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Infectious coryza, caused by Avibacterium paragallinarum, is an acute respiratory disease of poultry that can result in substantial morbidity, mortality, and economic losses. In March 2017, the Turlock branch of the California Animal Health and Food Safety laboratory system encountered an unusual clinical and pathologic presentation of infectious coryza in 6 live, 29-d-old, commercial broiler chickens that were submitted for diagnostic investigation. Antemortem evaluation revealed severe neurologic signs, including disorientation, torticollis, and opisthotonos. Swollen head-like syndrome and sinusitis were also present. Histologically, severe sinusitis, cranial osteomyelitis, otitis media and interna, and meningoencephalitis were noted, explaining the clinical signs described. A. paragallinarum was readily isolated from the upper and lower respiratory tract, brain, and cranial bones. Infectious bronchitis virus (IBV) was also detected by PCR, and IBV was isolated in embryonated chicken eggs. Based on sequencing analysis, the IBV appeared 99% homologous to strain CA1737. A synergistic effect between A. paragallinarum and IBV, resulting in exacerbation of clinical signs and increased mortality, may have occurred in this case. A. paragallinarum should be considered among the possible causes of neurologic signs in chickens. Appropriate media should be used for bacterial isolation, and the role of additional contributing factors and/or complicating agents should be investigated in cases of infectious coryza.

Streptococcal bacterial species represent common inhabitants of the intestinal tract of animals and humans with a potential for opportunistic infections. Streptococcosis has been identified in turkey poults ( Meleagris gallopavo), ducklings and goslings (Anatidae), broiler chickens, semimature-adult chickens ( Gallus gallus domesticus), and young and adult pigeons (Columbidae). However, the exact underlying factors that lead to bacterial invasion of the blood stream and tissue colonization have not been completely elucidated. The electronic database of the California Animal Health and Food Safety laboratory (Fresno, Tulare, and Turlock branches) was searched for necropsy cases in which streptococcosis was diagnosed in different avian species between January 2000 and August 2017. A total of 95 cases, involving both commercial operations and noncommercial premises, were analyzed. Streptococcus spp., Streptococcus bovis, and Streptococcus gallolyticus were identified from multiple organs, with macroscopic or histopathologic lesions (or both) indicative of septicemia in 23 (24%), 40 (42%), and 30 (32%) cases, respectively. Streptococcus pluranimalium and Streptococcus lutetiensis were also isolated from one (1%) and two (2%) cases, respectively. Turkey poults, broiler chickens, and ducklings were the most-commonly affected species with streptococcosis. Splenitis and hepatitis were the most-common lesions observed and these were the organs with the highest isolation rate. An overview of the clinical and pathologic presentation, and possible predisposing conditions associated with this bacterial infection, is provided.

This report documents the occurrence of a very virulent infectious bursal disease virus (vvIBDV) in Northern California commercial brown pullets. Diagnosis was made from multiple accessions from two neighboring and epidemiologically related ranches submitted to the California Animal Health and Food Safety (CAHFS) laboratory. Pullets, 11 and 14 wk of age from ranch A (rA) and ranch B (rB) respectively, were submitted from infectious bursal disease virus vaccinated flocks experiencing a drastic increase in mortality. The December 2008 outbreak resulted in 26% and 34% mortality on rA and rB respectively. Gross and histologic lesions characteristic of acute vvIBDV were observed. Gross lesions included edematous bursas, hemorrhages at the junction of the proventriculus and gizzard as well as hemorrhages on skeletal muscles. Microscopic lesions included severe lymphoid necrosis and inflammation in edematous bursas, lymphoid necrosis in thymus, spleen, Peyer's patches and cecal tonsils. Diagnosis of vvIBDV was confirmed by molecular characterization of the IBDV from bursas as well as viral pathogenicity in specific-pathogen-free birds. RT-PCR and nucleotide sequencing of the hypervariable region of the VP2 (vVP2) gene segment of the IBDV genome was performed on rA, rB and embryo passaged rA virions.The amino acids compatible with vvIBDV isolates: 222(Ala), 242(Ile), 256(Ile), 294(Ile) and 299(Ser) were reported from both ranches. In addition, nucleotide sequencing of a fragment of the VP1 gene demonstrated the viruses have the segment B genotype associated with highly pathogenic vvIBDV. Inocula of 10(5.5) 50% egg infective dose of vvIBDV virus from rA and rB were introduced orally into two groups (g1 and g2 respectively) of 4 wk 2-day-old SPF leghorns. At 4 days postinoculation, there was 100% (22/22) morbidity in g1 and g2; 91% (20/22) mortality in g1; 100% (22/22) mortality for g2; 0% (0/20) morbidity and 0% (0/ 20) mortality was reported in the control group. This is the first occurrence of vvIBDV reported from birds in the United States.

An outbreak of infectious catarrhal enteritis, associated with the flagellated protozoan Spironucleus meleagridis (syn. Hexamita meleagridis), is reported from a commercial flock of chukar partridges in California. The disease affected birds between the ages of 4 and 6 wk and resulted in diarrhea, listlessness, depression, and high mortality. Concurrent infection with other intestinal pathogens, including Cryptosporidia, group E Salmonella, long-segmented filamentous microorganisms (LSFMOs), and Rotavirus-like virus particles, was found in some but not all affected birds. Dermatitis of the face, shanks, and feet, suggestive of B-complex vitamin deficiency, was present in most affected birds as well. Flagellated protozoan parasites could be found in the lumen of the duodenum and jejunum and in the intestinal crypts. In some cases the flagellates were wedged between epithelial cells or were located intracellularly within cells of the mucosal epithelium and the intestinal lamina propria.

Egg production drops associated with western equine encephalitis (WEE) virus infection occurred in three turkey breeder flocks in California during summer 1993 and again in one flock the following year. Egg production losses totaled 8.76%, 9.57%, 9.71%, and 10.12% and were accompanied by an increase in small white-shelled and shell-less eggs. The outbreaks coincided with peak WEE virus activity in the state on the basis of statistics compiled by the California Department of Health Services on seroconversion rates in sentinel chicken flocks. Paired serum samples taken 2-3 wk apart showed increased titers to WEE between acute and convalescent sera in turkeys from three affected flocks. Convalescent sera were not available for testing from the fourth flock. WEE virus was isolated from one breeder hen submitted to the diagnostic laboratory during the early stages of the outbreak.

A mixed breed rooster, from a backyard flock of 13 chickens, was received at California Veterinary Diagnostic Laboratory System-Turlock Branch for postmortem examination. The bird presented with thickened, featherless, scab-encrusted skin around the head region. Numerous sticktight fleas were found attached to the encrusted skin. Microscopic evaluation of the skin revealed a lymphoplasmacytic reaction in the dermis with visible embedded flea mouthparts. Also noted histologically in this region were epidermal hyperplasia and ballooned epidermal cells containing intracytoplasmic inclusions indicative of fowl poxvirus.

The pathogenicity of a field isolate of western equine encephalitis (WEE) virus, which was recovered from a breeder hen during investigations of egg production drops in California turkey flocks, was tested in 2-wk-old turkey poults. No symptoms or mortality were observed in poults inoculated intramuscularly with 4.2 log10 50% embryo lethal doses of virus; however, the infection did result in mild to moderate lymphoid necrosis in the bursa of Fabricius and thymus glands beginning on the first day postinoculation. In addition, WEE virus could be isolated from the blood of infected poults for up to 3 days postinoculation.

Esophageal trichomoniasis has been rarely reported in chickens. At the California Veterinary Diagnostic Laboratory System-Turlock Branch, this disease was recently diagnosed in two cases submitted from backyard chicken flocks. The esophageal lesions observed were similar to those seen in several other important diseases of chickens. The causative trichomonad organisms were readily demonstrated on wet smears and by histologic studies. In both cases, the investigated flocks were afflicted with several concurrent diseases. California has experienced an increase in the number of small nontraditional chicken production operations. These facilities are sometimes in close proximity to commercial poultry operations and biosecurity barriers occasionally fail. The poor husbandry practices often used in these small flocks make them a potential reservoir for rare diseases such as trichomoniasis and also for disease organisms that are devastating to commercial poultry.

Outbreaks of enteritis associated with an unusual flagellated protozoan occurred in six California turkey flocks during the summer of 1992. Certain morphological and ultrastructural details of the parasite, which resembles Cochlosoma anatis, are illustrated with scanning and transmission electron micrographs. The flagellate attached to the intestinal mucosa by means of a sucker-like apparatus, and circular impressions of the sucker were created on the surface epithelium. Histological lesions were characterized by blunting and fusion of villi; cellular infiltration of the lamina propria with lymphocytes, plasma cells, histiocytes, and heterophils; and increased numbers of mitotic figures in crypt epithelium.

Infectious laryngotracheitis (ILT) was diagnosed as the cause of an outbreak of respiratory disease in broiler chickens in California. The classical form of ILT is characterized by dyspnea, gasping, coughing, and expectoration of bloody exudate. Most of the broilers submitted to the diagnostic laboratory showed a non-classical presentation of ILT, in which mucoid tracheitis and conjunctivitis were the most consistent lesions. Historically, most of the ILT cases diagnosed in our laboratory have consisted of layers with classical signs and lesions. It is not known whether this non classical presentation of ILT in broilers is due to differences in the way broilers respond to ILT infection or to the nature of the ILT virus isolate.

An outbreak of spirochetosis occurred in a flock of 75 game chickens in California during fall 1991. Affected birds were weak and anemic. Many had greenish diarrhea. Spirochetes were seen on Giemsa-stained blood smears and in silver-stained tissue sections of kidney, liver, and spleen. Splenomegaly, which is reported to be characteristic of fowl spirochetosis, was not observed in two acutely infected chickens.

An outbreak of diarrhea and neurological disease in California racing pigeons caused by avian paramyxovirus type 1 (PMV-1) is documented. Predominant clinical signs were polydipsia, ataxia, poor balance, torticollis, head tremors, inability to fly, and diarrhea that was unresponsive to therapy. Gross pathologic findings were often unremarkable or non-specific. The predominant histologic lesions were interstitial nephritis, chronic tubular necrosis, lymphoplasmacytic infiltration within the kidney, liver, and pancreas, and focal non-suppurative encephalitis. Pigeons from 20 submissions demonstrated characteristic clinical signs of PMV-1 infection. Pigeons from 17 submissions exhibited typical histopathology. Serologic evidence of PMV-1 infection was present in pigeons from 13 submissions, and PMV-1 was isolated from pigeons received in six submissions. None of these pigeons had been vaccinated against PMV-1.

Long-segmented filamentous organisms (LSFOs) are easily recognized gram-positive bacteria that infect several species of animals. The present study describes the epizootiological, clinical, and pathological characteristics of LSFOs in chicks, turkey poults, and quails in Georgia and California. LSFOs are most likely to be seen in young poultry that have gastrointestinal illnesses during winter. Concomitant infections with other bacteria and protozoans are common. Although inflammation and displacement of microvilli are characteristics of LSFO infections in these birds, LSFOs are not necessarily pathogens. They may be normal intestinal flora or commensal organisms that overgrow when certain unknown gastrointestinal conditions are correct or certain unknown events occur.

Six hundred fourteen meat turkeys were submitted for necropsy from 24 California ranches as part of the National Animal Health Monitoring System (NAHMS). Enteritis was the most frequent pathologic diagnosis in birds 18 days old or younger and the second most frequent diagnosis in birds 19-70 days old. Hemorrhagic enteritis was the most frequent diagnosis in birds aged 19-70 days. Tibial dyschondroplasia, bronchopneumonia, and ascaridiasis were ranked one through three in frequency of diagnoses in birds over 70 days of age. Salmonella was isolated from 71% of flocks tested, and Mycoplasma meleagridis was isolated from 33% of tested flocks over 70 days of age. Antibodies to several disease agents were detected, including hemorrhagic enteritis (100% of flocks over 70 days old) and Newcastle disease (63% of flocks over 70 days old).

Systemic trichomoniasis was responsible for severe morbidity and mortality in a commercial squab operation. Squabs of 1 to 3 weeks of age were primarily affected. Extensive caseous necrosis of the liver, heart, lung, and intestinal mesentery was observed grossly. Histologically, extensive heterophilic inflammation surrounded the necrotic areas and was observed perivascularly in areas that were uninvolved grossly. Numerous trichomonads were demonstrated in affected tissues with Bodian's silver stain.

Two cases of infectious coryza in meat chickens are reported. The first case involved 6-week-old broiler chickens in which only Haemophilus paragallinarum was isolated. The second case involved 11-week-old roaster chickens in which H. paragallinarum and Mycoplasma synoviae were isolated. Both farms were in close proximity to layer-chicken farms where infectious coryza had been previously diagnosed. In both cases, only certain houses on the farm were affected, and mortality in these houses increased slightly. At processing, the condemnation rates for affected houses were considerably higher than rates for unaffected houses. Condemnations for affected houses were mostly due to airsacculitis. A dissecting fibronopurulent cellulitis was a prominent lesion in the second case. This lesion could lead to confusion with chronic fowl cholera and swollen-head syndrome.

Outbreaks of Pasteurella anatipestifer infections in California turkey flocks were investigated and found to have a seasonal distribution, with a peak incidence in fall, coinciding with peak Culex mosquito populations. An experiment was conducted to test the hypothesis that mosquitoes may serve as vectors for P. anatipestifer infections in turkeys. Four 7-week-old turkey poults were exposed for 7 days to mosquitoes captured from turkey barns during a field outbreak of P. anatipestifer serotype 1 infection. One turkey developed serum antibodies to serotype 1, detectable by enzyme-linked immunosorbant assay, and was resistant to an intravenous inoculation of P. anatipestifer serotype 1 at 4 weeks postexposure. Giemsa-stained blood smears from this bird and from three 7-week-old turkeys inoculated intravenously with P. anatipestifer revealed the presence of rod-shaped bacteria in or on the surface of host erythrocytes. No such rod-shaped bodies were found on erythrocytes of an uninoculated control turkey.

A disease outbreak characterized by torticollis, incoordination, and depression was seen in a commercial broiler operation in California. Listeria monocytogenes was isolated from brain tissue with some degree of difficulty, and only after culturing directly from the brain stem. No evidence of concurrent disease was found, and the source of the outbreak was undetermined.