1. B. Nitrofurantoin (A) is a urinary antiseptic agent active against many of the Enterobacteriaceae. Nitrofurantoin has no effect on Toxoplasma or P. carinii, as both are protozoans. TMP-SMX (B) daily or three times a week has proved to prevent both PCP and toxoplasmosis in AIDS patients. Norfloxacin (C) and other second-generation fluo-roquinolones are known for their antipseudomonal and Enterobacteriaceae activity. The antimicrobial activity is exerted through inhibition of DNA gyrase A and type IV topoisomerase. Methenamine (D) is active against various Enterobacteriaceae; it has no activity against protozoa. Formaldehyde denatures proteins and is bactericidal. Nalidixic acid (E) is used in urinary tract infections caused by Enterobacteriaceae (e.g., E. coli, Klebsiella, and Proteus). It has no activity against protozoa.

2. B. Proteus species produce urease (A) that produces ammonia and urea, alkalizing urine. Urine requires acidification for effective therapy. Hippuric (B), mandelic, or ascorbic acids or methionine are urinary acidifying agents. The normal acidic urinary environment is disturbed by recurrent Proteus in fections. Catalase (C) is produced by staphylococcal spp. The catalase test differentiates Staphylococci from Streptococci. It has no urinary activity. Folic acid (D) is a water-soluble vitamin and has no effect on urinary pH or acidification. Humans cannot synthesize folic acid, which must be obtained from the diet. A coagulase enzyme (E) is produced by Staphylococcus aureus. Coagulase test differentiates S. aureus from other staphylococci .It has no urinary antimicrobial activity.

3. A. Sulfonamides (A) compete for bilirubin binding sites on plasma albumin and increase fetal blood levels of unconjugated bilirubin. Unbound bilirubin crosses the blood-brain barrier and can be deposited in the basal ganglia and subthalamic nuclei causing kernicterus, a toxic encephalopathy. Defective biliru-bin hepatic conjugation (B) is due to glucuronyl transferase deficiency resulting in Gilbert's syndrome. When seen in adults it usually presents with jaundice that is precipitated by fasting. Physiological jaundice (C) usually occurs in the newborn within a week of birth. It is due to the immature fetal acetyl-transferase system resulting in peripheral destruction of a large fetal red cell mass. Pregnancy-induced hepatic congestion (D), cholestasis, and acute cholecystitis are seen in pregnant women, not in the newborn. Primary biliary cirrhosis (E) is commonly seen in middle-aged women. It is a chronic progressive autoimmune disorder requiring steroids and sometimes liver transplant.

4. B. Humans cannot synthesize folic acid (A); diet is their main source. Sulfonamides selectively inhibit microbially synthesized folic acid. Incorporation (B) of PABA into microbial folic acid is competitively inhibited by sulfonamides. The TMP-SMX combination is synergistic because it acts at different steps in microbial folic acid synthesis. All sulfonamides are bacteriostatic. Inhibition of the transpeptidation reaction (C) involved in the synthesis of the bacterial cell wall is the basic mechanism of action of p-lac-tam antibiotics Changes in DNA gyrases (D) and active efflux transport system are mechanisms for resistance to quinolones. Structural changes (E) in dihydropteroate synthetase and overproduction of PABA are mechanisms of resistance to the sulfon-amides.

5. B. Acute urosepsis (A) is possible, but the patient's physical examination produced benign findings. Adding a broad-spectrum antibiotic has no benefit without evidence of active disease. Possible allergic reaction (B) to nitrofurantoin; it is appropriate to stop the drug immediately to guard against one of three potential pulmonary reactions: (l) acute pres entation with basilar infiltrate and pleural effusion,

(2) chronic progressive bilateral interstitial fibrosis;

(3) a subacute presentation. Nitrofurantoin-resistant E. coli infection (C) and urosepsis are possible in patients who are taking chronic prophylaxis, but his examination produced benign findings. Acute community-acquired streptococcal pneumonia (D) shows one or more lobar infiltrates on radiography. The patient described has bilateral interstitial fibro-sis. Nitrofurantoin-induced hemolysis (E) is possible in G6PD patients, but physical examination produced benign findings; G6PD patients usually present with hematuria.

6. B. Overproduction (A) of PABA is one of the resistance mechanisms of sulfonamides. Changes in the synthesis of DNA gyrases (B) is a well-described mechanism for quinolone resistance. Plasmid-mediated resistance (C) does not occur with quinolones. An active efflux system for transport of drug out of the cell has been described for quinolone resistance, but it is not plasmid mediated. Inhibition of structural blocks (D) in bacterial cell wall synthesis is a basic mechanism of action of p-lactam antibiotics. Inhibition of folic acid synthesis (E) by blocking different steps is the basic mechanism of action of sulfonamides.

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