Crit Care Nurse 2002 Oct; 22(5): 38-43
Clinical Article
Caring for a Patient With Listeria Endocarditis: Use of Antibiotic Desensitization
Lori Candela, RN, MS, EdD, CCRN
Lori Candela is an assistant professor of nursing at the University of Nevada, Las Vegas. She has 20 years of clinical experience and currently works with nursing students in acute care and community settings.
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Endocarditis due to Listeria monocytogenes is an uncommon bacterial infection.1 From 1955 until the end of 1996, only 58 cases had been reported.2 Despite the low prevalence, L monocytogenes is a deadly cause of endocarditis. In untreated cases, the mortality rate is 100%.2 Even with treatment, the mortality rate is 37%, compared with 14% for all types of bacterial endocarditis.3 Treatment ranges from aggressive antibiotic therapy to surgery. Although numerous antibiotic regimens have been used, ampicillin, often augmented by gentamicin, is recommended.1,4,5 A serious dilemma occurs when a patient with Listeria endocarditis is allergic to penicillin. In this situation, antibiotic desensitization may be used.
In this article, I describe the development of Listeria endocarditis and the role of antibiotic treatment. Included is a case in which the patient had antibiotic desensitization because of a suspected allergy to penicillin. I also discuss specific nursing management during antibiotic desensitization.
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DEVELOPMENT OF LISTERIA ENDOCARDITIS
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L monocytogenes is an opportunistic organism. Listeria infections are most apt to occur in persons who are immunosuppressed, for example, patients with acquired immunodeficiency syndrome, transplant recipients, and patients with long-term use of corticosteroids.6 The frequency of infection is also higher in pregnant women and in persons less than 1 month old or more than 60 years old. Patients who have diabetes, cardiovascular or renal impairment, cancer, high iron stores, or hypochlorhydria or who abuse alcohol or intravenous drugs are also at risk for Listeria infections.1,5
L monocytogenes is a small, facultative anaerobic, gram-positive bacillus found nearly everywhere in the environment.3,5 It is considered a hardy organism because of its ability to survive and multiply in a wide variety of temperatures and pH ranges.5 The usual source of transmission is contaminated food. The bacillus is found in bird, fish, and mammal feces. L monocytogenes has been cultured from many foods, including chicken, deli foods, and pasteurized milk. Refrigeration does not destroy the organism; in fact, it can multiply at temperatures as low as 4°C. Listeria can also be transmitted from mother to fetus. Less commonly, the bacterium can be transmitted cutaneously by contact with a contaminated source.1
Listeria infections are particularly aggressive because of the ability of the organism to escape immune detection through the use of host cells. After entering the body, usually through the gastrointestinal tract, the organism induces phagocytosis through the interaction of cell surface proteins with receptors found on host epithelial cells. Once inside the cell, 2 toxic elements, listeriolysis O and phospholipase, are released from the organism, allowing it to avoid intracellular death. The organism grows and multiplies within the cell cytoplasm. Through pushing against the cell membrane, L monocytogenes is ingested by other cells such as macrophages, enterocytes, and hepatocytes. Thus it is able to be transported without detection by antibodies, neutrophils, complement, or antibiotics in the extracellular fluid.5,6 The organism can travel anywhere, but it seems to have an affinity for the central nervous system, the placenta, and the heart. It can attack native or prosthetic heart valves, most often on the left side of the heart.1,6
Diagnosis of bacterial endocarditis is based on positive blood cultures and echocardiographic evidence of endocardial involvement. Signs and symptoms and diagnostic indicators of bacterial endocarditis7 are presented in Tables 1
and 2.
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CASE STUDY
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A 42-year-old man was admitted to the emergency department after a motor vehicle crash. His injuries included a hip dislocation, arm and leg fractures, concussion, and lacerations to the face and knee. He had been infected with human immunodeficiency virus for 15 years. Five years before admission, he had undergone a second aortic valve replacement because of congenital disease. He also had congestive heart failure, diet-controlled diabetes mellitus, and chronic renal insufficiency. His family provided the medical history and reported that he was allergic to penicillin. They did not know what the specific allergic response had been.
At the time of admission, the patient was receiving 100% oxygen via a nonrebreather mask, and oxygen saturation measured by pulse oximetry was 91% to 92%. He was alert with respirations 32/min, blood pressure 80/48 mm Hg, and axillary temperature 39.2°C. He had sinus tachycardia up to 138 beats/min with frequent preventricular contractions. He experienced an episode of ventricular tachycardia that required defibrillation and intubation.
Results of laboratory tests included white blood cell count 11.4 x 109/L, hematocrit 0.35, hemoglobin 119 g/L, and platelet count 191 x 109/L. His coagulation times were elevated: prothrombin time 34.8 seconds and partial thromboplastin time 65 seconds. Blood glucose level was 7.2 mmol/L (130 mg/dL). Serum levels of urea nitrogen and creatinine were 8.9 mmol/L (25 mg/dL) and 168 µmol/L (1.9 mg/dL), respectively. The preliminary results of blood cultures indicated infection with a gram-positive bacillus.
Transesophageal echocardiography revealed a moderate aortic perivalvular leak and severe left ventricular dysfunction. The calculated ejection fraction was 0.15 to 0.20. Findings on physical examination included bibasilar crackles, an S3 heart sound, and a clear prosthetic click.
Empiric treatment of endocarditis was started: vancomycin, rifampin, and levofloxacin. During the next 3 days, the patient remained febrile, with temperatures fluctuating from 38.9°C to 39.8°C. Final results of blood cultures included growth of L monocytogenes and sensitivity of the isolate to ampicillin and gentamicin.
Ampicillin and gentamicin are both excreted via glomerular filtration,8 which is normally 115 to 125 mL/min. The glomerular filtration rate can be determined from the creatinine clearance rate. In a patient with renal insufficiency, the glomerular filtration rate is 20% to 50% less than the normal rate.9 Consequently, drugs remain in the system longer, thereby increasing the chance of toxic reactions.8 The patient’s creatinine clearance was 1.93 mL/s (115.78 mL/min). In terms of renal function, his healthcare team thought that he could tolerate ampicillin and gentamicin.
A CD4 count of 0.34 x 109/L (34/µL) indicated that the patient had acquired immunodeficiency syndrome and was at high risk for opportunistic infections.10 Because his family had reported that he was allergic to penicillin, penicillin skin testing with controls was considered. The controls would be necessary to assess for true anergy. Anergy occurs in 80% or more of patients with CD4 counts less than 0.50 x 109/L (<50/µL).10 Therefore, the patient most likely would not have any skin reaction to the penicillin. Also, the patient was being given histamine blockers, which interfere with skin tests for penicillin allergy. In order to obtain accurate results, administration of the histamine blockers would have to be stopped and the drugs allowed to clear his system.
The members of the healthcare team considered the uncertain history of penicillin allergy and the current status of the patient. They decided to approach his family about the possibility of antibiotic desensitization with ampicillin.
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ANTIMICROBIAL ACTIVITY OF AMPICILLIN AND GENTAMICIN
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L monocytogenes is susceptible to ampicillin, penicillin,5 and amoxicillin.8 Although no clear consensus exists, ampicillin is often recommended in the treatment of Listeria endocarditis.1,4–6 Ampicillin affects a broader spectrum of organisms than penicillin does.8 Both antibiotics are considered bactericidal because they cause bacterial lysis.11 In Listeria, the drugs bind to penicillin-binding protein 3, causing disruption in the cell wall of the bacterium and ultimately death of the microorganism.5,8
Coadministration of gentamicin and ampicillin has a synergistic effect.2,5–7 The effectiveness against all 7 strains of L monocytogenes 24 hours after the start of therapy is greater with the combination of drugs than with either drug alone.5 Both antibiotics are recommended for patients who are more than 50 years old or have a compromised cardiac, respiratory, or immune system.5,6
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ANTIBIOTIC DESENSITIZATION
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As effective as it may be against Listeria, penicillin is still the antibiotic most often responsible for allergic reactions.12 In the United States, 0.7% to 10% of the population say they are allergic to penicillin.12–14 Of that number, only 10% to 30% have had skin tests that indicate an immediate-type hypersensitivity to the drug.14 Reactions to penicillin vary from mild gastric complaints to true anaphylaxis. Obtaining a clear, reliable history of drug allergies is often difficult.15
Antibiotic desensitization, also known as challenge testing or test dosing,12,14 is the administration of incrementally higher doses of drug until the full recommended dose is reached or until the patient has a noticeable reaction. No standard for dosing schedules exists; often, the schedules are developed through consultation with immunologists, allergists, and review of allergy texts and the literature.12 In addition, little agreement exists on the use of corticosteroids and/or antihistamines before antibiotic desensitization. The argument for their use is that they decrease the occurrence of reactions to the drug or the skin test antigen. However, the use of these drugs may only mask possible reactions.18 In the case presented, the patient was given a corticosteroid before the first dose of ampicillin (Table 3).
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NURSING MANAGEMENT DURING ANTIBIOTIC DESENSITIZATION
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Antibiotic desensitization requires strict nursing management. Up to two thirds of patients will have signs or symptoms of anaphylaxis. Hypersensitivity reactions may be fatal in 0.5% of patients.12 Table 4 lists the types of hypersensitivity and the associated signs and symptoms.14,17,19
As with desensitization schedules, no one protocol for nursing management during desensitization exists. In 1 report,20 desensitization was carried out with emergency medications and equipment at the bedside. The patient had a central venous catheter with multiple access lumens in place, and nursing personnel were aware of the potential for reaction.
Mild allergic reactions, such as flushing, pruritus, and rashes, may occur in as many as 30% of patients having antibiotic desensitization. These reactions can be managed by adjusting the dose (slowing the intravenous rate) and by use of antihistamines and corticosteroids. If a serious reaction such as severe asthma, hypotension, or laryngeal edema occurs, the drug flow should be stopped.18 Nurses should be prepared for the immediate use of epinephrine, vasopressive drugs, and full resuscitative measures. As soon as the patient’s condition is stable, the desensitization should be resumed, at a dose of at least one third the last dose given.18
In the case reported here, the patient, who was already in intensive care, was placed on 1-to-1 nurse-to-patient status. The physician explained the risks and benefits of antibiotic desensitization to his family. After their questions were answered, informed consent was obtained. Blood pressure, pulse, temperature, and respiratory rate beyond the rate set on the ventilator were measured initially and with each dose of ampicillin. Table 5 gives the specific nursing management used during the desensitization.
The patient tolerated the desensitization without any noticeable reaction. Gentamicin was added to the ampicillin regimen, and all other antibiotics were discontinued. After the desensitization, the patient was not given corticosteroids with each dose of antibiotics. He was treated with ampicillin and gentamicin for 14 days and had no signs or symptoms of allergy.
Importantly, patients may become resensitized to a drug once it has been discontinued for more than 12 hours. If drug therapy is temporarily interrupted or started again later, the entire desensitization procedure may have to be repeated.18
Blood cultures were repeated several days after the start of treatment with ampicillin and gentamicin. One week after the antibiotic desensitization, the patient had no growth of Listeria in blood cultures.
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SUMMARY
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Occurrence of Listeria endocarditis is rare, and the mortality rate is high, 100% in untreated cases. The use of antibiotics, specifically ampicillin, is considered a first-line treatment. Co-administration of ampicillin and gentamicin provides a synergistic effect in killing the bacteria.
Antibiotics are among the most common causes of hypersensitivity reactions. Of all antibiotics, penicillin is the one that most often causes a reaction. Skin testing adds time until treatment, and all patients with sensitivity to penicillin may not be detected. In the case presented, the patient had antibiotic desensitization with ampicillin. He did not have any allergic reactions to the drug. However, his history of allergy to penicillin was uncertain, so perhaps he did not have a true, serious penicillin allergy. Also, most likely he was anergic and could not mount an immune response to ampicillin, even if truly allergic. Therefore, his response may not be a typical response to antibiotic desensitization. Understanding possible hypersensitivity reactions can help guide the medical and nursing management of patients having antibiotic desensitization.
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Acknowledgments
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I thank Susan Kowalski, RN, PhD, for her thoughtful review of the manuscript and Don Frisch, PharmD, BCPS, for his suggestions for the development of this topic.
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References
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- Taege AJ. Listeriosis: recognizing it, treating it, preventing it. Cleve Clin J Med. 1999;66:375–380.[Medline]
- Spyrou N, Anderson M, Foale R. Listeria endocarditis: current management and patient outcome—world literature review. Heart. 1997;77:380–383.[Abstract/Free Full Text]
- Hood S, Baxter RH. Listeria endocarditis causing aortic root abscess and a fistula to the left atrium. Scott Med J. 1999;44: 117–118.[Medline]
- Castro Cabezas M, Cramer MJ, de Jongh BM, de Maat CEM. Listeria monocytogenes endocarditis in a patient with an aortic prosthetic valve. Neth J Med. 1996;48:15–17.[Medline]
- Temple ME, Nahata MC. Treatment of listeriosis. Ann Pharmacother. 2000;34:656–661.[Abstract]
- Lorber B. Listeriosis. Clin Infect Dis. 1997;24:1–11.[Medline]
- Giessel BE, Koenig CJ, Blake RL Jr. Management of bacterial endocarditis. Am Fam Physician. 2000;61:1725–1732, 1739.
- Edmunds MW, Mayhew MS. Pharmacology for the Primary Care Provider. St Louis, Mo: CV Mosby; 2000:63, 768–769, 771, 805.
- Porth CM. Pathophysiology: Concepts of Altered Health States. 5th ed. Philadelphia, Pa: Lippincott; 1998:581.
- Carmichael CG, Carmicheal JK, Fischl MA. HIV/AIDS: Primary Care Handbook. East Norwick, Conn: Appleton Lange; 1995:21, 70.
- Hopfer-Deglin J, Hazard-Vallerand A. Davis’s Drug Guide for Nurses. 5th ed. Philadelphia, Pa: FA Davis Co; 1997:76–79.
- Craig TJ, Mende C. Common allergic and allergic-like reactions to medications: when the cure becomes the curse. Postgrad Med. 1999;105:173–181.
- Penicillin allergies can go away. Mayo Clin Health Lett. September 1999;17:4.
- Lin RY. A perspective on penicillin allergy. Arch Intern Med. 1992; 152:930–937.[Medline]
- Dodek P, Phillips P. Questionable history of immediate-type hypersensitivity to penicillin in staphylococcal endocarditis: treatment based on skin-test results versus empirical alternative treatment—a decision analysis. Clin Infect Dis. 1999; 29:1251–1256.[Medline]
- Lacy CF, Armstrong LL, Goldman MP, Lance LL, eds. American Pharmaceutical Association Drug Information Handbook 1999 –2000. 7th ed. Hudson, Ohio: LexiComp; 1999:1355–1357.
- Segreti J, Trentholme GM, Levin S. Antibiotic therapy in the allergic patient. Med Clin North Am. 1995;79:935–942.[Medline]
- Patterson R, Grammar LC, Greenberger PA. Allergic Diseases: Diagnosis and Management. 5th ed. Philadelphia, Pa: Lippincott; 1997:355–256, 360–371.
- Czachor JS. Antibiotic troubleshooting in primary care. Hosp Pract. 1999;34:95–101.
- Papakonstantinou G, Bogner JR, Hofmeister F, Hehlmann R. Cefotaxime desensitization. Clin Investig. 1993;71:165–167.[Medline]
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DEVELOPMENT OF LISTERIA...
CASE STUDY
