Case Report Rapport de cas Pneumonia and gastritis in a cat caused by feline herpesvirus-1 Glenna F. McGregor, Karen Sheehan, Elemir Simko Abstract — We report a case of fatal respiratory and gastric herpesvirus infection in a vaccinated, adult cat with no known immunosuppression or debilitation. The disease was characterized by severe necrotizing bronchopneumonia, fibrinonecrotic laryngotracheitis, and multifocal necrotizing gastritis associated with eosinophilic intranuclear inclusion bodies and a large amount of feline herpesvirus-1 antigen detected with immunohistochemistry. Résumé — Pneumonie et gastrite chez un chat causées par l’herpèsvirus-1 félin. Nous signalons un cas d’atteinte respiratoire et gastrique mortel causé par l’infection à l’herpèsvirus chez un chat adulte vacciné sans immunosuppression ni affaiblissement. La maladie a été caractérisée par une bronchopneumonie nécrosante grave, une laryngotrachéite fibrinonécrosante et une gastrite nécrosante multifocale associée à des corps d’inclusion intranucléaire acidophiles et une grande quantité d’antigènes de l’herpesvirus-1 félin détectée par analyse immunohistochimique. (Traduit par Isabelle Vallières) Can Vet J 2016;57:147–150
F
eline herpesvirus-1 (FHV-1), also known as feline viral rhinotracheitis virus, is common in domestic cats worldwide. It typically results in variably severe conjunctivitis, rhinitis, and keratitis, and is becoming increasingly recognized as a cause of dermatitis, particularly on the nose and face (1). Following FHV-1 infection at least 80% of cats will remain latently infected for life; 45% of those cats will shed virus intermittently throughout life, subclinically or with recrudescence of, typically mild, clinical disease (1). There are only a handful of reported cases in domestic cats in which FHV-1 infection has resulted in more severe disease, predominantly in kittens or animals that were otherwise debilitated (2). These cases are usually characterized by severe necrotizing bronchiolitis accompanied by diffuse fibrinonecrotic bronchopneumonia (2–4). In one case the necrotizing bronchopneumonia and fibrinonecrotic tracheitis were severe enough to result in pneumomediastinum (3). There are also rare cases of hepatic necrosis associated with FHV-1 in young cats (4,5), 1 reported case of pancreatitis in a kitten (6), and a single case report of necrotizing gastritis, without respiratory tract lesions, in an adult cat (7). Here we report a unique
Department of Veterinary Pathology (McGregor, Simko), Department of Small Animal Clinical Sciences (Sheehan), Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan. Address all correspondence to Dr. Glenna McGregor; e-mail: [email protected] Use of this article is limited to a single copy for personal study. Anyone interested in obtaining reprints should contact the CVMA office ([email protected]) for additional copies or permission to use this material elsewhere. CVJ / VOL 57 / FEBRUARY 2016
and fatal case of concurrent necrotizing bronchopneumonia, laryngotracheitis, and gastritis caused by feline herpesvirus-1 and secondary bacterial infection in an adult vaccinated cat with no known immunosuppression or debilitation.
Case description A 6-year-old neutered male domestic shorthair cat was presented to the Veterinary Medical Center at the Western College of Veterinary Medicine in Saskatoon, Saskatchewan for acuteonset lethargy, anorexia, and exaggerated swallowing. The cat was housed predominantly indoors with 1 other cat, and had no history of previous illness. Booster vaccinations were 2 mo overdue, but up until then he had been fully vaccinated annually for rabies, feline herpesvirus-1, calicivirus, and panleukopenia virus. According to the owner, the other cat in the household had had a mild upper respiratory tract infection the previous week, which resolved without treatment. The initial physical and oral examination was unremarkable aside from an overweight body condition (body condition score 7/9) and dysphagia. Body temperature, measured rectally, was 38.5°C and other vital parameters were within normal limits. A complete blood cell count showed a mild regenerative left shift with mild toxic change suggestive of inflammation; a mild to moderate lymphopenia, suggestive of stress; and a mild elevation in total solids, suggestive of dehydration. Blood gas analysis was unremarkable. Tests for feline leukemia virus antigen (FeLV) and feline immunodeficiency virus antibody (FIV) were negative (SNAP FIV/FeLV Combo Test; IDEXX Laboratories, Westbrook, Maine, USA). Thoracic radiographs showed diffuse, transient gas dilation of the esophagus, mild widening of the pleural fissures and a diffuse moderate bronchial pattern. Abdominal radiographs showed 147
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Figure 1. Larynx. Cat. a — Note the multifocal areas of ulceration (arrows) and inflammation. Inset: inclusion bodies (arrowheads) within epithelial cells adjacent to areas of ulceration. H&E. b — Immunohistochemistry of the corresponding section of larynx displaying strong multifocal immunoreactivity for FHV-1.
Figure 2. Trachea. Cat. a — Note the denuded tracheal mucosa covered by a thick fibrinonecrotic exudate (asterisks), attenuation of the epithelium lining the tracheal glands (arrows) and numerous inflammatory cells infiltrating the tracheal wall. Inset: Inclusion bodies within the epithelial cells lining the tracheal glands (arrowheads). H&E. b — Strong immunoreactivity for FHV-1 in the epithelium of the trachea and tracheal glands.
marked gas-dilation of the stomach and mild diffuse gas-dilation of the intestines. Endoscopy of the upper gastrointestinal tract revealed marked laryngeal edema and a localized area of mild ulceration in the gastric mucosa; endoscopic mucosal biopsies of stomach and proximal duodenum were obtained. Prior to recovery from anesthesia, dexamethasone (Dexcort; Rafter, Rafter 8 Products, Calgary, Alberta), 0.1 mg/kg body weight (BW), IV, was administered in an effort to reduce laryngeal edema. Recovery from anesthesia was slow but unremarkable. Over the next 24 h, the cat was treated for laryngeal edema and gastritis with prednisolone (Prednisolone acetate; Vétoquinol, Lavaltrie, Quebec), 1 mg/kg BW, PO, q12h, Ranitidine (Ranitidine injection; Sandoz, Boucherville, Quebec), 2 mg/kg BW, IV, q8h, maropitant citrate (Cerenia injection; Zoetis, Kirkland, Quebec) once, Metoclopramide (Metoclopramide injection; Sandoz), 2 mg/kg BW, IV/24 h continuous rate infusion, buprenorphine, (Vetergesic: Champion Alstoe Animal Health, Whitby, Ontario), 0.02 mg/kg BW, IV, q8h, Sucralfate (Sulcrate suspension Plus; Aptalis Pharm Canada, Mont Saint Hilaire, Quebec), 2.5 mL, PO, q8h as well as intravenous fluids. The cat continued to decline and euthanasia was elected. On necropsy the entire larynx, particularly the arytenoids, was markedly edematous with numerous randomly distributed small, 1 to 2 mm diameter, white raised plaques. The tracheal and bronchial mucosa was diffusely ulcerated, hyperemic, and covered with fibrinonecrotic exudate. The dorsal aspect of the lungs and the accessory lung lobe were congested and slightly 148
firm; the accessory lobe was particularly affected and sank upon immersion in formalin. There was mildly increased prominence of the small airways on cross section, particularly evident in the accessory lung lobe. The gastric mucosa was mildly hyperemic and edematous. In the gastric fundus there were 3 small areas, ranging from 5 mm to 1 cm in diameter, of hemorrhage and erosion, where endoscopic pinch biopsies had been taken. Within the duodenum there was a small focal area about 5 mm in diameter of mucosal hemorrhage where another endoscopic biopsy had been taken. Numerous tissues from all organ systems were fixed in 10% neutral-buffered formalin, embedded in paraffin blocs, sectioned and stained with hematoxylin and eosin (H&E) according to routine histological procedure. Immunohistochemical staining was conducted at Prairie Diagnostic Services, Saskatoon, Saskatchewan using a commercial staining platform (Benchmark staining platform; Ventana Medical Systems, Tucson, Arizona, USA) and a streptavidin-biotin detection system (BMK iVIEW DAB Paraffin detection kit; Ventana Medical Systems). Epitope retrieval consisted of applying Protease 3 solution (Ventana Medical Systems) for 30 min. The primary antibody [mouse anti-feline herpesvirus (type 1) clone FHV7-7, custom monoclonals] was applied for 32 min at a dilution of 1:8000. Microscopically, the laryngeal mucosa was markedly edematous, infiltrated by a mixed population of inflammatory cells, and multifocally eroded and ulcerated. The epithelial cells adjacent to laryngeal ulceration frequently had 5 to 10 mm CVJ / VOL 57 / FEBRUARY 2016
CA S E R E P O R T
Figure 3. Lung. Cat. a — Severe neutrophilic necrotizing bronchopneumonia affecting airways (asterisks) and surrounding tissues. H&E. b — Strong immunoreactivity for FHV-1 in bronchial and bronchiolar epithelium.
Figure 4. Stomach. Cat. a — Area of necrosis within the gastric mucosa (asterisk). H&E. b — Multifocal areas of FHV-1 immunoreactivity corresponding to areas of necrosis within the gastric mucosa.
diameter eosinophilic intranuclear inclusion bodies with margination of chromatin (Figure 1a). Immunohistochemistry for FHV-1 displayed strong immunoreactivity in the ulcerated areas (Figure 1b). There was widespread ulceration and ballooning degeneration of the tracheal epithelium, which was overlain by a thick layer of fibrin, necrotic cellular debris and multiple aggregates of bacteria, both cocci and rods (Figure 2a). Large numbers of neutrophils, macrophages, lymphocytes, and plasma cells infiltrated the tracheal wall. There was multifocal loss and attenuation of the tracheal gland epithelium with numerous eosinophilic intranuclear inclusion bodies in the remaining epithelial cells and multifocal strong immunoreactivity with FHV-1 (Figure 2b). There was a severe pneumonia centered on airways in all lung lobes, particularly the accessory lung lobe (Figure 3a). Airways were filled with fibrin and necrotic cellular debris, aggregates of cocci bacteria, and sloughed epithelial cells. Most of the few remaining bronchial epithelial cells contained prominent eosinophilic intranuclear inclusion bodies. Similar inclusion bodies were present within epithelial cells lining the glands surrounding the larger airways. Fibrin, necrotic cellular debris, viable and degenerate neutrophils, macrophages, lymphocytes CVJ / VOL 57 / FEBRUARY 2016
and plasma cells surrounded and extended deeply into the pulmonary parenchyma around the airways. There was strong immunoreactivity for FHV-1 within the lung, particularly around large airways (Figure 3b). In the gastric mucosa, there were multifocal areas of necrosis with eosinophilic intranuclear inclusion bodies in the gastric glands (Figure 4a). These areas were strongly immunoreactive for FHV-1 (Figure 4b). The following tissues were examined and appeared histologically normal: brain, spleen, heart, adrenal gland, small intestine including duodenum, eye, eyelid, and conjunctiva. In the pancreas there were multifocal small nodules consistent with nodular pancreatic hyperplasia. Within the liver there was mild hepatocellular lipidosis and evidence of mild bile stasis. Immunohistochemistry for FHV-1 was negative on the following tissues: pancreas, eye, conjunctiva, spleen, liver, haired skin, thyroid gland, parathyroid gland, lymph nodes, bladder, kidney, heart, adrenal gland, duodenum, jejunum, ileum, colon, brain, and cervical spinal cord. Routine aerobic and anaerobic culture yielded 31 Streptococcus canis, 11 Pasteurella multocida, and 11 Pseudomonas spp. from the lung; 41 Streptococcus canis, 21 Pasteurella multocida, 149
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31 Pseudomonas spp. from the trachea, and 11 Streptococcus canis, 11 Pasteurella multocida, and 11 Pseudomonas spp. from the spleen. The morphological diagnoses assigned to these lesions were: acute, severe, fibrinonecrotic laryngotracheitis with intranuclear viral inclusion bodies; acute, severe, suppurative, necrotizing bronchopneumonia with intranuclear viral inclusion bodies and coccobacillli; and multifocal, acute, necrotizing gastritis with intranuclear viral inclusion bodies. These histologic and immunohistochemical findings are consistent with disseminated infection with FHV-1 with a secondary mixed bacterial infection. Terminal aspiration (based on mixed bacterial culture) or septicemia cannot be ruled out as contributing factors to the deteriorating clinical condition prior to euthanasia.
Discussion Feline herpesvirus-1 is a common cause of upper respiratory disease in domestic cats. The severity of the respiratory disease with concurrent necrotizing gastritis caused by FHV-1 in this cat is unusual, particularly since this was an adult cat that was FIV and FeLV negative and had no apparent underlying disease or immunosuppression. The majority of FHV-1 bronchopneumonia cases are in young kittens or, less commonly, in animals that are debilitated for another reason (2). It is also unusual to have such severe disease in an animal that had been vaccinated. Although booster vaccines were 2 mo overdue, protection from FHV-1 resulting from vaccination is thought to last much longer than the label duration of protection of 1 y, lasting at least 3 y, likely longer (8). Feline herpesvirus-1 is a homogenous virus with only mild differences in virulence between genotypes (9), so most of the variation in disease severity is thought to be due to host factors (1). However, in this case, no host factors were identified that seemed likely to predispose this cat to such severe disease. Other than a mildly to moderately overweight body condition, which seems unlikely to be related as most indoor cats are similarly overweight, no other abnormalities were apparent on clinical or detailed postmortem examination, and the cat had always been healthy with no instances of prior illness. Since both cats in this household were predominantly indoors with minimal contact with other cats, we hypothesize that the other cat in the household, which was reported by the owner to have a mild upper respiratory tract disease the previous week, was latently infected and, for unknown reasons, started
150
shedding virus which was transmitted through direct contact, resulting in disease. A second possibility is that this cat was latently infected and became ill resulting from reactivation of the latent infection. Reactivation and shedding is often triggered by corticosteroid treatment or stress (8). In this case there was no history of corticosteroid treatment and no identified potential stressors; however, it is possible that there was a cause of stress that was not apparent to the owner that resulted in viral reactivation in both cats. Feline herpesvirus-1 is fragile in the external environment and unstable as an aerosol, so the primary route of transmission is direct contact with another cat which is actively shedding the virus (1). A thorough literature search resulted in only 1 report of multifocal gastric mucosal necrosis associated with FHV-1 (7), although this reported case was not associated with the concurrent severe necrotizing bronchopneumonia and laryngotracheitis seen here. However, there is increasing interest in herpesviruses as a cause of chronic gastritis and gastric ulcer syndrome in humans (10). Feline herpesvirus-1 should be considered as a potential etiology of gastritis in cats, particularly in cats with concurrent respiratory disease. CVJ
References 1. Gaskell R, Dawson S, Radford A, Thiry E. Feline herpesvirus. Vet Res 2007;38:337–354. 2. Chvala-Mannsberger S, Bagó Z, Weissenböck H. Occurrence, morphological characterization and antigen localization of felid herpesvirusinduced pneumonia in cats: A retrospective study (2000–2006). J Comp Pathol 2009;141:163–169. 3. Maes S, Van Goethem B, Saunders J, Binst D, Chiers K, Ducatelle R. Pneumomediastinum and subcutaneous emphysema in a cat associated with necrotizing bronchopneumonia caused by feline herpesvirus-1. Can Vet J 2011;52:1119–1122. 4. Shields RP, Gaskin JM. Fatal generalized feline viral rhinotracheitis in a young adult cat. J Am Vet Med Assoc 1977;170:439–441. 5. Spradbrow PB, Carlisle C, Watt DA. The association of herpesvirus with generalized disease in a kitten. Vet Rec 1971;89:542–544. 6. Van Pelt CS, Crandell RA. Pancreatitis associated with feline herpesvirus infection. Comp Anim Prac 1987;1:7. 7. Breuer W, Hermanns W. Acute herpesvirus-gastritis in a cat. Dtsch Tierarztl Wochenschr 2003;110:158–160. 8. Thiry E, Addie D, Belák S, et al. Feline herpesvirus infection. ABCD guidelines on prevention and management. J Feline Med Surg 2009;11: 547–555. 9. Hamano M, Maeda K, Mizukoshi F, et al. Experimental infection of recent field isolates of feline herpesvirus type 1. J Vet Med Sci 2003; 65:939–943. 10. Krulevski˘ı VA, Petrovski˘ı AN, Anichkov NM, Novikova VP. Chronic gastritis and herpetic infections in subjects of different ages. Arkh Patol 2010;72:33–35.
CVJ / VOL 57 / FEBRUARY 2016
F
eline herpesvirus-1 (FHV-1), also known as feline viral rhinotracheitis virus, is common in domestic cats worldwide. It typically results in variably severe conjunctivitis, rhinitis, and keratitis, and is becoming increasingly recognized as a cause of dermatitis, particularly on the nose and face (1). Following FHV-1 infection at least 80% of cats will remain latently infected for life; 45% of those cats will shed virus intermittently throughout life, subclinically or with recrudescence of, typically mild, clinical disease (1). There are only a handful of reported cases in domestic cats in which FHV-1 infection has resulted in more severe disease, predominantly in kittens or animals that were otherwise debilitated (2). These cases are usually characterized by severe necrotizing bronchiolitis accompanied by diffuse fibrinonecrotic bronchopneumonia (2–4). In one case the necrotizing bronchopneumonia and fibrinonecrotic tracheitis were severe enough to result in pneumomediastinum (3). There are also rare cases of hepatic necrosis associated with FHV-1 in young cats (4,5), 1 reported case of pancreatitis in a kitten (6), and a single case report of necrotizing gastritis, without respiratory tract lesions, in an adult cat (7). Here we report a unique
Department of Veterinary Pathology (McGregor, Simko), Department of Small Animal Clinical Sciences (Sheehan), Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan. Address all correspondence to Dr. Glenna McGregor; e-mail: [email protected] Use of this article is limited to a single copy for personal study. Anyone interested in obtaining reprints should contact the CVMA office ([email protected]) for additional copies or permission to use this material elsewhere. CVJ / VOL 57 / FEBRUARY 2016
and fatal case of concurrent necrotizing bronchopneumonia, laryngotracheitis, and gastritis caused by feline herpesvirus-1 and secondary bacterial infection in an adult vaccinated cat with no known immunosuppression or debilitation.
Case description A 6-year-old neutered male domestic shorthair cat was presented to the Veterinary Medical Center at the Western College of Veterinary Medicine in Saskatoon, Saskatchewan for acuteonset lethargy, anorexia, and exaggerated swallowing. The cat was housed predominantly indoors with 1 other cat, and had no history of previous illness. Booster vaccinations were 2 mo overdue, but up until then he had been fully vaccinated annually for rabies, feline herpesvirus-1, calicivirus, and panleukopenia virus. According to the owner, the other cat in the household had had a mild upper respiratory tract infection the previous week, which resolved without treatment. The initial physical and oral examination was unremarkable aside from an overweight body condition (body condition score 7/9) and dysphagia. Body temperature, measured rectally, was 38.5°C and other vital parameters were within normal limits. A complete blood cell count showed a mild regenerative left shift with mild toxic change suggestive of inflammation; a mild to moderate lymphopenia, suggestive of stress; and a mild elevation in total solids, suggestive of dehydration. Blood gas analysis was unremarkable. Tests for feline leukemia virus antigen (FeLV) and feline immunodeficiency virus antibody (FIV) were negative (SNAP FIV/FeLV Combo Test; IDEXX Laboratories, Westbrook, Maine, USA). Thoracic radiographs showed diffuse, transient gas dilation of the esophagus, mild widening of the pleural fissures and a diffuse moderate bronchial pattern. Abdominal radiographs showed 147
R A P P O R T D E CA S
Figure 1. Larynx. Cat. a — Note the multifocal areas of ulceration (arrows) and inflammation. Inset: inclusion bodies (arrowheads) within epithelial cells adjacent to areas of ulceration. H&E. b — Immunohistochemistry of the corresponding section of larynx displaying strong multifocal immunoreactivity for FHV-1.
Figure 2. Trachea. Cat. a — Note the denuded tracheal mucosa covered by a thick fibrinonecrotic exudate (asterisks), attenuation of the epithelium lining the tracheal glands (arrows) and numerous inflammatory cells infiltrating the tracheal wall. Inset: Inclusion bodies within the epithelial cells lining the tracheal glands (arrowheads). H&E. b — Strong immunoreactivity for FHV-1 in the epithelium of the trachea and tracheal glands.
marked gas-dilation of the stomach and mild diffuse gas-dilation of the intestines. Endoscopy of the upper gastrointestinal tract revealed marked laryngeal edema and a localized area of mild ulceration in the gastric mucosa; endoscopic mucosal biopsies of stomach and proximal duodenum were obtained. Prior to recovery from anesthesia, dexamethasone (Dexcort; Rafter, Rafter 8 Products, Calgary, Alberta), 0.1 mg/kg body weight (BW), IV, was administered in an effort to reduce laryngeal edema. Recovery from anesthesia was slow but unremarkable. Over the next 24 h, the cat was treated for laryngeal edema and gastritis with prednisolone (Prednisolone acetate; Vétoquinol, Lavaltrie, Quebec), 1 mg/kg BW, PO, q12h, Ranitidine (Ranitidine injection; Sandoz, Boucherville, Quebec), 2 mg/kg BW, IV, q8h, maropitant citrate (Cerenia injection; Zoetis, Kirkland, Quebec) once, Metoclopramide (Metoclopramide injection; Sandoz), 2 mg/kg BW, IV/24 h continuous rate infusion, buprenorphine, (Vetergesic: Champion Alstoe Animal Health, Whitby, Ontario), 0.02 mg/kg BW, IV, q8h, Sucralfate (Sulcrate suspension Plus; Aptalis Pharm Canada, Mont Saint Hilaire, Quebec), 2.5 mL, PO, q8h as well as intravenous fluids. The cat continued to decline and euthanasia was elected. On necropsy the entire larynx, particularly the arytenoids, was markedly edematous with numerous randomly distributed small, 1 to 2 mm diameter, white raised plaques. The tracheal and bronchial mucosa was diffusely ulcerated, hyperemic, and covered with fibrinonecrotic exudate. The dorsal aspect of the lungs and the accessory lung lobe were congested and slightly 148
firm; the accessory lobe was particularly affected and sank upon immersion in formalin. There was mildly increased prominence of the small airways on cross section, particularly evident in the accessory lung lobe. The gastric mucosa was mildly hyperemic and edematous. In the gastric fundus there were 3 small areas, ranging from 5 mm to 1 cm in diameter, of hemorrhage and erosion, where endoscopic pinch biopsies had been taken. Within the duodenum there was a small focal area about 5 mm in diameter of mucosal hemorrhage where another endoscopic biopsy had been taken. Numerous tissues from all organ systems were fixed in 10% neutral-buffered formalin, embedded in paraffin blocs, sectioned and stained with hematoxylin and eosin (H&E) according to routine histological procedure. Immunohistochemical staining was conducted at Prairie Diagnostic Services, Saskatoon, Saskatchewan using a commercial staining platform (Benchmark staining platform; Ventana Medical Systems, Tucson, Arizona, USA) and a streptavidin-biotin detection system (BMK iVIEW DAB Paraffin detection kit; Ventana Medical Systems). Epitope retrieval consisted of applying Protease 3 solution (Ventana Medical Systems) for 30 min. The primary antibody [mouse anti-feline herpesvirus (type 1) clone FHV7-7, custom monoclonals] was applied for 32 min at a dilution of 1:8000. Microscopically, the laryngeal mucosa was markedly edematous, infiltrated by a mixed population of inflammatory cells, and multifocally eroded and ulcerated. The epithelial cells adjacent to laryngeal ulceration frequently had 5 to 10 mm CVJ / VOL 57 / FEBRUARY 2016
CA S E R E P O R T
Figure 3. Lung. Cat. a — Severe neutrophilic necrotizing bronchopneumonia affecting airways (asterisks) and surrounding tissues. H&E. b — Strong immunoreactivity for FHV-1 in bronchial and bronchiolar epithelium.
Figure 4. Stomach. Cat. a — Area of necrosis within the gastric mucosa (asterisk). H&E. b — Multifocal areas of FHV-1 immunoreactivity corresponding to areas of necrosis within the gastric mucosa.
diameter eosinophilic intranuclear inclusion bodies with margination of chromatin (Figure 1a). Immunohistochemistry for FHV-1 displayed strong immunoreactivity in the ulcerated areas (Figure 1b). There was widespread ulceration and ballooning degeneration of the tracheal epithelium, which was overlain by a thick layer of fibrin, necrotic cellular debris and multiple aggregates of bacteria, both cocci and rods (Figure 2a). Large numbers of neutrophils, macrophages, lymphocytes, and plasma cells infiltrated the tracheal wall. There was multifocal loss and attenuation of the tracheal gland epithelium with numerous eosinophilic intranuclear inclusion bodies in the remaining epithelial cells and multifocal strong immunoreactivity with FHV-1 (Figure 2b). There was a severe pneumonia centered on airways in all lung lobes, particularly the accessory lung lobe (Figure 3a). Airways were filled with fibrin and necrotic cellular debris, aggregates of cocci bacteria, and sloughed epithelial cells. Most of the few remaining bronchial epithelial cells contained prominent eosinophilic intranuclear inclusion bodies. Similar inclusion bodies were present within epithelial cells lining the glands surrounding the larger airways. Fibrin, necrotic cellular debris, viable and degenerate neutrophils, macrophages, lymphocytes CVJ / VOL 57 / FEBRUARY 2016
and plasma cells surrounded and extended deeply into the pulmonary parenchyma around the airways. There was strong immunoreactivity for FHV-1 within the lung, particularly around large airways (Figure 3b). In the gastric mucosa, there were multifocal areas of necrosis with eosinophilic intranuclear inclusion bodies in the gastric glands (Figure 4a). These areas were strongly immunoreactive for FHV-1 (Figure 4b). The following tissues were examined and appeared histologically normal: brain, spleen, heart, adrenal gland, small intestine including duodenum, eye, eyelid, and conjunctiva. In the pancreas there were multifocal small nodules consistent with nodular pancreatic hyperplasia. Within the liver there was mild hepatocellular lipidosis and evidence of mild bile stasis. Immunohistochemistry for FHV-1 was negative on the following tissues: pancreas, eye, conjunctiva, spleen, liver, haired skin, thyroid gland, parathyroid gland, lymph nodes, bladder, kidney, heart, adrenal gland, duodenum, jejunum, ileum, colon, brain, and cervical spinal cord. Routine aerobic and anaerobic culture yielded 31 Streptococcus canis, 11 Pasteurella multocida, and 11 Pseudomonas spp. from the lung; 41 Streptococcus canis, 21 Pasteurella multocida, 149
R A P P O R T D E CA S
31 Pseudomonas spp. from the trachea, and 11 Streptococcus canis, 11 Pasteurella multocida, and 11 Pseudomonas spp. from the spleen. The morphological diagnoses assigned to these lesions were: acute, severe, fibrinonecrotic laryngotracheitis with intranuclear viral inclusion bodies; acute, severe, suppurative, necrotizing bronchopneumonia with intranuclear viral inclusion bodies and coccobacillli; and multifocal, acute, necrotizing gastritis with intranuclear viral inclusion bodies. These histologic and immunohistochemical findings are consistent with disseminated infection with FHV-1 with a secondary mixed bacterial infection. Terminal aspiration (based on mixed bacterial culture) or septicemia cannot be ruled out as contributing factors to the deteriorating clinical condition prior to euthanasia.
Discussion Feline herpesvirus-1 is a common cause of upper respiratory disease in domestic cats. The severity of the respiratory disease with concurrent necrotizing gastritis caused by FHV-1 in this cat is unusual, particularly since this was an adult cat that was FIV and FeLV negative and had no apparent underlying disease or immunosuppression. The majority of FHV-1 bronchopneumonia cases are in young kittens or, less commonly, in animals that are debilitated for another reason (2). It is also unusual to have such severe disease in an animal that had been vaccinated. Although booster vaccines were 2 mo overdue, protection from FHV-1 resulting from vaccination is thought to last much longer than the label duration of protection of 1 y, lasting at least 3 y, likely longer (8). Feline herpesvirus-1 is a homogenous virus with only mild differences in virulence between genotypes (9), so most of the variation in disease severity is thought to be due to host factors (1). However, in this case, no host factors were identified that seemed likely to predispose this cat to such severe disease. Other than a mildly to moderately overweight body condition, which seems unlikely to be related as most indoor cats are similarly overweight, no other abnormalities were apparent on clinical or detailed postmortem examination, and the cat had always been healthy with no instances of prior illness. Since both cats in this household were predominantly indoors with minimal contact with other cats, we hypothesize that the other cat in the household, which was reported by the owner to have a mild upper respiratory tract disease the previous week, was latently infected and, for unknown reasons, started
150
shedding virus which was transmitted through direct contact, resulting in disease. A second possibility is that this cat was latently infected and became ill resulting from reactivation of the latent infection. Reactivation and shedding is often triggered by corticosteroid treatment or stress (8). In this case there was no history of corticosteroid treatment and no identified potential stressors; however, it is possible that there was a cause of stress that was not apparent to the owner that resulted in viral reactivation in both cats. Feline herpesvirus-1 is fragile in the external environment and unstable as an aerosol, so the primary route of transmission is direct contact with another cat which is actively shedding the virus (1). A thorough literature search resulted in only 1 report of multifocal gastric mucosal necrosis associated with FHV-1 (7), although this reported case was not associated with the concurrent severe necrotizing bronchopneumonia and laryngotracheitis seen here. However, there is increasing interest in herpesviruses as a cause of chronic gastritis and gastric ulcer syndrome in humans (10). Feline herpesvirus-1 should be considered as a potential etiology of gastritis in cats, particularly in cats with concurrent respiratory disease. CVJ
References 1. Gaskell R, Dawson S, Radford A, Thiry E. Feline herpesvirus. Vet Res 2007;38:337–354. 2. Chvala-Mannsberger S, Bagó Z, Weissenböck H. Occurrence, morphological characterization and antigen localization of felid herpesvirusinduced pneumonia in cats: A retrospective study (2000–2006). J Comp Pathol 2009;141:163–169. 3. Maes S, Van Goethem B, Saunders J, Binst D, Chiers K, Ducatelle R. Pneumomediastinum and subcutaneous emphysema in a cat associated with necrotizing bronchopneumonia caused by feline herpesvirus-1. Can Vet J 2011;52:1119–1122. 4. Shields RP, Gaskin JM. Fatal generalized feline viral rhinotracheitis in a young adult cat. J Am Vet Med Assoc 1977;170:439–441. 5. Spradbrow PB, Carlisle C, Watt DA. The association of herpesvirus with generalized disease in a kitten. Vet Rec 1971;89:542–544. 6. Van Pelt CS, Crandell RA. Pancreatitis associated with feline herpesvirus infection. Comp Anim Prac 1987;1:7. 7. Breuer W, Hermanns W. Acute herpesvirus-gastritis in a cat. Dtsch Tierarztl Wochenschr 2003;110:158–160. 8. Thiry E, Addie D, Belák S, et al. Feline herpesvirus infection. ABCD guidelines on prevention and management. J Feline Med Surg 2009;11: 547–555. 9. Hamano M, Maeda K, Mizukoshi F, et al. Experimental infection of recent field isolates of feline herpesvirus type 1. J Vet Med Sci 2003; 65:939–943. 10. Krulevski˘ı VA, Petrovski˘ı AN, Anichkov NM, Novikova VP. Chronic gastritis and herpetic infections in subjects of different ages. Arkh Patol 2010;72:33–35.
CVJ / VOL 57 / FEBRUARY 2016
