Diagnosis & Management of Diseases of Neonatal & Juvenile Camelids
ACVIM 2008
Erica C. McKenzie, BSc, BVMS, PhD, DACVIM
Corvallis, OR, USA

Introduction

A variety of diseases affect neonatal and juvenile camelids. Many are insidious but it is important to recognize and address these conditions as early as possible for the benefit of the owner, to improve treatment response and subsequent prognosis, and potentially to prevent clinical signs from developing in other animals at risk. Conditions that are frequently evident at birth and in the very early post partum period, including congenital cardiac defects and choanal atresia are addressed in a previous presentation.

Congenital Conditions

Urinary Tract Abnormalities

Normal camelid kidneys are smooth and elliptical, and usually easily identified on ultrasound examination. However, unilateral and bilateral renal agenesis have been reported.1,2 Affected animals may display progressive or poorly responsive azotemia. Bilateral agenesis also results in failure to urinate. Ultrasound examination identifies an absence of one or both kidneys, potentially with other concurrent urinary tract abnormalities. Contrast pyelography, surgical exploration and CT/ MRI might assist confirmation of the diagnosis. Abnormalities of the external genitalia are also reported, and their presence should warrant thorough examination of the urinary and reproductive tracts.

Azotemia is common in crias with problems such as gastrointestinal disease, and can be severe (BUN > 150 mg/dl, creatinine > 6 mg/dl). Resolution can require aggressive intravenous fluid therapy (50 to 120 ml/kg/day) and furosemide administration which may be given as a constant rate infusion (0.12 mg/kg loading dose then 0.12 mg/kg per hour for 8 hours).3 However frequent monitoring for complications including cerebral or pulmonary edema (especially in anuric or oliguric animals), and for electrolyte disturbances during furosemide administration (hyponatremia, hypochloremia and hypocalcemia) is critical.

Megaesophagus

Megaesophagus has been reported as an acquired condition of older camelids.4 However, the condition also occurs in young camelids and can be congenital, resulting from vascular ring anomalies.5 Multiple animals less than one year of age have presented to Oregon State University with esophageal dysfunction. Part or all of the esophagus may be affected, but the intrathoracic portion is commonly involved. Disease is frequently recognized around weaning as reliance on solid food increases. Clinical signs include salivation, regurgitation, dysphagia, ill thrift, anorexia and potentially signs of aspiration pneumonia. Esophageal waves may be prominent, and occasionally dyspnea may arise due to severe pneumonia, or obstruction of the nasal cavity with regurgitated feed.

Diagnosis is relatively uncomplicated although it should be kept in mind that sick and compromised camelids may display secondary esophageal dysfunction. Plain radiographs may reveal a dilated and/or feed filled esophagus. Endoscopy may identify feed material in the nasal cavity and esophagus, and/or esophageal dilation, but can be a very stressful procedure. Contrast radiography is usually forthcoming and assists identification of vascular ring anomalies. Fluoroscopy allows evaluation of swallowing as well as esophageal peristalsis, and can confirm or identify vascular ring anomalies that may not have been evident on contrast radiography. Treatment is unlikely to be successful unless dysfunction is mild or likely secondary to systemic illness. Thoracotomy on young camelids with vascular ring anomalies has been universally unsuccessful to date and esophageal dilation and dysfunction may persist after surgical intervention. Additionally, vascular ring anomalies can pursue several conformations in camelids and determining the surgical approach for thoracotomy procedures is therefore difficult. In animals with mild esophageal dysfunction, antibiotic therapy combined with feeding of digestible small particle feed stuffs like wet alfalfa leaves and pelleted feeds from a height can be considered.

Infectious Conditions

Coccidiosis

Five species of Eimeria are known to infest South American Camelids including Eimeria alpacae, E. lamae, E. macusaniensis, E. punoensis, and E. peruviana. Generally infection is self-limiting unless animals are in a heavily contaminated environment and subject to re-infection. Coccidia are contracted via feco-oral transmission and very heavy infestations may occur with few clinical signs in the host. However, E. macusaniensis in particular has recently been associated with severe and potentially fatal disease in naïve camelids of variable ages.6 Up to 22% of alpacas less than 1 year of age have been reported to be shedding E. macusaniensis, although usually in low numbers.7 Clinical signs of disease associated with E. macusaniensis infection include lethargy, weight loss, anorexia, and recumbency. Diarrhea is a frequent but not reliable clinical sign, possibly because lesions are primarily located in the jejunum and ileum. Common laboratory findings include high non-esterified fatty acid concentrations, hypoalbuminemia, hypoproteinemia, elevated serum AST, neutrophilia and eosinopenia as a result of severe damage to the small intestinal mucosa from the asexual multiplication stages of the parasite.6 Diagnosis can be made on saturated saline flotation or direct smear of fecal samples to identify the large, darkly staining oocysts which are ~ 3 to 4 times the size of other Eimeria sp. oocysts. Severe clinical signs, including death, can occur as much as 2 weeks before infection can be diagnosed by fecal testing, since E. macusaniensis has a substantially longer pre-patent period (~33-34 days) than other Eimeria (15-16 days).6 Treatment of Eimeria infection is generally directed at clinically affected animals using amprolium hydrochloride (10 mg/kg PO as a 1.5% solution, q 24 h) or sulfadimethoxine (110 mg/kg PO, q 24 h). Treatments are effective only against the immature stages and therefore may not have a significant impact on fecal oocyst count initially. Given the long prepatent period, it is prudent to treat E. macusaniensis infections for 10 to 15 days. Treatment should be directly administered to the animal rather than by medicating water supplies. Animals being treated with amprolium should receive thiamine hydrochloride (10 mg/kg, SC, q 24h) every 5 days during treatment.6

Cryptosporidiosis

Cryptosporidium can cause outbreaks of acute watery diarrhea in crias on intensively managed properties.8,9 Animals less than one month of age seem particularly susceptible and may be clinically affected as early as six days of age. Diarrhea is a hallmark sign, accompanied by weight loss and anorexia. Diagnosis is made from microscopic examination for oocysts, or fluorescent antibody staining of fecal smears, however, fecal testing should encompass investigation for concurrent infections with coronavirus, Giardia, coccidia, nematodes and helminths, which can occur concurrently.8 Clinical signs are self limiting in the majority of cases after approximately one week. Affected crias often require intensive supportive care including oral and intravenous nutritional support, intravenous fluids, and plasma transfusion. Weight loss despite supplemental feeding is a poor prognostic indicator.8 Azithromycin has been reported to reduce the duration of clinical signs and oocyst shedding in affected calves, but its efficacy in crias is unknown.10 Giardia infection can be determined from wet mount and immunostaining and should be treated with fenbendazole or metronidazole.

Myocplasma haemolama Infection

Infection is likely widespread and usually non-problematic. However, anemia may occur in heavily parasitized young or debilitated camelids. Diagnosis can be made by visualization of the organisms on blood smears made immediately after collection, however, PCR is more accurate and sensitive and can identify infection 48 hours before organisms are visible in blood smears. Infection is variably responsive to tetracycline.

Streptococcus zooepidemicus

Infection can result in septic peritonitis and/or pleuritis ('alpaca fever') usually in young camelids and pregnant females. Method of natural infection is possibly ingestion or inhalation and experimental intra-tracheal inoculation resulted in significant abdominal cavity disease in 5 of 6 llamas.11 Clinical signs include anorexia, lethargy, recumbency, and fever. Tachypnea and increased respiratory effort may be appreciated with thoracic cavity involvement. Abdominal cavity involvement can produce mild to dramatic signs of colic, resentment to abdominal palpation, tachycardia, shock and reduced defecation. Death occurs in 4 to 8 day without treatment. Diagnosis is based on ultrasound examination which reveals pleural and/or abdominal effusion and centesis samples have an elevated nucleated cell count comprised of neutrophils (variably degenerative) and chains of gram-positive streptococci. Cavity fluid glucose concentration may be considerably lower, and lactate higher, than systemic values, reflecting sepsis. CBC may reveal neutropenia or neutrophilia and hyperfibrinogenemia. In approximately 40% of clinical cases, contact with horses can be established and owners should be advised to feed horses in separate areas and to avoid nose-to-nose contact or communal pasture. Treatment with parenteral penicillin can be successful in animals identified early in the course or with mild to moderate clinical signs. Treatment should be continued until clinical signs and ultrasonographic abnormalities have resolved.

Chorioptic Mange

Chorioptes bovis infestation is frequently asymptomatic and anecdotally, clinical signs can be inversely proportional to the number of mites. Clinically affected camelids have alopecia, erythema, scaling and lichenification of the feet, limbs, trunk, perineal region and neck.12 Diagnosis is made via deep scrapings of the dorsal region of the interdigital space with microscopic examination for mites. The condition is difficult to treat and has shown limited response to repeated treatment with parenteral ivermectin. Additionally treatment with topical fipronil, eprinomectin or permethrin spray has been tried.12 A mixture of DMSO, ivermectin and gentamicin in mineral oil applied topically every 5 days for 3 treatments has also been recommended.

Septic Meningitis

Anecdotally, juvenile camelids are susceptible to bacterial meningitis even at several months of age. Histophilus somni, E. coli and Streptococcus sp. are among some of the pathogens that may be expected or isolated.13,14 Affected crias often present in recumbency and may have overt signs of central nervous dysfunction including nystagmus and respiratory acidosis. Diagnosis can be made on cerebrospinal fluid analysis. The atlanto-occipital space can be penetrated on the midline at the narrowest point of the cranial atlas using a 20G spinal needle, but general anesthesia is recommended which may potentially be detrimental to the patient. Alternatively, a lumbosacral CSF sample can be obtained by penetrating the subarachnoid space on midline 2cm caudal to last dorsospinous process of last lumbar vertebrae with a 20 gauge needle. In neonates the depth of the subarachnoid space may be only 2 to 2.5 cm from the skin. Spinal fluid from animals with bacterial meningitis has an elevated nucleated cell count (neutrophils) and protein.

Acquired Conditions

Lymphosarcoma

Lymphosarcoma is a relatively common neoplasm of camelids. In alpacas the average age at diagnosis is approximately 4 months, and llamas are usually diagnosed as mature adults.15 Peripheral lymphadenopathy is variable. Acute signs of lethargy, anorexia and recumbency may be appreciated although many animals are emaciated at presentation.15 Involvement of the liver, kidney and walls of the gastric compartments is frequently appreciable on abdominal ultrasound and biopsy of organs such as the liver may assist diagnosis if peripheral lymphadenopathy is absent. Lymphoblasts may also be identified in abdominocentesis and cerebrospinal fluid samples depending on the tissues affected.15,16 Approximately 20% of affected animals will have abnormal lymphocytes circulating in peripheral blood.

Gastrointestinal Obstruction

Several forms of gastrointestinal obstruction occur in juvenile camelids and determining whether surgical intervention is necessary can be a frustrating process. Phyto- and trichobezoars are the most prevalent abnormality although mineral encrusted concretions can also occur and may be visible on radiographs (usually in C1) as an incidental finding.17 Large bezoars can impact the gastric compartments, particularly C3 but occasionally also C1, resulting in anorexia, colic, decreased fecal passage, depression and death without surgical intervention. A palpable abdominal mass may be appreciated with large bezoars in the gastric compartments. Smaller bezoars may lodge in the duodenum, jejunum, spiral colon and transverse colon and cause similar signs. The spiral colon is a common site of obstruction due to its narrow diameter. Obstruction in proximity to the pylorus may promote hypochloremic metabolic alkalosis as in true ruminants, and high gastric chloride.17 Differential diagnoses include ulceration of C3, torsion of the spiral colon and jejunal intussusception. Diagnosis is based on clinical signs, abdominal radiographs (particularly useful for detecting large bezoars in C1), and abdominal ultrasound which may reveal distension of the small intestine, spiral colon and ascending colon depending on the site of obstruction. During surgical exploration the entire gastrointestinal tract should be carefully examined in case multiple bezoars are present.

Hypovitaminosis D

Crias are quite susceptible to this syndrome, particularly when born in autumn in geographic regions with long periods of inclement weather.18 Fall born crias enter a period of rapid growth (3 to 6 months of age) when serum vitamin D concentrations are in a seasonal slump. Dark coated animals are at greatest risk. Clinical signs generally present at 4 to 7 months of age and consist of lameness, reluctance to run and play, slow growth, excessive recumbency and angular limb deformity. Swollen costochondral junctions may be appreciated on palpation in addition to swollen carpi, tarsi and fetlocks. Laboratory findings include hypophosphatemia (< 4.5 mg/dl). Radiographs identify cortical thinning and metaphyseal flaring of long bones. Serum vitamin D concentrations <15 nmol/L support the diagnosis. Treatment includes administration of vitamin D (1500-2000 IU/kg IM or SC) and supplementation with oral phosphorus at 0.5 to 1gram per day may be beneficial.

Otitis Media

Otitis media is not uncommon in young camelids, and can also occur in mature animals.19 The condition may represent primary bacterial infection or in some cases, secondary infection associated with infestations of the spinose ear tick (Otobius megnini). It is not clear whether middle ear infection follows or precedes the concurrent otitis externa that is often present. Frequently, mixed bacterial populations are obtained on culture. Affected animals display head shaking and aural discharge, and signs of facial and vestibular nerve dysfunction can occur with progression. Radiographs confirm the involvement of tympanic bullae and document the severity of the changes, and the ear should be thoroughly examined with an otoscope or endoscope. Ticks can be manually removed or the animal treated with ivermectin. Bacterial otitis can be treated with a prolonged course (4-8 weeks) of daily ear cleaning, topical antibiotics (enrofloxacin, ceftiofur) and systemic antibiotics (florfenicol, ceftiofur, penicillin) which should be based on culture and sensitivity results where possible. With delayed treatment or severe infection nerve deficits are frequently permanent.

Diaphragmatic Paralysis

Diaphragmatic paralysis has been reported or observed in juvenile and young camelids.20 Signs include tachypnea, paradoxical respiration (inward movement of the abdominal cavity on inspiration) and respiratory acidosis. Affected animals may otherwise be relatively normal but display progressive dyspnea and respiratory acidosis. PCO2 may exceed 70 mmHg and may induce dullness. Radiographs, endoscopy, tracheal wash, BAL and lung biopsy rule out respiratory obstruction or infectious disease. Degeneration of the phrenic nerve is often histologically demonstrable at necropsy. Anecdotally, the condition has been suggested to respond to vitamin E supplementation, and administration of 500-1000 IU daily may be tried.

Idiopathic Nasal/Perioral Hyperkeratotic Dermatosis

Commonly referred to as 'munge' this condition tends to arise between 6 months to 2 years of age and presents as inflammation and crusting of the skin around the mouth and nares. Signs often resolve with topical iodine or systemic antibiotics. In refractory cases, topical glucocorticoids, intralesional triamcinolone, oral prednisone and oral zinc supplementation have been attempted.

Failure to Thrive/Bone Marrow Dysfunction

'Failure to thrive syndrome' has been described in crias that have a normal delivery and birth weight, but after several months cease to grow and may become emaciated and anemic.21 A subset of crias appear to exist that show poor growth and persistent neutropenia, but it is unclear if this comprises the same or a different syndrome. Affected animals should be treated for parasites, checked for oral cavity abnormalities and other medical problems, and serum IgG should be measured. Serum IgG < 400 mg/dl is considered characteristic for llama immunodeficiency syndrome in juvenile camelids.22 Treatment of ill-thrift animals can include blood transfusion, systemic antibiotics, iron supplementation, or in the case of neutropenia, pharmacologic stimulation of neutrophil production can be attempted (filgrastim 5 µg/kg SC q 24 h) but response is likely to be transient if treatment ceases. Bone marrow samples are readily obtained from the sternum with an 11 or 13G bone marrow needle under local anesthesia and sedation, but consistently characteristic abnormalities have not been identified. Recently several events have indicated that albendazole toxicity must be considered as a cause of acute, severe neutropenia especially if more than one animal is affected and therefore any history of anthelmintic administration to affected animals should be carefully investigated.

References

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Speaker Information
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Erica McKenzie, BSc, BVMS, PhD, DACVIM
Oregon State University
Corvallis, OR


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