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Diagnostic Approach to Rash and Fever in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Lee S. Engel, Charles V. Sanders, Fred A. Lopez
Management of TSS can be summarized by the seven “Rs” [134]. These include recognition, resuscitation, removal of the source of infection, rational choice of antibiotics, role of adjunctive treatment, review progress, and reduce risk of secondary cases in close contacts. Early recognition is important, owing to the high rate of morbidity and mortality associated with TSS. Resuscitation with aggressive fluid, respiratory, and inotropic support is important to curb the rapid progression to multi-organ failure. Source control is essential to stop the persistence of infection. Broad-spectrum antibiotics should be started as soon as possible. Benefits of adjunctive clindamycin therapy include inhibition of super-antigen production, improved tissue penetration, and an ability to overcome the “Eagle effect” associated with streptococcal infections. The “Eagle effect” occurs when stationary-growth-phase streptococci produce less penicillin-binding proteins and, in turn, render penicillin less effective [137]. Intravenous immunoglobulin has also been postulated to provide benefit; however, definitive data are lacking [138]. Household contacts of patients who suffer TSS may benefit from antibiotic prophylaxis, as there is an increased risk of invasive Group A streptococcal disease in these contacts [139].
Ciprofloxacin
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Jason Kwong, M. Lindsay Grayson
Quinolones initially kill bacteria rapidly, but with respect to some bacteria their activity lessens in vitro when the viable cell count is about 104 less than the initial inoculum numbers, or in some circumstances when bacteria are in a stationary phase of growth. Thus, quinolone bactericidal activity, depending on the bacterial species, is cell cycle specific, although this appears to be less so for ciprofloxacin and ofloxacin, at least against Gram-negative organisms (Eng et al., 1991; Hooper and Wolfson, 1993a). Bacterial killing tends to increase in rate and magnitude with increasing quinolone concentrations; however, above a maximum concentration of 30- to 60-fold above the MIC, the so called Eagle effect may occur for some fluoroquinolones, with a reduction in killing similar to the effect seen in some bacterial strains with excess penicillin concentration. Drugs such as chloramphenicol and rifampicin inhibit protein synthesis and are known to reduce bacterial killing by some quinolones, suggesting that some protein synthesis in addition to quinolone interference with DNA gyrase activity is necessary for cell death (Deitz et al., 1966; Crumplin et al., 1984). Interestingly, protein synthesis inhibitors such as rifampicin and chloramphenicol, although abolishing the bactericidal activity of nalidixic acid and norfloxacin, have only partial effect on fluoroquinolones such as ciprofloxacin, pefloxacin, ofloxacin, and lomefloxacin (Smith, 1984; Lewin et al., 1989a; Lewin and Amyes, 1990). Thus, these fluoroquinolones presumably possess other mechanisms of killing. In addition, anaerobic conditions inhibit fluoroquinolone killing, whereas oxygen reverses this effect (Lewin et al., 1991).
Cytolytic Vaginosis, Aerobic Vaginitis, and Desquamative Inflammatory Vaginitis
Published in William J. Ledger, Steven S. Witkin, Vulvovaginal Infections, 2017
William J. Ledger, Steven S. Witkin
The treatment of the Group A and B Streptococcus and S. aureus, will be guided in part by antibiotic susceptibility studies. The availability of clindamycin in a vaginal treatment form makes this a popular choice. Culture specimens should be sent to the laboratory with a request for clindamycin susceptibilities, for a portion of the Group B streptococcal isolates will be resistant.22 Alternative oral agents like penicillin or erythromycin can be prescribed instead. Group A streptococcal isolates should be regarded with caution, for their overgrowth can cause such serious clinical conditions as necrotizing fasciitis and TSS. This is a situation where antibiotic susceptibility studies can mislead the physician. The Group A Streptococcus is susceptible to penicillin and penicillin-like antibiotics, but if an early soft tissue infection with Group A Streptococcus is present, as in a vaginal laceration following vaginal birth, the Eagle effect must be kept firmly in mind. The high concentration of the Group A Streptococcus at the infection site markedly slows the replication of this bacteria and reduces the effectiveness of penicillin that acts on the cell wall of replicating bacteria.23 In this situation, clindamycin is the antibiotic of choice for two reasons. It is effective where high concentrations of the Group A Streptococcus exist, and, more important, it markedly diminishes toxin production of this organism24 and thus reduces the probability of serious systemic disease caused by the toxins of the Group A Streptococcus. The major concern about infections caused by the Staphylococcus is the life-threatening TSS caused by S. aureus. Two components need to be present for this to occur. The S. aureus strain in the vagina must produce the TSS toxin (TSST-1), and the patient must have no antibodies to the TSST-1.25 Antibiotic susceptibilities need to be done on the Staphylococcus isolates, but clindamycin is usually a good first choice in the situation.
Invasive Group A streptococcal postpartum endometritis associated with multi-organ infarctions: an uncommon case presentation and literature review
Published in Postgraduate Medicine, 2020
Mariam Riad, Elizabeth Thottacherry, Christina Crawley, Nessy Phillip-Abraham, Farrah Ibrahim
Antibiotic therapy aims at eradicating the infectious bacteria in the early stages. Penicillin remains the first-line treatment for TSS and clindamycin has been shown to have enhanced effects in vitro on suppressing exotoxin production [30]. Adjuvant clindamycin use has been found to have better outcomes than the use of penicillin alone [31]. It can be useful for counteracting the ‘Eagle effect,’ which is a paradoxically decreased bactericidal activity of high-dose penicillin [32]. Gall et al. reported no significant differences in effectiveness between treatment with ampicillin/sulbactam versus the combination of clindamycin and gentamicin [33]. Furthermore, antimicrobial resistance patterns and local antibiogram must be taken into consideration when individualizing therapy for the patient.
Streptococcal toxic shock syndrome in a returning traveller
Published in Acta Clinica Belgica, 2019
Stéphanie Note, Patrick Soentjens, Marie Van Laer, Philippe Meert, Peter Vanbrabant
As soon as STSS is diagnosed, antimicrobial treatment involving penicillin and clindamycin should be administered [1,12]. Since GAS remains sensitive to β-lactam agents, penicillin is a part of the first-line treatment [1,12]. Clindamycin is commonly added as it has shown to suppress superantigen production and possesses a better tissue penetration and longer post-antibiotic effect than penicillin, thereby improving survival [1,2,12,20,21]. Furthermore is clindamycin able to overcome ‘the Eagle effect’, e.g. the reduced effect of β-lactam antibiotics when large numbers of bacteria are present [12]. Monotherapy is not sufficient because of the increasing resistance of group A streptococci to macrolides and cross resistance is known [1,21].
Multidrug-resistant Candida auris: an epidemiological review
Published in Expert Review of Anti-infective Therapy, 2020
Arunaloke Chakrabarti, Shreya Singh
Only the isolates with mutations in FKS1 have been found to be resistant to echinocandins in some studies, highlighting the importance of gene sequencing in detection of resistant strains [105,106]. The AFST with caspofungin is reported to be particularly challenging since WT isolates have been seen to exhibit Eagle effect (also called the paradoxical growth effect) [105].