Listeria monocytogenes

Although uncommon as a cause of infection in the general population, the bacterium, Listeria monocytogenes, is an important foodborne cause of life-threatening bacteremia and central nervous system (CNS) infection in certain high risk groups. Listeriosis most often occurs in newborns, the elderly, pregnant women, and those with impaired cell-mediated immunity due to disease states, such as hematological malignancy or acquired immune deficiency syndrome (AIDS), or due to corticosteroid or other immunosuppressive therapy, as in the case of solid organ transplant recipients (10, 32, 51, 52, 72, 80, 81, 83, 89). Following ingestion of a large inoculum, L. monocytogenes can result in acute, self-limiting, febrile gastroenteritis in otherwise healthy people (23, 40, 73). Increasing interest in this organism has arisen from concerns about food safety following lethal foodborne outbreaks.

Listeria monocytogenes is a small, facultative anaerobic, nonsporulating, gram-positive rod. It grows best at temperatures of 30 to 37°C, but it grows well at colder (refrigerator) temperatures, and in the laboratory can be separated from other bacteria by taking advantage of this fact, a technique known as cold enrichment  (97). Routine culture media are effective for isolating L. monocytogenes from normally sterile body sites, such as blood, cerebrospinal fluid (CSF), or joint fluid, but not from stool. In clinical specimens, L. monocytogenes may not take up Gram's stain well and may appear gram-negative. Its morphology may also vary, and the bacterium may be seen as short rods, diplococci, or cocci. L. monocytogenes may be misidentified as a diphtheroid, Streptococcus, Enterococcus, or Haemophilus influenzae.

Listeria monocytogenes is an important cause of zoonotic disease in herd animals. It is widely distributed in nature and may be found in soil, on vegetation, and in the stool of healthy mammals, including humans (~5%) (89). The organism has been isolated commonly from foods, including raw vegetables, raw milk, fish, poultry, and meats, including fresh or processed chicken and beef available at supermarkets or deli counters.  Ingestion of contaminated foods appears to be the source of most human infection (83). Outbreaks of invasive disease (bacteremia and/or meningitis) (13) have been documented in association with coleslaw, milk, soft cheeses (15), pâté, ready-to-eat pork products, deli counter meats (15), smoked fish (66), butter (55), taco or nacho salads, and cantaloupes (61).

In the US, listeriosis was made a nationally reportable disease in 2000.  By 1993, following food industry regulations instituted to decrease the risk of foodborne listeriosis, the annual incidence had declined to approximately 4.4 cases per million population.  From 1996 through 2003, the incidence decreased 26%; estimated cases in the US were 2228 and 1803 in 1996 and 2003 respectively, and deaths were 462 and 378 (95).  Neonates and adults over the age of fifty years have higher infection rates. Pregnant women make up 30% of all cases and 60% of cases in the 10- to 40-year age group. Almost 70% of non-perinatal infections occur in those with hematologic malignancy, AIDS, bone marrow or solid organ transplants, or in those receiving corticosteroid therapy or anti-TNF agents. However, as many as one-fifth of all invasive listeriosis cases occur in apparently healthy persons, particularly those over age 60.

Non-perinatal listeriosis is almost always foodborne.  Listeriosis is a relatively rare foodborne illness (~1% of US cases) but carries a case-fatality rate of 16-20% (second only to Vibrio vulnificus at about 35%) and causes about 19-28% of all foodborne disease-related deaths (76). 

The CDC has established PulseNet (http://www.cdc.gov/pulsenet/), a network of laboratories that employ pulsed-field gel electrophoresis to subtype foodborne pathogens in order to detect disease clusters that may have a common source (90).  This system has proved effective in the early detection of listeriosis outbreaks.

Neonatal listeriosis typically presents in one of two ways, either as an early-onset sepsis syndrome usually associated with prematurity, or late-onset meningitis occurring at about two weeks of life in full-term infants. Early-onset disease represents in utero-acquired infection; in these cases, L. monocytogenes can be cultured from nearly all body sites, including, sometimes, the CSF.

Invasive listeriosis in the immunocompromised adult most often manifests as a bacteremia without obvious focus. In such cases, patients have non-specific complaints such as fever, malaise, myalgias, and back pain. Pregnant women are prone to developing listerial bacteremia with a 17-fold increase in risk (71). Bacteremia is the form of invasive listeriosis that complicates pregnancy; CNS infection is extremely rare in the absence of other risk factors.  Listeriosis during pregnancy may lead to spontaneous abortion or neonatal sepsis, but early antimicrobial therapy may lead to birth of a healthy child (8, 29, 44).  Fetal viability is low (29%) when infection occurs in the second trimester, but viability increases with each week of pregnancy and survival is likely when infection occurs late in the third trimester (95%) (29).

Endocarditis with L. monocytogenes can occur on both native and prosthetic valves and carries a high rate of septic complications.  

Persons who develop bacteremia with L. monocytogenes may progress to central nervous system (CNS) infection, most commonly manifested as meningitis. Listeria has a predilection for infecting brain tissue as well as the meninges, and unlike other common bacterial causes of meningitis, such as H. influenzae, S. pneumoniae, N. meningitidis, and group B streptococcus, can cause encephalitis or brain abscess. Brain abscess due to L. monocytogenes exhibits unusual features when compared with other bacteria: listerial brain abscess coexists with bacteremia in nearly all cases, and with meningitis in one-quarter. In addition, abscesses are often subcortical (24, 27).  

L. monocytogenes is the most common cause of bacterial meningitis in patients with lymphomas, organ transplant recipients, and patients treated with corticosteroids for any reason (52), and accounts for about 20% of bacterial meningitis in neonates as well as in those older than 60 years of age.  Mortality is 22%. Affected persons usually present with the classic acute symptoms of meningitis, but as many as one-half of patients may also have a subacute disease course more characteristic of tuberculous meningitis (9). Most have stiff neck, but 15 to 20% may not. Altered consciousness or focal neurologic findings, including ataxia, tremors, myoclonus, and seizures, may be seen, consistent with listeria's tropism for brain parenchyma; patients often have a true meningoencephalitis (22). CSF glucose is normal in over 60% of cases (9, 72), and mononuclear cells predominate in 30%. Gram stain of CSF reveals L. monocytogenes in only about 40% of cases, and even when seen, the organisms may be mistaken for pneumococci.

Listerial rhombencephalitis is an unusual form of listerial encephalitis involving the brain stem (2). Unlike other listerial CNS infections, rhombencephalitis usually occurs in healthy adults. The typical clinical picture is one of a biphasic illness with a prodrome of fever, headache, nausea, and vomiting lasting about 4 days followed by the abrupt onset of asymmetric cranial nerve deficits, cerebellar signs, and hemiparesis or hemisensory deficits, or both. About 40% of patients develop respiratory failure. Nuchal rigidity is present in about half, and CSF findings are only mildly abnormal with a positive CSF culture in about 40%. Almost two-thirds of patients are bacteremic. Magnetic resonance imaging is superior to computed tomography for demonstrating rhombencephalitis. Mortality is high, and serious sequelae are common in survivors.  

Localized infection may occur after hematogenous seeding (e.g. liver abscess, peritonitis, septic arthritis) or, rarely, following direct inoculation (e.g. conjunctivitis, self-limiting papulo-pustular skins lesions usually in veterinarians) (33, 52).  Recently, well-documented reports of foodborne outbreaks have demonstrated that ingestion of L. monocytogenes in sufficiently large inocula can result in a self-limited illness, consisting of fever, chills, diarrhea, abdominal cramps, and sometimes nausea and vomiting (3, 23,73, 75).   Symptoms follow exposure by one to two days, and last for about two days.

The clinical situations in which listeriosis should be considered are listed in Table 1. Diagnosis of listeriosis is best made by routine bacterial culture of specimens from usually sterile sites such as blood or CSF. Stool culture is recommended only when routine stool cultures are negative in the setting of an outbreak of gastroenteritis; many people have transient enteric colonization with L. monocytogenes without invasive disease. The laboratory must be advised that listerial infection is suspected since the organism is unlikely to be identified with routine stool culture media.  

Serologic testing for antibodies to listeriolysin O, the major virulence factor, is not useful in invasive disease, but may be helpful in retrospective identification of outbreaks of foodborne febrile gastroenteritis when routine cultures are negative. Real-time PCR of CSF for the hyl gene, which encodes listeriolysin O has been shown to be useful in diagnosis CNS listeriosis (50), including cases in which routine bacterial cultures were negative, but this test is not commercially available.

Magnetic resonance imaging is superior to computed tomography for demonstrating parenchymal brain involvement, particularly in the brainstem.

L. monocytogenes enters the human body through the gut, most often after ingestion of a contaminated food. The incubation period for invasive disease is ~30 days with a range of 11-70 days.  Gastrointestinal cells and macrophages phagocytose the organism and enclose it within a phagolysosome (47). Through the production of an exotoxin called listeriolysin O, the organism destroys the membrane of the phagolysosome and gains access to the cytoplasm. All pathogenic strains of L. monocytogenes produce listeriolysin O. Listeria actively divide in the cytoplasm, then migrate to the periphery of the cell using polymerization of host cell actin and push out the cell membrane forming pseudopods, which are taken up by adjacent host cells (84). The bacteria move from cell to cell in this fashion, repeating their life cycle (12, 38). 

Individuals transiently colonized in the gastrointestinal tract by L. monocytogenes may develop invasive infection after disruption of the integrity of the intestinal mucosa by infection with another pathogen (e.g. shigellosis) or mechanical disruption (e.g. colonoscopy).

After invasion through the gastrointestinal tract, listeriae may disseminate hematogenously to any body site, but show a particular tropism for the central nervous system.  Bacteria typically reach the CNS through the bloodstream, but in some instances (rhombencephalitis), infection may follow intra-axonal nerve spread of bacteria from peripheral sites such as the mouth directly to the CNS (25).

Resistance to infection with L. monocytogenes chiefly is dependent on T-cell lymphokine activation of macrophages but involves both innate and adaptive immune responses (100).  The adaptive response is predominantly cell-mediated as evidenced by the overwhelming clinical association between listeriosis and conditions that impair cell-mediated immunity, including lymphoma, pregnancy, corticosteroids or anti-TNF immunosuppression.  The frequency of listeriosis is not increased in persons with deficiencies in neutrophil numbers or function, splenectomy, complement deficiency, or immunoglobulin disorders.

Many antimicrobials show in vitro activity against L. monocytogenes.  One should be careful to equate susceptibility with clinical utility since some drugs that show excellent in vitro activity are inadequate to treat infection; cefazolin serves as an example. Summary susceptibilities for selected antimicrobials are shown in Table 2.

Synergy has been demonstrated both in vitro and in animal models when an aminoglycoside is added to ampicillin or penicillin  (4,  28, 56, 65, 68, 78). This synergistic effect is achieved by levels of aminoglycoside that can be achieved in the CSF with parenteral administration. In vitro antagonism was demonstrated when ampicillin was combined with tetracycline, erythromycin, chloramphenicol and rifampin (99).  In a rabbit model of meningitis, the addition of rifampin to ampicillin was equivalent to ampicillin alone; antagonism was not seen (79).

Recommendations for the treatment of infections with L. monocytogenes derive from in vitro data, animal models, and clinical experience with small numbers of patients compared with historical controls, for no well-controlled human trials have been performed to prove the superiority of one drug regimen to another. Many antimicrobials show in vitro activity against listerial isolates, but only a few agents have been proved clinically efficacious (43).

Twenty percent of bacterial meningitis in those over age 50 is caused by L. monocytogenes, therefore, empiric therapy for bacterial meningitis in all adults older than 50 years with a negative CSF Gram stain should include an antilisterial agent (either ampicillin or trimethoprim-sulfamethoxazole), especially in the absence of associated pneumonia, otitis, sinusitis, or endocarditis, which would suggest an alternative etiology. Recommendations for treatment of invasive listeriosis are found in Table 3. Meningitis doses should be used to treat all cases of invasive listeriosis, even in the absence of CNS or CSF abnormalities, because of the affinity of L. monocytogenes for the CNS. Patients with meningitis should be treated for no less than 3 weeks; bacteremic patients with normal CSF may be treated for 2 weeks. Patients with rhombencephalitis or brain abscess should be treated for at least 6 weeks and followed with repeated brain imaging studies. Endocarditis should be treated for 4 to 6 weeks.  

Based on wide clinical experience and demonstrated efficacy, ampicillin is generally preferred in treating confirmed cases of listeriosis (43, 65), although its superiority to penicillin or trimethoprim-sulfamethoxazole is questionable. Based on in vitro and in vivo studies, most authorities recommend the addition of an aminoglycoside to ampicillin for at least the first week in treatment of CNS infection (54, 70), although some have questioned the utility of adding an aminoglycoside (67). Penicillins, often described as bacteriostatic for listeriae, actually show delayed in vitro bactericidal activity (48 hours) at levels that are obtainable in the CSF (99). Vancomycin and imipenem also demonstrate this phenomenon.  

Relapses and treatment failures are reported in those with meningitis treated for less than two weeks (70). Therefore, treatment for 3 weeks is recommended for all cases of meningitis.

Endocarditis due to Listeria monocytogenes occurs on both native and prosthetic valves and carries a high frequency of embolic complications as well as a high mortality (48%). Early surgical intervention should be considered for those with major emboli. Listerial endocarditis, but not bacteremia per se, may be a clue to underlying gastrointestinal malignancy (52). It seems prudent to recommend colonoscopy for those with proved listerial endocarditis.

Joint infection typically involves prosthetic joints in compromised hosts and requires prosthesis removal for cure (16).

Most human listeriosis occurs in those with impaired cell-mediated immunity secondary to underlying disease or to immunosuppressive treatment, particularly with corticosteroids (51). Although it is not a common opportunistic infection in AIDS patients, the risk of listeriosis in these patients is several hundred times that of the general population. The treatment of invasive listeriosis is the same for both normal hosts and those with underlying diseases. Dosages and duration are determined by site of infection and need not be altered for underlying disease state.

In case of penicillin hypersensitivity, trimethoprim-sulfamethoxazole (TMP-SMX) is the treatment of choice. It is bactericidal (63, 98) and appears to be as effective as the combination of ampicillin and gentamicin (86). In one report (96) a boy with leukemia and listerial meningitis improved and was cured when he was switched to TMP-SX after failing to clinically respond to 7 days of IV amoxicillin and gentamicin. Rarely, oral TMP-SX has been reported as successful treatment for listerial bacteremia and meningitis, and transition from intravenous to oral therapy with TMP-SX may be appropriate for selected patients with likely good adherence (34, 77). Trimethoprim as monotherapy has also been described (37) in the treatment of bacteremia and meningitis with L. monocytogenes, usually following initial therapy with TMP-SMX. Patients with endocarditis should be desensitized and treated with ampicillin and gentamicin. A single dose of vancomycin or meropenem could be given while performing desensitization.  Those with CNS infection and allergy to both penicillins and sulfonamides could be treated with meropenem or given a single dose of vancomycin and then desensitized.  

In the absence of underlying immunosuppressive illness or treatment, pregnant women virtually never develop CNS infection. Therefore, a penicillin allergic pregnant woman, at a time in the pregnancy when sulfonamides should be avoided, reasonably could be treated with vancomycin, meropenem, or a macrolide

In cases of meningitis and endocarditis, and in patients with severely impaired T-cell function, most authorities recommend the addition of gentamicin to ampicillin for synergy, based on in vitro testing and animal models. Parenterally administered gentamicin provides synergistic levels of antibiotic in the CSF.

In one retrospective series (62), therapy with TMP-SMX plus ampicillin correlated with a much lower failure rate and fewer neurologic sequelae than ampicillin combined with an aminoglycoside. The data from this limited study are not compelling enough to recommend the combination of TMP-SMX and ampicillin, but they provide evidence that the combination is not antagonistic.  

Cephalosporins, commonly used in the treatment of bacterial meningitis, have limited activity against listeriae. Cephalosporins bind poorly to listeria's penicillin-binding protein 3, the primary target for ß-lactam antibiotics, while penicillin and ampicillin bind well. Many reports document treatment failures with cephalosporins, and patients have developed listerial meningitis while receiving cephalosporins for other reasons (53).

Several quinolones have good in vitro activity (21, 35, 42, 58, 59, 64, 94), and are rapidly bactericidal (35,  94).  In a rabbit model of listerial meningitis, moxifloxacin alone was equivalent to the combination of ampicillin and gentamicin (82); but clinical experience with quinolone therapy is minimal, and listerial meningitis may have developed, or at the very least progressed, during ciprofloxacin treatment (36). 

Chloramphenicol has been shown to have unacceptable failure and relapse rates and should not be used to treat infections with L. monocytogenes (20).  

Erythromycin and tetracycline have been reported to be effective, but are unreliable therapeutic options and should be avoided. Resistance to tetracycline, mediated by the acquisition of both plasmids and transposons, may be increasing (17, 18).  

Some clinicians have used vancomycin successfully to treat penicillin-allergic patients (6); others have reported the development of listerial meningitis in patients being treated with vancomycin (5).  Daptomycin is variably active in vitro; clinical experience is lacking, but MICs would indicate that daptomycin cannot be recommended to treat listeriosis (85, 87).  Linezolid has good in vitro activity (11, 39), but clinical experience is limited (48). Both imipenem and meropenem have been used successfully to treat cases of listeriosis (60). These agents attach to the same binding proteins as do penicillins and are highly active in vitro (39). Because imipenem may lower the seizure threshold, meropenem is preferred. Caution is advised because imipenem alone or with gentamicin was less effective than ampicillin or ampicillin plus gentamicin in a mouse model (45), and meropenem clinical failure has been documented (88).  Ertapenem is considerably less active than imipenem and meropenem and should not be used (49).

In vitro, rifampin demonstrates good activity (79), although it is not bactericidal. In addition, it effectively penetrates into phagocytic cells, making it, in theory, an attractive agent to treat an intracellular pathogen such as L. monocytogenes. Resistance may occur during monotherapy with rifampin, however, and, in an animal model of listerial meningitis, combination therapy with ampicillin and rifampin was no better than ampicillin alone (79). Clinical resistance has been described (19).

Clinically significant antimicrobial resistance has not been encountered, but vigilence is warranted because transfer of resistance from enterococcus to L. monocytogenes has been documented, tetracycline and quinolone resistance has emerged, and MICs for penicillin have risen slightly (69).  One center has reported a clindamycin resistance rate of more than 95% (74).

Some authors have suggested administration of intrathecal or intraventricular antimicrobials as an adjunct in the treatment of CNS infections, especially in the rare cases of brain abscess or rhombencephalitis that are not accompanied by meningitis. Insufficient data exist to recommend this therapy.  

Surgical treatment of CNS infections may be necessary, most commonly for the management of complicating hydrocephalus. In cases of listerial brain abscess, surgical intervention may not be necessary, as numerous case reports exist of successful treatment with antimicrobial therapy alone. Brain abscesses can be treated with antibiotics and followed with serial brain imaging studies.  

Iron is a virulence factor for L. monocytogenes, and clinically, iron overload states are risk factors for listerial infection. Therefore, in patients with listeriosis and iron deficiency, it seems prudent to withhold iron replacement until antimicrobial therapy is complete.  

Corticosteroids appear to be important adjunctive agents in treating the most common forms of bacterial meningitis. Their role in the treatment of listerial CNS infection in unknown, but they should probably be avoided when the diagnosis of listerial meningitis is clear, because impairment of cellular immunity from corticosteroid therapy is a major risk factor for the development of listeriosis.  

Extracorporeal membrane oxygenation has been used to support neonates with severe respiratory failure due to listeriosis until there was improvement of their necrotizing lung infection with antimicrobial therapy (41).  

Febrile gastroenteritis due to L. monocytogenes is self-limited with a typical duration of no more than two days. No data exist concerning antimicrobial efficacy in this illness and treatment is not warranted.

The utility, or even the feasibility, of eradicating gastrointestinal colonization as a means to prevent invasive disease is unknown. However, asymptomatic people at high risk for listeriosis, known to have ingested a food implicated in an outbreak, reasonably could be given several days of oral ampicillin or TMP-SMX.

Patients with bacteremia, meningitis, or endocarditis can be treated for the durations outlined in Table 3. Those with a good clinical response to antibiotics (defervescence, improvement in mental status, negative repeat blood cultures, etc.) do not require repeat studies to determine a treatment endpoint. Those with rhombencephalitis and brain abscesses should be followed clinically and with serial MRI or CT studies. Duration of therapy for these patients should be at least 6 weeks, but should be continued until the patient is clinically stable and the brain imaging study shows resolution of lesions or a small, residual, stable lesion after initial improvement.

There are no vaccines currently available for listerial infection.

Guidelines for preventing listeriosis are similar to those for preventing other food-borne illnesses. In general, one should thoroughly cook raw food from animal sources, wash raw thoroughly before eating, keep uncooked meats separate from vegetables and from cooked foods and ready-to-eat foods, avoid raw (unpasteurized) milk or foods made from raw milk, and wash hands, knives, and cutting boards after each handling of uncooked foods.

People at high risk for listeriosis may choose to avoid soft cheeses such as feta, Brie, Camembert, blue-veined, and Mexican-style cheese such as queso fresco. Hard cheeses, processed cheeses, cream cheese, cottage cheese, and yogurt are safe. Leftover foods or ready-to-eat foods, such as hot dogs, should be cooked until steaming hot. It is best to avoid foods from deli counters, such as prepared salads, meats, and cheeses, or at least to thoroughly reheat cold cuts until they are steaming hot before eating.  

Listeriosis is effectively prevented by trimethoprim-sulfamethoxazole given as Pneumocystis prophylaxis to organ transplant recipients or to individuals with HIV infection (26). In areas with a high prevalence of AIDS, the widespread use of TMP-SX for Pneumocystis prophylaxis appears to have resulted in a marked decline in nonperinatal listeriosis (10).  

Second episodes of neonatal listerial infection are virtually unheard of, and intrapartum antibiotics are not recommended for women with a history of perinatal listeriosis.  

Except from infected mother to fetus, human to human transmission of listeriosis does not occur; patients do not need to be isolated.

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Tables

Table 1. Clinical Settings in Which Listeriosis Should Be Considered Strongly in the Differential Diagnosis

Neonatal sepsis or meningitis

Meningitis or parenchymal brain infection in patients with hematological malignancies, AIDS, organ transplantation, or corticosteroid immunosuppression, or those receiving anti-TNF agents

Meningitis or parenchymal brain infection in adults older than 50 years

Meningitis with a subacute presentation or simultaneous infection of the meninges and brain parenchyma

Subcortical brain abscess

Fever during pregnancy

Blood, CSF, or other normally sterile specimen reported to have "diphtheroids" on Gram stain or culture

Foodborne outbreak of febrile gastroenteritis when routine cultures fail to identify a pathogen

Table 2.  Antimicrobial Susceptibilities of Listeria monocytogenes*

	MIC (ug/ml)
Drug	Range	50%	90%
Ampicillin	0.03-1	0.5	0.5
Penicillin	0.06-2	0.5	1
Oxacillin	0.5-4	1	2
Piperacillin	0.5-2	1	2
Clindamycin	0.25-4	1	2
Chloramphenicol	2-8	4	8
Erythromycin	0.1-1	0.5	1
Clarithromycin	0.06-0.5	0.5	0.5
Rifampin	0.008-0.25	0.06	0.25
Tetracycline	0.5-4	1	2
Sulfamethoxazole	16-32	16	32
Trimethoprim	0.03-0.12	0.06	0.12
Trimethoprim-sulfamethoxazole	0.012-0.5	0.5	0.5
Gentamicin	0.25-2	0.5	1
Cefazolin	1-4	2	4
Ceftriaxone	4->128	128	>128
Ceftazidime	128->128	128	>128
Cefipime	4-64	64	64
Imipenem	0.5-4	2	4
Meropenem	0.064-0.25	0.125	0.19
Vancomycin	0.5-2	1	1
Ciprofloxacin	0.5-2	1	2
Levofloxacin	0.25-2	0.5	1
Moxifloxacin	0.064-1	0.5	1
Daptomycin	1-8	2	4
Linezolid	0.75-3	2	3

* Data are adapted from references 1, 7, 21, 30, 31, 35, 39, 42, 46, 57-59, 63, 64, 85

Table 3.   Intravenous Therapy of Invasive Listerial Infection

SYNDROME	ANTIBIOTIC*	DOSAGE**	INTERVAL	MINIMUM
Meningitis	Ampicillin	200 mg/kg	q4h	3wk
	plus Gentamicin	3 mg/kg	Q8h
Brain abscess or rhombencephalitis	Ampicillin	200 mg/kg	q4h	6wk
	plus Gentamicin	3 mg/kg	Q8h
Endocarditis	Ampicillin	200 mg/kg	q4h	6wk
	plus Gentamicin	3 mg/kg	Q8h
Bacteremia	Ampicillin	200 mg/kg	q4h	2wk

*  Penicillin allergic patients without endocarditis can be treated with trimethoprim-sulfamethoxazole alone, using 15-20mg/kg of trimethoprim daily at 6-8 hour intervals.  Patients with endocarditis should be desensitized to ampicillin and treated as above.

** Maximum daily dose of ampicillin should not exceed 15 grams

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Listeria monocytogenes

In the 1890s, pathologists in France and Germany noted gram-positive rods that likely were Listeria monocytogenes in tissue sections from deceased patients.  In 1911, Hülphers, a Swedish observer, isolated an organism from necrotic foci in a rabbit liver which he named Bacillus hepatis. Again, this organism most likely represented L. monocytogenes. The first description of L. monocytogenes is credited to Murray and colleagues from England who isolated a bacterium from the livers of sick rabbits and guinea pigs and, in 1926, published a paper titled, “A disease of rabbits characterized by large mononuclear leukocytosis caused by a hitherto undescribed bacillus Bacterium monocytogenes (n. sp.).”  The following year, in South Africa, Pirie isolated an identical bacterium from livers of gerbils and named the organism Listerella hepatolytica.  In 1940, after acknowledging that the name  Listerella had been assigned to an unrelated organism in 1906, the genus name was changed to Listeria.

Clinical listeriosis appears to have been recognized in sheep and cattle in Germany and in the US in the latter 1920s.  In 1933, Gill described an illness in sheep that he named “circling disease,” a descriptive term for the hemiparesis that caused animals to walk in circles. Gill later isolated L. monocytogenes from domesticated farm animals for the first time when he recovered the organism from the brain of an affected sheep.  The first isolation of the organism from a human came from a soldier with meningitis in 1924, but the bacterial isolate was not identified as L. monocytogenes until 1942. Credit for the first report of human infection due to L. monocytogenes usually is given to Nyfeldt who, in 1929, isolated the bacterium from persons with a mononucleosis-like illness.  Until the discovery of the Epstein-Barr virus almost 40 years later, L. monocytogenes was considered by many to be the cause of infectious mononucleosis, and it was so indicated in standard texts and medical dictionaries. 

The strong association of human listeriosis with hematologic cancer was recognized in publications during the 1970s, and the association with impaired cell-mediated immunity and corticosteroid immunosuppression was widely recognized in the 1980s.  Demonstration that human infection typically has a foodborne source came in a 1983 publication describing a 1981 outbreak in the maritime provinces of Canada that was traced to contaminated coleslaw made from locally farmed cabbages.  Subsequently, numerous foodborne outbreaks of bacteremia and CNS infection have been described. In recent years, the unique intracellular pathogenesis of L. monocytogenes has been investigated in detail, including the ability of this organism to polymerize host cell actin and move from cell to cell without encountering phagocytic neutrophils, complement, or antibodies.