A two-year-old male alpaca was presented to the Hospital for Large Animals at Cummings Veterinary Medical Center for acute weakness and inability to rise. The animal had lost 5 lbs body weight over the past two weeks, and was found down in his field the morning of presentation.
On presentation, the alpaca was mentally dull, extremely weak and exhibited open-mouth breathing. He was unable to stand or support his head in an upright position, and his body condition score was low at 2/5 (normal is 3-3.5/5). Additionally, an elevated heart rate of 120 bpm (normal is 60-90) was noted, while respiratory rate and temperature were within normal limits. Mucous membranes and ocular conjunctiva appeared pale pink. Initial bloodwork revealed multiple abnormalities, including changes consistent with dehydration in the face of anemia (Packed Cell Volume or PCV 25%), hypoproteinemia (total serum protein level 4.0 g/dL), profound hypoglycemia (<20 mg/dL), marked hyperlactatemia (lactate level 18 mmol/L; normal <2 mmol/L), severe metabolic acidosis (pH 7.12; normal 7.35 – 7.45), mildly increased kidney values and mild electrolytes abnormalities. Soon after admission, the alpaca exhibited seizure activity, controlled with administration of diazepam. He was given oral dextrose and administered intranasal oxygen while an IV catheter was being placed. Intravenous fluid therapy was initiated with dextrose and sodium bicarbonate supplementation to address the dangerously low blood sugar and blood pH level.
At this point, what is your differential diagnosis?
Striking abnormalities in this alpaca are the combination of weakness with severe metabolic acidosis, mild anemia, and profoundly low blood glucose levels. To note, true hypoglycemia is very rare in adult camelids based on their tendency to show hyperglycemic stress responses upon handling. Furthermore, camelids are known for their innate insulin resistance in comparison to other species, which contributes to disorders of both fat metabolism (lipemia) and glucose dysregulation (hyperglycemia). Sepsis (systemic infection) is the most common cause of hypoglycemia in neonates but is less likely to be encountered in adults. The specific challenge of this case relates to whether metabolic abnormalities (lactic acidosis with hypoglycemia) are the primary cause of the animal’s weakness and seizure activity, or whether an underlying, primary neurological cause is present. Common causes of severe lactic acidosis may relate to hypoperfusion, hypoxemia, severe anemia, increased cellular production of lactate, forestomach acidosis or sepsis in camelids.
The acute onset of clinical signs should be interpreted with caution, as camelids may merely show subtle clinical signs, even in the presence of severe disease. The onset of illness is therefore often insidious and may go unnoticed initially. Overall, recumbency (inability to rise) is an unspecific clinical sign and may be observed as a result of abdominal discomfort or neurologic, musculo-skeletal, cardiopulmonary or metabolic causes. In addition, recumbency as a result of a traumatic, infectious, or toxic disease should be considered depending on the history and clinical presentation of the patient. This makes the diagnostic workup particularly challenging and many of these conditions require immediate attention.
It is important to recognize that open mouth breathing is not always related to hypoxemia or respiratory distress in camelids, but may be considered a behavioral stress response in many situations. For this reason, supplemental oxygen therapy is often initiated in emergency situations until hypoxemia can be ruled out through further diagnostic testing.
What would be your next step?
Collection of cerebrospinal fluid (CSF) from the lumbosacral space was performed under mild sedation, after initial fluid resuscitation and stabilization of the patient. Analysis (cytology) of the CSF fluid was unremarkable, which ruled out many infectious or inflammatory causes of neurological disease. Forestomach fluid analysis was also within normal limits, with a pH of 7 and moderately active protozoa, eliminating the presence of forestomach acidosis. Complete bloodwork showed a leukocytosis with neutrophilia (increase in inflammatory cells), as well as high AST (aspartate aminotransferase) and CK (creatinine kinase) levels, most likely related to recumbency. Below is a microscopic view (x100) of the blood smear:
What is your final diagnosis?
This slide was remarkable by the amount of Mycoplasma haemolamae organisms, a 0.5 to 1 µm blood organism (bacterium) that attaches to erythrocytes but can also be seen free in plasma. Notice its coccoid, rod-shaped or ring-shaped (left top of image); they appear singly, in pairs or in clumps. Also note the elliptical shape and small size of the camelid erythrocyte. Mycoplasma haemolamaeMycoplasma haemolamae is a blood pathogen that can cause a variety of abnormalities, including anemia, metabolic acidosis, profound hypoglycemia, and hyperlactemia associated with sudden population growth of the organisms in the bloodstream, which can overwhelm the host's immune response. M. hemolamamae are gram-negative bacteria that attach to erythrocyte walls but do not penetrate host cells. The presumed mechanism for its pathogenicity include glucose consumption, activation of inflammatory and immune response and accelerated removal of parasitized erythrocytes (extravascular hemolysis). The prevalence in camelids in North America is thought to range from 10% to 30%. The definitive mode of transmission is unknown. However, biting insects are suspected to play a role as vectors (parasite vehicle). There is also increasing evidence of transplacental or parturient transmission (during pregnancy or delivery).[1,4,5] M. haemolamae infection has been reported in all ages of both llamas and alpacas. If an individual is infected, it is likely that the rest of the herd is too. However, Mycoplasma does not typically cause clinical illness in the adult alpaca. The disease may be seen in animals that are stressed, immunocompromised, heavily parasitized, or in poor body condition. Other risk factors for clinical disease are JLID (juvenile llama immunodeficiency syndrome), corticosteroids administration, concurrent Anaplasma phagocytophilum infection, or any other condition causing debilitation. Clinical signs of the disease include lethargy, weight loss, decreased fertility and sometimes death. Anemia is the most common finding but is not always present and can be transient; speculated mechanism are hemolysis, immuno-mediated destruction and inhibition of red blood cell regeneration. Infection is sometimes associated with hypoglycemia, especially when bacteremia is severe. The most sensitive test (best detection ability) to diagnose Mycoplasma haemolamae infection is a PCR (Polymerase Chain Reaction, a molecular test) performed on whole blood. Alternatively, parasites can be seen on a blood smear after staining. However, subclinical infections are unlikely to be detected with this method. Blood smears should be made as soon as possible after blood collection and before refrigeration (parasites fall off the erythrocytes quickly). PCR has been shown to be positive 2 to 5 days before parasites can be seen on a blood smear and to stay positive after visible parasitemia has resolved.
How would you treat this condition?
Intravenous oxytetracycline until clinical infection is cleared and PCV stabilizes.
Typically, M. haemolamae exhibits sensitivity to oxytetracycline. In severe cases, this drug should be administered slowly (diluted) intravenously to maximize efficacy. Alternatively, if clinical signs are not as severe, long-acting oxytetracycline can be administered subcutaneously every 48 hours at the farm. Treatment is expected to resolve clinical signs, but alpacas often remain carriers of Mycoplasma. A stressful event or a decrease in immunity can lead to recrudescence or ease re-infection. Early antibiotic discontinuation can facilitate drug resistance, which is why the antibiotic course should not be stopped before the clinical infection is actually cleared. A mycoplasma PCR can be submitted shortly after discontinuing antibiotic therapy, as persistent infection or recurrence of anemia may warrant use of alternate antimicrobial choices (such as enrofloxacin or macrolide antibiotics).
Treatment should also be aimed at decreasing environmental stress, resolving other health concerns and, in case of treatment failure, investigating immunodeficiency. In severe cases (e.g. PCV less than 12%) a whole blood transfusion can be life-saving. Transfusion reactions are rare (especially in animals receiving their first transfusion) and commercial products are available in the absence of a healthy donor animal.
Treatment and Outcome
Treatment with intravenous oxytetracycline was immediately initiated and the animal improved quickly. By the next morning, he was standing, walking, and eating more normally. Pantoprazole and thiamine administration were pursued to counteract secondary C3 ulcerations and potential polioencephalomalacia as a consequence to low feed intake. Kidney values had returned to normal by the day after admission (initial abnormalities were attributed to dehydration). However, the total serum protein level had decreased to a critical level of 3.0 g/dL. To prevent any complications related to a low colloid oncotic pressure (such as edema formation), the alpaca was given two units of plasma over the course of several hours. His protein level increased to >4.0 g/dL and remained stable during subsequent hospitalization. A fecal analysis revealed 3,000 eggs per gram of Moniezia spp (tapeworms), likely the cause of his low serum protein. A five-day course of fenbendazole (Panacur) was initiated. Two days after admission, very few Mycoplasma organisms could be seen on a repeated blood smear, indicating a good response to the oxytetracycline therapy. A subsequent recheck CBC showed that the neutrophil count had normalized and no parasites could be identified on the blood smear on day four. On serum chemistry, AST was still mildly elevated but had significantly decreased, while CK values were normal.
The alpaca was discharged seven days after admission for further care at home with subcutaneous pantoprazole, thiamine and long-acting oxytetracycline (LA 200), and made a full recovery.
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Sophie Sage, DVM, IPSAV is a Large Animal Medicine Resident at the Hospital for Large Animals. She received her veterinary education at the National Veterinary school of Lyon (France), then completed an internship in equine medicine at the Faculty of Veterinary Medicine of Montreal. When not working, she enjoys skiing, hiking, traveling, and horseback riding.
The Hospital for Large Animals is home to the largest veterinary critical care and diagnostic center for horses and farm and fiber animals in New England. The hospital provides 24-hour intensive care, medical and surgical services by its board-certified veterinary specialists in Internal Medicine and Critical Care in its state-of-the-art facility. Dr. Daniela Bedenice is also the only board-certified specialist in Large Animal Emergency and Critical Care in New England.
24-hour emergency/critical care includes full medical and surgical services (e.g. management of colic or colitis, trauma patients, respiratory distress). Advanced intravenous care, parenteral nutrition, blood and plasma transfusion, dialysis, intensive cardio-vascular monitoring, airway support, mechanical ventilation, and transfaunation for ruminants and camelids are some of the treatments offered.”