Two overtly healthy Himalayan cats from a single household were brought to the veterinary hospital for annual dental cleaning and prophylaxis. The cats were siblings and were housed strictly indoors. Cat 1 was a 6-year-old castrated male that weighed 3.6 kg (7.9 lb); cat 2 was a 5-year-old spayed female that weighed 2.9 kg (6.4 lb). The medical history of cat 1 was unremarkable, whereas in cat 2, lymphocytic-plasmacytic colitis had been diagnosed 2 years previously by means of endoscopic biopsy. As a result, both cats were fed a diet of lamb and green peas,a and clinical signs in cat 2 had been stable since the diagnosis had been made. Both cats received annual vaccinations and regular veterinary care. During a recent examination, both cats were noticed to have mild to moderate dental tartar with mild gingivitis.
Results of a complete physical examination, including pulmonary auscultation, prior to dental cleaning and prophylaxis were unremarkable, except that cat 2 was noticed to have stenotic nares. Results of preanesthetic laboratory testing were also unremarkable with the exception of high blood calcium concentrations (12.6 and 14.3 mg/dL in cats 1 and 2, respectively; reference range, 7.8 to 11.3 mg/dL).
Both cats had a history of being fractious and difficult to handle. Thus, no preanesthetic medications were administered, and both cats were anesthetized by placing them in an induction chamber and exposing them to 5% isoflurane. In each cat, anesthetic induction was smooth without evidence of struggling. Once the righting reflex was lost, each cat was removed from the induction chamber and intubated with a cuffed, 3.5-mm endotracheal tube. Lidocaine was not used for endotracheal intubation.
Cats were connected to a nonrebreathing anesthetic circuit, and anesthesia was maintained with 2% isoflurane. An IV catheter was placed in the left cephalic vein, and administration of lactated Ringer's solution was started at a maintenance rate. Anesthetic monitoring was performed with a pulse oximeter that used a rectal reflectance probe and with a blood pressure cuff applied to the tail. Cats were allowed to breathe spontaneously, but a sigh was performed manually approximately every 4 to 5 minutes, with maximum airway pressure between 10 and 15 cm H2O. The cats were moved from left to right lateral recumbency as the procedure progressed.
Dental cleaning in cat 1 proceeded without incident until the procedure was almost complete. While polishing the teeth, the dental technician noticed frothy blood in the endotracheal tube and the procedure was halted. At this time, oxygen saturation measured by means of oximetry was > 95% and blood pressure was within reference limits. Before the procedure could be continued, additional blood was noticed in the endotracheal tube. Therefore, the procedure was terminated, and anesthesia was discontinued. A sterile red rubber catheter attached to a surgical vacuum unit was advanced down the endotracheal tube, and approximately 3 to 4 mL of bloody fluid was collected.
Thoracic radiography was performed while the cat recovered from anesthesia and revealed diffuse pulmonary infiltrates consistent with alveolar hemorrhage in the dorsocaudal lung fields (Figure 1). As a result, the cat was given vitamin K (15 mg, SC) and placed in a heated recovery cage; fluid administration was continued at a maintenance rate. The cat recovered from anesthesia without further incident. No more hemorrhage was seen, but the endotracheal tube was found to be covered with coagulated blood when removed. Following extubation, the cat seemed comfortable in the recovery cage and was clinically eupneic.
The events for cat 2 were similar to those for cat 1, with the exception that laser rhinoplasty was performed prior to initiation of dental cleaning. Again, frothy blood was noticed in the endotracheal tube near the completion of the dental cleaning. As with cat 1, the procedure was halted and the endotracheal tube was suctioned. Again, approximately 3 to 4 mL of bloody fluid was aspirated. Thoracic radiographs revealed diffuse alveolar infiltrates similar to those seen in cat 1.
Vitamin K (15 mg, SC) was administered, and cat 2 was placed in a recovery incubator for monitoring. The cat remained dyspneic, demonstrating open-mouth breathing, and supplemental oxygen bubbled through saline solution was administered.
Cat 1 was discharged later the same day. However, after returning home, the owners thought that the cat's breathing was labored and brought the cat back to the hospital. On reexamination, the cat appeared to be resting comfortably but moist rales were noticed bilaterally during auscultation over the dorsal lung fields. As a result, it was decided to hospitalize the cat overnight for monitoring. On the assumption that both cats had a condition similar to exercise-induced pulmonary hemorrhage in horses, for which there is no specific treatment,1 it was decided to monitor the cats overnight while maintaining them in a quiet, low-stress environment and providing supplemental oxygen as needed.
The following morning (ie, day 2), both cats were resting comfortably. Cat 2 was removed from the oxygen cage and returned to a standard ward for continued monitoring. In cat 1, however, recheck radiography revealed that the infiltrates had either expanded or migrated from the dorsocaudal lung fields to the cranioventral lung fields (Figure 2). Later that afternoon, cat 1 became dyspneic and was transferred to an oxygen cage and supportive treatment was initiated. An IV catheter was placed, and administration of 0.45% NaCl with 5% dextrose was started at a maintenance rate. In addition, dexamethasone (0.5 mg/kg [0.23 mg/lb], IV), furosemide (6 mg/kg [2.7 mg/lb], IV), cimetidine (6 mg/kg, slow IV), and aminophylline (4 mg/kg [1.8 mg/lb], SC) were administered. The cat's condition stabilized with these treatments, and the cat appeared clinically to be eupneic, but approximately 7 hours later, the cat developed hemoptysis followed by respiratory and cardiac arrest. Attempts at resuscitation were unsuccessful.
The initial treatment for cat 2 was identical to that for cat 1. The PCV was 32% on day 3, compared with a PCV of 36% prior to anesthesia, and the total solids concentration was 6.4 g/dL, compared with a concentration of 6.8 g/dL prior to anesthesia, suggesting that there had been minimal loss of blood into the lungs. In anticipation of hospital discharge, treatment was changed to oral administration of prednisone (5 mg, q 24 h) and theophylline (25 mg, q 24 h), although IV administration of furosemide was continued. Prothrombin time (8.5 seconds; reference range, 6 to 11 seconds) and partial thromboplastin time (15.8 seconds; reference range, 10 to 25 seconds) were within reference limits, as was the platelet count (230,000 platelets/μL; reference range, 200,000 to 500,000 platelets/μL). On day 4, the cat's PCV was again 32%, the cat was taking food when offered by hand, and the cat appeared eupneic. Therefore, the cat was discharged.
Cat 2 was reexamined on day 6. Results of thoracic auscultation were unremarkable, and no infiltrates were seen on thoracic radiographs. On day 9, the owner reported that the cat was doing well and breathing normally but had a finicky appetite. The poor appetite was attributed to treatment with theophylline, and drug administration was discontinued. At this time, the PCV was 34%. A CBC revealed leukocytosis (33,000 WBCs/μL; reference range, 5.5 to 19.5 WBCs/μL) characterized by neutrophilia (21,000 neutrophils/μL; reference range, 2,500 to 12,500 neutrophils/μL), lymphocytosis (9,360 lymphocytes/μL; reference range, 400 to 6,800 lymphocytes/μL), monocytosis (2,080 monocytes/μL; reference range, 150 to 1,700 monocytes/μL), and basophilia (150 basophils/μL; reference range, 0 to 100 basophils/μL). The platelet count was 214,000 platelets/μL. The cat's condition appeared stable, and the cat was not febrile (rectal temperature, 38.4°C [101.2°F]). Therefore, the leukogram was attributed to a combination of steroid administration and resolving inflammation in the lungs. On the basis of these findings, it was decided to begin decreasing the prednisone dosage.
The owner called on day 12 to report that the cat had an improved appetite but had vomited 3 times that morning, with the last vomitus having a tinge of blood. On examination, the cat was lethargic but still eupneic. The owner did not want to hospitalize the cat for IV fluid therapy, so lactated Ringer's solution was administered SC, as well as a dose of cimetidine (15 mg). The cat was discharged, and the owner was advised to administer amoxicillin-clavulanic acid (62.5 mg, PO, q 12 h) and cimetidine (50 mg, PO, q 8 h).
On day 14, the owners took the cat to another hospital for a second opinion. The following day (day 15), the owners chartered a plane to take the cat for a third opinion at yet another hospital. The cat died later that evening, several hours after the flight.
Gross necropsy findings for cat 1 included severe, diffuse pulmonary edema and hemorrhage in both lungs. Edema fluid was evident in the bronchi and bronchioles, and a small amount of blood-tinged fluid was seen in the trachea and nasal passages. There were no other gross abnormalities and no other evidence of hemorrhage anywhere else in the cat. Histologic examination of lung tissue revealed that the pulmonary architecture had been completely effaced by hemorrhage, fibrin deposition, and large numbers of mixed inflammatory cells. Bacterial culture of a lung specimen yielded a pure growth of Pasteurella spp.
Necropsy of cat 2 revealed bronchopneumonia; bacterial culture of lung specimen yielded β-hemolytic Streptococcus spp and Klebsiella pneumoniae. The pathologist indicated that the lung lesions appeared to be acute (ie, of ≤ 3 days' duration) and secondary to aspiration. No other evidence of hemorrhage was seen on the gross examination. Microscopically, lung specimens included multifocal areas where bronchioles and surrounding alveoli were partially or completely filled with fibrin, large numbers of bacteria, and abundant cellular debris.
Serum that had been collected and banked from each cat was sent to the Mary Ann Swetland Center of Environmental Health at the Case Western Reserve University School of Medicine for mold toxin analysis. Samples were analyzed for mycotoxin-serum protein adducts by means of adduct detection.2 In brief, following exhaustive digestion of serum proteins with pronase, affinity chromatography was performed with polyclonal anti–satratoxin G antibodies that selectively bind macrocyclic trichothecenes and their amino acid and peptide adducts. Adducts were eluted and identified by means of matrix-assisted, laser desorption, time-of-flight mass spectrometry.
Serum samples from both cats were positive for satratoxin G adducts, biomarkers for the toxin produced by Stachybotrys chartarum, also known as “toxic black mold.” Cysteinyl–satratoxin G and lysyl–satratoxin G adducts were found in the serum of cat 1 (Figure 3). Similarly, the adduct of lysine with satratoxin G was detected in the serum of cat 2. Lysine–satratoxin G adducts containing potassium were detected in serum from both cats, along with 2 dipeptidyl–satratoxin G adducts.
To validate findings for the 2 affected cats, serum samples from 6 healthy blood-donor cats living in a mold-free environment in Denver, Colo, were also tested. None of the 6 control cats had satratoxin G adducts in their serum.
IVD, Royal Canin, St Charles, Mo.
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