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Treatment Acinetobacter baumannii Infections

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Acinetobacter baumannii: Epidemiology, Antimicrobial Resistance, and Treatment Options

Abstract

Multidrug-resistant Acinetobacter baumannii is recognized to be among the most difficult antimicrobial-resistant gram-negative bacilli to control and treat. Increasing antimicrobial resistance among Acinetobacter isolates has been documented, although definitions of multidrug resistance vary in the literature. A. baumannii survives for prolonged periods under a wide range of environmental conditions. The organism causes outbreaks of infection and health care–associated infections, including bacteremia, pneumonia, meningitis, urinary tract infection, and wound infection. Antimicrobial resistance greatly limits the therapeutic options for patients who are infected with this organism, especially if isolates are resistant to the carbapenem class of antimicrobial agents. Because therapeutic options are limited for multidrug-resistant Acinetobacter infection, the development or discovery of new therapies, well-controlled clinical trials of existing antimicrobial regimens and combinations, and greater emphasis on the prevention of health care–associated transmission of multidrug-resistant Acinetobacter infection are essential. Visit to: acinetobacterbaumannii.com

 

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Epidemiology

Risk factors for colonization or infection with multidrug-resistant Acinetobacter species include prolonged length of hospital stay, exposure to an intensive care unit (ICU), receipt of mechanical ventilation, colonization pressure, exposure to antimicrobial agents, recent surgery, invasive procedures, and underlying severity of illness [1, 3]. Widespread environmental contamination is often demonstrated, and outbreaks of infection have been traced to respiratory care equipment, wound care procedures, humidifiers, and patient care items [4–13]. Wilks et al. [8] reported a recent outbreak of multidrug-resistant Acinetobacter infection, with environmental contamination found on curtains, laryngoscope blades, patient lifting equipment, door handles, mops, and keyboards. Medical equipment has been implicated, emphasizing the need for special attention to disinfection of shared items and extra caution with respiratory care and wound care procedures [4, 5, 7]. One or more epidemic Acinetobacter clones often coexist with endemic strains, making it difficult to detect and control transmission. https://academic.oup.com/cid/article/46/8/1254/362279

 

Symptoms of Acinetobacter infection

Acinetobacter causes a variety of diseases, ranging from pneumonia to serious blood or wound infections, and the symptoms vary depending on the disease. Acinetobacter may also “colonize” or live in a patient without causing infection or symptoms, especially in tracheostomy sites or open wounds.

 

Transmission of Acinetobacter infection

Acinetobacter poses very little risk to healthy people. However, people who have weakened immune systems, chronic lung disease, or diabetes may be more susceptible to infections with Acinetobacter. Hospitalized patients, especially very ill patients on a ventilator, those with a prolonged hospital stay, those who have open wounds, or any person with invasive devices like urinary catheters are also at greater risk for Acinetobacter infection. Acinetobacter can be spread to susceptible persons by person-to-person contact or contact with contaminated surfaces.

 

Prevention of Acinetobacter infection

Acinetobacter can live on the skin and may survive in the environment for several days. Careful attention to infection control procedures, such as hand hygiene and environmental cleaning, can reduce the risk of transmission.

 

Treatment

Carbapenems. Increasing antimicrobial resistance leaves few therapeutic options, and there are no well-designed clinical trials to compare treatment regimens for multidrug-resistant Acinetobacter infection. Available data are from in vitro, animal, and observational studies. Carbapenems remain the treatment of choice if isolates retain susceptibility to this antimicrobial class. The Meropenem Yearly Susceptibility Test Information Collection (MYSTIC) surveillance program has documented discordance that favors imipenem as the more potent agent, compared with meropenem, for treatment of multidrug-resistant Acinetobacter infection [78, 79]. The converse result was reported in Greece [80]. Efflux pumps may affect meropenem to a greater degree, whereas specific ²-lactamases hydrolyze imipenem more efficiently [80]. Susceptibility testing of imipenem does not predict susceptibility to meropenem or vice versa [78]. Unfortunately, carbapenem-resistant Acinetobacter isolates are increasingly reported worldwide.

²-Lactamase inhibitors. ²-Lactamase inhibitors, particularly sulbactam, have intrinsic activity against many Acinetobacter strains. The presence of a ²-lactam agent (e.g., ampicillin) in combination with the ²-lactamase inhibitor does not appear to contribute activity or synergy [81, 82]. Monotherapy with sulbactam is not recommended for severe Acinetobacter infection. However, Wood et al. [83] reported successful use of sulbactam to treat 14 patients with multidrug-resistant Acinetobacter ventilator-associated pneumonia, finding no difference in clinical outcomes between sulbactam-treated patients and 63 patients who received imipenem. Levin et al. [84] reported a cure rate of 67% using ampicillin-sulbactam to treat carbapenem-resistant Acinetobacter infection, but good patient outcomes were associated with lower severity of illness. The results of antimicrobial susceptibility tests (e.g., with agar dilution or the Etest) of ²–lactam/²-lactamase combinations at fixed concentrations must be interpreted with caution, because they may indicate susceptibility when an isolate is actually resistant [82].

Tigecycline. Tigecycline, a relatively new glycylcycline agent, has bacteriostatic activity against multidrug-resistant Acinetobacter species [85, 86]. High-level resistance to tigecycline has been detected among some multidrug-resistant Acinetobacter isolates, and there is concern that the organism can rapidly evade this antimicrobial agent by upregulating chromosomally mediated efflux pumps [68, 87–91]. Peleg et al. [89] reported 2 cases of multidrug-resistant Acinetobacter bacteremia that occurred while patients were receiving tigecycline for another indication. Two recent studies documented overexpression of a multidrug efflux pump in Acinetobacter isolates with decreased susceptibility to tigecycline [92, 93]. Given these findings and concern about whether adequate peak serum concentrations can be achieved, tigecycline is best reserved for salvage therapy, with administration determined in consultation with an infectious diseases specialist [89].

Aminoglycosides. Aminoglycoside agents, such as tobramycin and amikacin, are therapeutic options for infection with multidrug-resistant Acinetobacter isolates that retain susceptibility. These agents are usually used in conjunction with another active antimicrobial agent. Many multidrug-resistant Acinetobacter isolates retain intermediate susceptibility to amikacin or tobramycin; resistance to this class of agents is increasingly associated with aminoglycoside-modifying enzymes or efflux pump mechanisms.

Polymyxin therapy. Given limited therapeutic options, clinicians have returned to the use of polymyxin B or polymyxin E (colistin) for the most drug-resistant Acinetobacter infections [94, 95]. Colistin acts by disturbing the bacterial cell membrane, thus increasing permeability, leading to cell death [94]. Colistin is bactericidal against Acinetobacter species, and its effect is concentration dependent [95]. Resistance to polymyxins has been reported, possibly as a result of outer cell membrane alterations or an efflux pump mechanism [65, 66, 94, 95]. Observational studies have reported rates of cure or improvement for colistin of 57%–77% among severely ill patients with multidrug-resistant Acinetobacter infections, including pneumonia, bacteremia, sepsis, intra-abdominal infection, and CNS infection [96–99]. Although high-quality pharmacokinetic data are lacking, colistin is reported to have relatively poor lung and CSF distribution, and clinical outcomes vary for different types of infections [96]. Despite an overall “good outcome” rate of 67%, Levin et al. [96] found a lower response rate of 25% for patients with pneumonia due to multidrug-resistant, gram-negative bacilli who were treated with parenteral colistin. Other studies have reported more favorable clinical response rates (56%–61%) for parenteral colistin treatment of multidrug-resistant Acinetobacter ventilator-associated pneumonia [100–103].

There are case reports of successful treatment of multidrug-resistant Acinetobacter meningitis with parenteral colistin, but its efficacy for this condition remains unclear [104, 105]. Several case reports and case series report the use of intraventricular or intrathecal polymyxin therapy, with or without parenteral therapy, for the treatment of gram-negative bacterial meningitis [104, 106–108]. A recent review of 31 reports involving 64 episodes of gram-negative bacterial meningitis found a cure rate of 80%, including cure for 10 (91%) of 11 patients with Acinetobacter meningitis [109]. The majority of patients received systemic antimicrobial therapy in addition to local administration of polymyxin. Neurologic toxicity occurred primarily in reports published before 1970, and the most common manifestation was meningeal irritation, which was apparently dose-dependent and reversible [109]. Overall, there is insufficient evidence to draw conclusions regarding the efficacy, safety, or pharmacokinetic properties of colistin for treatment of CNS infection, although it remains an important option for salvage therapy [104].

Data are lacking on the pharmacokinetics, pharmacodynamics, and toxicodynamics of colistin. Earlier methods of measuring serum concentrations of the drug were unable to adequately distinguish concentrations of colistimethate, the nonactive prodrug, from concentrations of colistin [95]. There are inconsistencies among manufacturers regarding the recommended dosing of colistin and the units of measurement employed [95]. Data suggest that current recommended dosing regimens may lead to serum levels of colistin that are less than the MIC for Acinetobacter infection [95]. These problems highlight the need for careful pharmacologic studies and the importance of attention to formulation and dosing in clinical care and research studies.

Synergy and combination therapy. A lack of controlled clinical trials makes it difficult to evaluate the role of synergy or combination therapy for multidrug-resistant Acinetobacter infection. Most available data are from uncontrolled case series, animal models, or in vitro studies. The studies summarized in table 2 investigated various combinations of rifampin, sulbactam, aminoglycoside agents, colistin, carbapenems, and other agents against multidrug-resistant Acinetobacter infection [102, 110–123].

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Treatment and Diagnostic Streptococcus agalactiae Infection

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Streptococcus agalactiae morphology culture and cell structure

 

Streptococcus agalactiae belongs to serological group B streptococcal (GBS) due to the antigen characteristics. Morphologically it is gram- positive, round -bearing chains in bacteria. On sheep blood nutrient media containing form around the colonies haemolysis (beta- hemolysis). Hemolysis is but usually less pronounced than that of group A streptococci. Visit: streptococcus-agalactiae.com

 

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Epidemiology

 

Group B streptococcus (GBS), also known as Streptococcus agalactiae,was once considered a pathogen of only domestic animals, causing
mastitis in cows. Although asymptomatic vaginal carriage of GBS was described in 1935, the first report of GBS sepsis in a neonate was not reported until 1964. Since the 1970s, GBS is recognized as one of the most common causes of neonatal infectious morbidity and mortality in developed countries. GBS causes significant maternal and perinatal morbidity, asymptomatic bacteriuria in pregnancy, and urinary tract and other infections in the adult nonpregnant population. The virulence of S. agalactiae is related to the polysaccharide toxin it produces. Immunity is mediated by antibodies to the capsular polysaccharide and is serotype specific. Several serotypes are known, including Ia, Ib, Ic, II, III, IV, V, VI, VII, and VIII.

 

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Pathogenesis and clinical pictures

 

S. agalactiae colonizes in the body of some animals, including cow, sheep, and humans without causing any harm.  The habitat of this microorganism is largely confined to the intestine and vagina in human and the mammary gland of cows and sheep. This microorganism also colonizes in the genital and/or intestinal tract of about 10-30% of pregnant women.[7] However, some can actually cause diseases in their neonates or immunocompromised mammals. S. agalactiae is the common cause of inflammation or fibrosis of mammary glands and adjacent areas in cows and sheep colonizing the surface of the teat and
duct sinuses. This species causes invasive bacterial infections in mostly neonates and rarely immunocompromised adults, most notably septicemia,  neumonia, and meningitis colonizing different locations including the faces, the nose, the umbilical cord, the ears, feces. Infection is spread between cows and/or sheep through the milker's hand, contaminated instrument, and the mouth of calves. Once infected, these mammals are likely to lose their reproductive capacity due to blocked milk channels through inflammation. Infection in humans is through genital and/or intestinal tract of pregnant women either during pregnancy or delivery and from other neonates or members of the hospital staff in the maternity hospital. "The interaction of this bacteria
with host protein and and the entry into host cells thereby represent important virulence traits."

 

 

 

Therapy

 

The neonatal sepsis due to GBS is because of the serious prognosis of the disease with a combination of penicillin G [(PENICILLIN GRUNENTHAL others) 300,000 IU / kg bw / day in 4-6 divided doses ] or ampicillin [(BINOTAL others) 200 mg / kg bw / day in 3 divided doses ] with an aminoglycoside [eg As gentamicin (Refobacin etc.) ] for at least 5 days treated (pronounced synergism between penicillins and aminoglycosides). Cephalosporins are an alternative to the penicillins. Isolates with reduced susceptibility to b-lactam antibiotics or high levels of resistance to gentamicin come in Germany practically inexistent. The natural sensitivity of B-streptococci to penicillins but by a factor of 10 lower than that of group A streptococci. The percentage of isolates with resistance to erythromycin (Erythrocin, etc.) in all group B streptococci is given as approximately 10%.

 

In the detection of a B streptococcal colonization between the 35th and 37th week of pregnancy is suggested chemoprophylaxis at the time of birth. In question penicillin G are (initially 5 million IU iv and then 2.5 million IU iv every 4 hours until delivery) or ampicillin (2 g IV at the beginning and then 1 g IV every 4 hours until delivery). In penicillin allergy can clindamycin [(Sobelin others) 900 mg iv ] every 8 hours - not expressly approved in Germany with this indication) or erythromycin (500 mg administered intravenously every 6 hours) until delivery. With the use of erythromycin (about 10% in this country) should previously a sensitivity test can be performed to prevent a failure of prophylaxis of infection due to the resistance situation.

 

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patient #223

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I've been here so long, locked inside this hell so long ago, I don't know if I even existed before I opened my eyes in this prison. I don't even know if there is a world beyond these walls. Everything is so hazy in my mind, I'm not sure what is real and what is a dream, though the doctors tell me it is all in my mind, and the people who come to me aren't real. I'm told they don't' exist, but they tell me things that are to be, and whisper in my ears at night, words of future events. I've tried telling someone, anyone, but the therapy and the experiments have left me nothing but a consciousness that barley hangs on, and feels as it fades with each treatment. I am locked in my mind now, with no one to hear me, but myself and the grey people who still visit me. I no longer try, but keep it locked inside, just as they have me locked in here, with hope that I'll be cured and free, but I'm so scared I fear I'll never be able to stand among men again as a human..but as a freak, a monster of their creating. In this place, I spend my time, and the time is soon that I will be free of my own doing, whether in death or life. They have a plan for me, and Soon that plan will be revealed.