AMPROCOX WS

Indications

• Coccidiosis in poultry
• Coccidiosis in livestock
• Prevention of coccidial infections in animals

Dosage

Children: Refer to veterinary guidelines for specific dosing for younger animals, as it may vary according to weight and age.

Adults: Refer to veterinary guidelines for specific dosing based on the type of animal and severity of infection.

Mechanism of action

Amprolium acts as a thiamine antagonist, inhibiting the uptake of thiamine in the protozoa. This leads to depletion of thiamine within the parasites, which is essential for their energy metabolism and growth. The lack of thiamine disrupts several metabolic pathways, ultimately resulting in the death of the parasitic organisms.

Pharmacodynamics

Amprolium exhibits selective toxicity towards protozoa by exploiting the differences in thiamine metabolism between the host and the parasite. The drug's action is primarily coccidiostatic, preventing the development and reproduction of Eimeria species. The effectiveness of amprolium is influenced by factors such as the specific strain of Eimeria, the dosage administered, and the duration of treatment.

Pharmacokinetics

Amprolium is well absorbed after oral administration, with peak plasma concentrations occurring within a few hours. It is primarily metabolized in the liver, and its metabolites are excreted mainly through the urine. The drug has a relatively short half-life, necessitating multiple doses for effective treatment. The pharmacokinetic profile may vary between species, and veterinary guidelines should be followed for specific dosing regimens.

Adverse effects

• Anorexia
• Weight loss
• Neurological signs including ataxia
• Thiamine deficiency symptoms

Precautions

• Use with caution in animals with pre-existing neurological conditions
• Monitor for signs of thiamine deficiency

Pregnancy

There are no adequate and well-controlled studies in pregnant animals. Use with caution.

Breast-feeding

Not established. Caution is advised.

Storage

Store in a cool, dry place, away from light.

Formulations

• Oral powder
• Oral solution

Indications

• Bacterial infections in veterinary medicine
• Coccidiosis in poultry
• Treatment of certain protozoal infections

Dosage

Children: Refer to the relevant prescribing information for specific dosing guidelines as per clinical condition.

Adults: Refer to the relevant prescribing information for specific dosing guidelines as per clinical condition.

Mechanism of action

Sulfaquinoxaline acts as a competitive antagonist of para-aminobenzoic acid (PABA), a key substrate in the bacterial synthesis of folic acid. By inhibiting the enzyme dihydropteroate synthase, sulfaquinoxaline prevents the incorporation of PABA into dihydropteroic acid, which is the precursor of folic acid. This inhibition disrupts the formation of folic acid necessary for DNA synthesis, thus hindering bacterial cell multiplication. Mammalian cells, which utilize preformed folic acid, are not affected by this mechanism.

Pharmacodynamics

The pharmacodynamics of sulfaquinoxaline are characterized by its ability to inhibit bacterial growth through the blockade of folic acid synthesis. It demonstrates a bacteriostatic effect, meaning it stops bacteria from multiplying rather than killing them directly. The efficacy of sulfaquinoxaline depends on the susceptibility of the bacteria involved and is influenced by the presence of PABA in the environment, which can compete with the drug.

Pharmacokinetics

Sulfaquinoxaline is well absorbed from the gastrointestinal tract and achieves therapeutic levels in the serum. It has a distribution that allows it to penetrate tissues and body fluids. The drug is metabolized in the liver and excreted primarily through the kidneys. The pharmacokinetic profile can be influenced by factors such as the presence of other substances that may compete for absorption or metabolism.

Contra-indications

• Hypersensitivity to sulfonamides
• Severe hepatic or renal impairment
• Porphyria

Adverse effects

• Allergic reactions including rash, itching, and fever
• Gastrointestinal disturbances such as nausea and vomiting
• Hematological effects including leukopenia, thrombocytopenia, and aplastic anemia
• Kernicterus in newborns
• Crystalluria

Interactions

• May enhance the effects of anticoagulants such as warfarin
• Potentially decreases the effectiveness of oral contraceptives
• Can increase the toxicity of methotrexate
• May interact with other drugs that affect renal function

Precautions

• Use with caution in patients with renal impairment
• Monitor for signs of blood dyscrasias
• Adequate hydration is important to prevent crystalluria
• Caution in patients with a history of asthma or allergic reactions

Pregnancy

Use during pregnancy only if clearly needed, as sulfonamides can cross the placenta and may cause harm to the fetus.

Breast-feeding

Breastfeeding is not recommended while taking sulfaquinoxaline due to potential adverse effects on the infant.

Storage

Store at room temperature, away from moisture and heat.

Formulations

• Tablets
• Suspensions
• Injectable forms

Mechanism of action

Bacteriostatic. Sulfonamides interfere with the biosynthesis of folic acid in bacterial cells; they compete with paraaminobenzoic acid (PABA) for incorporation in the folic acid molecule. By replacing the PABA molecule and preventing the folic acid formation required for DNA synthesis, the sulfonamides prevent multiplication of the bacterial cell. Susceptible organisms must synthesize their own folic acid; mammalian cells use preformed folic acid and, therefore, are not susceptible. Cells that produce excess PABA or environments with PABA, such as necrotic tissues, allow for resistance by competition with the sulfonamide. /Sulfonamides/ Sulfonamides are structural analogs and competitive antagonists of para-aminobenzoic acid (PABA) and thus prevent normal bacterial utilization of PABA for the synthesis of folic acid (pteroylglutamic acid). More specifically, sulfonamides are competitive inhibitors of dihydropteroate synthase,the bacterial enzyme responsible for the incorporation of PABA into dihydropteroic acid, the immediate precursor of folic acid. Sensitive microorganisms are those that must synthesize their own folic acid; bacteria that can utilize preformed folate are not affected. Bacteriostasis induced by sulfonamides is counteracted by PABA competitively. Sulfonamides do not affect mammalian cells by this mechanism, since they require preformed folic acid and cannot synthesize it. /Sulfonamides/