at 2-6 months old, November to April at 1000- 1500 IU/kg every 6 weeks, Adults at least twice in the winter period, Constant Vit d intake through feed

60
Q

Clinical signs of rickets in camelids

A

○ Lameness
○ Shifting weight
○ Increased recumbency
○ Poor growth
○ Poor body condition
○ Abnormal gait
○ Ataxia
○ Fractures
○ Anaemia

61
Q

Osteomyelitits in camelids

A

Young animals (2-3 years of age)

Acute lameness- not related to trauma, although in some cases could be traumatic

Endogenous origin of bacteria seeding in bone causing lysis and sequestrum

Mild cases are responsive to antibiotics (penicillin or florfenicols are usually first line) but many require surgery to remove the sequestrum.

If chronic may lead to sequestrum formations

Surgical removal

62
Q

Septic arthritis in camelids

A

Any joint

Crias more frequent (even in spine) but multiple joint affected can be seen in adults too.

Approach like horses

Antimicrobials

63
Q

Anaemia in camelids

A

Pale mucus membranes, dull and lethargic animals

Normal PCV 25-45%
○ Below 20% is significant
○ Transfusion trigger 14%

Main causes:
○ Blood borne disease
§ Blood borne bacteria
§ Candidatus Mycoplasma haemolamae (formerly Eperythrozoon)
§ Gram neg bacteria
○ Blood sucking parasites
§ Haemonchus contortus
§ Trichuris
○ Compartment ulcers (refer to ulcers)
○ Iron deficiency
○ Chronic disease (infections)

Treatment:
○ Transfusion trigger 14%- whole blood
○ Treat cause
○ Mycoplasma haemolamae: oxytetracycline 10%
○ Haemonchus/Trichuris: Moxidectin/Fenbendazole
§ refer to diarrhoea treatment with Parasitosis.
○ Iron deficiency: Can treat with oral iron (Red cell)

64
Q

Polioencephalomalacia/CCN in camelids

A

Most commonly caused by Thiamine deficiency, but can be caused by other factors (sulfur toxicity, lead toxicity, rapid influx/exit of sodium (hypo/hyper Natraemia), these are usually non thiamine responsive.

Thiamine deficiency can occur from dysbiosis- grain overload, ingestion of thiaminase containing plants or medications (such as Levamisoles, Benzamidazoles).

Treatments- performed with no testing (no testing available a part from at post mortem..):
○ Thiamine
○ Dexamethasone
○ NSAIDs

65
Q

Clinical signs of polioencephalitis/CCN in camelids

A

○ Depression
○ Head pressing
○ Opistotonus
○ Cortical blindness (no menace with intact PLR)
○ Wandering aimlessly,
○ Tremors of head and neck/ muscle fasciculations
○ Ataxia
○ Circling
○ Seizures

66
Q

Dystocia in camelids

A

Usually early morning births

Over 6 hours lack of progression of stage 2; frequent alternation between standing and recumbency; abnormally coloured vaginal discharge

Causes:
○ Malpositioning
○ Faetal maternal disproportion
○ Poor cervical dilation
○ Torsion
○ Uterine inertia
○ Twins

Treatment
○ Gentle manipulation, sterile gloves, plenty of lube
○ Snares or sheep ropes
○ Very long necks and legs so gentle traction to avoid uterine tearing
○ C-section possible
§ In crush
§ Under GA (referral)

67
Q

Uterine torsion in camelids

A

fairly common especially in the last trimester of pregnancy

Rolling or C section

68
Q

Retained placenta in camelids

A

Usually passed within 60 min post partum (some cases up to 4 hrs)

Examine to make sure complete and presence of villi

Treat like a mare, urgency!
§ Oxytocin
§ Removal of placenta
§ Uterine flush
§ Antimicrobials
§ NSAIDs

69
Q

Uterine/vaginal prolapse in camelids

A

Like a sheep, and buhner suturing

perform epidural (1-2 ml procaine or lidocaine)

70
Q

Induction of parturition in camelids

A

Only if cria >330 days gestation

Only if torsion has been ruled out

PGF2lpha (CL depended)

Do not give steroids (associated with intrauterine death)

71
Q

Congenital abnormalities in cria

A

Fairly common

Atresias:
§ Choanal atresia
§ Atresia ani/coli
§ Vulvar atresia
§ Naso lacrimal duct atresia
Cleft palate
Wry face
Polydactyly
Hermaphroditism
Cardiac abnormalities (VSD/ASD/PDA)

72
Q

Umbilical hernias in cria

A

May self resolve if smaller than 1 cm with growth.

Can be supported with abdominal bandaged as the cria is growing.

Surgical correction also an option

73
Q

FPT in cria

A

Common

Common secondary diseases:
○ Navel infections
○ Urachal abscesses
○ Joint infections
○ Neonatal septicaemia
○ Sepsis

IgG levels can be measured with snap test, SRID or zinc turbidity test.

If orphans or agalctia
○ <24 hours
○ Frozen alpaca colostrum
○ Cow or goat colostrum
○ Fed at 10% BW
○ 60-90ml per feeding

Plasma transfusion can be performed in cases where FPT is confirmed or suspected already 24-48 hrs of age

Donor choice usually: male, good BCS, ideally vaccinated prior transfusion, can take 300 ml from an alpaca/500 ml from a llama (max 1% of BW). Spin down and give slowly IV (prior catheterisation) making sure to check vitals during the process. If prior collection and stored viable for 2 years in freezer.

74
Q

Neonatal septicaemia in cria

A

Treatment can be done in field but severe cases should be hospitalised/referred

Signs:
○ Abnormal behaviours
○ Failure to suckle
○ May not be febrile (normal temp 37.8-38.9)
○ Injected MM
○ Poor growth rate

Antimicrobials usually used:
○ Amoxicillin clavulanic acid
○ Sulfonamides
○ Oxytetracyclines
○ Ceftiofur and quinolones- last resorts and ideally based on blood culture

NSAIDs
○ Meloxicam
○ flunixin

Fluids
○ Supportive, crystalloids (5% dextrose)

Plasma transfusion, even in face of treatment

75
Q

Hyponatraemia/hypernatraemia in cria

A

Presents with neurological signs, head pressing, open wide stance, depression

76
Q

Hypoglycaemia in cria

A

Severe depression, increased recumbency, poor suckling reflex

77
Q

Hyperglycaemia in cria

A

Due to stress, can also occur with no clinical signs
Associated with insulin resistance

78
Q

Hyperosmolar syndrome in cria

A

Restricted fluid intake

Associated with steroids administration

Usually presents with neurological signs and severe depression, head pressing.

Small ruminants II (3 decks)

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