John J. Andrews

Comparative Pathogenicity of Nine US Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) Isolates in a Five-Week-Old Cesarean-Derived, Colostrum-Deprived Pig Model:

One hundred forty-six 5-week-old cesarean-derived, colostrum-deprived (CDCD) pigs were inoculated intranasally with 1 of 9 US porcine reproductive and respiratory syndrome virus (PRRSV) isolates. Differences were found in severity of clinical respiratory disease, rectal temperatures (P ≤0.001), gross lung lesions (P ≤ 0.001), and microscopic lung lesions (P ≤ 0.05). Gross lung lesions were generally most severe 10 days postinoculation and were distributed primarily in the cranial, middle, and accessory lobes and ventromedial portion of the caudal lung lobes. Mean gross lung lesion scores estimating the percentage of lung affected by pneumonia at 10 days postinoculation ranged from 16.7% ± 2.8% (xX ± SEM, n = 10) for isolate ISU-51 to 62.4% ± 5.7% (n = 10) for isolate ISU-28. Microscopic lung lesions were characterized by hyperplastic and hypertrophied type 2 pneumocytes, septal infiltration by mononuclear cells, and accumulation of necrotic alveolar exudate. Lymph node follicular hyperplasia and focal necrosis was seen with all 9 isolates. This CDCD pig model was useful for demonstration of significant differences in pathogenicity among US PRRSV isolates. This difference in pathogenicity may help explain the variation in severity of clinical disease observed in field outbreaks of porcine reproductive and respiratory syndrome and should provide for meaningful comparison of PRRSV genotypes.

Immunohistochemical Identification of Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) Antigen in the Heart and Lymphoid System of Three-week-old Colostrum-deprived Pigs

Porcine reproductive and respiratory syndrome virus (PRRSV) antigens were detected by a streptavidin-biotin complex technique in tissues of 3-week-old colostrum-deprived pigs that had been inoculated intranasally with PRRSV and had developed moderate respiratory disease. Moderate, multifocal, tan-colored consolidation of the lungs and severe enlargement of the lymph nodes were noted at necropsy. Severe interstitial pneumonia characterized by type 2 pneumocyte proliferation, septal infiltration with mononuclear cells, and accumulation of macrophages and necrotic cells in alveolar spaces was observed at 4 and 9 days postinoculation. Moderate multifocal perivascular lymphohistiocytic myocarditis was observed at 9 days postinoculation. Marked lymphoid follicular hyperplasia and follicular necrosis in the tonsil, spleen, and lymph nodes was observed. A monoclonal antibody that recognizes a conserved epitope of PRRSV nucleocapsid protein was used as primary antibody for immunohistochemistry. Antigen was readily detected in alveolar macrophages in the lung and in endothelial cells and macrophages in the heart. Macrophages and cells resembling dendritic cells in tonsil, lymph nodes, thymus, and spleen also stained intensely positive for viral antigen. PRRSV appears to replicate primarily within macrophages in the respiratory and lymphoid systems of the pig.

Development of a Streptavidin-Biotin Immunoperoxidase Procedure for the Detection of Porcine Reproductive and Respiratory Syndrome Virus Antigen in Porcine Lung

Boos J, Esiri MM: 1986, Pathological features of encephalitis. In: Viral encephalitis: pathology, diagnosis and management, pp. 1-27. Blackwell Scientific, Boston, MA. Calisher CH: 1983, Taxonomy, classification, and geographic distribution of California serogroup bunyaviruses. Prog Clin Biol Res 123:1-16. Craig GB Jr: 1983, Biology of Aedes triseriatus: some factors affecting control. Prog Clin Biol Res 123:329-341. Defoliart GR: 1983, Aedes triseriatus: vector biology in relationship to the persistence of La Crosse virus in endemic foci. Prog Clin Biol Res 123:89-104. Early E, Peralta PH, Johnson KM: 1967, A plaque neutralization method for arboviruses. Proc Soc Exp Biol Med 12:5741747. Godsey MS Jr, Amoo F, Yuill TM, Defoliart GR: 1988, California serogroup virus infections in Wisconsin domestic animals. Am J Trop Med Hyg 39:409-416. 11.

Experimental reproduction of Haemophilus parasuis infection in swine: clinical, bacteriologic, and morphologic findings

Haemophilus parasuis is a common cause of polyserositis and polyarthritis in swine. Little is known about the mucosal and systemic sites of replication and lesions which follow an aerosol exposure to H. parasuis. In this experiment 5–week-old cesarean-derived, colostrum-deprived (CDCD) pigs were inoculated intranasally with an inoculum containing 2 × 109 colony-forming units of H. parasuis. Two principals and one control pig were necropsied at 12, 36, 84, and 108 hours postinoculation (PI) and samples obtained for bacteriologic culture and microscopic examination. Inoculated pigs developed clinical signs of inappetence, reluctance to move, lameness, and a serous nasal discharge. Macroscopic findings included a fibrinous polyserositis and polyarthritis 36 hours PI which became progressively more severe at 84 and 108 hours PI. No lung lesions were grossly visible. Microscopic lesions included a mild purulent rhinitis at each post inoculation interval and fibrinous to fibrinopurulent synovitis and serositis at 36, 84, and 108 hours PI. A focal suppurative bronchopneumonia was observed in one pig examined at 36 hours PI. The nasal cavity and trachea were the only mucosal sites from which H. parasuis was reisolated. Haemophilus parasuis was isolated from the blood and systemic sites at 36, 84, and 108 hours PI. Findings presented indicate that intranasal inoculation of 5-week-old CDCD pigs with H. parasuis results in clinical signs and lesions of polyserositis and polyarthritis typical of field cases and is a useful model for the study of H. parasuis pathogenesis. The results also suggest that H. parasuis initially colonizes the nasal mucosa.

Experimental Reproduction of Pneumonia in Gnotobiotic Pigs with Porcine Respiratory Coronavirus Isolate AR310

The pathogenicity of porcine respiratory coronavirus (PRCV) isolate AR310 was determined for gnotobiotic pigs. PRCV-AR310 was isolated from the intestines of a nursery pig from a herd with endemic transmissible gastroenteritis. The AR310 isolate was plaque purified and cell culture propagated, passed once in a gnotobiotic pig, then used as inoculum for a gnotobiotic pig pathogenicity study. Eight pigs were inoculated oronasally with 2 × 106 plaque-forming units of PRCV-AR310. Eight pigs served as controls and received cell culture medium. Two pigs from each group were necropsied at 3, 5, 10, and 15 days postinoculation (DPI). There was moderate multifocal to coalescing reddish tan consolidation of 60% of the lung by 10 DPI. Microscopic examination revealed a necrotizing and proliferative bronchointerstitial pneumonia characterized by necrosis, squamous metaplasia, dysplasia, proliferation of airway epithelium, mononuclear cell infiltration of alveolar septa, mild type II pneumocyte proliferation, and lymphohistiocytic alveolar exudation. The microscopic lesions were mild by 3 DPI, moderate by 5 DPI, severe by 10 DPI, and mostly resolved by 15 DPI. No lesions were observed in the intestines of these pigs. There was no clinical respiratory disease. Control pigs remained normal and had no lesions. PRCV was isolated from the lungs but not from the intestines of inoculated pigs. PRCV was not isolated from the lungs or intestines of control pigs. PRCV was also isolated from the nasal and rectal swabs of inoculated but not of control pigs.

West Nile Virus Infection in Free-Ranging Squirrels in Illinois

West Nile virus (WNV) infection was diagnosed in 13 gray squirrels (Sciurus carolinensis) and 3 fox squirrels (Sciurus niger) that were observed with neurologic signs before death or found dead. All 16 had gliosis throughout all sections of the brain. Most had lymphoplasmacytic encephalitis or meningoencephalitis, many with admixed neutrophils. Neuronal necrosis and neuronophagia were also prominent features. West Nile virus antigen was demonstrated in the brain, spleen, heart or kidney in 10 of 13 gray squirrels and 3 of 3 fox squirrels by immunohistochemistry. Nucleic acid amplification tests (NAATs) confirmed the presence of WNV in the brain or spinal cord of 10/10 gray squirrels and 1/3 fox squirrels tested. Viral levels were quantified in various tissues of selected gray squirrels, and titers were highest in spleen and brain, with no virus detected in serum. This is the first description of lesions associated with WNV infection in gray and fox squirrels.

Immunohistochemical Detection of Porcine Reproductive and Respiratory Syndrome Virus Antigen in Neurovascular Lesions

At necropsy, no gross lesions were observed except for reddish consolidation of approximately 10% of the anterioventral portions of the lungs in 1 pig. Likewise, no significant gross lesions were seen in the tissues submitted from the sow. Results of experimental studies indicate that PRRSV infection is a multisystemic disease characterized initially by viremia with subsequent virus distribution and replication in multiple organs, causing interstitial pneumonia, lymphadenopathy, myocarditis, and encephalitis. 5-8,16,18 Nervous signs are uncommonly reported and are described as incoordination, paresis, splay-leggedness, and tremors in young pigs. Characteristic PRRSV-induced central nervous system (CNS) lesions include encephalitis with lymphohistiocytic perivascular cuffing, gliosis, and less often mild vasculitis.

Primary Hepatic Hemangiosarcoma with Pulmonary Metastasis in a New Zealand White Rabbit

In dogs, pathologic fractures of the vertebrae,4 extradural masses,3 and hyperviscosity due to the presence of high concentrations of paraproteins within the blood have all been associated with neurologic signs.5 The presenting signs of dysphagia and ptyalism in this horse were attributed to neoplastic involvement of the trigeminal nerve. To our knowledge, these clinical signs have not been previously reported in plasma cell myeloma in the horse. In humans, Waldenstrom’s macroglobulinemia can cause a peripheral neuropathy that is characterized by a marked monoclonal gammopathy of IgM. In some patients, the IgM acts as an antibody to various glycolipids or glycoproteins in the myelin, such as myelin-associated glycoprotein, and can cause complement-mediated demyelination.1,6 This condition has not been reported in horses but could explain the distribution of neoplastic cells and subsequent dysphagia. Marek’s disease in chickens can produce a similar neoplastic infiltration by lymphoproliferative cells into peripheral nerves.5 The distribution of the neoplastic cells in this horse was very unusual because the plasma cell infiltrate did not involve the bone marrow or the usual tissues involved in equine extramedullary plasmacytomas (typically liver, spleen, or lymph nodes). Rather, the neoplastic cells were most prevalent in nervous and connective tissue.

Atypical Hypoplastic Left Ventricular Syndrome in a Calf

An 8-day-old male Angus calf was presented to the University of Illinois, Veterinary Teaching Hospital, Urbana, IL, for lethargy, weakness, and poor suckle reflex. Clinical evaluation revealed a strong left-sided heart murmur and a split S2 sound. The calf died within 48 hours. Necropsy revealed a combination of the following cardiac defects: left ventricular hypoplasia, high ventricular septal defect, left auricular atresia with mitral valve aplasia, patent foramen ovale, patent ductus arteriosus, and pulmonary trunk atresia. Mild suppurative pneumonia with pulmonary edema and congestion were also present. This combination of defects appears to be similar to the hypoplastic left heart syndrome in humans and is reported here for the first time in cattle.