Association of bronchopneumonia with sinusitis due to Bordetella bronchiseptica in an experimental rabbit model.

An animal model for rhinogenic sinusitis was developed in rabbits naturally colonized with Bordetella bronchiseptica. It was found that ostial occlusion predisposes the sinus to invasion with this opportunistic bacterium and subsequent sinusitis as a result of reduced local host defense. In addition to the inflammatory lesions in the sinus, bronchitis and pneumonia were found in 84% of the experimental rabbits, suggesting that ostial dysfunction can also contribute to infectious disease of the lower respiratory tract. In such a model it is possible to study the significance of asymptomatic carriage of potential pathogens after ostial occlusion.

The role of B-cells in experimental myasthenia gravis in mice.

Myasthenia gravis (MG) and experimental autoimmune myasthenia gravis (EAMG) are caused by auto-antibodies against the nicotinic acetylcholine receptor (AChR) at the postsynaptic membrane. To evaluate the extent to which the humoral immune response against AChR operates in the pathogenesis of EAMG, we immunized B-cell knockout (microMT) and wild type C57BL/6 mice with AChR in complete Freund's adjuvant. The ability of AChR-primed lymph node cells to proliferate and secrete IFN-gamma in response to AChR and its dominant peptide alpha 146-162 were intact in microMT as in wild type mice. Similar levels of mRNA for IFN-gamma, IL-4 and IL-10 in AChR-reactive lymph node cells were detected in microMT and wild type mice. However, microMT mice had no detectable anti-AChR antibodies and never developed clinical EAMG. We conclude that B-cells are critically required for the genesis of clinical EAMG, but not for AChR-specific T-cell priming.

Experimental autoimmune myasthenia gravis induction in B cell-deficient mice.

Experimental autoimmune myasthenia gravis (EAMG) is an animal model for human myasthenia gravis (MG). Autoantibody-induced functional loss of nicotinic acetylcholine receptor (AChR) at the postsynaptic membrane is an important pathogenic feature of both MG and EAMG. To evaluate the extent at which the humoral immune response against AChR operates in the pathogenesis of EAMG, we immunized B cell knockout (muMT) and wild-type C57BL/6 mice with AChR and complete Freund's adjuvant. The ability of AChR-primed lymph node cells to proliferate and secrete IFN-gamma in response to AChR and its dominant peptide alpha146-162 were intact in muMT mice as in wild-type mice. Similar amounts of mRNA for IFN-gamma, IL-4 and IL-10 in AChR-reactive lymph node cells were detected in muMT and wild-type mice. However, muMT mice had no detectable anti-AChR antibodies and remained completely free from clinical EAMG. We conclude that B cells are critically required for the genesis of clinical EAMG, but not for AChR-specific T cell priming.

Effect of systemic pretreatment with betamethasone on the bacterial flora, inflammatory response, and polyp formation in experimentally infected rabbit maxillary sinus mucosa.

To investigate possible effects of corticosteroids on polyp formation and local bacterial colonization, pneumococcal sinusitis was experimentally induced in rabbits pretreated with betamethasone or saline. After 7 days, macroscopic polyps were counted post-mortem and on histologic slides after serial sectioning. Histologic sections were also examined with light microscopy. Macroscopic polyps were significantly fewer in animals given betamethasone, while there was no difference regarding the number of microscopic polyps. Ingrowth of pathogenic microorganisms was found in five of eight rabbits given placebo but in none of the animals treated with corticosteroids (P < 0.05). The reduced number of pathogenic strains in these animals may be explained by a better-preserved local host defense. The lower number of macroscopic polyps in the same animals could be because of a delayed mucosal repair and subsequent polyp formation.

B cell-deficient muMT mice as an experimental model for Mycoplasma infections in X-linked agammaglobulinemia.

B cell-deficient muMT mice were investigated as an experimental model for human X-linked agammaglobulinemia (XLA). Mice were intranasally infected with Mycoplasma pulmonis and in 16 out of 17 muMT mice, dissemination of the bacteria from the airways was observed. More than 50% of these mice developed arthritis and/or changes in periarticular tissues. Mycoplasmal infection in muMT mice thus resembles the disease seen in XLA patients implying the usefulness of the model.

Differential susceptibility to Mycoplasma pulmonis intranasal infection in X-linked immunodeficient (xid), severe combined immunodeficient (scid), and immunocompetent mice.

Mice with the scid mutation are highly susceptible to Mycoplasma pulmonis infection and develop a disseminated disease. In order to study the contribution of humoral immunity to the immune response, M. pulmonis was inoculated intranasally to X-linked immunodeficient (xid) mice. Severe combined immunodeficient (scid) and immunocompetent CBA mice were used as controls. The mice were killed and necropsied at day 30 or 37 post-infection. Samples from the nose, lungs and joints were taken for bacteriological and histological examination. Rhinitis was observed in all mouse strains. Chronic purulent bronchopneumonia was diagnosed in some of the CBA mice. Xid mice did not show severe lung lesions, despite the presence of numerous mycoplasma organisms in the lungs, in contrast to immunocompetent mice, which developed lung pathology. Scid mice showed less signs of pneumonia, but unlike in xid and CBA mice, there was spread of mycoplasmas from the respiratory tract and severe pathological changes in the joints. Our results indicate that B and/or T lymphocytes protect against dissemination of M. pulmonis from the airways. Innate immune reactions and/or bacterial virulence factors seem to contribute to the development of joint lesions, whereas IgG3 and IgM antibodies might be involved in lung pathology.

Intranasal inoculation of Mycoplasma pulmonis in mice with severe combined immunodeficiency (SCID) causes a wasting disease with grave arthritis.

Mycoplasma pulmonis or Myc. pneumoniae were inoculated intranasally to C.B-17 scid/scid mice (severe combined immunodeficient (SCID) mice). Immunocompetent C.B-17 mice were inoculated as controls. During the observation period of 5 weeks the mice were killed and necropsied. Mycoplasma pulmonis was recovered from all of the inoculated mice, and dissemination to various tissues increased with time. SCID mice, unlike immunocompetent mice, did not show lung lesions but exhibited severe inflammatory changes of the joints. Mycoplasma pulmonis, however, was isolated both from the lungs and the articular lesions. In addition, SCID mice infected for more than 3 weeks suffered from a pronounced loss of weight and emaciation. In the experiment with Myc. pneumoniae the agent could be reisolated, but lesions were not found in any of the infected mice. Mycoplasma pulmonis infection in SCID mice may be useful as a model of arthritis in immunodeficient humans.

Persistence of polyomavirus in adult SCID C.B-17 mice.

C.B-17 mice with the Severe Combined Immune Deficiency (SCID) mutation were infected with the naturally occurring murine polyomavirus. Using the Polymerase Chain Reaction (PCR) technique, persistence of polyomavirus was followed in different tissues of the mice between 24 hours and 2 months post infection (p.i.). Viral DNA appeared by 3-5 days and was detected in all studied organs by 3 weeks p.i. From 4 weeks to 2 months p.i. viral DNA was present at high levels in all studied organs in all of the animals. As controls normal C.B-17 and A/Sn mice were used. Viral DNA appeared by 2-4 days. The infection reached a peak around 1 week p.i. This was followed by a clearing stage and viral DNA was no longer detectable by 4-5 weeks p.i. Most organs studied with PCR were also examined histologically, but no lesions were observed. Consequently persistence and organ distribution of polyomavirus in adult SCID mice differs greatly from that in normal adult mice.

In vitro susceptibility of "Campylobacter upsaliensis" to twenty-four antimicrobial agents.

The in vitro susceptibility of 41 strains of "Campylobacter upsaliensis" to 24 antimicrobial agents was determined using a broth microdilution procedure. Most isolates were susceptible to the fluoroquinolones and beta-lactam antibiotics tested, but all strains were resistant to trimethoprim (MBCs greater than or equal to 128 micrograms/ml) and teicoplanin (MBCs greater than or equal to 32 micrograms/ml). These agents may be useful in a selective isolation medium for "Campylobacter upsaliensis".

Rapid radiometric detection of mycobacterial growth from smear-positive tissue samples from pigs.

Rapid demonstration of mycobacteria in slaughter pigs is important for medical, epidemiological and economic reasons. The Bactec radiometric system detected more mycobacteria in less time than conventional culture on solid medium.

Gizzard erosions as a cause of mortality in White Leghorn chickens.

Increased mortality connected with gizzard erosions has been observed in several flocks of White Leghorn chicks in Sweden. Bacterial infection of the gizzard wall was a common finding in chicks that had died from the disease. Infection with Clostridium perfringens is supposed to be the main cause of mortality, but the primary cause of the gizzard lesions has not been established.

Campylobacter in the dog: a clinical and experimental study.

Faecal samples from 54 dogs with diarrhoea and 54 control dogs were cultured for Campylobacter, Salmonella and Yersinia species and controlled for enteric viruses. The campylobacter were identified as either C jejuni/coli or C upsaliensis. In the diarrhoeic group 16 dogs (29.6 per cent) were positive for campylobacter, 10 C upsaliensis and six C jejuni/coli. Concomitant infection with parvovirus was evident in six of the dogs with diarrhoea and campylobacter-positive faecal cultures. In the control group 13 dogs (24.1 per cent) were positive for campylobacter; three of the isolates were C upsaliensis and six C jejuni/coli. Four isolates could not be identified. The most prominent clinical findings in naturally occurring cases were an acute onset of vomiting (12 of 16), diarrhoea (16 of 16) which was often haemorrhagic (nine of 16) and a raised rectal temperature. Dogs were infected experimentally with both C jejuni (three dogs) and C upsaliensis (three dogs). The challenge strains could be identified in faecal samples from all the dogs, but clinical signs of diarrhoea were seen in only one dog infected with C jejuni. Soft faeces was passed by one dog infected with C upsaliensis. It is concluded that C jejuni/coli or C upsaliensis are either primary pathogens or, after predisposing factors such as virus infections, act as secondary pathogens. It also seems probable that Campylobacter species are present in the intestinal flora of the normal dog.

Extraction and determination of adenosine 5'-triphosphate in bovine milk by the firefly luciferase assay.

The release of ATP from somatic cells in milk with the detergent Triton X-100 was optimized for assay with firefly luciferase. A small volume of milk (40 microliters) is added to 0.8 ml of 0.2% Triton X-100 in 100 mM Tris, 4 mm EDTA, pH 7.8. After approximately 1 min, 0.2 ml of luciferase reagent is added and the emission of light is measured in a luminometer. Results are calibrated with an ATP standard. This single method gave high yields of ATP from somatic cells in milk without interference from bacterial ATP. Extracts could be stored or transported prior to assay without deterioration of results. A close correlation was found between somatic cell count and ATP in milk samples collected at a farm as well as in milk samples from a cow with experimental mastitis. Results are promising for future use for diagnosis of mastitis but further work and field testing has to be done before it can be used on a wider scale.

Serum antibodies to Leptospira bratislava in Swedish pigs and horses.

Sera from 116 and 89 Swedish pigs and horses respectively were examined for the presence of antibodies to L. bratislava. Antibodies were found in 18.1 and 49.4% respectively of pigs and horses examined. Presence of serum antibodies was not associated with clinical signs of infection.

Salmonella isolated from animals and feed stuffs in Sweden during 1978-1982.

Regulations concerning the control of Salmonella in animals are more strict in Sweden than in most other countries, though a certain liberalization took place in 1982. The main purpose of these regulations is to prevent transmission of Salmonella infections from animals to man. Veterinarians and laboratories are obliged to report all Salmonella cases to the veterinary authorities. The cases are recorded by the Swedish Board of Agriculture. During the period of this report, 1978-1982, 1266 outbreaks of Salmonella in animals were recorded in Sweden. Isolated strains belonged to 78 different serotypes. The most frequent serotypes were S. typhi-murium (38.5% of the recorded cases) and S. dublin (37%). S. dublin was isolated mainly from cattle, while S. typhi-murium was isolated from a wide range of animal species. Next in frequency are some serotypes isolated mainly from chicken, at rates around 2%: S. livingstone, S. liverpool, and S. agona. Of the 78 isolated serotypes, 25 were never isolated before from animals in Sweden. There were 687 outbreaks of Salmonella recorded in cattle. Predominant serotypes are S. dublin (67% of the outbreaks in cattle) and S. typhi-murium (28%). The outbreaks of S. dublin, like earlier in the sixties and seventies, occurred mainly in south-eastern Sweden. The recorded occurrence of Salmonella in swine continued to decrease. During this period only 37 outbreaks were diagnosed. Of these more than half were caused by S. typhi-murium. S. choleraesuis was isolated from 6 cases only.(ABSTRACT TRUNCATED AT 250 WORDS)

Genetic and phenotypic characteristics of a new group of Campylobacter isolated from pigs and cattle.

Five intestinal strains of Campylobacter isolated from pigs and cattle are described. The strains grew in anaerobic as well as in micro-aerobic environment; they were catalase positive and resistant to nalidixic acid but sensitive to cephalothin and metronidazole. They had a mean G+C content of 35.4 mol %. DNA-DNA-hybridizations showed that the group was homogeneous: about 50% related to C. fetus ss fetus and less than 25% related to other Campylobacter species.

A serological survey of antibodies against Francisella tularensis in some Swedish mammals.

Tularemia occurs in Sweden as an epizootic among the mountain hare. Little is known about the occurrence of the disease in other animals in this country. For this reason serum samples from 28 cattle, 83 moose, 110 beavers and 97 mountain hares were investigated for the presence of antibodies against Francisella tularensis. The antibody levels against F. tularensis found in moose and cattle were generally low and also in a low incidence. This indicates that these species are not susceptible to tularemia and not involved in the epizootiology of this disease. Beaver titres were found to vary from 1:20 to 1:1 000. Twenty-one % of the investigated sera showed titres higher than 1:100. This indicates that infections are common in the species and that the Scandinavian beaver plays an important role in the epizootiology of tularemia. It could well act as a reservoir for the disease. Ninety-six of the 97 tested sera from the mountain hare were negative. In one serum was a titer of 1:20 seen. This low titer was regarded as non-specific. The absence of titers against F. tularensis in this species could be explained by the high susceptibility to this disease. This indicates that the mountain hare is not a reservoir for tularemia in Sweden. It is one of the most susceptible and the dominating species involved in tularemia epizootics, but it is not the normal reservoir for F. tularensis.

Concomitant occurrence of Campylobacter and parvoviruses in dogs with gastroenteritis.

In 1979 a canine parvovirus infection was widespread among dogs in Sweden. During the epizootic faecal samples were taken for bacteriological examination from 77 hospitalised dogs at an animal clinic. Forty-nine of the dogs had signs of gastroenteritis and they were all infected with canine parvovirus according to serological investigations. The remaining 28 dogs were referred to the clinic for other reasons. Campylobacter was isolated from 23 out of the 49 dogs with gastroenteritis and from 4 out of 28 dogs lacking symptoms of enteritis. The significance of these findings is discussed.