Thirty-eight tracheobronchial aspirates (TBA) were collected from twenty 1 to 6-month-old foals, which were free of clinical signs of respiratory tract or other infectious disease. We collected TBA from 9 of the foals 3 times when they were approximately 8, 16, and 24 weeks old. Aspirates were examined cytologically after staining with modified Wright-Giemsa, Gram, toluidine blue, and prussian blue stains. Aerobic bacterial culturing was performed on all aspirates. Of the 20 initial TBA, 4 (20%) were normal cytologically on the basis of previously defined criteria for TBA from clinically normal horses, 6 (30%) had a high percentage of eosinophils (> 5%), 8 (40%) were classified as indicative of subacute inflammation, and 2 (10%) were classified as indicative of acute inflammation. Nine (45%) were positive for mast cells and none were positive for hemosiderin-laden macrophages (hemosiderophages). Of the 9 foals from which samples were collected at 16 and 24 weeks of age, results were similar, except for an increase in the number of TBA classified as indicative of chronic inflammation (33% and 22% respectively) and the number positive for hemosiderophages (33% and 88%, respectively). One TBA was considered nondiagnostic because of pharyngeal contamination. Culturing of 12 of the 37 aspirates (32%) yielded a potential microbial pathogen. Only 2 were positive cultures from the same foal. The following organisms were isolated: beta-hemolytic Streptococci spp (4), Actinobacillus/Pasteurella spp (4), Rhodococcus equi (2), unidentified nonenteric Gram-negative rod (1), and Escherichia coli (1). Thirty-four of the 37 aspirates (92%) yielded light growth of various organisms considered to be nonpathogenic and normal inhabitants of the upper respiratory tract. It was concluded that the presence of inflammatory cells, eosinophils, and mast cells in the tracheobronchial aspirates from clinically normal foals is a common finding. These cytologic findings were consistent in the samples collected from foals at 8, 16, and 24 weeks of age. It was also concluded that bacteria with recognized pathogenicity can be isolated from TBA from clinically normal foals and were most frequently isolated from 1- to 2-month-old foals or those with cytologic evidence of inflammation, even in the absence of clinical signs of respiratory tract disease.

The pharmacokinetics and bioavailability of rifampin were determined after IV (10 mg/kg of body weight) and intragastric (20 mg/kg of body weight) administration to 6 healthy, adult horses. After IV administration, the disposition kinetics of rifampin were best described by a 2-compartment open model. A rapid distribution phase was followed by a slower elimination phase, with a half-life (t1/2[beta]) of 7.27 +/- 1.1 hours. The mean body clearance was 1.49 +/- 0.41 ml/min.kg, and the mean volume of distribution was 932 +/- 292 ml/kg indicating that rifampin was widely distributed in the body. After intragastric administration of rifampin in aqueous suspension, a brief lag period (0.31 +/- 0.09 hour) was followed by rapid, but incomplete, absorption (t1/2[a] = 0.51 +/- 0.32 hour) and slow elimination (t1/2[d] = 11.50 +/- 1.55 hours). The mean bioavailability (fractional absorption) of the administered dose during the first 24 hours was 53.94 +/- 18.90%, and we estimated that 70.0 +/- 23.6% of the drug would eventually be absorbed. The mean peak plasma rifampin concentration was 13.25 +/- 2.70 microgram/ml at 2.5 +/- 1.6 hours after dosing. All 6 horses had plasma rifampin concentrations > 2 microgram/ml by 45 minutes after dosing; concentrations > 3 microgram/ml persisted for at least 24 hours. Mean plasma rifampin concentrations at 12 and 24 hours after dosing were 6.86 +/- 1.69 microgram/ml and 3.83 +/- 0.87 microgram/ml, respectively. We tested 162 isolates of 16 bacterial species cultured from clinically ill horses for susceptibility to rifampin. All strains of coagulase-positive staphylococci, Streptococcus zooepidemicus, Str equi, Str equisimilis, Rhodococcus equi and Corynebacterium pseudotuberculosis were highly susceptible to rifampin (minimal inhibitory concentration [MIC] less than or equal to 0.25 microgram/ml).

We attempted to determine whether weaning is required for induction of diarrhea in pigs with postweaning enterotoxigenic Escherichia coli infection. Three-week-old newly weaned pigs and their suckling littermates were inoculated with the K88+ enterotoxigenic E coli strain M1823B. Fourteen of 21 weaned and 12 of 20 suckling pigs were genetically resistant to intestinal adhesion by the K88+ strain of E coli; they remained healthy, and gained weight at similar rates. Both groups of K88-resistant pigs gained weight faster, and shed fewer bacteria of strain M1823B in their feces, than did their K88-susceptible counterparts. Diarrhea developed in K88-susceptible pigs in the weaned (6 of 7 pigs) and suckling (4 of 8 pigs) groups, and 1 of the 4 affected suckling pigs died from complications resulting from diarrhea. The incidences of diarrhea, weight gain rates, and the numbers of strain M1823B shed in feces of susceptible weaned and suckling pigs were not significantly (P > 0.05) different. Diarrhea scores of susceptible weaned pigs were significantly (P < 0.02) higher than those of susceptible suckling pigs on the second day after inoculation. In this experimental model, it was concluded that weaning is not required for induction of diarrhea, but may modestly increase its severity.

Fifty raw ewe’s and goat’s milk samples (25 of each) were examined for total viable, psychrotrophic count and the presence of foodborne pathogenic microorganisms. The obtained results revealed that the mean total bacterial counts/ml were 1.9 x103 and 1.4 x103 in the examined samples, respectively. Psychrotrophic bacteria could be detected in all examined samples (100.0 %) with mean values of 7.8 x10 and 6.3 x10/mL, respectively. Staphylococci, Enterococci, and E. coli , were detected in (52.0 & 84.0 %), (44.0 & 36.0 %) and (36.0 & 44.0 %) of the examined samples with mean values/ml of (7.2 x10 & 6.1 x10), (2.5 x10 & 2.4 x10) and (3.0 x10 & 2.1x10), respectively. The predominant isolated bacterial strains were Staphylococcus aureus, Staphylococcus epidermidis, Enterococcus faecalis, Enterococcus faecium and E. coli, at percentages of (24.3 & 19.2 %), (16.2 & 32.7 %), (10.8 & 13.5 %), (19.0 & 17.3 %) and (29.7 & 17.3 %) of total isolates, respectively. On the other hand, Clostridium perfringens, Campylobacter jejuni, Corynebacterium bovis and Salmonellae failed to be detected in all examined samples. The sanitary and public health importance of these organisms as well as preventive measures to improve the quality of milk and safeguard the consumers from infection were discussed.

The present study describes the clinical, serological and bacteriolological findingsin calves from two beef herds experiencing outbreaks of pneumonia. The clinical signs were nasal discharge, cough, pyrexia and increased respiratory rates. The morbidity and mortality rates over a month period were 40.72% and 15.63% respectively. Laboratory investigations revealed that bovine viral diarrhea virus (BVDV) was involved in and probably initiated both outbreaks as indicated by a significant increase in antibody titers against BVDV in sera of convalescent calves (paired serum samples). No antibodies bovine herpesvirus-1 (BHV-1), bovine respiratory syncytial virus (BRSV) and parainfluenza-3 (BPIV-3) viruses were detected in both acute and convalescent sera. Mycoplasma bovis was concurrently demonstrated in lungs of affected calves as it was isolated from 13 (81.25%) of examined lungs suggesting that there may be a synergism between bovine viral diarrhea virus and Mycoplasma bovis in the pathogenesis of pneumonia. A total of 15 (68.18%) isolates of Mannheimia haemolytica, 5 (22.73%) Pasteurella multocida, 1 (4.54%) Pseudomonase aerugenosa, 3 (13.64%) Staphylococcus aureus, 3 (13.64%) Actinomycis pyogenes, 1 (4.54%) Klebsiella pneumonae, 1 (4.54%) Streptococcus pneumonae, 2 (9.09%) E. coli and 2 (9.09%) Aspergellus fumigatus were recovered from lungs of calves suffering from pneumonia.

The aim of this study was to compare the effects of cryopreservation at approximately -196 °C in liquid nitrogen (N) and freezing at approximately -20 °C in a freezer, on the viability and survival of eight different mastitogenic bacteria inoculated in milk. Bacteria were frozen at approximately -20 °C in a freezer and cryopreserved at approximately -196 °C in liquid nitrogen. An effective preservation method was needed for follow-up samples from cows identified in the South African National Milk Recording Scheme (NMRS) with somatic cell counts above 250 000 cells/mL milk. The organisation responsible for sample collection of the NMRS milk samples also provides producers with liquid nitrogen for their semen flasks at the collection sites. This existing mode of storage and transport could therefore be utilised.Ten samples of each organism were thawed and cultured bi-weekly until week 18 for both temperature treatments. An additional sampling was performed at week 30 for samples frozen at approximately -20 °C. Freezing and cryopreservation did not impair subsequent isolation of Streptococcus dysgalactiae, Streptococcus uberis, Enterococcus faecalis, Staphylococcus aureus (STH) (phage type lytic group III) or Sta. aureus (STA) (phage typed, other than lytic group III). Survival was indicated by the isolation of bacteria from samples, and viability by the strength of growth of the bacteria isolated. The survival of Streptococcus agalactiae decreased after week 12 and Escherichia coli after week 16 of freezing, but both organisms survived under cryogenic preservation until week 18. Coagulase-negative staphylococci survived until week 18 for both freezing and cryogenic preservation.Both storage methods could thus contribute to the improvement of a pro-active approach towards udder health management in South African dairy herds.

The prevalence rate of bacterial isolates of public health importance in pigeons was (28.16%). The incidence of bacterial pathogens differed according to health status of examined pigeons and ages either squabs or adults, as it gave the higher incidence in freshly dead squabs (33.33%) and in adults (28.57%) followed by diseased squabs (31.03%) and adults (26.67%) then finally slaughtered pigeons (25.56%). There was a wide range of bacterial pathogens isolated from nasal and cloacal swabs of diseased pigeons including C. jejuni, Citrobacter freundii, D. pneumoniae, E. coli, K. oxytoca, K. pneumoniae, Mannheimia haemolytica, P. aeruginosa, Salmonella spp, S. aureus and Y. enterocolitica. There were variations between the incidence and the species of pathogens isolated from cloacal and nasal swabs either in squabs or in adults K. oxytoca, Mannheimia haemolytica and Y. enterocolitica never isolated from adult. It was appeared that the deaths usually occurred due to combination of more than one bacterium. On the examination of internal organs slaughtered pigeons, there were differences in the incidences of bacterial isolation form different organs. Serological identification of most prevalent isolates revealed 5 Salmonella serovars including, 3 P. aeruginosa serogroups and 6 E. coli serogroups. All examined pathogens were sensitive to enrofloxacin followed by gentamicin then ciprofloxacin. In contrast, streptomycin then erythromycin and colistin sulphate showed the lowest effect. Among the isolates tested, P. aeruginosa was resistant to the most used antibiotics..Most isolated strains of E. coli, P. aeruginosa, Salmonella spp. and Y. enterocolitica from pigeons were elaborating enterotoxin. S. paratyphi A and S typhimurium var. copenhagen were 100% enterotoxigenic followed by S. typhimurium(83.33%) , E. coli O8 and Ps. aeruginosa I (75%) in each. On other hand, lower enterotoxin production was observed in Ps. aeruginosa A (46.15%) and E. coli O111 (44.44%).

Diarrhoea in growing-finishing pigs is a common problem of commercial pig farms. Among many causative factors, porcine circovirus type 2 (PCV2) is one considered an important pathogen in modern pig production. The aim of the study was to verify if PCV2 was responsible for antibiotic non-responsive diarrhoea and wasting in pigs. A total of 13 dead pigs aged between 12 and 15 weeks from three Polish farms with persistent herd symptoms suggestive of PCV2 infection were provided for evaluation. Sections of lymph nodes and intestines were analysed by in situ hybridization (ISH) for PCV2 and histopathological examination. Faeces and intestinal scrapings were tested for Lawsonia intracellularis and Brachyspira hyodysenteriae by real-time PCR and for parasitic infection by flotation and decantation. ISH and histopathological examination showed that all pigs were PCV2 systemic disease negative. Swine dysentery was confirmed by real-time PCR on two farms, and proliferative enteropathy on one farm. In histological examinations, erosions of the caecal and colonic mucosa were found, together with cysts and trophozoites of Balantidium coli. The protozoa were present in the intestinal lumen and mucosa. B. coli cysts were identified in faeces from all examined pigs. These results suggest that monitoring of B. coli infections should be an additional measure of control and prevention of gastrointestinal tract disorders in modern swine husbandry.

Coinfection of goose parvovirus (GPV) and duck circovirus (DuCV) occurs commonly in field cases of short beak and dwarfism syndrome (SBDS). However, whether there is synergism between the two viruses in replication and pathogenicity remains undetermined. We established a coinfection model of GPV and DuCV in Cherry Valley ducks. Tissue samples were examined histopathologically. The viral loads in tissues were detected by qPCR, and the distribution of the virus in tissues was detected by immunohistochemistry (IHC). Coinfection of GPV and DuCV significantly inhibited growth and development of ducks, and caused atrophy and pallor of the immune organs and necrosis of the liver. GPV and DuCV synergistically amplified pathogenicity in coinfected ducks. In the early stage of infection, viral loads of both pathogens in coinfected ducks were significantly lower than those in monoinfected ducks (P < 0.05). With the development of the infection process, GPV and DuCV loads in coinfected ducks were significantly higher than those in monoinfected ducks (P < 0.05). Extended viral distribution in the liver, kidney, duodenum, spleen, and bursa of Fabricius was consistent with the viral load increases in GPV and DuCV coinfected ducks. These results indicate that GPV and DuCV synergistically potentiate their replication and pathogenicity in coinfected ducks.

Fowl adenovirus can cause important diseases in chickens such as inclusion body hepatitis, hepatitis hydropericardium syndrome, and gizzard erosion and ulceration. Inclusion body hepatitis has been regularly reported from many countries. This is the first case report from Turkey, describing an outbreak of inclusion body hepatitis in broiler farms due to fowl adenovirus-8b (FAdV-8b). Broiler flocks with mortality about 10% were visited in Turkey, and necropsy was performed on dead birds. Samples were subjected to PCR assay to detect FAdV and other viral pathogens. After sequencing, phylogenetic analysis was performed and the nucleotide sequences of hexon genes were compared with the FAdV sequences data available in GenBank. Clinical signs such as anorexia, depression, ruffled feathers, huddling, and greenish diarrhoea were observed. Mortality started at the 8ᵗʰ day of age and ranged from 10% to 14%. Necropsy showed severe hepatitis, jaundice, and pancreatitis. The main necropsy findings included a pale, enlarged, haemorrhagic, and friable liver along with swollen and haemorrhagic kidneys and spleen. PCR and sequence analysis revealed the presence of fowl adenovirus serotype 8b (FAdV-E). This is the first report on characterisation and the pathological lesions associated with FAdV in broilers in Turkey. Our findings suggest that FAdV strains could be an emerging pathogen in Turkish broilers and could actively contribute to hepatitis and immunosuppression.