Camelidae

Question 1

What are the six camelid species and their scientific names?

Answer 1

Camelidae Taxonomy (Terio)

A. “Old World” Camelids (Camelus spp.)

1. Dromedary camel (Camelus dromedarius)
2. Bactrian camel (Camelus bactrianus)

B. “New World” Camelids

1. Lama spp. = llama (Lama glama) and guanaco (Lama guanicoe)
2. Vicugna spp. = Alpaca (Vicugna pacos) and vicugna (Vicugna vicugna)

Question 2

Describe the dentition of Old world and New World Camelids

Question 3

Describe the gastrointestinal anatomy of camelids.

Answer 3

• Foregut fermentation
• 3 compartment stomach (C1, C2, C3) – not analogous to ruminants
  
  • All have glandular epithelium
• Greater omental sling is absent
• Spiral colon has 5 coils

Zoo Path

• Foregut fermentation in three-compartment stomach
  
  • C1 = in left abdomen with cranial and caudal sacs with glands on ventral surfaces
  • C2 = most of mucosa is glandular with deep crests/bands
  • C3 = entirely glandular with a net-like appearance
  • pH drops abruptly (6.5 to 2.0) as you move to caudal C3 with red, smooth mucosa and gastric glands
• Green-black gastroliths are common, incidental findings in saccules of C1 and C2
• Liver has fringed edges

Question 4

Describe the male and female reproductive anatomy of camelids.

What is the Dulaa?

What is the poll gland?

Answer 4

1. Male anatomy:
   
   1. Sigmoid flexure in their fibrocartilaginous penis
   2. Accessory organs: prostate, paired bulbourethral glands
   3. Dorsal urethral diverticulum makes urinary catheterization impossible
   4. Poll gland in male camels secretes fluid on the back of the head
   5. D_ulaa in male dromedary camels is a diverticulum of the ventral soft palate that can fill with air and extrude from the oral cavity_
2. Female anatomy:
   
   1. Bicornuate uterus with diffuse, epitheliochorial, microcotyledonary placenta
   2. Fetal epidermal membrane covers the surface of the fetus when it is near term
   3. Attached to fetus at mucocutaneous junctions, coronary band, footpad, and umbilicus

Question 5

Compare and contrast camelids and ruminants.

What animal groups have foregut fermentation?

How does their hematology vary?

How does their skull and feet anatomy differ?

Describe the GI anatomy of teh two groups

How does their reproductive anatomy & physiology differ?

How does their urogenital anatomy differ?

How does disese susceptiblity differ?

How does reproductive behavior differ?

Answer 5

• Foregut fermentation and multicompartmental stomachs – camelid, hippo, kangaroo, colobus monkey, peccary
• Parallel evolution between Camelidae and ruminantia
• Camelids are quite resistant to many regulated ruminant diseases
• Llama and alpaca can become infected by inoculation with FMD, but not when cohabiting with infected swine (unlike cattle)
• Camelids have shown resistance to acquiring TB
• Natural Brucella abortus does not occur in llamas and alpacas
• There are no reports of transmission of any regulated ruminant disease from camelids to ruminants. They are not a threat to the livestock industry because they either have total resistance to infection or minimal susceptibility to infectious and parasitic diseases of ruminants

Question 6

Describe the housing of camelids.

Do they have any particular requirements?

Answer 6

Husbandry (Fowler 8)

· Camelids – can be housed as other domestic livestock

· NWC – minimal housing – protection vs inclement weather

· Guanacos & Vicuñas social animals

Camels adapted to heat and dehydration (97.7-107.6F)

o Able to sustain 25% of body weight loss as a result of dehydration

o Can rehydrate immediately

§ Elliptical erythrocytes able to swell to 240% of normal without rupturing

§ Reabsorbs water from bladder

§ Feces become desiccated

§ Milk becomes less concentrated

· NWC adapted to cool weather and not heat tolerant

Question 7

Describe the nutrition of camelids.

How does their body condition change in the wild over time?

Answer 7

Nutrition (Fowler 8)

• OWC & NWC have non unique requirements
• Good quality of grass hay or mixed grass, and legume hay
  
  • Supplemental feeding with concentrate is usually not necessary except for growing juveniles, working animals and lactating females
  • Camelids consume 1-2% BW in dry matter when consuming good quality forage
• Maintenance diet 10-14% crude protein and 50% to 55% total digestible nutrient (TDN’s).
  
  • Late gestation or heavy gestation, females should consume 60-65% TDN
• Camelids on native pasture fluctuate body weight- lose weight
  
  • NWC feast or famine – gain a lot of weight during rainy season, then use stores during dry season

Question 8

Describe your preventative medicine protocol for camelids.

Answer 8

Preventative Medicine (Fowler 8)

• Monitor parasitic loads and manage like other hoofstock
• · Vaccination - vary by location but should include:
• o Tetanus,
• o Leptospirosis
• o Enterotoxemia types D and C
• o Rabies

Question 9

Describe the physical restraint of camelids

Answer 9

Restraint (Fowler 8)

· Camelid offensive and defensive behaviors include spitting, biting,kicking

o Spitting – spew content of C1

o No place is safe around untrained camel since front legs can kick any direction and hindlimbs can reach far forward

o NWC- spit and kick

§ Kick sweep forward and outwards

· Can use kushing for restraint

· Can use chutes/stocks

Question 10

Describe procedures for chemical restraint of camelids.

How long shoudl they be fasted for?

What are the best sites for vascular access?

Descrbie the intubation of camelids.

Answer 10

Restraint and Handling

• Fast prior to general anesth to minimize regurgitation, aspiration, and bloat (12-18 hr fast for llama and alpaca, 24-36 hour fast for camels). Withhold water for a portion of that time.
• Do not fast nursing juveniles
• Halter train camelids and towel over nostril and mouth to reduce spitting
• Camel can be restrained in stocks, eased into sternal with ropes around forelimbs, or trained to cush

Instrumentation

• Most common venous access site is jugular vein – restraint in chute or stanchion significantly helps
• Jugular vein located at the bisection of a line drawn caudally from the lower jaw with a line drawn ventrally from the base of the ear.
  
  • Thick skin in this area, but better separation between jugular and carotid artery
  • Cerebral injury reported following inadvertent intracarotid injection – hard to differentiate arterial vs venous due to brightness of venous blood in SA camelids
  • Recommended to make skin incision before catheter placement
• Alt sites for catheter – lateral thoracic vein (adult), cephalic or saphenous (Juv), auricular vessels

Intubation

• Llama and alpaca – visual orotracheal intubation with animal in sternal and head extended with long narrow laryngoscope. Lidocaine arytenoids.
  
  • Nasotracheal intubation – via ventral medial nasal meatus
    
    • Smaller tube and potential for hemorrhage, but can be left in place until fully recovered
    • Phenylephrine can be given topically to minimize hemorrhage
    • Camelids are nasal breathers – minimizes upper airway obstruction risk in recovery period
• Camel – intubation blindly or by manual palpation of arytenoid cartilages

Question 11

Describe the monitoring and supportive care of camelids undergoing anesthesia.

How do you monitor depth of anesthesia in camelids?

How is blood pressure monitored?

How is positioning important for camelids?

How do you address bloat?

Answer 11

Monitoring

• Monitoring depth can be challenging as they maintain ocular reflexes at nearly all planes of anesthesia
  
  • Globe rotates periodically but bears little correlation with movement in response to noxious stimuli.
  • Eyelid aperture 🡪 increases with increasing depth of anesthesia in llamas. Jaw tone useful in camelids, along with preputial/rectal tone, drooping of lower lip, relaxation of neck and abdominal/tail musculature
• Invasive BP monitoring – auricular, medial saphenous, carpal, cranial tibial, or middle coccygeal arteries.
  
  • BP tends to decrease with increasing inhalation anesthetic depth
• HR: 60-120 (lower if alpha 2 used) in alpaca/llama. HR 40-50 in camels (bradycardia and second-degree AV block observed with alpha 2.
• Healthy llama and alpaca typically have PCV from mid-20s.
• Monitor abdominal distention, regurgitation, and nasal edema

Support

• Pull lower forelimb forward in lateral recumbency and support upper limbs in natural position (not hanging). Use padding (air or foam mattresses)
• Llama and alpaca may become hypoxic during injectable protocols 🡪 oxygen supplementation recommended, especially at altitude. Camels prone to hypoxemia due to body mass and O2 should always be supplemented
  
  • Hose placed in ventromedial nasal meatus up to the medial canthus
• Uncommon in llama or alpaca, but camel may bloat so placement of a bloat tube can help to reduce the influence on venous return and pulmonary function.
  
  • Head positioned to allow drainage of regurgitant fluid and minimize edema. Obligate nasal breathers 🡪 nasal edema can become problematic
  • Phenylephrine can be placed into nasal passages prior to extubation.
• If food material observed from nose 🡪 ensure ET cuff inflated and perform gentle lavage

Question 12

Describe the following nutritional diseases in camelids:

Obesity & hyperglycemia - why does this occur easily? What are some metabolic consequences?

Thiamine deficiency - what lesion is associated?

Vitamin E & Selenium Deficiency - what lesions are associated?

Zinc deficiency - what lesions are seen?

Answer 12

Noninfectious Diseases (Terio)

Nutritional

1. Obesity & Hyperglycemia in NW camelids
   
   1. Easily overfed because of efficient digestion evolved for poor quality diet
   2. Increased fat in subcutis, hyperlipemia
   3. Hepatic lipidosis is especially common in pregnant/lactating NW camelids
   4. Increased risk for infertility and hyperthermia
   5. Develop poor glucose tolerance, partial insulin resistance, and low circulating insulin
   6. Persistent hyperglycemia → dehydration from glucosuria and glucose diuresis
2. Polioencephalomalacia (cerebral cortical necrosis) is associated with thiamine (B₁) deficiency
3. Diets that increase thiaminase-producing bacteria (grain, amprolium) increase risk
   
   1. Vitamin E and Selenium Deficiency
4. Skeletal muscle degeneration and necrosis, esp. In intercostals, diaphragm, and tongue
5. Cardiac necrosis can lead to sudden death
   
   1. Other differentials for sudden death with cardiac myonecrosis = oleander and ionophore toxicity
   2. Overweight animals can develop fat necrosis with vitamin E and selenium deficiency
6. Zinc responsive dermatosis is most common in adult, black NW camelids
   
   1. Hyperpigmentation and thickening on face, ventrum, thorax, and inguinal region

Question 13

Describe the congential defects of camelids.

What skeletal defects are common?

What about craniofacial defects?

What is the most common congenital defect?

Answer 13

Congenital/Genetic

1) Most common NW camelid congenital defects = angular limb deformity, polydactyly, hemivertebra, and cranial dysgenesis
2) Congenital deafness is seen sometimes in alpacas with white hair and blue irises
3) Choanal atresia (bony partition between nasal cavity and pharynx = lethal defect

Skeletal Defects

• Angular limb deformity
  
  • Carpal valgus most prevalent
  • Carpal varus, metacarpophalangeal valgus, femorotibial valgus have also been seen
  • Nutrition appears to be a factor in some cases, possibly a sequala to rickets and associated cortical thinning
  • Carpal valgus may be present at birth but should correct over a month – so recheck at that time if present
  • Radiographic lesions include a wedge-shaped radial epiphysis, with the base of the wedge on the medial aspect of the carpus
  • PVC splints can be used on the carpus on animals <2 months of age; unlikely to be effective after 15 months of age
• Patellar Luxation
  
  • Causes crias to stand in a crouched position
  • Stifle is thickened, patella is palpated in medial position rather than in the dorsal groove fo the femur
  • Laxity of the tibiopatellar and femoropatellar ligaments may cause the patella ot lodge on the medial or lateral ridge of the trochlea
• Polydactyly & Syndactyly
  
  • Hereditary
  • Polydactyly more common than syndactyly

Craniofacial Defects

• Choanal atresia
  
  • Membranous or osseous partition between nasal and pharyngeal cavities
  • Agenesis of facial bones results in shortening of the face and muzzle and doming of the forehead (often mistaken as hydrocephaly)
  • Complete occlusion of nasal passageway causes characteristic breathing pattern – Air is sucked in, cheeks force air into the pharynx with lips closed, and then air is forced out on expiration
  • This causes crias to have difficulty breathing while nursing – aspiration pneumonia is a common sequela and chewing on fiber due to hunger results in trichobezoars
• Jaw Dysgenesis
  
  • Common, hereditary (brachygnathism etc)
  • Alpacas have continuously growing incisors – proper alignment of the teeth usually doesn’t cause a problem
  • Retained deciduous incisors is a common problem in llamas

Reproductive System Defects

• Hypogenesis or Agenesis of Uterus results in stenosis that predisposes them to mucometra
• Male defects – testicular hypoplasia, cryptorchidism, testicular cysts, penile hypoplasia, persistence of penile frenulum, curvature of the penis

Digestive Tract Defects

• Atresia ani, atresia coli
• Megaesophagus

Cardiovascular Defects

• Ventricular septal defect (VSD) – common in llamas. Suspicion based on murmur should be confirmed by echo

Question 14

What are the causes of ovarian hydrobursitis in camels?

What lesions are associated with hyperthemia? Which camelids are susceptible?

Where do ulcerations most commonly occur in camelids? Where are they most likely to perforate?

What is the most common neoplasia of camelids?

Answer 14

Age-Related/ Degenerative

1. Overextension of metacarpo/metatarsophalangeal joints (dropped fetlocks) is common
2. Prolonged recumbency → ulceration and infection of the sternal callosity

Inflammatory Non-Infectious

1. Ovarian hydrobursitis in dromedary camels is seen in up to 15% of dromedary camels
   
   1. Estrogen-rich, hemorrhagic fluid
   2. Chlamydia abortus may be a cause

Miscellaneous

1. Hyperthermia
   
   1. OW camelids are resistant
   2. NW camelids are very susceptible
   3. Lesions = petechial hemorrhages, hyperemia, thrombosis, pulmonary edema/congestion, renal/hepatic necrosis
2. Idiopathic superficial necrolytic dermatitis
   
   1. Non-pruritic, intermittent erythematous, crusting vesicles
3. Gastric Ulceration
   
   1. Along margins of saccules in C-1 and C-2
   2. Linear ulcers in C-3 along longitudinal pleats
   3. Ulcers in distal C-3 are most likely to perforate
4. Neoplasia is relatively rare
   
   1. Lymphosarcoma is the most common

Question 15

What poxviruses affect camelids?

Which is OIE reportable?

How are these spread?

How is this diagnosed and treated?

What are the typical inclusion bodies associated with camelpox and parapox?

What papillomaviruses affect camelids?

Answer 15

• Viral camel pox
  
  • Poxviridiae, Orthopoxvirus cameli
  • OIE reportable disease
  • zoonotic
  • Most common viral disease of Bactrian and dromedary
    
    • Not in US or Australia
  • Spread by direct contact
  • CS:
    
    • Pustules on nostrils, lips, eyelids and oral and nasal mucosa
  • Dx:
    
    • ELISA
  • Mgt:
    
    • Vaccine
  • Other viruses seen Parapoxvirus (contagious ecthyma (orf)), papillomatosis, Bovine virus diarrhea virus, peste des petites ruminants (paramyxovirus), FMD,, EEE, WNV, MERS-CoV

Zoo Path

• Camelpox = zoonotic, OIE-reportable
  
  • Most common virus in camels
  • Macules, papules, and vesicles on head, nostrils, ear margins, lips, gentialia, and eyelids
  • Transmission is direct or inhalation from secretions
  • Inclusions are NOT typical
• Parapoxvirus = contagious ecthyma = contagious pustular dermatitis = “orf”
  
  • Epidermal proliferation in the oral commissures of crias/calves and teats of dams
  • Eosinophilic intracytoplasmic inclusion bodies
  • Zoonotic with reported anthropozoonosis
  • Associated with housing near small ruminants
• Papillomatosis = Camelus dromedarius papillomavirus types 1 and 2
  
  • Can be confused with parapox or camelpox
  • No inclusions

Question 16

What is an important infectious differential for sudden blindness in a Llama?

How did this animal get this infection?

What are histologic lesions?

Answer 16

1) DNA Viruses

• Equine herpesvirus (EHV-1)
  
  • In all camelids as “spill-over” from nearby equids
  • Neurologic signs, especially blindness
• Retinal degeneration
  
  • Equine Herpes virus 1 (transmission unknown)
    
    • Clinical signs
      
      • Blindness, non-responsive pupils, encephalitis
    • Dx:
      
      • Exam, retinal degeneration
      • Eosinophilic intranuclear inclusion bodies in endothelium and neurons
    • Mgt:
      
      • Vaccination in face of epizootic
      • Blindness is permanent

Question 17

What type of virus is bovine viral diarrhea virus?

How does this virus affect New World camelids?

What about OW camelids?

Answer 17

Bovine viral diarrhea virus (BVDV)

• Flaviviridae, Pestivirus
• NW camelids commonly have in utero infection leading to abortion or birth of persistently infected offspring
• Alpacas – abortion, BVDV positive tissues, chronic poor doing crias, stillbirth, neonatal death
• OW serology studies suggest exposure, but disease has not been described
• Experimental infection in alpacas <2 → lymphocytopenia with viremia and nasal shedding with no clinical signs

Question 18

What type of virus is peste des petites ruminants?

What clincial signs have been reported in camelids?

What species is this disease seen in most commonly?

Answer 18

Peste de petites ruminats (PPR)

• Paramyxoviridae, Morbillivirus
• Signs: fever, dehydration, oral ulcers, diarrhea, lymphadenopathy, dermatitis, corneal ulceration, conjunctivitis, respiratory disease (pulmonary congestion, edema, pneumonia), renal tubular necrosis
• Reported in dromedary camels

Question 19

What type of virus is foot and mouth disease?

What species of camelids are susceptible to this disease?

What are the clinical signs and lesions in camelids?

Answer 19

Foot and mouth disease (FMD)

• OIE-reportable
• Picornaviridae, Aphthovirus
• Dromedary camels are resistant; Bactrians play a small role in the transmission of the disease in Central Asia; NW camelids can contract the disease but are less susceptible than cows/sheep and stop shedding after 14 days and don’t remain carriers.
• Signs: vesicles and ulcers on the tongue, dental pads, oral cavity, palate, lips, nostril, coronary band, and interdigital space – undermining of footpads, teats, and pillars of C-1 and C-2

Question 20

What type of virus is vesicular stomatitis?

How does this disease affect camelids?

What are the clinical signs?

Answer 20

Vesicular Stomatitis (VS)

• Rhabdoviridae, Vesiculovirus
• Vesicular and erosive lesions similar to FMD (vesicles, fever, recumbency)
• Only one case reported in a NW camelid; none in OW

Question 21

What taxa are susceptible to borna disease virus?

What are the clincal signs in camelids?

What lesions are present?

Answer 21

Borna disease virus

• Bornaviridae, bornavirus
• Seen in NW camelids, horses, and donkey in eastern Europe
• Signs: anorexia, weight loss, loss of libido, and stretching convulsions
• No gross lesions; non-suppurative enchephalomyelitis and perivascular cuffing

Question 22

What types of viruses are Eastern Equine Encephalomyelitis and West Nile virus?

What are the clinical signs in camelids?

What are differentials for these signs?

Which camelids appear most susceptilbe?

What are the lesions associated with these diseases?

Answer 22

Eastern equine encephalomyelitis (EEE) and West Nile virus (WNV)

• Arboviruses (Alphavirus, Flavivirus)in NW camelids
• Signs: Fever, seizures, ataxia, recumbency, and high mortality rate
• Differentials: listeriosis, rabies, polioencephalomalacia, meningeal nematodiasis
• No gross lesions; histo includes polioencephalitis with lymphocytis perivascular cuffs, neutrophil infiltration, multifocal neuronal and glial necrosis and edema

Question 23

What two viruses cause diarrhea in camelids?

How prevalent are these diseases?

Are there any risk factors that predispose animals to infection?

Answer 23

Rotavirus and coronavirus cause diarrhea in young NW camelids

• Rotavirus (Reoviridae) – Coronavirus (Coronaviridae)
• Prevalence of rota up to 98% on some farms: 42% of diarrhea in young NW camelids due to corona
• OW camelids affected too.
• Failure of passive transfer is a predisposing factor

Question 24

What type of virus causes Middle Eastern Respiratory Syndrome?

What species transmit it?

Are there any lesions in those animals?

Can other animals get the disease?

An outbreak of a similar virus occurred in alpacas - what animals were most susceptible and what lesions were seen?

Answer 24

Middle Eastern Respiratory Syndrome

• MERS coronavirus = camel flu = zoonotic, OIE-reportable disease
• More transmission among young camels
• No lesions in camels
• Experimental infection of alpacas shows they can get infected and transmit it as well

Novel Alpaca Coronavirus

• Outbreak in 2007 – mostly in pregnant animals
• Lesions – pulmonary congestion, edema, and pleural effusion; histo – diffuse bronchointerstitial pneumonia with fibrin deposition and hyline membranes

Question 25

What is the cause of caseous lymphadenitis in camelids?

How is this disease transmitted?

What are the clinical signs?

How is it diagnosed and treated?

Answer 25

• Pseudotuberculosis, caseous lymphadenitis
  
  • Corynebacterium pseudotuberculosis
    
    • Also, Staph aureus, Corynebacterium pyogenes, E coli, Rhodococcus
  • Spread by ingestion, inhalation, direct contact with wounds
  • Common and widespread
  • CS
    
    • Lymph node abscessation
      
      • Deep abscesses in camels are rare
  • Dx
    
    • Culture and clinical signs
  • Txt:
    
    • Penicillin
    • Isolate affected animals

Question 26

What is teh cause of hemorrhagic disease in camils?

How are camels exposed to this disease?

What are the clinical signs?

How is it diagnosed and treated?

Answer 26

• Hemorrhagic diathesis or hemorrhagic disease
  
  • Bacillus cereus toxin
    
    • B cereus usually nonpathogenic but associated with food poisoning in humans
    • Toxic syndrome seen in racing camels fed green alfalfa
    • CS:
      
      • Fever, anorexia, agranulocytosis
      • Colic, atony of C1
      • Swollen submandibular lymph nodes
      • +/- CNS signs
    • Dx:
      
      • Hx (racing, fresh alfalfa)
      • Hemorrhage of serosa and mucosa of abdominal and thoracic organs
    • Txt
      
      • Avoid manure fertilized alfalfa
      • Sanitation

Question 27

What is the etiologic agent of brucellosis in camelids?

Which camelids are most commonly affected?

What is the most common clinical sign?

What lesions are associated with this disease?

Answer 27

• Brucellosis
  
  • Common in OW camels (OIE reportable)
  • Zoonotic transmission via consumption of unpasteurized milk
  • Dromedary camels – B melitensis (rare B abortus)
  • Less common in NWC
  • CS:
    
    • Abortion
    • Placental retention rare

Brucellosis

• Brucella melitensis, abortus = OIE-reportable
• Gram - facultatively intracellular bacteria
• Most common in OW camelids
• Abortion (wihtout placental retention) = most common clinical sign
  
  • Necrosis, suppurative inflammation, and fibrosis of the chorion

Question 28

What bacteria are common causes of mortality in neonatal camelids?

Are there any predisposing factors?

At what age are crias susceptible to the varying diseases?

Answer 28

• Enterotoxemia
  
  • Clostridium perfringes type A
    
    • Clinical signs:
      
      • Sudden death, colic, bloat, seizures, coma
      • Neonatal disease in alpacas
    • Dx: Monoclonal Ab, PCR
    • Mgt:
      
      • Correct environment
      • Abx for secondary infection
  • Clostridium perfringes type C &D
    
    • Young NW camelids
    • Similar to A but see more diarrhea

Neonatal Infections (best documented in NW camelids)

• Escherichia coli → neonatal diarrhea and sepsis
  
  • Failure of passive transfer – usually within first week of age
• Clostridium perfringens type A → enterotoxemia (at 2-3 wks old as clostridial antibodies wane)
• Clostridium perfringens type C → enterotoxemia and diarrhea
• Clostridium perfringens type D
• Lesions – neutrophil, lymphocyte, plasma cell infiltration of lamina propria, crypt abscesses, and adherent Gram-negative coccobacilli to enterocytes

Question 29

What mycoplasma infects camelids?

What species are particularly susceptible?

How is this diagnosed?

Answer 29

Mycoplasma haemolamae = endemic, intra-erythrocytic Mycoplasma of NW camelids

• Small bacteria on the edge of the red blood cell membrane
• Signs: weight loss, lethargy, anemia
• Diagnosis with blood film or PCR
• Vertical transmission is possible

Question 30

What bacterial infections are common causes of infertility in New World camelids?

What additional bacteria affect NW camelid fertility?

What about OW camelids?

Besides reproductive loss, what are the other lesions associated with Alpaca Fever?

What is the etiologic agent of Alpaca Fever?

Answer 30

• E coli and Streptococcus equi ssp zooepidemicus (Alpaca fever)
  
  • common causes of endometritis in NWC
  • CS:
    
    • Endometrial ulceration, neutrophilic infiltrate, intraglandular aggregates of debris
      
      • Chronic – fibrosis, glandular atrophy, infertility
  • Other causes of abortion: Leptospirosis, toxoplamosis, chlamydiosis, brucellosis, trypanosomiasis (more common in Middle East and Africa)

Reproductive infections = common source of infertility

• Escheria coli, Streptococcus equi ssp. Zooepidemicus → endometritis
• NW camelis: leptospirosis, toxoplasmosis, chlamydiosis
• OW camelids: mastitis, brucellosis, trypanosomiasis (in Middle East and Africa)

Alpaca fever = Streptococcus equi ssp. Zooepidemicus

• Very high mortality
• Most common in young animals in South America → polyserositis
• Adults have chronic abscesses

Question 31

What is the etiologic agent of Johne’s disease?

What are the clinical signs and lesions of this disease in camelids?

Answer 31

Johne’s disease = Mycobacterium avium subsp. paratuberculosis

• Signs: severe weight loss and diarrhea
• Lesions: Abdominal lymphadenopathy, granulomas in lungs, liver, and LN
• Histo – expansion of lamina propria and mesenteric and ileocecocolic lymph nodes with bacteria laden macrophages

Question 32

What is the etiologic agent of tuberculosis in camelids?

Which species are more affected?

What are the lesions?

How do the lesions differ in camelids compared to ruminants?

Answer 32

Tuberculosis = Mycobacterium tuberculosis, bovis = OIE-reportable disease

• Primarily affected OW camelids
• Granulomatous tubercles with central caseous necrotic core and mineralization surrounded by macrophages, lymphocytes, plasma cells, and neutrophils within a capsule
• Giant cells are rarely present in camelid lesions as compared to ruminants

Question 33

What is the most significant fungal disease of camelids?

What is the etiologic agent?

How is this disease transmitted?

What are the clinical signs?

How is this disease diagnosed?

How is it treated?

Answer 33

• Coccidioidomycosis
  
  • Coccidiodes immitus
    
    • C immitis – soil fungal
  • Clinical signs
    
    • Dyspnea, dermatidis
  • Dx
    
    • Culture
    • Cytology
    • AGID
    • CF
  • Mgt
    
    • Poor prognosis
    • Fungicidal antibiotics (amphotericin B)

Coccidioidomycosis = Coccidioides immitis, posadasii

• Most significant fungal disease of NW camelids
• Endemic to SW US and desert areas of Mexico and South America
• Transmission: Inhalation of arthrospores
• Signs: respiratory disease (most common), or disseminated
• Endospores can be zoonotic

Question 34

Describe the life cycle and clincial signs associated with Lamanema chavezi infestation in New World camelids.

What are the effects of Haemonchus & Trichuris infestation in camelids?

Describe the life cycle and lesions associated with Parelaphostrongylus tenuis infestation in camelids.

What are the two main flukes affecting camelids? What lesions do they cause?

Answer 34

• Metazoa
  
  • Lamanema chavezi = trichostrongylid nematode
    
    • High mortality in NW camelids
    • Signs: severe hemorrhagic enteritis, hepatic necrosis
      
      • Catarrhal and hemorrhage enteritis from larvae migration
      • Coagulative necrosis, hemorrhage, and abscessation of the liver
    • Definitive host = mountain viscacha (a South American rodent)
      
      • Larvae are ingested, penetrate GI, migrate to lung and liver.
  • Haemonchus contortus causes blood and protein loss through damage to C-3 mucosa
  • Trichuris spp. = whipworms → unthriftiness in camelids
    
    • Ova are very environmentally stable
  • Parelaphostrongylus tenuis = meningeal worm → neurologic signs in camelids
    
    • Definitive host = white-tailed deer
    • Intermediate host = terrestrial snails and slugs
    • Peripheral eospinophilia and increased eosinophils in CSF is suggestive
    • Lymphoplasmacytic perivascular cuffs, hemosiderin-laden macrophages, eosinophils, meningitis, mineralization, giant cells, glial scars, and tracts of necrosis and inflammation
  • Liver flukes = Fasciola hepatica and Dicrocoelium dendriticum
    
    • Most commonly cause chronic hepatic infection with biliary stasis in NW camelids
    • Can also cause acute bile stasis, liver injury, and death
    • Gross – hepatic fibrosis, ascites, nodules, mineralization, absecces
    • Histo – fibrosis with biliary hyperplasia

Question 35

What three protozoa commonly affect camelids?

What are the clincal signs associated with infection?

Answer 35

• Protozoa
  
  • Eimeria spp. = apicomplexan parasite
    
    • E. macusaniensis → anorexia, diarrhea, death in young NW camelids
    • Additional species can cause disease in OW camelids
  • Cryptosporidia = apicomplexan parasite in young camelids → neonatal diarrhea
    
    • Diagnose with acid fast stain of feces
  • Trypanosoma evansii = nagana = surra
    
    • Affects OW camelids in Asia and Africa
    • Acute syndrome (surra): fever, anemia, edema, paresis/paralysis, abortion, mastitis → death
    • Chronic syndrome: intermittent fever, anemia, edema, weight loss
    • Check blood smears during febrile episodes to increase sensitivity
    • Intermediate host = tsetse fly
    • Camels can also be affected by T. brucei and T. congolensis

Question 36

What ectoparasites are common in camelids?

Answer 36

• Ectoparasites
  
  • Oestrus ovis = nasal bot → sneezing, discharge, dyspnea in NW camelids
  • Cephalopina titillator = camel bot
    
    • Nasopharyngeal mucous membranes are congested with mucus and fibrin
    • Primary host = OW camelids
  • Mange mites can affect fiber quality
    
    • Sarcoptes scabiei = most common

Question 37

Describe urolithiasis in camelids.

Describe the male anatomy that makes them predisposed to obstruction.

What are the clinical signs of urethral obstruction?

How is urolithiasis diagnosed?

How is it managed?

What are some complications from urolithiasis?

Answer 37

Urolithiasis

• Associated with high concentrated feed diets
• Male urinary anatomy
  
  • At the ischium, the pelvic urethra only has a tiny orifice that allows urine to pass
  • A dorsal urethral recess at that site makes passage of a urinary catheter impossible – into the bladder at least – the new camelid book recommends trying, with the goal of hyrdopulsing the stone/plug back into the bladder, the new camelid book also suggests that it is possible – but must just be very difficult
  • The sigmoid flexure is the most common site of obstruction in ruminants, in camelids it’s the small orifice at the pelvic penis, followed by the narrow urethra as it enters the glans penis
• Clinical Signs
  
  • Prior to bladder rupture – colic, dysuria, urine dribbling, hematuria, anuria, distended bladder, pulsation of the urethra
  • Following bladder rupture – colic, depression, anorexia, anuria, uroperitoneum, distended abdomen, uremia
    
    • Llamas become frenzied and thrash when urine enters the abdominal cavity, but will calm down as the pain subsides
• Diagnosis
  
  • Bloodwork – hemoconcentration, elevated BUN, hypophosphatemia, hypercalcemia, hypermagnesemia, hyperkalemia, hypercreatininemia, hypochloremia
  • Uroabdomen confirmation – creatinine > 15 mg/dL (serum 3 mg/dL), potassium > 185 mmol/L
• Management
  
  • Breeding males are the most commonly affected
  • Perform urethrostomy over the urolith – return to breeding is poor to unfavorable
  • New camelid book recommends tube cystotomy as the initial management to relieve the pressure on the bladder
• Complications
  
  • Ruptured bladder or urethra, urethral stricture from stone or surgical trauma, chronic cystitis, recurrence of calculi

Question 38

Describe gastroenterolithiasis in camelids.

What types of stones do they get?

How are they diagnosed?

How are they managed?

Answer 38

Gastroenterolithiasis

• Terminology
  
  • Bezoar – derived from words meaning antidotes (apparently useful in arsenic poisoning)
  • Gastrolith – stomach stone
  • Enterolith – intestinal stone
  • Phytobezoar – plant sone
  • Trichobezoar – hair ball
• Etiology
  
  • Mineral stones – Commonly found in the saccules of the camelid stomach
  • Phytobezoars – become major intestinal instructions at the narrowing of the spiral colon
  • Trichobezoars – camelids seldom lick anything, however crias with difficulty breathing while nursing (choanal atresia) often develop habits of chewing the fiber of the mother’s coat to stay full
• Clinical Signs
  
  • Enterolith concretions appear to be incidental
  • Bezoar obstruction is similar to other intestinal obstructions – anorexia, lack of defecation, colic, refusal to drink, depression – without surgery, animal may die in 2-5 days
• Diagnosis
  
  • C-1 concretions may be seen on radiographs
  • Bloodwork may indicate inflammation, dehydration
  • Abdominal fluid may help diagnose peritonitis
• Therapy
  
  • If obstructed, remove surgically
  • Sand impaction – repeated doses of mineral oil or dioctyl sulfonate & neostigmine

Question 39

What are ionophores? What is their mechanism of action?

What are the clinical signs associated with toxicity in dromedary camels?

How is diagnosed?

What are some differentials for this disease?

Answer 39

Fowler 6 Ch 5 – Ionophores: Salinomycin Toxicity in Camelids

Mechanism of Action

• Naturally occurring antimicrobial drugs with wide range of activity (produced by Actinomycetales)
  
  • Widely used for coccidia control in cattle, poultry, and pigs
  • Maintain intestinal balance during times of high-volume concentrate feeding
• Interfere with ion exchange at the cell membrane
• Biliary secretion with no renal clearance
• Predilection of striated muscle cells because of the high concentration of Ca ions and extreme activity involving movement of ions
  
  • Overdosage most often causes clinical signs associated with skeletal muscle dysfunction and myocardial dysfunction
• Overdosages reported in numerous species
  
  • Differences in species sensitivity to ionophores
  • Most often monensin, lasalosid, and salinomycin

Clinical Signs of Overdosage

• Vary among species and are dose dependent
• Muscoskeletal, cardiopulmonary, neurologic, smooth muscle (GI: anorexia, diarrhea)
• Acute death without signs is possible
• Chapter reports on a group of 120 dromedary camels that received a single dose of salinomycin that was an accidentally contaminant in the feed
  
  • Weakness, incoordination 🡪 recumbancy within 4-6 hours
  • SQ edema and myoglobinuria, excessive lacrimation, stiff gait
  • All 120 showed clinical signs and 58 died (80% of the deaths within 2 weeks)
  • Of the surviving camels, half remained ambulatory and the other half became recumbent and required up to 10 weeks to regain voluntary ambulation
  • Lower mortality in calves 7 months or less
  • Necropsy
    
    • Skeletal muscle edema, pale streaking of myocardium, fatty liver dz, hemorrhagic enteritis
• Chapter reports an outbreak in 10 herds of alpacas in Ohio fed a contaminated diet
  
  • Acute death and acute rhabdomyolysis were dominant clinical syndrome during first 5 days
  • Myocardial injury, cardiopulmonary failure, and death were later dominant syndrome

Diagnosis, Treatment, Etc.

• Diagnosis based mainly on feed analysis (rumen and feces may yield positive test)
• Marked increases in CK, LDH, and AST
• DDx: clostridial myosistis, Se toxicity or deficiency, Vit E deficiency, mycotoxins, severe muscle trauma (e.g. capture myopathy, compartment syndrome)
• No antidote. Treaments to decrease absorption may or may not help.
• Supportive care
• Long-term effects may be present due to lasting myocardial fibrosis
• Ideally feeds for use in camelids, horses, and other high-risk species should be mixed at mills where no feed additives are used

Question 40

A recent study evaluated the neonatal disorders of New World camelids.

What are some common presentations of neonatal NW camelids?

What factors were associated with increased odds of death?

What factos were associated with increased hazard of death?

What proportion of neonates survive with appropriate care?

Answer 40

J Am Vet Med Assoc 2021;258:892–898

Investigation of neonatal disorders in New World camelids and factors associated with death during and after hospitalization of affected crias

Stephanie L. Frank dvm Brad B. Nelson dvm, ms, phd Katharine M. Simpson dvm, ms Timothy N. Holt dvm Robert J. Callan dvm, ms, phd Eileen S. Hackett dvm, ms, phd (Reviewed by AJC)

OBJECTIVE To assess signalment, clinical findings, and treatments for New World camelids (NWCs) hospitalized for evaluation and treatment of neonatal disorders and investigate associations between these factors and death during and after hospitalization.

ANIMALS 267 NWCs ≤ 30 days of age.

PROCEDURES Medical records of a veterinary teaching hospital were retrospectively reviewed to identify NWCs admitted for evaluation and treatment of neonatal disorders between 2000 and 2010. Signalment, physical examination data, diagnostic findings, treatments, and outcomes were recorded. Factors were examined for association with death during hospitalization and the overall hazard of death by use of multivariable logistic regression and Cox proportional hazards analysis, respectively.

RESULTS The sample comprised alpacas (n = 255) and llamas (12). Median age at admission was 3 days, and median hospitalization time was 2 days; 208 of the 267 (77.9%) neonatal NWCs survived to hospital discharge. Factors associated with increased odds of death during hospitalization included prematurity or dysmaturity, hypothermia, sepsis, toxic changes in neutrophils, and undergoing surgery. The odds of death during hospitalization also increased as anion gap increased. After discharge, 151 of 176 (85.8%) animals had follow-up information available (median follow-up time, 2,932 days); 126 (83%) were alive and 25 (17%) had died. Prematurity or dysmaturity, congenital defects, sepsis, oxygen administration, and undergoing surgery as a neonate were associated with an increased hazard of death; the hazard of death also increased as serum chloride concentration at the time of hospitalization increased.

CONCLUSIONS AND CLINICAL RELEVANCE Results suggested the prognosis for survival during and after hospitalization is good for most NWCs hospitalized because of neonatal disorders.

Key Points:

• Common presentations for neonatal NWCs: prematurity/dysmaturity, congenital defects, poor regulation of body temperature, and blood glucose concentration, FPT and sepsis.
  
  • Crias born after dystocia or C-section have increased risk for hypoglycemia and FPT
• Objective – evaluate the type and distribution of disorders as well as diagnostic tests and treatments performed
• Primary diagnosis was multiple disorders followed by FPT, prematurity/dysmaturity, sepsis and congenital
  
  • Most common congenital disorder was choanal atresia
• ~80% of neonates survived to hospital discharge
  
  • Factors associated with increased odds of death: prematurity/dysmaturity, hypothermia, sepsis, toxic changes in neutrophils, increased anion gap and surgery
  • Increased hazard of death associated with prematurity/dysmaturity, congenital defects, sepsis, oxygen administration, increasing Cl concentration and surgery.
• Factors associated with decreased odds of death during hospitalization: increased hospitalization time, FPT, enema, increasing TP
  
  • As hospital time and serum IgG during hospitalization increased, the hazard of death decreased.
• Primary cause of death from necropsy records was sepsis
• ~80% were still alive at the time of follow-up survey and ~90% reached their expected potential

Take home: Prognosis for survival is good for more NWCs hospitalized because of neonatal disorder and have a good chance of reaching their intended use long-term.

Question 41

A recent study described the management of obstructive urolithiasis in a Bactrian camel.

What clinical signs are associated with urethral obstruction?

What are the most common uroliths in camels?

What surgical procedures were performed to manage this animal?

Why is cystotomy difficult in camels?

Answer 41

Rosser, J. M., Jacob, S. I., & Brounts, S. H. (2019). Use of tube cystostomy in the surgical management of obstructive urolithiasis in a Bactrian camel. Journal of the American Veterinary Medical Association, 254(7), 868-873.

Abstract: CASE DESCRIPTION A 6-year-old castrated male Bactrian camel was evaluated because of a 14- hour history of oliguria and stranguria that progressed to anuria.

CLINICAL FINDINGS Perineal urethral pulsations and intermittent tail flagging with no accompanying urination were observed. Ultrasonography of the urethra revealed multiple hyperechoic foci with shadowing artifact indicative of calculi present in the penile urethra distal to the sigmoid flexure. Rectal palpation revealed a pulsating hard urethra and intact distended urinary bladder. Further clinical examination was not possible because of challenges associated with handling the camel.

TREATMENT AND OUTCOME Urethral catheterization through a perineal urethral incision failed to achieve urinary bladder decompression. Tube cystostomy was performed to prevent bladder rupture. Urethrocystography performed 3 days after surgery revealed a urethral rupture at the level of the prepuce. Five weeks after surgery, the camel could urinate a steady stream via the urethrotomy site. Seven weeks after surgery, the cystostomy tube was removed, and the urethrotomy site was modified to provide a permanent urethral opening via perineal urethrostomy. During 6 years of subsequent periodic follow-up by telephone, the owner reported that the camel continued to do well and urinate through the revised opening.

CLINICAL RELEVANCE To the authors’ knowledge, this is the first detailed description of a tube cystostomy in an adult camel with obstructive urolithiasis that includes information on the patient’s long-term outcome. This technique was a viable option in the surgical management of obstructive urolithiasis in this camel and may be useful for other large camelids as well.

• • Urethral obstruction from urolithiasis in large animals
    
    • clinical signs: stranguria, hematuria, urethral pulsation, peripreputial edema from rupture, colic-like signs (tachypnea, tachycardia), oliguria progressing to anuria
    • Camels - Silica calculi most commonly reported, single or multiple
    • Small ruminants - Struvite and apatite calculi, single or multiple
    • Large ruminants - Phosphate calculi from high-grain diets, single calculus in cattle
    • Prevention: control P:Ca ratio in diet, include high-quality, high-fiber roughage, increase water intake, +/- ammonium chloride to acidify the urine
• Tube cystostomies in cattle and small ruminants- short-term success 76-90%, long term 86%
• Camel bladder sits within pelvic cavity, dorsal to the ventral abdominal wall
  
  • Difficult to see on transabdominal ultrasound and to reach for cystostomy
• Alternatives
  
  • Perineal urethrotomy - high rate of post-op complications (stricture), unsuitable for breeding animals
  • Minimally invasive tube cystostomy in standing or laterally recumbent small ruminants via left paralumbar fossa approach
  • Laparoscopic-assisted tube cystostomy also reported, requires dorsal recumbency and Trendelenburg position
  • Laser lithotripsy - depends on urethra large enough to pass laser in endoscope, positioning it on the calculi, and hardness of the calculi
    
    • Proximal urethra in ruminants cannot be evaluated due to sigmoid flexure and urethral recess (on the dorsal urethra at the level of the ischium)
    • Often have to do cystotomy concurrently to remove calculi that were flushed retrograde back into the urinary bladder and can’t be retrieved with a wire basket
• Bloodwork changes: hypercalcemia (13), hyperphosphatemia (12.7), hypokalemia (3)
• Perineal urethrotomy performed first but only leaked small amount of urine with pulsations
  
  • Sedation: xylazine 0.3 mg/kg IV, coccygeal epidural 2% lidocaine in cush position then xylazine 0.3 mg/kg and butorphanol 0.1 mg/kg boluses IV (aural vein IV catheter)
  • Midline incision 10 cm ventral to anus, extending 8 cm to ischial arch
  • Suspect unsuccessful due to inflammation - became patent later when swelling reduced
  • Urethral catheterization from urethrotomy site also unsuccessful
• Tube cystostomy to decompress bladder, used equine bronchoalveolar lavage tube (10 mm od with inflatable cuff, sterile)
  
  • Pen G 22,000 U/kg, ceftiofur 2.2 mg/kg SQ, flunixin 1.1 mg/kg IV, ketamine 2.2 mg/kg IV, diazepam 0.1 mg/kg IV, iso vis ET tube
  • 12 cm incision left paralumbar fossa (10 cm ventral to left tuber coxae), 3 cm tunneled incision through ventrolateral left paralumbar fossa, stab incision into bladder just cranioventral to left lateral ligament of the bladder, introduced BAL tube, inflated the cuff with sterile saline, sutured tube to skin, lavaged peritoneal cavity and suctioned, closed lap site in 4 layers (transverse abd, int abd oblique, ext abd oblique, skin
  • Phenazopyridine 4 mg/kg PO q8h - topical analgesia on the mucosa of the urinary tract
• Urethrotomy to remove last calculi, conversion to permanent urethrostomy at perineal urethrotomy site due to scar tissue formation at previous urethral rupture site
  
  • Detomidine 0.1-0.125 mg/kg IM, Telazol 2-4 mg/kg IM, ketamine 2.2 mg/kg IV, iso via ET tube, ceftiofur CFA 6.6 mg/kg SQ, meloxicam 1 mg/kg PO q24h
• Successful tube cystostomy to aid in obstructive urolithiasis in an adult camel with long-term follow-up.
  
  • Alternative to urethrotomy or urethrostomy
• Camels - Silica calculi, single or multiple, prevent with high-fiber roughage diet +/- ammonium chloride (acidify urine)

Question 42

A recent study described a novel surgical technique to treat complete membranous choanal atresia in an alpaca cria.

What is choanal atresia?

Is it common in camelids?

How was this alpaca cria treated?

Were there any complications with treatment?

Are camelids obligate nasal breathers?

Answer 42

Pader, K., Burns, P. M., Brisville, A. C., Rousseau, M., Blond, L., Truchetti, G., … & Francoz, D. (2017). Use of a novel surgical approach for treatment of complete bilateral membranous choanal atresia in an alpaca cria. Journal of the American Veterinary Medical Association, 250(9), 1036-1041.

CASE DESCRIPTION

A 4-hour-old 6.3-kg (13.9-lb) female alpaca cria was evaluated because of severe respiratory distress and difficulty nursing since birth.

CLINICAL FINDINGS

The cria had open-mouth breathing and cyanotic membranes, with no air- flow evident from either nostril. Supplemental oxygen was delivered, and the patient was anesthetized and intubated orotracheally; a CT evaluation of the head confirmed bilateral membranous obstruction of the nasal cavities, consistent with complete bilateral choanal atresia.

TREATMENT AND OUTCOME

Choanal atresia was treated with an endoscopically assisted balloon- dilation technique, and temporary tracheostomy was performed. Stenosis recurred, requiring revision of the repair and intranasal stent placement 3 days after the first surgery. The tracheostomy tube was removed the next day. Complications during hospitalization included mucoid obstruction of the tracheostomy tube, granulation tissue development in the trachea near the tracheostomy site, mucoid stent obstruction, aspiration pneumonia, and presumed partial failure of passive transfer of immunity. The stents were removed 2 weeks after admission, and the cria was discharged 3 days later. The owner was advised that the animal should not be bred. At last follow-up 3 years later, the alpaca was doing well.

CLINICAL RELEVANCE

Surgical treatment with a balloon-dilation technique and placement of nasal stents with endoscopic guidance were curative in this neonatal alpaca with bilateral membranous choanal atresia. Computed tomography was useful to determine the nature of the atresia and aid surgical planning. Because a genetic component is likely, owners should be advised to prevent affected animals from breeding.

• Choanal atreasia – congenital membranous or bony obstruction at caudal aspect of choanae that blocks communication between nasal cavities and pharynx
  
  • Most common congenital maxillofacial defect in camelids – 0.75% of llama and 0.48% of alpaca births
• Camelids are primary but not obligate nasal breathers

Question 43

A recent study described the medical management of an osseous sequestrum in an alpaca cria.

What predisposing factors in this case led to the sequestrum?

How was this case managed?

Answer 43

Medical management of an osseous sequestrum in an alpaca cria.

Oman RE, Adkins PR, Reed SK.

Journal of the American Veterinary Medical Association. 2021;258(12):1394-1397.

CASE DESCRIPTION A 2-month-old 12.0-kg (26.4-lb) sexually intact male alpaca was evaluated for a 1-week history of progressive forelimb lameness with no known history of trauma.

CLINICAL FINDINGS The cria had toe-touching lameness in the right forelimb with a firm swelling at the distal dorsomedial metacarpal region. Signs of pain were elicited on palpation of the swollen region. There was no associated wound or draining tract. Radiographic examination revealed soft tissue swelling and osteomyelitis of the distal portion of the third metacarpal bone with a possible medial cortical sequestrum.

TREATMENT AND OUTCOME The cria was hospitalized and treated with meloxicam (1 mg/kg [0.45 mg/lb], PO, q 72 h) and ceftiofur sodium administered SC (2.2 mg/kg [1 mg/lb], q 12 h for 8 days) and by means of regional limb perfusion (1.25 mg/kg [0.57 mg/lb], IV, q 48 h for 8 days). Lameness and swelling improved, and the cria was discharged from the hospital with meloxicam (1 mg/kg, PO, q 72 h for 2 weeks) and ceftiofur crystalline free acid (1.5 mg/kg [0.68 mg/kg], SC, q 5 d for 2 weeks). At a recheck examination 17 days later, there was radiographic evidence of a well-defined 3.4 × 0.3-cm osseous sequestrum in the distal aspect of the affected third metacarpal bone. The owner declined further treatment and elected to monitor the cria at home. One year later, radiographic examination revealed nearly complete resolution of the sequestrum.

CLINICAL RELEVANCE Results for this patient suggested that osseous sequestra in some camelids may resolve following medical treatment without surgical intervention.

Background

• 2 mo old Suri alpaca, toe-touching lame R forelimb, firm warm painful swelling, medial cortical sequestrum on rads
  
  • Suspected inadequate passive transfer of immunity, hematogenous osteomyelitis
• Regional limb perfusion with ceftiofur sodium, systemic ceftiofur and meloxicam
• 1 year later nearly complete resolution on rads

Key Points

• First report of resolution of a sequestrum in an alpaca cria with medical management only
• Location on 3rd metacarpal bone allowed continued limb support by 4th metacarpal bone
• Minor food producing species affect antimicrobial choice, exempt from major food species restriction on extralabel use of celphalosporins

Conclusions: medical management with RLP has promise as a less expensive and invasive treatment for osseous sequestrum in alpaca cria

Question 44

A recent study evaluated the piroplasms of dromedary camels.

What are piroplasmids? What are some species examples?

What clinical signs do they cause? How are they transmitted?

How common were these in the camels?

Answer 44

Bahrami, S., Tabandeh, M. R., & Tafreshi, A. R. G. (2017). Prevalence and molecular identification of piroplasmids in Iranian dromedaries (Camelus dromedarius). Journal of Zoo and Wildlife Medicine, 48(4), 1026-1030.

Abstract: Camels (Camelus dromedarius) are important, multipurpose local animals in Iran. Despite their importance, camelid parasitic diseases have not received adequate attention in the veterinary literature. The present study investigated the prevalence of, and molecularly identified, camel piroplasms in Iran. Blood samples from 248 camels from five different regions of Iran were screened for the presence of piroplasmid infection using an 18SrRNA polymerase chain reaction (PCR) sequencing method. Of the 248 samples, 16 were positive for piroplasms via PCR (6.45%). Ten PCR amplicons with expected sizes were sequenced for molecular characterization. Three camels were infected with Babesia caballi and seven with Theileria equi. Statistical analysis showed that age, sex, and location were not risk factors for infection with piroplasmids in camels.

• Piroplasmids – tick-borne apixomplexan parasites.
  
  • i.e. babesia, Theileria, Cytauxzoon.
  • CS – Variable, acute fever, anemia, edema, dyspnea, death, or asymptomatic.
  • Parasitemia not consistent on blood smear.
  • Ixodid tick vectors.
  • Two camelid-specific species – Theileria camelensis, Theileria dromedarii.
    
    • Questionable taxonomy.
• Overall prevalence 16/248 = 6.45%.
• Age, sex, location not risk factors.
• Camels are a possibly a reservoir for equine piroplasms i.e. T. equi and B. caballi. Similar ticks on both camels and horses, also dogs may play a role.

Takeaway: Overall prevalence for piroplasmids in camels in five geographic regions of Iran 6.45%; Age, sex, location not risk factors in this study.

Question 45

A recent study evaluated the acute phase and hemostatic responses of dromedary camels.

What are some common inflammatory indicators?

What are some positive and negative acute phase proteins?

What are acute phase proteins sepcifically in camels?

Animals chronically infected with corynebacterium showed what changes with their acute phase proteins and TEG profiles?

Answer 45

Greunz, E. M., Krogh, A. K., Pieters, W., Ruiz, O. A., Bohner, J., Reckendorf, A., … & Bertelsen, M. F. (2018). The acute-phase and hemostatic response in dromedary camels (Camelus dromedarius). Journal of Zoo and Wildlife Medicine, 49(2), 361-370.

Abstract: Acute-phase reactants indicate inflammation and are increasingly used in veterinary medicine to indicate and to monitor progression of disease. Hemostasis and inflammation have interconnected pathophysiologic pathways and influence each other on different levels. This study established observed normal ranges for acute-phase reactants and for coagulation and thromboelastographic (TEG) parameters in 49 dromedary camels (Camelus dromedarius) and assessed the response to chronic and acute inflammation. Chronically infected animals suffering from lymph abscessation due to Corynebacterium spp. had significantly higher concentrations of the acute-phase reactants haptoglobin (P < 0.005) and fibrinogen (P < 0.013) and an increased clot strength characterized by an increase of the TEG parameters MA (P < 0.039), representing the maximum amplitude of the clot strengths, and G, the global clot strength (P < 0.022), compared to healthy animals. When the acute-phase and hemostatic responses of 10 males receiving a gonadotropin-releasing hormone vaccine and of 9 males that were surgically castrated over 7 days were studied, haptoglobin proved to be a minor positive acute-phase protein, with moderate levels in healthy animals. It increased significantly after both vaccination and castration and remained elevated 7 days postinsult. The negative reactant ironsignificantly decreased over the 7-day period after castration, whereas a similar decrease following vaccination lasted less than 3 days. Fibrinogen reacted as a positive, minor reactant, with a significant increase and a peak on days 3–5, with higher values seen after castration. Prothrombin time showed a slight shortening at days 5–7, and the TEG parameters MA and G showed significantly increased values, similar to fibrinogen. The acute-phase protein serum amyloid A showed poor repeatability, suggesting that the assay was not reliable.

• Inflammatory indicators – iron, TP, APPs.
  
  • Iron decreases, nonspecific for bacterial infection.
  • Immunoglobulins increase TP.
  • APP – Major have immediate increase and > 10x normal, normalize shortly. Minor havesmaller gradual response, longer lasting.
    
    • Positive APPs – fibrinogen, SAA, haptoglobin.
    • Negative APPs – Albumin.
• Hemostasis and inflammation.
  
  • Cytokines (IL1, 6), protein synthesis (fibrinogen, factor VIII).
  • Direct interaction between cells – platelets, leukocytes, endothelial cells.
  • Evaluation via PT, PTT, fibrinogen, TEG.
• In camels:
  
  • Generally accepted that haptoglobin, fibrinogen, SAA positive APPs.
  • Albumin negative APP.
• Objective:
  
  • Characterize development of hemostatic parameters and APP reactants over 7 days after acute onset of trauma and assess difference in parameters between healthy and chronically infected camels.
  • Establish normal ranges of hemostatic parameters and APPs.
• Corynebaccterium camels had > haptoglobin and fibrinogen.
  
  • Also higher WBC counts, significant difference in MA and G TEG parameters.
• Prospective study, > haptoglobin in all castrated camels, remained increased through 7 days.
  
  • Also > fibrinogen, < iron.
  • No difference in SAA.
• Haptoglobin is a minor positive APP in camel, unlike cattle (major).
• Camels with chronic inflammation showed significantly higher fibrinogen (positive minor APP).
• Iron levels not significantly altered in chronically infected camels (unlike horses), but is considered a negative reactant in acute onset inflammation in camels.
• Albumin did not significantly decrease in chronically infected or during prospective study.
• APTT and PT no significance difference.
• No significant changes in TEG parameters for initiation of clot formation.
• In chronically infected animals, MA and G are increased, representing strength of the formed clot (which is consistent with increased fibrinogen which is important in clot formation).

Question 46

A recent paper described gastric pythiosis in a bactrian camel.

What is pythium? What types of disease does it typically cause?

What lesions were present in this camel?

Answer 46

Heck, L. C., Bianchi, M. V., Pereira, P. R., Lorenzett, M. P., de Lorenzo, C., Pavarini, S. P., … & Sonne, L. (2018). Gastric pythiosis in a bactrian camel (bactrianus camelus). Journal of Zoo and Wildlife Medicine, 49(3), 784-787.

Brief Communication

Abstract: Pythium insidiosum, an aquatic oomycete, causes chronic lesions in the skin and digestive tract of multiple species. A captive-bred Bactrian camel (Camelus bactrianus) showed clinical signs of lethargy and weight loss in a clinical course of 30 days, with no response to treatment. At necropsy, the abdominal cavity had approximately 32 L of a yellow, turbid fluid with fibrin. The third compartment of the stomach (C-3) showed a focal area of rupture covered with fibrin. Close to this area, the C-3 wall was thickened and firm, demonstrating irregular, yellow, and friable areas on cut surface (kunkers). Microscopically, these corresponded to necrosis, characterized by a central amorphous eosinophilic material, surrounded by a pyogranulomatous inflammatory infiltrate and fibrosis. Negatively stained hyphae were observed at the periphery of the necrotic areas, which showed marked immunostaining for P. insidiosum. Pythiosis in camelids may involve the stomach, resulting in peritonitis and death.

• Family Camelidae. Order Artiodactyla, suborder Tylopoda.
  
  • New world – Lama spp, Vicugna spp.
  • Old world – Camelus bactrianus and C. dromedaries.
  • Foregut fermentation, three-compartment stomach (C1, C2, C3).
    
    • Analogous to rumen, reticulum, omasum, abomasum of ruminants.
    • All three compartments contain some glandular mucosa, unlike ruminants which have three aglandular stomachs.
• Pythium insidiosum.
  
  • Kingdom Stramenopila.
  • Chronic disease with lesions on skin, GIT, systemic.
  • Reported in horses, dogs, cattle, sheep.
  • Previously described in C. dromedaries – skin, vulva, C3.
• 3yo M C. bactrianus – lethargy and wt loss, 30 days no improvement, died.
  
  • Nx – 32L yellow turbid peritoneal fluid, fibrin, C3 focal rupture, marked thickening of wall, intramural nodular lesions, multifocal to coalescing yellow, irregular firm but friable masses compatible with kunkers intermixed with firm white tissue.
    
    • Kunkers – unique components of these lesions, common in equine pythiosis due to tendency of horses to respond with abundant eosinophilic inflammation that becomes necrotic.
  • Probable infection from consumption of contaminated water containing infective zoospores (most common route in dogs).
  • Feeding changes or episodes of gastric acidosis predispose for fungal invasion.
  • Gastric pythiosis should be a ddx for camelids with CS of wt loss, vomiting, diarrhea, apathy, assoc with prolonged exposure to flood and conditions favoring penetration of the agent. Other ddx GI FB, neoplasia, zygomycosis.
    
    • Zygomycosis caused by Conidobolus spp.
  • Affects mainly rhinopharyngeal region, sheep.
  • Larger hyphae and bulbous dilatations not present in P. iniodisum (smaller, irregular branching of hyphae). GMS and IHC to confirm.

Question 47

A recent study described black oil sunflower seed toxicity in New World Alpacas.

What clinical signs were seen in these animals?

What clinicopathologic chnges were present in these animals?

How were these animals treated? What was their prognosis?

What lesions were present on necropsy?

How did this intoxication differ from grain overload?

Answer 47

McKenzie, E. C., Guerra, J. C., Middleton, J. R., Kim, D. Y., Williams, F., Garcia, T. M., & Russell, D. S. (2021). Black oil sunflower seed ingestion associated with renal azotemia, gastroesophageal ulceration, and a high mortality rate in four alpacas and two llamas. Journal of the American Veterinary Medical Association, 259(4), 406-414.

CASE DESCRIPTION

4 alpacas and 2 llamas (11 months to 11 years old) from 2 properties were examined for lethargy (6/6), salivation and regurgitation (4/6), and recumbency (3/6). Signs developed approximately 48 to 72 hours after accidental access to black oil sunflower seeds.

CLINICAL FINDINGS

3 alpacas died suddenly prior to treatment and were necropsied. One llama survived, and 1 alpaca and 1 llama died after days of medical treatment. All 3 treated animals had systemic inflammatory signs including tachycardia, fever, and hematologic changes. Biochemical anomalies included azotemia, hyperglycemia, hyponatremia, hypochloremia, and hypoalbuminemia. Necropsy identified numerous sunflower seeds in the gastrointestinal tract of all 5 animals that died, with pulmonary congestion (5/5 animals), mild centrilobular vacuolar hepatic degeneration (4/5), and erosions of the esophagus (3/5) and first (3/5) and third (1/5) compartments of the forestomach. Renal tubular necrosis was found in the 2 animals that died on day 4 of treatment.

TREATMENT AND OUTCOME

One llama responded successfully to intensive medical management including supplemented IV fluid therapy, oral and partial parenteral nutrition, and administration of antimicrobials, furosemide, and insulin and was clinically normal with plasma biochemical analysis values within reference range 12 weeks later. Vitamin D, oxalates, heavy metals, and mycotoxins were excluded as the cause of clinical signs on the basis of screening of uneaten seeds and tissue samples and gastric content from the treated llama that died.

CLINICAL RELEVANCE

Inadvertent large volume black oil sunflower seed ingestion resulted in a high mortality rate in camelids. A specific toxic principle was not identified. Feeding this product to camelids is not recommended to avoid the risk of accidental overingestion and subsequent disease

Key Points:

• Not grain overload – gastric pH was normal, seeds are more fatty than carbohydrate rich
• No evidence of known toxins – likely some other toxic principle within the seeds not yet identified
• Black oil sunflower seed ingestion in camelids carries a guarded prognosis

Take Home Message: Don’t feed camelids sunflower seeds

Question 48

A recent study investigated the prevalence of anaplasmosis in dromedary camels.

What blood cell is affected by Anaplasma phagocytophilum?

What is the most common tick vector?

What are the clinical signs of anaplasmosis in camels?

How prevalent was anaplasmosis in the Iranian camels investigated?

Answer 48

Bahrami, S., Hamidinejat, H., & Tafreshi, A. R. G. (2018). First molecular detection of Anaplasma phagocytophilum in dromedaries (Camelus dromedarius). Journal of Zoo and Wildlife Medicine, 49(4), 844-848.

Abstract: Anaplasma phagocytophilum infects a wide variety of wild and domestic animals and causes an emerging zoonotic tick-borne disease. There are no available data regarding the presence of A. phagocytophilum in camels (Camelus dromedarius). Therefore, the objective of this study was to investigate the prevalence of A. pagocytophilum in Iranian camels. Whole blood of 207 camels from five geographical regions of Iran was tested for A. phagocytophilum using polymerase chain reaction (PCR), nested PCR, and specific nested PCR based on 16S rRNA. The overall prevalence of infection in tested animals was 34.2% (71/207). Sex was not identified as a risk factor for A. phagocytophilum infection, but analysis revealed significant differences in age and region. In conclusion, Iranian camels can be potential reservoirs for A. phagocytophilum, and Iran must be considered an enzootic area for this infection as indicated by the high subclinical infection rate in camels.

• A. phagocytophilum forms morulae in granulocytes, not erythrocytes
• Ixodes is the most common tick vector (others include dermacentor, Haemophysalis, Hyalomma, Rhipicephalus)
• Infection is most common in sheep, cattle, and deer
• CS – fever, dullness, anorexia, sudden drop in milk yield, weight loss, coughing, abortion, stillbirth, infertility
• Higher prevalence in camels than in cattle in Iran may be due to poor level of hygiene, medicine, and less economic importance

Take Home: 34% of camels in Iran are positive for Anaplasma phagocytophilum

Question 49

A recent study investigated the pharmacokinetics and pharmacodynamics of buprenorphine and sustained-release buprenorphine in alpacas.

How long did plasma buprenorphine concentrations stay above therapeutic levels in alpacas?

Answer 49

Dooley, S. B., Aarnes, T. K., Lakritz, J., Lerche, P., Bednarski, R. M., & Hubbell, J. A. (2017). Pharmacokinetics and pharmacodynamics of buprenorphine and sustained-release buprenorphine after administration to adult alpacas. American journal of veterinary research, 78(3), 321-329.

OBJECTIVE

To determine pharmacokinetics and pharmacodynamics of buprenorphine after IV and SC administration and of sustained-release (SR) buprenorphine after SC administration to adult alpacas.

ANIMALS

6 alpacas.

PROCEDURES

Buprenorphine (0.02 mg/kg, IV and SC) and SR buprenorphine (0.12 mg/kg, SC) were administered to each alpaca, with a 14-day washout period be- tween administrations. Twenty-one venous blood samples were collected over 96 hours and used to determine plasma concentrations of buprenorphine. Pharmacokinetic parameters were calculated by use of noncompartmental analysis. Pharmacodynamic parameters were assessed via sedation, heart and respiratory rates, and thermal and mechanical antinociception indices.

RESULTS

Mean ± SD maximum concentration after IV and SC administration of buprenorphine were 11.60 ± 4.50 ng/mL and 1.95 ± 0.80 ng/mL, respectively. Mean clearance was 3.00 ± 0.33 L/h/kg, and steady-state volume of distribution after IV administration was 3.8 ± 1.0 L/kg. Terminal elimination half-life was 1.0 ± 0.2 hours and 2.7 ± 2.8 hours after IV and SC administration, respectively. Mean residence time was 1.3 ± 0.3 hours and 3.6 ± 3.7 hours after IV and SC administration, respectively. Bioavailability was 64 ± 28%. Plasma concentrations after SC administration of SR buprenorphine were below the LLOQ in samples from 4 alpacas. There were no significant changes in pharmacodynamic parameters after buprenorphine administration. Alpacas exhibited mild behavioral changes after all treatments.

CONCLUSIONS AND CLINICAL RELEVANCE

Buprenorphine administration to healthy alpacas resulted in moderate bioavailability, rapid clearance, and a short half-life. Plasma concentrations were detectable in only 2 alpacas after SC administration of SR buprenorphine.

• Plasma concentrations >0.7 ng/mL are considered therapeutic in other species
  
  • Obtained >0.7 ng/mL for about 1.3 hours
• Much higher clearance and shorter half life

Take home: Buprenorphine doesn’t last long enough to be useful

Question 50

A recent described a CT protocol for evaluation of dentition in alpacas.

What types of dental disease are common in alpacas?

What was the optimum scanning protocol?

Answer 50

Optimized computed tomography protocol for assessment of dentition in alpacas

Caroline V. Fulkerson DVM, MS; Chee Kin Lim DVM, BVSc, MMedVet; Aubrey N. Baird DVM, MS; Ann B. Weil DVM, MS; Hock Gan Heng DVM, MVS, MS; Beatrice Gutierrez-Crespo DVM; George E. Moore DVM, PhD

AJVR • Vol 79 • No. 3 • March 2018

Abstract:

OBJECTIVE To determine the optimal protocol for acquisition of CT images of the dentition in alpacas. ANIMALS 3 healthy adult male alpacas.

PROCEDURES Each alpaca was anesthetized with an IM injection of a combination of ketamine, xylazine, and butorphanol and positioned in sternal recumbency on the CT couch with its legs folded in a natural cush position and its head positioned within the isocenter of the gantry of a 64-slice CT scanner. Images were acquired by means of 6 protocols (sequential and helical modes at slice thicknesses of 1.25, 2.5, and 5 mm). Five images (2 molar, 2 premolar, and mandibular incisor teeth) were selected from each protocol for evaluation by 3 veterinary radiologists. For each image, tooth root visibility and sharpness and image noise artifact were subjectively evaluated on a 3-point scoring system.

RESULTS Slice thickness significantly affected tooth root visibility and tooth root sharpness but did not affect image noise artifact. Acquisition mode significantly affected tooth root visibility and tooth root sharpness as well as image noise artifact. Tooth root visibility and sharpness did not differ significantly between the helical and sequential images when the slice thickness was 1.25 mm. Image noise artifact was greater for helical images than sequential images but did not differ by slice thickness within either acquisition mode.

CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that for a 64-slice CT scanner, the optimal protocol for the acquisition of CT images of the dentition in alpacas was a sequential scan with a slice thickness of 1.25 mm

Summary:

Introduction:

• Dental disease – common in alpacas
  
  • tooth root abscesses, mandibular osteomyelitis, malocclusion, fractured teeth, uneven teeth, overgrown teeth, worn teeth, and persistent deciduous teeth
• alpaca skull rads - sedation and a minimum of 4 views
• CT superior to evaluate skull – decreased time of procedure because no need to re-position, increased contrast resolution, lack of superimposition of soft tissue and osseous structures, and the ability to reconstruct multiplanar and 3-D volume rendering images
• Alpacas difficult to intubate – small trachea, deep oral cavity

M + M:

• CT scans performed on alpacas using injectable anesthesia (ketamine 4-6 mg/kg, xylazine 0.4-0.6 mg/kg, and butorphanol 0.1 mg/kg) in cushed with neck extended position
• Each alpaca underwent 6 scan protocols, 3 sequential scans with slice thicknesses of 1.25 (S1.25), 2.5 (S2.5), and 5 (S5) mm and 3 helical scans with slice thicknesses of 1.25 (H1.25), 2.5 (H2.5), and 5 (H5) mm

Conclusion/results

• Injectable anesthesia provided adequate restraint for CT
• optimized CT protocol for the acquisition of diagnostic images of the dentition for alpacas by means of a 64-slice CT scanner was a sequential mode with a slice thickness 1.25 mm (S1.25 protocol)
  
  • superior quality images for evaluation of tooth roots
  • less image noise artifact than images acquired in the helical mode
  • 1.25 mm slice thickness provided better visualization of tooth roots and demarcation of the dental and alveolar bone margins
• Image noise artifact - image graininess caused by variation in the number of x-ray photons emerging from the patient that are recorded by the photon detectors
  
  • As slice thickness decreases, z-axis resolution improves but there is an increase in image noise artifact because fewer photons reach the x-ray detector
• Helical scanning - uses different start and end point for each slice and requires an additional data processing step to create an image = interpolation - can result in reconstruction artifacts
  
  • Sequential scanning does not require interpolation
• Results of the present study indicated that image noise artifact was not significantly affected by slice thickness but was significantly affected by image acquisition mode (sequential or helical)
• Multiplanar reconstruction for helical scans is superior to that for sequential scans
• optimal protocol for the acquisition of images of dentition by means of a 64-slice CT scanner was a sequential scan with a slice thickness of 1.25 mm and use of a high-frequency reconstruction algorithm
  
  • if multiplanar reconstruction images desired, recommend an additional helical scan

Question 51

A recent paper described the placement of a transphyseal screw for correction of bilateral varus deformities in an alpaca cria.

When are surgical techniques (hemicircumferential periosteal transection & elevation, transphyseal screw placement) considered in varus or valgus cases?

What are some potential complications with these procedures?

How did this cria do?

Answer 51

McQuillan, S., Vermedal, H., O’Leary, J. M., Chandler, C., & Kearney, C. (2021). Transphyseal screw placement with and without hemicircumferential periosteal transection and elevation for correction of severe bilateral carpal varus deformities in an alpaca cria. Journal of the American Veterinary Medical Association, 259(9), 1057-1062.

CASE DESCRIPTION

A 2.5-month-old 17.5-kg female alpaca cria was presented for evaluation and treatment of severe bilateral carpal varus deformities.

CLINICAL FINDINGS

No lameness was evident at a walk, and neither carpal varus deformity could be corrected by means of manipulation. Radiography revealed severe varus of the left (27°) and right (21°) carpal regions. No additional conformational abnormalities were detected.

TREATMENT AND OUTCOME

A single 2.7-mm transphyseal cortical screw was placed in the distolateral aspect of the radius in each limb. On reexamination 8 weeks after screw placement, the left carpal varus deformity had corrected from 27° to 2.6°, and the left transphyseal screw was removed. The right carpal varus deformity had improved but was still present (18°), and hemicircumferential periosteal transection and elevation was performed on the mediodistal aspect of the right radius. Five weeks after the second surgery, the right carpal varus deformity had corrected to 2.4°, and the right transphyseal screw was removed. Six months after the second screw removal, both thoracic limbs remained straight, the cria had a normal gait, and the owner was happy with the cosmetic result.

CLINICAL RELEVANCE

Placement of a single transphyseal cortical screw with or without the addition of hemicircumferential periosteal transection and elevation can provide a favorable outcome in skeletally immature alpacas with severe carpal varus deformities.

Key Points:

• Surgical techniques for tx of ALD include growth acceleration techniques (physeal stimulation, HCPTE – hemicircumferential periosteal transection and elevation) and growth retardation techniques (transphyseal bridging and single transphyseal screw implants).
• If conservative management is unsuccessful or the angulation is > 10 deg in animals < 3 mos old, surgical tx often consists of HCPTE combined with partial ulnar ostectomy.
• Complications associated with single transphyseal screw placement in equids – Septic physitis, metaphyseal collapse following implant removal.
• Successful correction using single transphyseal cortical screw on one side + hemicircumferential periosteal transection and elevation on the other side in a cria.

Question 52

A recent study described disseminated toxoplasmosis in a dromedary camel.

What causes encysted tachyzoites to divide?

Why is toxoplasmosis a concern in camels in the middle east?

What were the lesions seen in this case?

Answer 52

Journal of Zoo and Wildlife Medicine 48(3): 937–940, 2017

DISSEMINATED TOXOPLASMOSIS IN A CAPTIVE ADULT DROMEDARY CAMEL (CAMELUS DROMEDARIUS)

Jennifer Riley, D.V.M., Michael M. Garner, D.V.M., Dipl. A.C.V.P., Matti Kiupel, Dr vet. med., Dr habil, Ph.D., Dipl. A.C.V.P., and Elizabeth E. Hammond, D.V.M., Dipl. A.C.Z.M.

Abstract: An 11-yr-old dromedary camel (Camelus dromedarius) at a zoo in south Florida presented with diarrhea while being treated with enrofloxacin and dexamethasone for a chronic skin condition. Three weeks after initiation of therapy with dexamethasone, the camel developed diarrhea, which worsened despite treatment with antibiotics. The animal became increasingly debilitated, developed hemorrhagic diarrhea, declined rapidly over the next 3 days, and died despite aggressive fluid therapy and supportive care. Histologic examination revealed intralesional protozoal tissue cysts consistent with Toxoplasma gondii in the intestines, lungs, and liver, as well as lymphoid depletion of the spleen suggesting immunosuppression. To the author’s knowledge this is the first reported case of disseminated toxoplasmosis that clinically manifested as hemorrhagic enterocolitis in a camel.

Key Points:

• Toxoplasma
  
  • Tachyzoites divide when immunosuppressed resulting in tissue necrosis and inflammation
  • Concern with camels due to the consumption of camel milk and meat in some countries
  • High incidence of seroprevalence in camels, but not many clinical reports
• Single dose of steroids given in this animal - may have contributed to immunosuppression, but other factors could have caused this
• C3 hemorrhagic ulcers in camelids (seen in this case) can be caused by stress, high-grain diets, and NSAIDs

Take Home: Disseminated toxoplasmosis can occur in immunosuppressed dromedaries