Doses Of Sulfadiazine Research Articles

The study of the influence of tetracycline and sulfadiazine on biomethane production from manure and apple pomace

Anaerobic digestion is the most popular technic for obtaining biomethane from substrates like cow manure and other organic materials, however, chlortetracycline (CTC) and sulfadiazine (SDZ) which are commonly used in animal husbandry and present in cow manure can adversely affect biomethane yields. In this paper, the results of the influence of an increasing dose of CTC between 10 and 1000 mg×kg−1 and dose of SDZ between 10 and 500 mg×kg−1 on biomethane yield and kinetics for co-fermentation of cow manure and apple pomace experiment was presented. The obtained data during 21 days of lasting batch tests performed under mesophilic conditions allowed the determination of kinetics parameters of biomethane production according to the modified Gompertz model. The biomethane yield for the experiment with CTC differs from 233 to 353 mlCH4, while for the experiment with SDZ from 396 to 455 mlCH4. The kinetics parameters varied in a broad range. The ymax, λ, and Rm were 232–531 ml, 18–66 ml d−1, and –2.9-(–1.7) d for CTC, and 533–653 ml, 20–21 ml d−1, and –4.5-(–0.8) d for SDZ, respectively. With the high antibiotics dose, the biomethane yield decreased due to the inhibitive effect on microorganisms. The experiment showed that antibiotics had an inhibitory effect on biomethane production, at high doses. The biomethane yield had been reduced by 32.3 % at 1000 mg×kg−1 of CTC and by 13.9 % at 500 mg×kg−1 of SDZ. Interestingly, small doses (<100 mg×kg-1) did not affect significantly methane yield and sometimes increased it. Obtained results showed that the co-fermentation of apple pomace and manure performance may be affected by high doses of antibiotics. Depending on the dose and the antibiotic type it affects the biomethane yield, production rate, or lag phase differently.

Pollutant removal performance and microbial responses of pure moving bed biofilm reactor to the successional sulfadiazine exposure

Pure Moving bed biofilm reactor (pure MBBR) with biofilm as biomass core is a viable process for treating antibiotics. The influences of sulfadiazine (SDZ) on pure MBBR have yet to be investigated in depth. This study examined the responses of biofilm exposure to different doses of SDZ (0, 1, 3, 5, 7 and 10 mg/L) in the pure MBBR. Under continuous-flow conditions, pure MBBR held a high SDZ removal rate, but SDZ significantly inhibited COD and TN removal. However, 1–3 mg/L SDZ could enhance NH4+-N and TP removal. And these observations were confirmed by biomass analysis and multi-omics sequencing data. SDZ accelerated the sloughing and renewal of aerobic biofilm, thus shortening the solids residence time. The biofilm communities were strongly shifted by SDZ and the activity of autotrophs was less inhibited by SDZ than that of heterotrophs. Meanwhile, SDZ did not alter the biofilm's primary nitrogen metabolism mechanism, while disrupting the ratio of denitrification genes to nitrification genes. SDZ effectively promoted the gene expression of amoCAB and hao, but restrained norBC. The increased abundance of resistance genes Sul1–3 was a major reason for the biofilm could adapt to the high concentration of SDZ. Overall, the pure MBBR could operate well when SDZ was below 3 mg/L. This study provided new insight into antibiotic wastewater treatment through pure MBBR.

Genetic Polymorphisms and Phenotypic Profiles of Sulfadiazine-Resistant and Sensitive Toxoplasma gondii Isolates Obtained from Newborns with Congenital Toxoplasmosis in Minas Gerais, Brazil.

BackgroundPrevious Toxoplasma gondii studies revealed that mutations in the dhps (dihydropteroate synthase) gene are associated with resistance to sulfonamides. Although Brazilian strains are genotypically different, very limited data are available regarding the susceptibility of strains obtained from human to sulfonamides. The aim of this study was to evaluate the efficacy of sulfadiazine (SDZ) against Brazilian isolates of T. gondii and verify whether isolates present polymorphisms in the dhps gene. We also investigated whether the virulence-phenotype and/or genotype were associated with the profile of susceptibility to SDZ.MethodsFive T. gondii isolates obtained from newborns with congenital toxoplasmosis were used to verify susceptibility. Mice were infected with 104 tachyzoites and orally treated with different doses of SDZ. The mortality curve was evaluated by the Log-rank test. The presence of polymorphisms in the dhps gene was verified using sequencing. A descriptive analysis for 11 Brazilian isolates was used to assess the association between susceptibility, genotype, and virulence-phenotype.ResultsStatistical analysis showed that TgCTBr03, 07, 08, and 16 isolates were susceptible to SDZ, whereas TgCTBr11 isolate presented a profile of resistance to SDZ. Nineteen polymorphisms were identified in dhps exons. Seven polymorphisms corresponded to non-synonymous mutations, with four being new mutations, described for the first time in this study. No association was found between the profile of susceptibility and the virulence-phenotype or genotype of the parasite.ConclusionsThere is a high variability in the susceptibilities of Brazilian T. gondii strains to SDZ, with evidence of drug resistance. Despite the large number of polymorphisms identified, the profile of susceptibility to SDZ was not associated with any of the dhps variants identified in this study. Other genetic factors, not yet determined, may be associated with the resistance to SDZ; thus, further studies are needed as a basis for a more adequate toxoplasmosis treatment.

Histopathological changes and biochemical analysis of sulfadiazine injected in egg in chicken embryo pectoral muscles

This study aimed to investigate the effects of different doses of sulfadiazine on embryonic chicken pectoral muscles. In total, 100 fertile eggs were obtained and divided into five groups of control (no injection) and sulfadiazine injection at doses of 2, 10, 30, and 70 mg/kg. After hatching, pectoral muscle tissues were harvested from the newly hatched chickens for histopathological examination and measurement of oxidative stress parameters. Microscopic examination of pectoral muscle samples indicated that sulfadiazine administration changed the histopathological structure of chicken pectoral muscles only at very high doses (30 and 70 mg/kg). Major histopathologic events associated with sulfadiazine cytotoxicity were multifocal degeneration, necrotic tissue changes, and inflammatory cell infiltration (predominantly mononuclear cells) around degenerated and necrotic muscle fibers. Moreover, sulfadiazine at doses of 10, 30 and 70 mg/kg increased malondialdehyde level and decreased glutathione, ferric reducing antioxidant power, and total carotenoid, which indicated oxidative damage in broiler skeletal muscles. Therefore, it could be concluded that in-egg administration of up to 10 mg/kg of sulfadiazine is safe for chicken embryo, whereas dosage of 30 mg/kg (or above) is considered highly toxic.

Efficacy of epiroprim (Ro11-8958), a new dihydrofolate reductase inhibitor, in the treatment of acute Toxoplasma infection in mice.

Toxoplasma gondii is a major cause of focal encephalitis in patients with acquired immunodeficiency syndrome. Epiroprim, an inhibitor of dihydrofolate reductase, was evaluated in vitro and in a mouse model of acute infection for activity against T. gondii. The 50% inhibitory concentration (IC50) of epiroprim for T. gondii dihydrofolate reductase was 0.9 micromole, similar to that of pyrimethamine, but epiroprim was 650-fold more selective than pyrimethamine for T. gondii compared with human dihydrofolate reductase. While intraperitoneally administered epiroprim (300 mg/kg/day for 14 days) alone was ineffective in mice acutely infected with the RH strain of T. gondii, 100% survival was seen when it was combined with orally administered sulfadiazine (375 mg/kg/day), which alone was also ineffective. Increases in survival were seen in combination with doses of sulfadiazine as low as 0.375 mg/kg/day. Orally administered epiroprim combined with dapsone also prolonged survival. Thus epiroprim is an active and potentially less toxic alternative pyrimethamine for the treatment of toxoplasmosis.

Nonionic block copolymers potentiate activities of drugs for treatment of infections with Toxoplasma gondii.

We studied the interaction between drugs and the nonionic block copolymers CRL 8131 and CRL 8142 in the treatment of toxoplasmosis in murine models of the disease. Treatment of acute toxoplasmosis with copolymers alone caused slight prolongation of time to death but not survival. In contrast, significant survival occurred when mice were treated with either copolymer combined with doses of sulfadiazine, pyrimethamine, clindamycin, or atovaquone, which did not prevent mortality when used alone. Treatment with CRL 8131 plus sulfadiazine or pyrimethamine resulted in 50 or 40% survival, respectively. Treatment with the same copolymer plus a dose of clindamycin that protected 40% of the mice when used alone resulted in 100% survival. Treatment of toxoplasmic encephalitis with CRL 8131 plus an ineffective dose of atovaquone reduced the inflammation and numbers of Toxoplasma gondii cysts in the brain. Studies to investigate the drug-enhancing activity of CRL 8131 revealed that mice immunized with toxoplasma lysate plus copolymer had lymphocyte proliferation responses to T. gondii antigens significantly higher than those in mice immunized with lysate alone. Challenge of immunized mice with a lethal inoculum of T. gondii resulted in significant survival. Administration of CRL 8131 alone appeared to cause a down-regulation in the production of gamma interferon and up-regulation in the production of interleukin-2. No differences were noted in the production of tumor necrosis factor alpha between mice treated with CRL 8131 and controls.

Rifabutin is active in murine models of toxoplasmosis.

Rifabutin, a semisynthetic derivative of rifamycin S, was examined alone and in combination with other drugs for activity in treatment of systemic toxoplasmosis and toxoplasmic encephalitis in murine models. One hundred percent of the mice infected with a lethal inoculum of tachyzoites or cysts of Toxoplasma gondii were protected against death by treatment with doses of 400 or 300 mg of rifabutin per kg administered alone for 10 days. Doses of 200 mg/kg protected at least 80% of the mice, and doses of 100 mg/kg protected 10 to 40% of the infected mice against death. Doses of 50 mg/kg were not protective but caused a delay in time to death. Combination of nonprotective (50-mg/kg) or slightly protective (100-mg/kg) doses of rifabutin with doses of sulfadiazine, pyrimethamine, clindamycin, or atovaquone that did not confer any protection against death from toxoplasmosis when administered alone resulted in remarkable enhancement of the in vivo activities of all of these drugs. Seventy-five percent of the infected mice survived when treated with 100 mg of rifabutin per kg per day combined with the ineffective dose of 10 mg of pyrimethamine per kg. A dose of 50 mg of rifabutin per kg in combination with the ineffective dosages of clindamycin (25 mg/kg/day), atovoquone (5 mg/kg/day), and sulfadiazine (80 mg per liter of drinking water) protected at least 80, 60, and 60% of the mice against death, respectively. The inflammatory responses in the brains of mice treated for 30 days with 200 mg of rifabutin per kg per day were significantly reduced compared with those in the brains of untreated controls. These observations suggest that clinical trials with rifabutin for treatment and prevention of human toxoplasmosis may be justified, particularly when the drug is used in combination with other drugs with activity against T. gondii.

Pharmacokinetic Studies with Trimethoprim and Different Doses of Sulfadiazine in Healthy Human Subjects

Concentrations of sulfadiazine were compared with those of sulfamethoxazole after combination treatment of sulfonamide plus trimethoprim. Sulfadiazine was used in doses of 1.6, 1.0 or 0.6 g ini, and t

An Evaluation of Antimalarial Combinations against Plasmodium berghei in the Mouse

The suppressive action of various doses of chloroquine, amodiaquine, primaquine, and pyrimethamine on the development of parasitemia in mice infected with Plasmodium berghei was investigated. After the dose-suppression curve was established for each of the four drugs, various combinations of two and three drugs were compared with equivalent doses of single drugs. Test mice were infected intravenously with 1 million parasitized red blood cells. Drugs were administered by stomach tube daily for 5 consecutive days, beginning on the day of infection (day 0). Parasitemia was evaluated from blood smears made on day 6 of infection. Average per cent parasitemia for animals within test groups was used to compare the effect of various drug treatments. By the test procedure employed, combinations of chloroquine, amodiaquine, primaquine, and pyrimethamine were not superior to single drug treatments in suppression of the development of parasitemia in mice infected with P. berghei. The joint suppressive action of combinations of two or three of these drugs was additive, or less than additive, and no evidence of synergism was observed. In the treatment of human malaria various combinations of drugs have been used in an effort to enhance therapeutic effects. Combinations of drugs have been employed to reduce the relapse rate in P. vivax infections through their joint action on both erythrocytic and exoerythrocytic phases of the parasite. Other objectives of combining drugs include (1) suppression of the development of drugresistant strains, (2) reduction of overall toxicity to the host, and (3) enhancement of the suppressive activity, thereby reducing the dosage requirement. In experimental malarial infections the suppressive effect of drug combinations has been compared with the effect of single drugs in order to assess the potency of the combination and also to study the nature of combined drug action. Roehl (1926) demonstrated that in avian malaria pamaquine combined with quiReceived for publication 30 July 1963. * Office of the Director, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda 14, Maryland. tPresent address: Department of Pharmacology, University of Tennessee, School of Medicine, 874 Union Avenue, Memphis 3. nine was more effective than quinine alone in delaying the appearance of parasites. The enhanced action of this combination since has been demonstrated clinically. Proguanil and sulfadiazine, when given concurrently to chicks infected with P. gallinaceum, were found to be synergistic by Greenberg and his associates (1948). The effective dose of proguanil could be reduced to 1/4 if combined with 1/32 to 164 the effective dose of sulfadiazine. Later Greenberg (1949) showed that other compounds are synergistic with proguanil and that these drugs, like sulfadiazine, are all inhibitors of p-aminobenzoic acid. Reilly et al. (1950) studied the action of drug combinations on Plasmodium lophurae in chicks and found the joint suppressive effect of quinine and quinacrine as well as quinacrine and pamaquine to be additive, whereas quinine combined with pamaquine and possibly quinine with pentaquine are synergistic in their joint suppressive effects. Subsequently, Bishop and McConnachie (1952) reported that no synergism was observed between pamaquine and quinine, when tested in combined doses, upon active infections of P. gallinaceum in chicks. Bishop (1956) observed no potentiation of drug action

Optimum dose of sulfadiazine in treatment of pneumococcic pneumonia

Optimum dose of sulfadiazine in treatment of pneumococcic pneumonia

The Effect of Chemotherapy on the Duration of the Carrier State Following Scarlet Fever

THE utilization of chemoprophylaxis in the control of infections spread by the respiratory tract is a recent development that is gaining ever wider application. In 1939 it was shown that sulfanilamide was effective in preventing streptococcal upper respiratory infections and relapses in rheumatic fever.1 2 3 Kuhns et al.4 found that sulfadiazine, when given prophylactically, diminished meningococcal carrier rates as well as the incidence of meningococcal meningitis. During the course of a scarlet-fever epidemic in a United States naval station, the routine administration of prophylactic doses of sulfadiazine to healthy contacts appeared to be effective in checking its spread.5 Conflicting reports have . . .

OPTIMUM DOSE OF SULFADIAZINE IN TREATMENT OF PNEUMOCOCCIC PNEUMONIA

Extensive experience with the sulfonamide drugs in clinics throughout the United States has established sulfadiazine as the drug of choice in the treatment of pneumococcic pneumonia because of its greater efficacy and lower toxicity.1Hence it is important to establish its optimum dose in order that it may be used with maximum effectiveness. The initial dose of sulfadiazine usually advocated is 4 or 5 Gm.2However, it varies from 23to 711Gm. A maintenance dose of 1 Gm. every four hours is usually given,4although 1 Gm.5 or 2 Gm.1ievery six hours have also been used. It has been demonstrated1ithat, since sulfadiazine is excreted slowly, a proportionately higher dose given every six hours is as effective in maintaining adequate blood concentrations as is a four hourly dose. Early in the use of sulfadiazine, its administration by the intravenous route was reserved for critically ill

Some Chemotherapeutic Properties of Sulfaquinoxaline.

SummarySulfaquinoxaline was found to be active against certain bacteria both in vitro and in vivo. Single daily doses of this drug were more effective than single daily doses of sulfadiazine or sulfathiazole. These findings may be explained by the fact that sulfaquinoxaline remains in the blood for long periods of time.

ACUTE URINARY SUPPRESSION FOLLOWING SULFADIAZINE THERAPY

Acute urinary suppression following the administration of sulfadiazine is rare but is a severe complication of use of the drug. The attendant development of uremia may lead to a fatal termination if urinary drainage is not reestablished immediately. In a review of recent literature, urinary suppression from sulfadiazine has been reported but once. 1 Renal colic and both gross and microscopic hematuria have been mentioned not infrequently following its use. 2 So far, no cases of anuria following the administration of sulfanilamide have been reported. The following is a report of a case in which acute urinary suppression developed following average doses of sulfadiazine: L. E., a white man aged 26, single, American, a night club operator, entered the surgical service Feb. 23, 1942 for removal of an orbital tumor on the left side. General physical examination was not remarkable. The blood pressure was 120 systolic and 80 diastolic. There

INTRAVENOUS USE OF SODIUM SULFADIAZINE IN THE TREATMENT OF PNEUMOCOCCIC PNEUMONIA

In previous papers we have reported on the behavior of sulfadiazine (2-[paraaminobenzenesulfonamido]-pyridine) in normal subjects, 1 and its use in the treatment of pneumococcic pneumonia. 2 Oral therapy with sulfadiazine 2 was supplemented with intravenous administration of the sodium salt of sulfadiazine in certain instances when rapid elevation of the level of the drug in the blood was desired. The behavior of the drug when given by vein suggested that administration of the entire dose of sulfadiazine by the intravenous route might be advantageous. Observations on the intravenous use of sodium sulfadiazine 3 without oral therapy in the treatment of pneumococcic pneumonia are described in the present paper. MATERIAL AND METHOD Intravenous Administration of Sodium Sulfadiazine to Normal Subjects. —As a guide to the therapeutic use of sodium sulfadiazine the fate of this compound administered by vein was first investigated in normal subjects (table 1). Five adult males with normal