Prevalence of Campylobacter jejuni in selected domestic and wild birds in Louisiana.

Prevalence of Campylobacter jejuni was determined in a selected population of domestic and free-living birds submitted for necropsy to the Louisiana State Veterinary Medical Diagnostic Laboratory. The 445 cases examined included 13 orders of birds and yielded C. jejuni in 45 cases, representing an isolation rate of 10.1%. Prevalence was highest in Galliformes (25.2%), followed by Anseriformes (12.9%) and Columbiformes (8.3%). Only one isolation was made out of 179 Psittaciformes examined. Penner serotypes 1, 2, 4, and 16 were most commonly identified among the C. jejuni isolates. This study emphasizes the importance of Galliformes as reservoirs of C. jejuni. The commonality of these serotypes with isolates derived from humans suggests the zoonotic potential of Galliformes in relation to human campylobacteriosis. The isolation rate of 12.9% in Anseriformes implicates free-living and migratory waterfowl as carriers of C. jejuni. Results confirm that Psittaciformes represent a low risk of C. jejuni infection in humans.

Role of litter in the transmission of Campylobacter jejuni.

Autoclaved or non-autoclaved used broiler litter that was experimentally contaminated with Campylobacter jejuni was capable of infecting specific-pathogen-free chicks maintained in modified Horsfall isolators. Artificially infected chicks became fecal shedders of C. jejuni, resulting in contamination of both autoclaved and non-autoclaved used broiler litter. Fecal shedding of C. jejuni by litter-reared, artificially infected chicks persisted for at least 63 days after chicks were transferred to an isolation unit with a wire floor, which prevented coprophagy. C. jejuni was consistently recovered from water and litter in units housing directly and indirectly infected birds, indicating environmental contamination. These experiments demonstrate the potential role of litter in the perpetuation and transmission of C. jejuni infection in commercial chickens.

Transmission of Campylobacter jejuni by the housefly (Musca domestica).

Houseflies (Musca domestica) were infected with Campylobacter jejuni after being confined for 5 days in a Horsfall isolator containing 25-day-old chickens known to be fecal excretors of the organism. Contaminated flies, when subsequently transferred to a second unit, transmitted C. jejuni to specific-pathogen-free chickens. Allowing a sample of 32 houseflies to ingest C. jejuni in a liquid suspension resulted in recovery rates of 20% from the feet and ventral surface of the body and 70% from the viscera. These experiments demonstrated the potential role of flies in the dissemination of avian campylobacteriosis.

Encephalitis attributed to dactylariosis in Japanese quail chicks (Coturnix coturnix japonica).

Dactylaria gallopava was isolated from brain tissue of 1-to-3-week-old quail chicks. Successive batches demonstrated elevated (15-20%) mortality preceded by incoordination and lateral recumbency. Chicks exhibited cerebellar and cerebral encephalitis characterized by brown-red discoloration of affected brain tissue. Decontamination of setters and hatchers resulted in abrupt cessation of mortality in subsequent placements, implicating incubators as the source of infection.

The occurrence of Clostridium perfringens in the intestine of chicks.

Commercial broiler chicks brooded either on wire or on used or new litter demonstrated a 75% (62/75) incidence of recovery of "perfringens-like" colonies from the intestine during a 5-week period. Eleven Clostridium spp. were identified from among these "perfringens-like" organisms, which were cultured on SPS selective agar medium. Clostridium perfringens was positively identified only infrequently (five isolates) from among the "perfringens-like" colonies. In contrast, "perfringens-like" colonies were not recovered from the intestinal contents of specific-pathogen-free chicks reared in an isolation unit. However, C. perfringens was isolated from the yolk sac of one embryonated egg and from the intestine of a single 7-day-old chick, indicating the possibility of vertical transmission of this potential pathogen.

The occurrence of Aeromonas hydrophila in avian diagnostic submissions.

Twenty isolations of Aeromonas hydrophila were made from 15 species of free-living, commercial, and companion birds submitted for routine diagnostic postmortem examination. Seventy percent of the isolations were made from November through March during the 25-month survey period.

Chronic obstructive pulmonary disease in horses in Louisiana.

OBJECTIVE: To evaluate chronic obstructive pulmonary disease of horses in Louisiana by assessing the signalment, history, environmental factors, clinical signs, and treatment of such horses. DESIGN: Epidemiologic mail survey. SAMPLE POPULATION: 83 of 240 veterinarians contacted by mail agreed to take part in the survey. Veterinarians contacted were listed as mixed-animal or equine practitioners in the 1991/1992 directory of the Louisiana Veterinary Medical Association or had submitted a specimen from a horse to the Louisiana Veterinary Medical Diagnostic Laboratory within the past 2 years. PROCEDURE: The survey contained 47 questions designed to elicit information from owners and veterinarians about horses reported to have chronic obstructive pulmonary disease (COPD). Questions were included to evaluate age, breed, sex, vaccination history, respiratory disease history, environment of primary activity, level of exercise, primary residence (pasture or stall), condition of pasture or barn, type and condition of feed, clinical signs, concurrent conditions, and treatment regimen prescribed. Information from the returned forms was analyzed by using a microcomputer program designed for epidemiologic data. RESULTS: Of the 83 veterinarians who agreed to participate, 31 returned 71 completed questionnaires for horses affected with COPD. Most affected horses were mature in age, kept on pasture, and had developed clinical signs during the summer months. The most consistent clinical signs were dry coughing, slight serous nasal discharge, labored expiratory effort, and flaring nostrils. CLINICAL IMPLICATIONS: Summer pasture-associated obstructive pulmonary disease appears to be precipitated by factors different than those associated with the traditionally diagnosed form of COPD and, thus, successful management measures may also vary.

Etiology and pathogenesis of necrotic enteritis.

Sporulated oocysts of Eimeria acervulina were administered orally to cage-housed broilers at a dose of 3.5 X 10(5) resulted in mild subclinical coccidiosis. Clostridium perfringens incorporated in feed at a level of 2.5 X 10(8) organisms/g. produced lesions characteristic of necrotic enteritis. Mortality of 8% (7/80) occurred in birds fed a ration inoculated with Cl. perfringens alone. Mortality of 35% (28/80) was observed in birds which received an oral dose of E. acervulina and which were fed simultaneously with a ration containing Cl. perfringens. Birds which were fed an inoculated ration two days after an oral dose of E. acervulina showed 41% (33/80) mortality. Birds which received an inoculated ration for two days before administration of an oral dose of E. acervulina demonstrated 18% mortality (15/80). Birds which were fed an inoculated ration four days after an oral dose of E. acervulina showed 10% mortality. Infection with E. acervulina reduced the pH of intestinal contents with a simultaneous depression in serum protein. A 39% increase in intestinal passage time from 178 to 248 minutes occurred on the fifth day after infection with E. acervulina. These experiments suggest that necrotic enteritis, attributed to proliferation of a toxigenic strain of Cl. perfringens, followed intestinal stasis and minimal lesions induced by mild intestinal coccidiosis.

Salmonella colonization in commercial pet turtles (Pseudemys scripta elegans).

An epidemiological survey was conducted on two commercial turtle farms in southern Louisiana to determine the reason for an apparent increase in the prevalence of Salmonella spp. in turtle hatchlings at the time of pre-export certification examination. Pond water was consistently found to be contaminated (6/36 samples) with either Salmonella newport, S. arizonae, or S. poona. Environmental specimens obtained from eggs and turtle hatcheries (204 specimens) failed to yield Salmonella spp. A sample comprising 197 hatchlings, derived from a batch previously demonstrated to be contaminated, showed a salmonella prevalence of 12%, with S. arizonae and S. poona the only serotypes isolated. Four serotypes of Salmonella sp. isolated by a certifying laboratory in 1988, and 20 salmonella isolates obtained from hatchling turtles, were all resistant to gentamicin. The emergence of gentamicin resistance in Salmonella spp. isolated from turtles will reduce the effectiveness of preventive measures in use in Louisiana since 1984.

Leukemia-associated AML1/ETO (8;21) chromosomal translocation protein increases the cellular representation of PML bodies.

Promyelocytic leukemia (PML) nuclear bodies are important components of nuclear architecture that are functionally linked to aberrant gene expression and disease. To understand the mechanisms that modify subnuclear distribution and regulatory activities of PML domains in leukemia, we performed immunofluorescence microscopy with a panel of normal diploid cells and established cell lines. We analyzed the representation and intranuclear distribution of PML domains. We find that multiple biological parameters contribute to heterogeneity in the subnuclear organization of PML domains in a broad spectrum of cell types. The subnuclear organization of PML domains was also evaluated following transient transfection with a series of vectors expressing normal hematopoietic and leukemia-related transcription factors. Our results show that expression of a chimeric transcription factor encoded by the tumor related chromosomal translocation (8;21) involving the AML1 and ETO loci is sufficient to cause reorganization of PML domains. This finding increases our understanding of the mechanisms by which the AML1/ETO protein may contribute to modified gene expression linked to the onset and progression of t(8;21) related acute myelogenous leukemia.

A novel, nerve growth factor-activated pathway involving nitric oxide, p53, and p21WAF1 regulates neuronal differentiation of PC12 cells.

During development, neuronal differentiation is closely coupled with cessation of proliferation. We use nerve growth factor (NGF)-induced differentiation of PC12 pheochromocytoma cells as a model and find a novel signal transduction pathway that blocks cell proliferation. Treatment of PC12 cells with NGF leads to induction of nitric oxide synthase (NOS) (Peunova, N., and Enikolopov, G. (1995) Nature 375, 68-73). The resulting nitric oxide (NO) acts as a second messenger, activating the p21(WAF1) promoter and inducing expression of p21(WAF1) cyclin-dependent kinase inhibitor. NO activates the p21(WAF1) promoter by p53-dependent and p53-independent mechanisms. Blocking production of NO with an inhibitor of NOS reduces accumulation of p53, activation of the p21(WAF1) promoter, expression of neuronal markers, and neurite extension. To determine whether p21(WAF1) is required for neurite extension, we prepared a PC12 line with an inducible p21(WAF1) expression vector. Blocking NOS with an inhibitor decreases neurite extension, but induction of p21(WAF1) with isopropyl-1-thio-beta-D-galactopyranoside restored this response. Levels of p21(WAF1) induced by isopropyl-1-thio-beta-D-galactopyranoside were similar to those induced by NGF. Therefore, we have identified a signal transduction pathway that is activated by NGF; proceeds through NOS, p53, and p21(WAF1) to block cell proliferation; and is required for neuronal differentiation by PC12 cells.

The t(8;21) chromosomal translocation in acute myelogenous leukemia modifies intranuclear targeting of the AML1/CBFalpha2 transcription factor.

Targeting of gene regulatory factors to specific intranuclear sites may be critical for the accurate control of gene expression. The acute myelogenous leukemia 8;21 (AML1/ETO) fusion protein is encoded by a rearranged gene created by the ETO chromosomal translocation. This protein lacks the nuclear matrix-targeting signal that directs the AML1 protein to appropriate gene regulatory sites within the nucleus. Here we report that substitution of the chromosome 8-derived ETO protein for the multifunctional C terminus of AML1 precludes targeting of the factor to AML1 subnuclear domains. Instead, the AML1/ETO fusion protein is redirected by the ETO component to alternate nuclear matrix-associated foci. Our results link the ETO chromosomal translocation in AML with modifications in the intranuclear trafficking of the key hematopoietic regulatory factor, AML1. We conclude that misrouting of gene regulatory factors as a consequence of chromosomal translocations is an important characteristic of acute leukemias.