Lawrence J. Kunz

Genitourinary tuberculosis: Clinical features in a general hospital population

Abstract Seventy-eight patients with genitourinary tuberculosis were evaluated during a 12 year period. Active tuberculosis was confined to the genitourinary tract in all but 10 patients. Aside from five cases of miliary tuberculosis, most genitourinary infections developed from the breakdown of granulomes acquired earlier during transient dissemination from a primary pulmonary infection. Patients with genitourinary tuberculosis exhibited features of local organ dysfunction rather than systemic symptoms of infection; fever, weight loss and anorexia were uncommon. Seventy-one per cent of the patients with active tuberculosis of kidneys, ureters and bladder presented because of urinary tract symptoms. Twenty per cent were asymptomatic and were detected because of abnormal urinary sediments. The diagnosis of genitourinary tuberculosis should be suspected on the basis of an abnormal urinalysis (hematuria and/or pyuria) with negative routine cultures, and a positive tuberculin skin test. Intravenous pyelograms disclosed abnormalities in most patients but were rarely diagnostic. Serial intravenous pyelograms disclosed increasing ureteral obstruction during chemotherapy in three patients. Multiple drug chemotherapy is the mainstay of treatment, but reconstructive surgery remains important. Male genital tuberculosis may result from direct spread from infected urine or from hematogenous seeding. Our nine patients presented with a mass lesion in the epididymis, testicle or prostate. Female genital tuberculosis results from hematogenous seeding, with fallopian tube involvement most common. Infertility, pelvic pain or abnormal vaginal bleeding were the initial symptoms. Endometrial curettage is important for the diagnosis of tuberculosis endometritis, and tuberculosis salpingitis often requires laparotomy for diagnosis.

Antibiotic Synergism Against Listeria monocytogenes

The effectiveness of ampicillin, penicillin, streptomycin, and gentamicin against 20 strains of Listeria monocytogenes was studied in vitro. For all strains, the minimal bactericidal concentration (MBC) of both ampicillin and penicillin was much higher than the minimal inhibitory concentration (MIC). The MBC of both streptomycin and gentamicin was close to the MIC, but relatively high concentrations of these antibiotics were necessary to inhibit the growth of most of the strains of Listeria. The combination of penicillin plus streptomycin was synergistic against 19 of 20 strains and in the remaining strain produced enhanced killing (but of less magnitude than our criterion for synergism). Combinations of penicillin plus gentamicin, ampicillin plus streptomycin, and ampicillin plus gentamicin produced enhanced killing against all strains tested. No antagonism was observed when ampicillin or penicillin was combined with streptomycin or gentamicin.

Endocarditis due to group D streptococci. Comparison of disease caused by streptococcus bovis with that produced by the enterococci.

Abstract The group D streptococci include the nonenterococcal Streptococcus bovis in addition to the classic enterococci. Endocarditis due to Strep. bovis has received little previous attention in the medical literature. A review of all cases of group D streptococcal endocarditis seen at the Massachusetts General Hospital between 1964 and 1973 revealed 14 cases caused by Strep. bovis and 15 by enterococci. There were only minor differences in the clinical presentations of endocarditis caused by these two groups of organisms. Although it contains the group D antigen Strep. bovis behaved like Strep. viridans in producing endocarditis. Moreover, the strains of Strep. bovis in this study were much more susceptible to penicillin than the enterococci. Therapy of severe enterococcal infections requires penicillin plus an aminoglycoside antibiotic whereas the present study strongly suggests that penicillin alone is adequate therapy for endocarditis due to Strep. bovis.

Extrarespiratory streptococcal infections. Importance of the various serologic groups.

IN the 1940s Rantz1 and Foley2 reported on the frequent isolation from clinical specimens of streptococci belonging to serologic groups other than A. During the last two decades, however, the atte...

Resistance to gentamicin, tobramycin and amikacin among clinical isolates of bacteria☆

Susceptibility to the administration of gentamicin, tobramycin and amikacin was determined for all isolates of aerobic and facultative gram-negative bacilli submitted for testing to the clinical bacteriology laboratory of the Massachusetts General Hospital between July 1, 1974, and June 30, 1976. In this 24-month period more than 46,000 isolates of bacteria were tested by the single-disc diffusion (Bauer-Kirby) method. Resistance to one or more of the aforementioned aminoglycosidic aminocyclitol antibiotics was found among 4,114 stains. Correlation with quantitative susceptibility test methods revealed that disc-diffusion methods using 10 microng discs accurately predicted resistance to gentamicin and tobramycin, but overestimated the prevalence of resistance to amikacin by 20 to 60%. Most of the gentamicin-resistant Enterobacteriaceae in this study were also cross-resistant to tobramycin but were susceptible to amikacin. Many gentamicin-resistant strains of Ps. aeruginosa were susceptible to both tobramycin and amikacin. Resistance to amikacin tended to be of relatively low magnitude (most had minimal inhibitory concentrations (MICs) between 31 and 125 microng/ml), but organisms which were resistant to the administration of amikacin were usually resistant to the other two aminoglycosidic antibiotics as well.

Resistance to Six Aminoglycosidic Aminocyclitol Antibiotics Among Enterococci: Prevalence, Evolution, and Relationship to Synergism with Penicillin

Two hundred and three recent clinical isolates of enterococci were tested for susceptibility to streptomycin, kanamycin, amikacin, gentamicin, sisomicin, and tobramycin. Depending upon the source of the isolate, 36 to 54% of the enterococci demonstrated high-level resistance (minimal inhibitory concentration, >2,000 μg/ml) to streptomycin, 16 to 49% to kanamycin, and 0 to 14% to amikacin. None of the strains was highly resistant to gentamicin, sisomicin, or tobramycin. A comparison with isolates of enterococci obtained in 1968 revealed that there has been a decrease in prevalence of high-level resistance among organisms isolated from wound cultures in 1976. However, no decrease in resistance to streptomycin or kanamycin was demonstrated among blood or urine isolates. Penicillin, combined with gentamicin, sisomicin, or tobramycin, was synergistic against all 10 strains of Streptococcus faecalis subjected to formal testing. For streptomycin and kanamycin, the presence or absence of synergism with penicillin correlated with the absence or presence of high-level aminoglycoside resistance. High-level resistance to amikacin was seen in only 1 of the 10 strains. Nonetheless, combinations of penicillin plus amikacin failed to produce synergistic killing against 6 of the 10 strains. Indeed, the combination was synergistic only against those four strains that were susceptible to high levels of kanamycin.

Susceptibility of Clinical Isolates of Bacteria to Cefoxitin and Cephalothin

The susceptibility of 4,929 unselected clinical isolates of bacteria to cefoxitin and cephalothin was determined by the single-disk method, using a computer-associated electronic zone analyzer to obtain, record, and process measurements of sizes of zones of inhibition. Both cefoxitin and cephalothin were effective against most gram-positive strains, including Staphylococcus aureus, S. epidermidis, micrococci, and all streptococci except enterococci. The three strains of Listeria monocytogenes tested were susceptible to cephalothin but resistant to cefoxitin. There was little difference between the cefoxitin and cephalothin susceptibility of Salmonellae, Citrobacter sp., Enterobacter sp., Proteus mirabilis, and Pseudomonas sp. Cefoxitin was more effective then cephalothin against Escherichia coli, Klebsiella sp., Serratia sp., indole-positive Proteus sp., Providence sp., Flavobacter sp., Herellea vaginicola, and Mima polymorpha. Cefoxitin also appeared to exhibit enhanced activity, as compared with cephalothin, against Bacteroides sp. Thus cefoxitin appears to have a very broad antibacterial spectrum which is greater than that of cephalothin, especially against gram-negative strains.

Excretion of Coxsackie Virus (Conn. No. 5 Strain) in the Urine of Infected Mice.

Conclusion Infant mice infected with the Conn. No. 5 strain of Coxsackie virus eliminate virus in the urine. The infectious titer of urine obtained on the 2nd day after intraperitoneal inoculation is 10-5,6. Adult mice with pancreatic disease caused by Conn. No. 5 virus may also excrete virus in the urine.

Evaluation of a Computer-Associated Electronic Zone Analyzer in Single-Disc Antimicrobial Susceptibility Testing

A computer-associated electronic zone analyzer was evaluated for use in measuring zones of inhibition for single-disc antimicrobial susceptibility testing. This unit gave measurements which were reproducible and comparable to those obtained by the standard manual technique. By feeding results directly into the computer, this system eliminates errors in interpretation of zone sizes and in transcription of results to clinical reports. It has also been shown to eliminate possible sources of observer bias. In routine high-volume use, this system has resulted in a substantial saving of man-hours of work. Images

Pancreatic Disease in Mothers of Suckling Mice Infected with Connecticut No. 5 Strain of Coxsackie Virus.

Summary Mothers of suckling mice may spontaneously become infected with Conn.-5 strain of Coxsackie virus, following inoculation and infection of their young with this virus. They develop pancreatic lesions and, in some cases, hepatic lesions identical with those produced after intraperitoneal injection of virus. This condition can be reproduced experimentally in adult mice of either sex by feeding them with the carcasses of infected suckling mice.