Pleural fluid may be obtained from healthy camelids or more readily from those with subacute to chronic hypoproteinemia.¹ Fluid is best obtained approximately one third to half way up the thorax, at the sixth or seventh intercostal space. The area should be clipped, aseptically prepared, and infused with local anesthetic. A needle, cannula, or chest tube may be used, depending on how much fluid is expected, and how flocculent it is likely to be. Normal pleural fluid contains less than 1500 nucleated cells per microliter (cells/µL), with lymphocytes making up at least 80% of these cells.¹ Pleural fluid usually has protein concentrations less than 2.7 grams per deciliter (g/dL), but as with abdominal fluid, outliers are possible.

Imaging studies are useful for assessing the upper airway and lung. Conventional radiography or cross-sectional techniques are useful for the bony and cartilaginous structures of the head. Intranasal contrast material may be used, if occlusion is suspected. Radiography and cross-sectional studies may be used to assess the lung, with the cross-sectional studies being more useful than radiography for finding small focal lesions such as tumors, abscesses, or granulomas. Transthoracic ultrasonography is most useful for identifying pleural fluid or when parenchymal disease is extensive or against the body wall.

Supplemental Oxygen and Ventilation

Although camelids often appear relatively vigorous in spite of hypoxemia, it is generally accepted that they are healthier and have more efficient body functions when oxygenation is closer to normal. Thus, similar rules apply as in other species: camelids with an arterial partial pressure of oxygen (PaO₂) less than 60 millimeters of mercury (mm Hg) are candidates for supplemental oxygen, and camelids with PaCO₂ greater than 60 mm Hg are candidates for mechanical ventilation. In neonates or other small camelids, oxygen cages may be used. For larger camelids or for crias kept near their mothers, intranasal oxygen is often effective and well tolerated. Soft rubber catheters or specialized breathing tubes may be tabbed into one nostril so that the distal end in the nostril is approximately at the level of the medial canthus of the eye. Pure oxygen may be delivered at approximately 0.75 to 1.5 liters per hour L/hr per 9 kilograms kg (20 lb), with the higher volumes used in acute or severe cases. Delivered oxygen may be gradually decreased over 1 to 5 days as the clinical condition or blood gas values improve.

Mechanical ventilation also follows the principles used in other species. The ventilator or breathing bag may be hooked to an endotracheal tube or tracheostomy tube, with the latter necessary for animals with an intact gag or chew reflex or a collapsed upper airway.

Diseases of the Respiratory Tract

Retropharyngeal Lymphadenopathy

Enlargement of the retropharyngeal lymph nodes may lead to occlusion of the upper airway and dysphagia. This finding is relatively rare in camelids and may be the result of neoplastic change or infection. The most common neoplasm of the area is lymphoma.³ The most common infection is likely to be Corynebacterium pseudotuberculosis, although this is more likely to affect the submandibular lymph nodes, rather than the retropharyngeal nodes.^4,5 Penetrating foreign bodies may also lead to infection in that area with a variety of bacteria introduced.

Masses may become large enough to be appreciated from the outside or may require deep palpation of the upper neck. A small amount of external pressure may cause an exacerbation of stridor or dyspnea. Endoscopy, ultrasonography, or imaging studies may also reveal the mass lesion, and facilitate aspiration or biopsy. Treatment for the primary disease may be all that is necessary, but if the camelid has dyspnea or dysphagia, lancing of the abscesses or tracheostomy may provide relief.

Nasal Bots

Infestations of the caudal nasal passages and dorsal pharyngeal region by nasal bots larvae from sheep (Oestrus ovis) or deer (Cephenemyia sp.) have been reported.6–8 Reports of deer nasal bots are currently confined to the western parts of the United States (California, Colorado, Oregon). Infestation occurs during fly season. Populations of the definitive host (sheep, deer) are usually found nearby. Both genera of fly are viviparous and deposit live larvae near the external nares of the host. Larvae colonize the upper airway leading to an exudative, granulomatous reaction and enlargement of adjacent soft tissue (Figure 37-4). On maturation, larvae are sneezed or coughed back onto the ground and develop into flies.

Figure 37-4 Cephenemyia larvae within the larynx of a llama.

Most reports involve individual camelids, but herd outbreaks have occurred. Clinical signs are mainly from the physical narrowing of the upper airway. These include sneezing, coughing, respiratory stridor mainly on inspiration, nasal discharge possibly with mild epistaxis, exercise intolerance, and open mouth breathing. Pulmonary auscultation is usually normal but is complicated by sounds referred from the upper airway. Affected camelids are afebrile and have normal clinical pathology data except for the changes caused by stress. Most cases occur in adults, but one case of a 9-month-old llama has been reported. Many also have a history of treatment failure with antibiotics.

Definitive diagnosis of Cephenemyia infestation is by endoscopic examination. Individuals or groups of larvae may be seen. They are often found within a pouch of soft tissue on the dorsal nasopharyngeal wall. This pouch may also be seen radiographically. Oestrus ovis are less commonly reported but have a predilection for the dorsal nasal turbinates and sinuses in sheep. These areas are inaccessible to endoscopy. Oestrus ovis larvae may be distinguished from Cephenemyia sp. by examining the two dark peritremes at the posterior (exposed) end. Peritremes are circular in Oestrus with a central button and kidney-shaped in Cephenemyia with buttons aligned with the medially oriented lesser curvature.

Treatment depends on the severity of signs. Mildly affected camelids may be treated with ivermectin, which often resolves the infestation within 2 weeks. More compromised camelids may require more aggressive intervention. Removal of larvae one at a time using the endoscope’s biopsy instrument is time consuming but effective.

Upper Airway Malformations

Congenital upper airway malformations are relatively common in New World camelids. Among the more common are choanal atresia (10.4% of reported congenital defects in one study), wry face (7%), and cleft palate (3%).⁹ Subepiglottic cysts and hypoplastic trachea are less common. All of these impede air flow or heighten risk of aspiration.

Choanal atresia is anatomically well described. It results from failure of the buccopharyngeal membranes to completely rupture during the early second trimester of fetal development, leaving membranous or bony obstructions over one or both nasal passages (Figure 37-5). Camelids with unilateral lesions may thrive into adulthood, showing little more than a heightened respiratory rate, open-mouthed breathing, or dyspnea when stressed. Bilaterally affected neonates are born with little or no ability to breathe nasally. Thus, clinical signs start immediately or soon after birth. Affected crias typically display open-mouthed breathing, with the lips pulled away from the mouth, stertor (inspiratory or expiratory), and pronounced nostril flaring (Figure 37-6). They often have difficulty eating and are at high risk for aspiration. Air flow at the nostrils is absent or reduced, and soft rubber tubes cannot be passed nasally beyond the level of the eye. Definitive diagnosis may be achieved by endoscopic examination with a pediatric endoscope (up to approximately 6 mm diameter), plain radiography, contrast radiology, in which approximately 5 to 10 milliliters (mL) of contrast (preferably an organic iodide to reduce risk of aspiration complications) is instilled into each nasal passage and the nose held in dorsal extension (Figure 37-7), or more advanced imaging techniques that allow the nasal passages to be displayed in slices. Aerophagia and hyperinflated lungs may also be seen. Endoscopy or contrast radiography reveals imperforate membranes or bony obstruction. Mucoid fluid may obscure the actual obstruction. Plain radiography reveals bony obstruction only and may be difficult to interpret. Clinical pathology data reflect stress or secondary aspiration pneumonia. Blood oxygenation is usually poor. Tracheostomy or surgical repair are possible and provide immediate relief, but camelids frequently outgrow these stomata and repeated procedures may be necessary.¹⁰

Figure 37-5 Choanal atresia is a neonate. The arrow marks the bony occlusion of the airway.

Figure 37-6 Open-mouthed breathing in an alpaca cria with choanal atresia. The nostrils moved in synchrony with inspiration in spite of no air flow.

Figure 37-7 Contrast radiographs of a cria with choanal atresia. Five to 10 milliliters (mL) of iohexol are placed in each nostril, and the nose held in an elevated position.

Much of the controversy surrounding choanal atresia involves questions of heritability. Researchers have been unable to define a specific mode of inheritance. Camelids that have given rise to previous offspring with choanal atresia appear to be more likely to have subsequent affected offspring compared with camelids that never have had affected offspring. In contrast, breeding affected camelids rarely leads to the birth of affected offspring.

Cleft palate is relatively common in camelids, some of which also have other congenital malformations.⁹ The airway is not specifically narrowed with this disorder. Aspiration is the greatest danger. Affected camelids frequently cough after eating and may have milk come out the nose. Some clefts are large enough to be seen on oral examination, although many affect only the caudal palate and require endoscopy to diagnose. Surgical repair is uncommon but may be successful with the smaller clefts.¹¹ Camelids with large defects tend to aspirate at a very young age, whereas those with smaller defects may thrive for a longer period. No information is available concerning heritability in camelids.

Fungal Rhinitis and Sinusitis

True fungal infections of the nasal passages are rare in New World camelids. Turbinate infection by Rhizopus spp., together with nodular pneumonia and meningoencephalitis, was identified in a single llama with various cranial nerve deficits and eventually weight loss.¹²

Sinus infection with osseous proliferation and facial deformation was associated with an Aspergillus-like organism in a llama.¹³ Infections of the sinus or nasal passages may be difficult to diagnose. Most lead to bone deformation, bone lysis and proliferation, and soft tissue densities that may be seen on radiographs or cross-sectional imaging studies. Smaller masses or those involving the airway may be identified by endoscopy. Biopsy with or without fungal culture is necessary to distinguish these masses from tumors.

Infection on the skin of the nares by Conidiobolus coronatus in two llamas led to proliferation of tissue, chronic nasal discharge, and eventual occlusion of the nasal passages.14,15 Conidiobolus is a tropical fungus and most common in the Gulf Coast region in the United States, but one infected llama was a lifelong resident of Illinois. Diagnosis was achieved by histopathologic examination of tissue sections and fungal culture. Systemic antifungal medications have been used successfully in other species, but in the single treated llama case report, infected tissue was surgically removed after iodides and topical fungicides failed to resolve the lesion.

Snake Bite

Although snake envenomation affects several organ systems, the propensity for camelids to be bit on the lips or nose warrants the discussion here. Bites occur during seasons of snake activity, usually late spring and the summer. Most reports involve the Western diamondback in California or the smaller prairie rattlesnake in Colorado.16,17 The venom of these snakes contains a combination of enzymatic and nonenzymatic toxins. The overall effects are local tissue digestion, anticoagulation, hemolysis, vasculopathy, and hypotension. Eastern diamondbacks have a more hemolytic effect, and the Mojave rattlesnake has a presynaptic paralytic neurotoxin. Neurotoxin also is present sporadically in other species of pit vipers. In addition to the venom, bites are also often contaminated with a variety of microorganisms, including Pseudomonas aeruginosa, Clostridium, and Bacteroides fragilis.

Affected camelids generally have severe local swelling, which, in the case of bites on the face, may cause severe lip, nose, and eyelid edema and occasionally tracks to the laryngeal region and neck. Swollen areas often exude sanguinous fluid, and close inspection may reveal paired fang marks. Hemorrhagic diathesis appears to be more common in camelids bit in Colorado than in California. Swelling may also occlude air flow, leading to dyspnea, nostril flare, stridor, and tachypnea and cause dysphagia. Systemic signs of envenomation include bruxism, signs of shock, hyperthermia, tachycardia, cardiac arrhythmias, recumbency, lethargy, ileus, and anorexia. Further obtundation and other neurologic signs, respiratory signs, and colic may occur with progression of envenomation. Obviously, if the bite is on another part of the body such as a leg, signs referable to that body part will be present, possibly in the absence of respiratory signs. Local signs often worsen over the first 48 to 96 hours.

Although not yet described, Mojave rattlesnake bites would be likely to cause much less severe local inflammation, but they cause progressive neuromuscular weakness and respiratory paralysis.

Blood examination reveals evidence of stress, inflammation, muscle damage, and possibly cardiopulmonary or renal failure. Neutrophilia and neutropenia are both possible, usually with concurrent left shift and lymphopenia. Anemia, thrombocytopenia, and hypofibrinogenemia may also be seen. As with other camelid diseases, hypoalbuminemia, hyperglycemia, and hypokalemia are common. Increases in muscle enzymes are often dramatic and may be accompanied by increases in liver enzymes. Azotemia and acidosis are common in more severely affected camelids. Coagulation profiles may reveal the hypocoagulable state.

Treatment may be multimodal and extensive. Airway preservation is often the primary goal and may be achieved through nasotracheal intubation or tracheostomy in severely affected camelids. Characteristically, tracheostomy sites or other skin breaks bleed persistently. Because of the progression of lesions, camelids not requiring immediate airway intervention should still be kept under observation, in case some future intervention is necessary. Even in apparently hydrated camelids, some form of fluid therapy is helpful in preventing thrombotic complications. The finding of hepatic lipidosis in one affected camelid suggests some may benefit from specific treatments against this condition. However, the risk of edema is even higher in camelids with snake bite than in the general population, so any fluids must be given at a judicious rate and sometimes accompanied with a colloid, blood, or blood products. Given the tendency toward tissue swelling, any neck wrap must be loose and assessed frequently, lest it should become constricting.

Broad-spectrum antibiotics with good anaerobic coverage are recommended because of the contaminated nature of the bites and the risk of translocation across a compromised bowel. A tetanus toxoid is also recommended.

Antiinflammatory medications may aid in reducing the swelling and some of the effects of the toxins. Generally, when veterinary treatment is initiated, nonsteroidal medications are preferable to corticosteroids or antihistamines. Corticosteroids are often used in a last-ditch effort and may be indicated in some forms of shock; especially when repeated, they also suppress the immune system during a period of possible sepsis. Antihistamines are unlikely to be of value beyond the peracute stage and may worsen hypotension.

Local wound care should be performed on weeping or necrotizing lesions. Fasciotomy may also release internal pressure and prevent secondary lesions. The use of antivenin has not been explored extensively. It appears to improve survival in most species but usually must be given within hours of envenomation. In one report, a camelid appeared to have an anaphylactic reaction to equine-derived antivenin.¹⁶ Use of ovine-derived antivenin has not been reported.

Reported survival of moderate to severely affected camelids is about 50%. Death occurs secondary to cardiopulmonary failure, asphyxiation, or septic shock. Necropsies have revealed extensive local necrosis, hemorrhage, edema, and congestion, laryngeal edema, third-compartment ulceration with possible perforation, intestinal thrombosis, multifocal ecchymoses, pneumonia, endocarditis, pericarditis, myocarditis, peritonitis, hepatic lipidosis, and hemorrhage, edema, or congestion of a variety of internal organs.

The possibility of survival is higher in less severely affected camelids. A proportion of snakebites results in little to no venom injection and hence may result in minor clinical signs or may never be noticed. Prevention revolves around avoiding contact between camelids and venomous snakes. One report infers that bites occur overnight or in the morning, which suggests a preventative role to housing camelids overnight.