Development of turbinate lesions and nasal colonization by Bordetella bronchiseptica and Pasteurella multocida during long-term exposure of healthy pigs to pigs affected by atrophic rhinitis.

Natural transmission of atrophic rhinitis from pigs from a herd with an endemic atrophic rhinitis problem to pigs from a herd free of atrophic rhinitis was demonstrated. Six replicates each with five pigs from the endemic atrophic rhinitis herd (Group A) and five pigs from the atrophic rhinitis-free herd (Group B) were housed together from 5 wk of age, with each replicate kept in isolation rooms maintained at optimal and controlled environmental conditions. Three replicates each with six pigs/room from the atrophic rhinitis-free herd (Group C), served as nonexposed controls. Group C pigs remained healthy and had no turbinate atrophy at either 10 or 17 wk of study (atrophic rhinitis score = 0 on a 0 to 3 scale). Group A pigs had a mean atrophic rhinitis score of 1.85 +/- 0.84, and group B pigs developed atrophic rhinitis to a mean score of 1.57 +/- 0.70. The isolation rate and quantity of Pasteurella multocida found on nasal swabs was directly related to lesions while those for Bordetella bronchiseptica were inversely related to turbinate atrophy. Of the various types of P. multocida evaluated, nontoxigenic type A and toxigenic type D were both directly related to atrophic rhinitis while nontoxigenic type D strains were not. No toxigenic type A P. multocida strains were isolated.     

Bordetella bronchiseptica and toxigenic type D Pasteurella multocida as agents of severe atrophic rhinitis of swine

Bordetella bronchiseptica and toxigenic type-D Pasteurella multocida were cultured from pigs in each of five herds diagnosed as having severe atrophic rhinitis (AR). B. bronchiseptica alone, P. multocida alone, or both organisms isolated from four herds were inoculated intranasally into 1-week-old gnotobiotic pigs which were necropsied 4 weeks post-inoculation (PI). Nasal turbinate atrophy in B. bronchiseptica-inoculated pigs was moderate to severe, while P. multocida-inoculated pigs had slight to severe atrophy. Pigs inoculated with both organisms had moderate to complete turbinate atrophy. P. multocida was reisolated at necropsy from all pigs receiving the organism except those having no turbinate damage. B. bronchiseptica and P. multocida from a fifth herd were simultaneously inoculated into six naturally farrowed 6-day-old SPF pigs. Necropsy performed 4 weeks PI revealed severe to complete turbinate atrophy. Nasal turbinates were normal for control pigs in both experiments.     

Bordetella bronchiseptica isolations from the nasal cavity of pigs in relation to atrophic rhinitis.

The occurrence of Bordetella bronchiseptica and atrophic rhinitis was studied during a one-year period in four Danish sow herds. In three of the heards, the epidemiological studies revealed a relation between the occurrence of B. bronchiseptica in 3--10-week-old pigs and the presence and severity of atrophic rhinitis at slaughter. In the fourth herd no such relation was found.     

Expression of a truncated Pasteurella multocida toxin antigen in Bordetella bronchiseptica

Mild or subclinical respiratory infections caused by Bordetella bronchiseptica are widespread in pigs despite multiple control efforts. Infection with virulent B. bronchiseptica strains is a common risk factor in the establishment of toxin-producing strains of Pasteurella multocida in the nasal cavity of pigs leading to the disease, atrophic rhinitis (AR). This study was designed to explore the possibility of expressing a protective epitope of P. multocida toxin (PMT) in B. bronchiseptica to create single-component mucosal vaccine to control atrophic rhinitis in pigs. To achieve this, a P. multocida toxin fragment (PMTCE), that was non-toxic and protective against lethal challenge in mice, was cloned into a broad-host-range plasmid, PBBR1MCS2, and introduced into B. bronchiseptica by electroporation. The Pasteurella gene construct was placed under the regulatory control of a promoter region that was separately isolated from B. bronchiseptica and appears to be part of the heat shock protein gene family. B. bronchiseptica harboring the plasmid under antibiotic selection expressed the 80kDa PMTCE as determined by PAGE and Western blot with a PMT-specific monoclonal antibody. When introduced into the respiratory tracts of mice, B. bronchiseptica harboring the plasmid construct was reisolated in declining numbers for 72h post-inoculation. Antibody responses (IgM, IgA and IgG) to B. bronchiseptica were detected in serum and respiratory lavage, but PMTCE-specific antibodies were not detected. While further refinements of PMT expression in B. bronchiseptica are necessary, this study provides a basis for the development of a single-component, live-attenuated vaccine against atrophic rhinitis.     

Efficacy of Bordetella bronchiseptica bacterin in controlling enzootic atrophic rhinitis in swine.

The efficacy of a Bordetella bronchiseptica bacterin was evaluated in 2 commercial swine herds affected with mild and severe enzootic atrophic rhinitis (AR). In the 1st herd study, (mild AR), the degree of clinical AR, nasal turbinate evaluation, blood serum titer to B bronchiseptica antigen, and adjusted days from birth to 100 kg were determined for individual pigs. Bacterin inoculation reduced the incidence and severity of gross turbinate atrophy 57% and reduced clinical AR over 93%. Inoculated swine had an average blood serum-agglutinating titer greater than 1:2,793 and noninoculated (control) swine had an average titer of 1:112. Increased serum titer significantly (P less than 0.05) correlated with decreased degree of nasal turbinate atrophy. Inoculated and control pigs reached 100 kg in an average of 171 and 178 days after birth, respectively. In the 2nd study (severe enzootic AR), inoculated and control pigs were individually evaluated for clinical AR and total average daily weight gain. Inoculation reduced clinical AR over 90%. The total average daily gain for the inoculated and control pits was 435.84 g and 340.50 g, respectively. Inoculated pigs and control pigs reached 100-kg market weight in 184 and 238 days, respectively.     

Indirect fluorescence antibody studies of porcine cytomegalo virus infections in the Netherlands

Summary Sera from 683 pigs of 41 swine herds with clinical atrophic rhinitis (A R), from 477 pigs of 37 herds with no A R history, from 267 breeding sows and breeding boars for slaughtering, from 22 boars at an artifical insemination centre, and from 103 SPF pigs were tested for the presence of antibodies to porcine cytomegalo virus (PCMV). The herds examined were spread all over the Netherlands. For the presence of antibodies to PCM V the indirect fluorescence antibody test was used. To obtain the antigen, the PCMV had been grown in pig lung macrophage cultures in Petri dishes for 10-12 days. These macrophages were dropped into the wells of slides. The serum dilution 1:20 of all the 103 sera from SPF pigs were negative, but 93 per cent of the other sera were positive. No marked differences were found between swine herds with clinical atrophic rhinitis and herds with no A R history. The FA titres in both types of herds seem to be at a comparable level.     

Experimental atrophic rhinitis in 2 and 4 month old pigs infected sequentially with Bordetella bronchiseptica and toxigenic type D Pasteurella multocida.

Experimental infections with Bordetella bronchiseptica and/or toxigenic type D Pasteurella multocida were studied in 2- and 4-month-old primary specific-pathogen-free pigs. None of the 2-month-old pigs inoculated with B. bronchiseptica or P. multocida alone developed turbinate atrophy. All the pigs inoculated with B. bronchiseptica (10(7) CFU/head) and P. multocida (10(9) CFU/head for 5 consecutive days) together, however, developed clinical and post-mortem signs of atrophic rhinitis (AR) similar to the naturally occurring disease. Slight to severe turbinate atrophy was observed in the 4-month-old pigs inoculated with B. bronchiseptica and P. multocida (at the same concentration as above) at necropsy.     

Serum haptoglobin concentration in growing swine after intranasal challenge with Bordetella bronchiseptica and toxigenic Pasteurella multocida type D.

The acute phase reaction, in association with progressive atrophic rhinitis (AR), was monitored for 3 wk using serum haptoglobin (HPT) quantification in thirty-six, 15 kg swine after intranasal challenge with varying doses of Pasteurella multocida type D (toxigenic strain) and Bordetella bronchiseptica. The challenge doses were administered alone or in combination with pigs divided into 9 isolated treatment groups. Increasing doses of B. bronchiseptica were associated with lower serum HPT (P < 0.05), whereas increasing doses of P. multocida tended to increase serum HPT (0.05 < P < 0.10). Significant and positive correlation of mean HPT and AR score was found in these pigs; increased AR scores were associated with elevated mean HPT concentration (r = 0.41, P < 0.01). A significant interaction between P. multocida and B. bronchiseptica dose indicated that increasing the dose of B. bronchiseptica, for a fixed P. multocida dose, was associated with less AR (P < 0.05). The AR scores were greater in pigs given P. multocida, than B. bronchiseptica alone. These results indicate that a complex interaction between Pasteurella multocida and Bordetella bronchiseptica causes progressive atrophic rhinitis and alters serum HPT concentration in swine.     

Pasteurella multocida and Bordetella bronchiseptica in atrophic rhinitis and pneumonia in swine.

A total of 163 pigs from nine farrow-to-finish herds representing various levels of atrophic rhinitis (AR) were selected for postslaughter examination of AR and pneumonia. Nasal swabs and lungs were cultured for detection of Bordetella bronchiseptica and Pasteurella multocida. Seventy-three pigs were examined at eight weeks of age and 90 contemporaries at six months of age. Mean AR scores were 1.21 and 1.11 for the eight week and six month old pigs, respectively (0 = normal, 3 = severe). In individual pigs increasing AR score was related to increasing pneumonia score in eight week old pigs but not in six month old hogs. In eight week old pigs, B. bronchiseptica and P. multocida were isolated more frequently from pigs with higher AR scores. From nasal swabs of six month old hogs, Bordetella was almost never recovered while Pasteurella was frequently isolated score. Toxigenic type DP. multocida was isolated from nasal cultures of only seven (4%) pigs and from lung cultures of only one pig. Pasteurella was never isolated from lungs of the eight week old pigs and Bordetella never from the six month old hogs. The isolation rate of P. multocida, predominantly type A, from lungs of six month old pigs increased from 11% in grossly normal lungs to 86% in lungs with severe pneumonia. Pigs from one herd free from lesions of AR and pneumonia were also examined; type AP. multocida was isolated from nasal cultures of one of six eight week old pigs. Somatic antigens of P. multocida were determined for 94 nasal and 20 lung isolates. Somatic serovar 3 was found in 93% of the nasal isolates and in all lung isolates.(ABSTRACT TRUNCATED AT 250 WORDS)     

A comparative study of the complement fixation test for mycoplasma hyopneumoniae in SPF and non-SPF herds of swine in Illinois

Serum samples from 458 swine from eight specific pathogen-free (SPF) herds swine were compared to samples from 178 swine from eight non-SPF herds in Illinois using the complement fixation (CF) test for Mycoplasma hyopneumoniae antibodies. In SPF herds, 9.4% of the samples gave positive test results, compared to 51.7% of the samples from non-SPF herds. The range of reactor rates in SPF herds was 0–26.9% and in non-SPF herds 3.4–100%. Used on herd basis with some modification, the CF test should be useful in monitoring state and nationally accredited SPF swine herds.     

Induction of nasal turbinate atrophy in germ-free pigs, using Pasteurella multocida as well as bacterium-free crude and purified dermonecrotic toxin of P multocida

To establish the role of the dermonecrotic toxin (DNT) of Pasteurella multocida in the cause and pathogenesis of atrophic rhinitis, germ-free pigs were inoculated with several strains of P multocida, crude DNT, or purified DNT. In some experiments, the aforementioned inocula were combined with Bordetella bronchiseptica. All DNT-producing P multocida strains induced severe turbinate atrophy. Histologic examination of the remnants of the nasal turbinates revealed intact, but undulated, ciliated epithelium and numerous osteoclasts. Inflammation was minimal or absent. A DNT-producing B bronchiseptica strain induced only mild turbinate atrophy. The lesions were characterized histologically by loss of cilia and ciliated cells and by an infiltration of predominantly mononuclear cells. Bone formation seemed impaired. Turbinate lesions were most severe in pigs infected with a combination of B bronchiseptica and a DNT-producing P multocida strain. Intranasal administration of sterile DNT-containing culture filtrate of P multocida or purified DNT of P multocida did not result in turbinate atrophy. In contrast, turbinate atrophy developed when these preparations were injected IM or when intranasal administration of DNT was preceded by inoculation of B bronchiseptica.     

Protection of piglets against atrophic rhinitis by vaccinating the sow with a vaccine against Pasteurella multocida and Bordetella bronchiseptica

The efficacy of a new vaccine against atrophic rhinitis in pigs was tested in the Netherlands and Denmark. The vaccine contained protein dO (a truncated Pasteurella multocida toxin which is immunogenic and non-toxic), inactivated Bordetella bronchiseptica whole cells, and an adjuvant. The sows were either vaccinated intramuscularly with 2 ml of the vaccine at six to eight and two to four weeks before expected farrowing or left unvaccinated as controls. All the piglets were challenged intranasally with B bronchiseptica when three to seven days old and with P multocida three to four days later. Pigs born to the vaccinated sows performed significantly better than pigs born to the control sows when judged on growth, average daily weight gain and snout scores. The challenge organisms were reisolated more frequently from the control pigs than from the pigs in the vaccinated group. The vaccinated sows and their progeny developed high titres of antibodies against B bronchiseptica and P multocida toxin.     

Polymorphism of pertactin gene repeat regions in Bordetella bronchiseptica isolates from pigs

Bordetella bronchiseptica pertactin (prn) is an outer membrane protein which has been implicated as both an adhesin and a protective antigen that induces immunity against atrophic rhinitis in pigs. Previous studies demonstrated extensive heterogeneity of the prn sequence within two distinct regions of amino acid repeats for B. bronchiseptica isolated from the United States and Europe. By deducing the amino acid sequences of the repeat regions of the prn gene from recent isolates from Korea, two region 1 variants and five region 2 variants were identified. Five pertactin types were distinguished based on combinations of variants of both regions. Interestingly, none of the field isolates have the same pertactin type as the B. bronchiseptica P4 strain widely used to vaccinate pigs.     

In vitro susceptibility of some porcine respiratory tract pathogens to aditoprim, trimethoprim, sulfadimethoxine, sulfamethoxazole, and combinations of these agents

The in vitro antimicrobial activities of aditoprim (AP), a new dihydrofolate reductase (DHFR) inhibitor, trimethoprim (TMP), sulfadimethoxine (SDM), sulfamethoxazole (SMX), and combinations of these drugs against some porcine respiratory tract pathogens were determined by use of an agar dilution method. The minimal inhibitory concentrations (MIC) of these agents were determined twice against Bordetella bronchiseptica (n = 10), Pasteurella multocida (n = 10), and Actinobacillus pleuropneumoniae (n = 20) strains isolated from pigs suffering from atrophic rhinitis or pleuropneumonia. All B bronchiseptica strains were resistant to AP and TMP. The MIC50 values of AP and TMP for P multocida were 0.25 and 0.06 microgram/ml, respectively, and for A pleuropneumoniae, 1 and 0.25 microgram/ml, respectively. The MIC50 values of SDM and SMX for B bronchiseptica were 4 and 1 micrograms/ml, respectively; for P multocida, 16 and 8 micrograms/ml, respectively; and for A pleuropneumoniae, 16 and 8 micrograms/ml, respectively. The investigated combinations of the DHFR inhibitors and the selected sulfonamides had synergism for the A pleuropneumoniae strains; the MIC90 values of the combinations were less than or equal to 0.06 microgram/ml. Potentiation was not observed for the B bronchiseptica and the P multocida isolates. The MIC of the combinations against B bronchiseptica and P multocida corresponded respectively to the concentrations of the sulfonamides and the DHFR inhibitors in the combinations. For A pleuropneumoniae, 2 types of strains were used (25% of serotype 2 and 75% of serotype 9). Type-2 strains had lower susceptibility than type-9 strains to AP and TMP as well as to SDM and SMX (at least a fourfold difference in MIC between the 2 types of strains).(ABSTRACT TRUNCATED AT 250 WORDS)     

Prevention and treatment of atrophic rhinitis in pigs with Getroxel, chlorquinaldol and oxytetracycline.

The sensitivity of ten Bordetella bronchiseptica and ten Pasteurella multocida strains, each isolated from cases of atrophic rhinitis (AR), was examined in tube dilution test. Getroxel, chlorquinaldol and oxytetracycline and the former two ones combined with trimethoprim inhibited the growth of both species in vitro. The minimum inhibitory and the minimum bactericidal concentration was less than 0.5 microgram/ml. When efficacy was tested in SPF in the group fed a combination of Getroxel, chlorquinaldol and oxytetracycline (60 mg, 240 mg and 360 mg/kg of feed, respectively), P. multocida disappeared from the nasal cavity by the end of a 30-day treatment. B. bronchiseptica was reisolated in low numbers from 2 out of 9 piglets. The daily body mass gain was by 7.9% higher and the feed conversion rate was by 19% better than in the control group. After slaughter, only mild signs of AR were seen in 3 out of 9 piglets treated with the above-mentioned drug combination, while in the control group severe lesions were observed in 8 out of 9 pigs. In treated commercial herds P. multocida disappeared from the nasal cavity of the piglets by the end of the treatment (42nd day of life), but the B. bronchiseptica strains could not be completely eliminated. Due to the treatment, mortality between 2 and 6 weeks of age decreased by 0.8-7.6%. Daily body mass gain was, on the average, 16.4% higher, the amount of feed needed for 1 kg body mass gain was by 15.3% lower and the duration of fattening was by 30.8 days shorter than in the control groups.     

猪萎缩鼻炎研究进展

猪萎缩性鼻炎是猪的一种重要的呼吸系统疾病 ,该病给养猪业造成了重大的经济损失 ,其病原是支气管败血波氏杆菌和产毒素多杀性巴氏杆菌。支气管败血波氏杆菌引起非进行性萎缩性鼻炎 ,而产毒素多杀性巴氏杆菌引起进行性萎缩性鼻炎。二者在致病机理、临床症状、病理变化、流行病学和控制方法等方面存在很大差异。鉴于环境因素和病原因子在此病发生过程中均起一定作用 ,对本病的控制应是多种措施的综合。     

Effects of intranasal inoculation of porcine reproductive and respiratory syndrome virus, Bordetella bronchiseptica, or a combination of both organisms in pigs

OBJECTIVE: To examine effects of co-infection with porcine reproductive and respiratory syndrome virus (PRRSV) and Bordetella bronchiseptica in pigs. ANIMALS: Forty 3-week-old pigs. Procedure-30 pigs (10 pigs/group) were inoculated with PRRSV, B bronchiseptica, or both. Ten noninoculated pigs were control animals. RESULTS: Clinical signs, febrile response, and decreased weight gain were most severe in the group inoculated with both organisms. The PRRSV was isolated from all pigs in both groups inoculated with virus. All pigs in both groups that received PRRSV had gross and microscopic lesions consistent with interstitial pneumonia. Bordetella bronchiseptica was cultured from all pigs in both groups inoculated with that bacterium. Colonization of anatomic sites by B bronchiseptica was comparable between both groups. Pigs in the group that received only B bronchiseptica lacked gross or microscopic lung lesions, and B bronchiseptica was not isolated from lung tissue. In the group inoculated with B bronchiseptica and PRRSV, 3 of 5 pigs 10 days after inoculation and 5 of 5 pigs 21 days after inoculation had gross and microscopic lesions consistent with bacterial bronchopneumonia, and B bronchiseptica was isolated from the lungs of 7 of those 10 pigs. CONCLUSIONS AND CLINICAL RELEVANCE: Clinical disease was exacerbated in co-infected pigs, including an increased febrile response, decreased weight gain, and B bronchiseptica-induced pneumonia. Bordetella bronchiseptica and PRRSV may circulate in a herd and cause subclinical infections. Therefore, co-infection with these organisms may cause clinical respiratory tract disease and leave pigs more susceptible to subsequent infection with opportunistic bacteria.     

Relationship to growth performance of pneumonia and atrophic rhinitis lesions detected in pigs at slaughter among four seasons.

A commercial swine herd was selected for study, because pigs at slaughter repeatedly had lung lesions consistent with enzootic pneumonia and had snout lesions typical of atrophic rhinitis. Pigs born during various seasons of the year were allotted to 4 investigations and were evaluated from birth to slaughter. Individual lungs and snouts were identified and collected at the slaughter plant and later examined for gross lesions of bronchopneumonia and atrophic rhinitis, respectively. Each lesion was scored, and the following comparisons were made within investigations: prevalence and mean scores for lung lesions; prevalence and mean grades for snout lesions; correlations between lung lesion scores and growth indicators; correlations between snout lesion grades and growth indicators; and correlations between lung lesion scores and snout grade scores. Included in the growth indicators were average daily gain during the growing phase, average daily gain during the finishing phase, average daily gain during growing and finishing phases, and days to attain 104.5 kg of body weight. Prevalence of lung or snout lesions, mean values for lung lesion scores, mean values for snout lesion grades, and mean values for the various growth indicators were tested for statistical differences among the 4 investigations. Prevalence of lung lesions was highest (96%) for winter-slaughtered and lowest (81%) for autumn-slaughtered pigs. Mean scores for lung lesions were 7% (summer), 5% (autumn), 9% (winter), and 16% (spring). Prevalence of snout lesions was highest (85%) for spring-slaughtered pigs and lowest (42%) for autumn-slaughtered pigs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Infectious and rearing-system related risk factors for chronic pleuritis in slaughter pigs

Chronic pleuritis (CP) in Danish pigs for slaughter is by far the most frequent finding at the routine post-mortem meat inspection. An initial investigation published in 1990 demonstrated infectious and management-related risk factors. Serological testing for additional infectious agents, as well as the need to consider the effect of disease clustering at the herd level, required a re-analysis of the data.

Our re-analysis used a representative sample of 4800 pigs originating from 623 Danish herds. Each pig was examined for the presence of CP and progressive atrophic rhinitis (PAR). The gender of the pig, the weight of the carcass, and the herd of origin were also recorded. Individual blood samples were examined for seropositivity for Actinobacillus pleuropneumoniae (AP) serotypes 2, 6, 7, 12, Haemophilus parasuis, Mycoplasma hyopneumoniae (MYC) and swine influenza (SI). Herd-level information retrieved through a questionnaire included health status, production type, herd size (i.e. pigs per year) and vaccination procedures.

Associations between CP and infectious, individual and herd-related factors were investigated by logistic regression with random effects. Among pigs from herds with conventional health status, seropositivity for AP serotypes 2 and 6, and MYC had odds ratios (ORs) of CP of 9.0, 1.6 and 1.8, respectively. Neither seropositivity for AP serotype 7 nor SI were associated with CP by themselves, but interacted: OR of CP of 5.3 (1.8) when present at the same time among pigs exhibiting (not exhibiting) PAR. An association of PAR with CP was found, and PAR interacted with AP serotype 7: OR=10.0 (4.3) when both factors were present among pigs exposed (non-exposed) to SI. The OR (0.97) for an increase of carcass weight by 1 kg was negligible.

In pigs from specific pathogen-free (SPF) herds, seropositivity for MYC and herd size were associated with CP. Moreover, for a herd size of 1000 pigs, CP was associated with exposure to MYC by an OR of 3.3 (decreasing to 1.9 when the herd size was increased by 1000). Farrow-to-finish as opposed to finishing herd had an OR of CP of 3.2.

In conventional herds, seropositivity for AP serotype 2 and MYC were associated with 51% and 29% of the occurrence of CP. In SPF herds, farrow-to-finish as opposed to finishing herds was associated with 47% of the occurrence of CP. Seropositivity for MYC was associated with 33% (39%) of the occurrence of CP in herds with a size > (≤) 1500 pigs.     

In vitro antimicrobial activity of sulfonamides against some porcine pathogens

The minimal inhibitory concentrations (MIC) of sulfonamides were determined against Bordetella bronchiseptica (n = 10), Pasteurella multocida (n = 10), Haemophilus pleuropneumoniae (n = 20), and Streptococcus suis (n = 10) strains isolated from pigs with atrophic rhinitis, pneumonia, or meningitis. Sulfonamides tested in an agar dilution method were sulfachloropyridazine, sulfadiazine, sulfadimethoxine, sulfamethazine, sulfadoxine, sulfisoxazole, sulfamerazine, sulfamethoxazole, sulfamethoxypyridazine, sulfanilamide, sulfatroxazole, and sulfisomidine. Results indicated that monotherapy of S suis infections with sulfonamides should not be encouraged because the MIC50 of all sulfonamides investigated was greater than 32 micrograms/ml. The MIC50 of the sulfonamides against B bronchiseptica ranged from 0.5 to 8 micrograms/ml, against P multocida from 2 to 32 micrograms/ml, and against H pleuropneumoniae from 8 to 64 micrograms/ml. The MIC50 of sulfachloropyridazine, sulfadiazine, sulfadimethoxine, sulfamerazine, and sulfamethoxazole for the gram-negative bacteria did not exceed 16 micrograms/ml. Among these compounds, sulfamethoxazole had the highest activity. The frequently prescribed sulfamethazine had an overall low antimicrobial activity.