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Treatment and prevention of typhoid fever
Author
Elizabeth L Hohmann, MD
Section Editor
Stephen B Calderwood, MD
Deputy Editor
Elinor L Baron, MD, DTMH
Disclosures
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Jan 2013. | This topic last updated: jul 13, 2012.
INTRODUCTION — Typhoid fever and paratyphoid fever (also known as enteric fever, but
collectively referred to here as typhoid fever) are severe systemic illnesses characterized by
sustained fever and abdominal symptoms. The treatment and prevention of typhoid fever will be
reviewed here. The epidemiology, pathogenesis, clinical manifestations, and diagnosis of typhoid
fever are discussed separately. (See"Pathogenesis of typhoid fever" and "Epidemiology,
microbiology, clinical manifestations, and diagnosis of typhoid fever".)
ANTIBIOTIC THERAPY — Treatment of typhoid fever has been complicated by the development and rapid dissemination of typhoidal organisms resistant to ampicillin, trimethoprimsulfamethoxazole, and chloramphenicol. In recent years, development of creeping resistance to fluoroquinolones has resulted in more challenges.
Multidrug-resistant strains — Multidrug-resistant (MDR) strains have caused numerous outbreaks
in the Indian subcontinent, Southeast Asia, Mexico, the Arabian Gulf, and Africa [1,2]. These
patterns of resistance are reflected in travelers returning to the United Kingdom and the United
States. In 1999, 26 percent of S. typhi strains characterized at a United Kingdom reference lab were MDR strains [3], and 17 percent of 293 strains evaluated by the Centers for Disease Control and Prevention (CDC) from 1996 to 1997 were resistant to five drugs [4]. In contrast, a study from India has reported the "reemergence" of sensitivity to older drugs: 67 percent of 60 S. typhi blood isolates and 80 percent of 20 S. paratyphi blood isolates from 2001 through 2004 were sensitive
to chloramphenicol [5,6].
Resistance patterns have led to a shift toward the third generation cephalosporins, azithromycin,
and fluoroquinolones as empiric therapy for typhoid fever while awaiting the results of antimicrobial
susceptibilities.
A report of 113 S. typhi strains collected in India from 1987-2006 demonstrated possible “MIC
creep” for ceftriaxone, though no frank resistance. A gradual increase in ceftriaxone MIC has been
observed in five-year increments: 0.047 mcg/mL, 0.098 mcg/mL, 0.211 mcg/mL, and 0.365 mcg/mL for ceftriaxone MIC [7].
Two isolates of S. paratyphi B expressing extended-spectrum beta-lactamases have been reported
from Turkey [8].
Fluoroquinolone-resistant organisms — Nalidixic acid-resistant organisms with decreased
susceptibility to the clinically important fluoroquinolones have become a major problem worldwide.
Isolated cases of high-level resistance to ciprofloxacin have been reported from India in S. paratyphi
and S. typhi (MICs of 8 mcg/mL to 16 mcg/mL) [9-11].
Nalidixic acid-resistant S. typhi (NARST, NaR, or NALR) have decreased ciprofloxacin sensitivity
and are less effectively treated with fluoroquinolones, especially with the use of a "short course" of
three to five days, which is very effective against susceptible organisms. The clinical impact of NaR
organisms is illustrated by the following studies:
· A retrospective review of 150 patients from Vietnam showed that patients infected with NaR
S. typhi defervesced more slowly (256 versus 84 hours) and more frequently required
retreatment (33 versus 0.8 percent) than those infected with nalidixic acid-sensitive
organisms [12].
· Pooled data from several studies of almost 500 bacteremic patients treated with two, three,
or five days of ofloxacin, found that those patients with NaR strains who got ofloxacin had
greater rates of clinical treatment failure than those treated with comparator drugs
(eg, ceftriaxone, azithromycin, or cefixime) [13].
· Additional reports from other parts of the world identified treatment failures with
fluoroquinolones for enteric fever caused by nalidixic acid-resistant S. typhi and S.
paratyphi that tested susceptible to the quinolones [14-16].
· An open label, randomized study in 88 Vietnamese patients with bacteremia due to NaR or
MDR S. typhi strains compared oral treatment with azithromycin (1 g daily for five days)
to ofloxacin (200 mg twice daily for five days) [17]. There was no difference in clinical cure
rate between the regimens, but patients with NaR S. typhi treated with ofloxacin took longer
to defervesce and had a higher rate of positive stool cultures following therapy compared
with those receiving azithromycin (41 versus 0 percent). Early convalescent fecal shedding
may spread the organism in a community even if few of these individuals become chronic
carriers.
This situation has been further complicated by the emergence of newer mechanisms of resistance
to fluoroquinolones [18]. Some isolates may have decreased sensitivity to clinically important
fluoroquinolones, but appear to be sensitive to nalidixic acid, calling into question the reliability of
using NaR as a marker of FQ resistance. As a result, both the Clinical and Laboratory Standards
Institute (CLSI) and European Committee on Antimicrobial Susceptibility Testing (EUCAST) have
revised the fluoroquinolone breakpoints for extra-intestinal Salmonella isolates. CLSI standards now
designate Salmonella isolates with aciprofloxacin MIC ≥1 mcg/mL as resistant (formerly MIC 2 to 4
mcg/mL), MIC 0.125 to 0.5 mcg/mL as intermediate, and MIC ≤0.064 mcg/mL as susceptible.
Laboratories in the United States are in the process of implementing such changes [18].
S. typhi isolates should be screened for resistance to nalidixic acid and, when possible, directly
tested for ciprofloxacin or ofloxacin sensitivity utilizing the new breakpoints as described above [18-
20]. However, the latter may be technically challenging especially in resource-limited settings.
Infectious disease consultation should be considered for such cases if clinicians are not familiar with
typhoid fever and its treatment.
When possible, patients with enteric fever caused by NaR organisms or organisms with
decreased ciprofloxacin or ofloxacin sensitivity should ideally be treated with a nonquinolone drug.
However, it is important to note that alternatives are expensive, sometimes not available, and may
require parenteral administration. Alternative treatments that are likely to be investigated more in the future include azithromycin, imipenem, the newer fluoroquinolones, higher doses of
fluoroquinolones, and combination therapies.
Antimicrobial regimens — Typhoid fever is usually treated with a single antibacterial drug. The
optimal choice of drug and duration of therapy are uncertain [12,21,22]. Antibiotic selection depends upon local resistance patterns, patient age, whether oral medications are feasible, the clinical setting, and available resources. In some circumstances, older agents such as chloramphenicol, ampicillin, or trimethoprim-sulfamethoxazole may be appropriate, but these
drugs are generally not used widely because of high levels of resistance. Oral chloramphenicol is
no longer available in the United States but is still used in other parts of the world. Successful
treatment in uncomplicated cases usually results in clinical improvement within three to five days. It
is reasonable to begin with a parenteral agent and then complete therapy with an oral drug once
symptoms improve.
Adults — Drugs of choice for the treatment of typhoid fever in adults include [23]:
· A fluoroquinolone such as ciprofloxacin (500 mg twice daily) or ofloxacin (400 mg twice
daily), either orally or parenterally for 7 to 10 days. The fluoroquinolones should not be used
as a first-line treatment for typhoid fever in patients from South Asia or other regions with
high rates of fluoroquinolone resistance unless antibiotic susceptibility data demonstrate
fluoroquinolone or nalidixic acid sensitivity [14,15]. (See 'Fluoroquinolone-resistant
organisms' above.)
· A beta-lactam such as ceftriaxone (2 to 3 g once daily) parenterally or cefixime (20 to 30
mg/kg per day orally in two divided doses) for 7 to 14 days.
Alternative agents for adult patients who cannot be treated with the above antimicrobials, and for
fluoroquinolone resistant isolates include:
· Azithromycin (1 g orally once followed by 500 mg once daily for five to seven days, or 1 g
orally once daily for five days) [24-27].
· Chloramphenico l 2 to 3 g per day orally in four divided doses for 14 days.
Fluoroquinolones appear to have therapeutic advantages over beta-lactams for the treatment of
uncomplicated typhoid fever and are now considered by many experts to be the drug of choice for
fully susceptible organisms in patients who can take these drugs. Quinolones are bactericidal and
concentrated intracellularly and in the bile. Ciprofloxacin, ofloxacin, and pefloxacin are widely
available and efficacious:norfloxacin is very poorly absorbed and should not be used. When treating
fully susceptible organisms, the quinolones may result in more rapid defervescence than betalactam
agents or chloramphenicol because of more rapid elimination of intracellular bacteria [28,29].
An open label randomized trial of 82 children randomized to receive cefixime (20 mg/kg per day
divided twice daily for five days) or ofloxacin (10 mg/kg per day divided daily for five days)
demonstrated more rapid resolution of fever in the ofloxacin group (4.4 versus 8.5 days) [30]. There was one treatment failure in the ofloxacin group compared with 10 treatment failures and one
relapse in the cefixime group. Another open label randomized trial among patients older than 15
years demonstrated that ofloxacin (200 mg orally twice daily for three days) was superior
to ceftriaxone (3 g intravenously once daily for three days) [29].
Azithromycin is capable of achieving excellent intracellular concentrations, and its use for treatment
of typhoid fever has been increasing as a result of rising fluoroquinolone resistance. There are no
standard microbiological breakpoints for determining Salmonellae MICs in routine clinical practice;
in research studies MICs are typically 4 to 32 mcg/mL. These values typically exceed serum drug
levels; azithromycin is concentrated intracellularly at levels 50 to 100 greater than serum levels [31].
The first report of azithromycin resistance (MIC by E-test 64 mcg/mL) in S. paratyphi A resulting in treatment failure was reported in a traveler returning from Pakistan to Great Britain. The patient was successfully treated with a two week course of IV ceftriaxone, 2 g daily [32].
In a study of 358 Vietnamese patients with infection due to resistant isolates (96 percent of isolates
were resistant to nalidixic acid and 58 percent were multidrug resistant), outcomes among those
treated with seven days of gatifloxacin or azithromycin were essentially equivalent [33]. A large
open label randomized controlled trial of gatifloxacin (10 mg/kg once daily for seven days)
versus chloramphenicol (75 mg/kg/day in four divided doses for 10 days) for uncomplicated, cultureproven
typhoid fever showed equivalent cure and relapse rates in children and adults in Nepal. The
authors concluded that gatifloxacin should be the preferred treatment for enteric fever in developing
countries because of its shorter treatment duration and fewer adverse events (14 versus 24 percent
of patients) [34].
Children — In patients with severe systemic illness, therapy should be initiated with a parenteral
agent. Current drugs of choice and dosing regimens for the treatment of typhoid fever in children
differ depending on local practice preferences. For these reasons, we present treatment regimens
used in the United States [35,36] and those used in endemic countries (eg, Southeast Asia) [23].
The practice preference in the United States for typhoid fever in children include one of the following treatment regimens [35,36]:
· A beta-lactam such as:
· Ceftriaxone 100 mg/kg per day intravenously once daily, maximum 4 g per day for
10 to 14 days.
· Cefotaxime 150 to 200 mg/kg per day intravenously in three to four equally divided
doses, maximum 12 g per day for 10 to 14 days.
· Cefixime orally 20 mg/kg per day orally in two divided doses, maximum 400 mg per
day for 10 to 14 days.
· A fluoroquinolone (See 'Fluoroquinolone-resistant organisms' above.)
· Ciprofloxacin 30 mg/kg daily, maximum 1000 mg either orally or parenterally for 7 to
10 days.
· Ofloxacin 30 mg/kg daily, maximum 800 mg per day, either orally or parenterally for
7 to 10 days.
· Azithromycin 10 to 20 mg/kg to 1 g maximum once daily for five to seven days.
· In children with infection due to a fully susceptible S. typhi strain, one of the following
alternative regimens may be used:
· Chloramphenico l 75 mg/kg per day divided every six hours, maximum 3 g per day
for 14 to 21 days.
· Amoxicillin 100 mg/kg per day divided every eight hours, maximum 4 g per day for
14 days.
· Trimethoprim-sulfamethoxazole 8 to 12 mg/kg trimethoprim/40 to 60 mg/kg
sulfamethoxazole per day divided every six hours, maximum 320 mg trimethoprim/1600
mg sulfamethoxazole per day for 14 days.
The practice preferences for children treated outside the United States, particularly in endemic
countries in Southeast Asia, more closely mirror treatment regimens used for adults and include one
of the following [23]:
· For fluoroquinolone-sensitive strains (see 'Fluoroquinolone-resistant organisms' above):
· Ciprofloxacin 15 mg/kg daily, maximum 1000 mg and 800 mg per day either orally
or parenterally for 10 to 14 days.
· Ofloxacin 15 mg/kg daily, maximum 800 mg per day either orally or parenterally for
10 to 14 days.
· In children with infection due to a fully susceptible S. typhi strains, one of the following
alternative regimens may be used:
· Chloramphenico l 100 mg/kg per day divided every six hours, maximum 3 g per day
for 14 to 21 days.
· Ampicillin 100 mg/kg per day divided every eight hours, maximum 4 g per day for
10 to 14 days.
· Trimethoprim-sulfamethoxazole 8 mg/kg trimethoprim/40 mg/kg sulfamethoxazole
per day divided every six hours, maximum 320 mg trimethoprim/1600 mg
sulfamethoxazole per day for 10 to 14 days.
· Alternative agents in children with infection due to multiple drug-resistant isolates, including
nalidixic acid-resistant S. typhi, include:
· Ceftriaxone 60 mg/kg per day intravenously once daily, maximum 2 g per day.
· Cefotaxime 80 mg/kg per day intravenously in three to four equally divided doses,
maximum 12 g per day for 10 to 14 days.
· A fluoroquinolone using a higher dose such as, ciprofloxacin or ofloxacin (20 mg/kg
daily, maximum 1000 mg and 800 mg per day, respectively), either orally or parenterally
for 10 to 14 days.
· Azithromycin 10 to 20 mg/kg to 1 g maximum for five to seven days.
Differences in practice preferences in children are in part due to concern in the United States about
the use of fluoroquinolones because of cartilage toxicity of these drugs in immature animals [37,38].
Large series have found no evidence of acute adverse bone or joint events [39] or of adverse
effects on growth [40] in humans. These findings are reassuring and suggest that, for a serious
illness such as infection with MDR S. typhi, a fluoroquinolone may be reasonably used in children
when other less toxic agents are not available or appropriate [41].
The optimal duration of third generation cephalosporin therapy in children has not been firmly
established, but the following observations have been made:
· A seven day course does not appear to be sufficient. In two randomized trials, seven days
of ceftriaxone (50 to 75 mg/kg per day) resulted in relapse within four weeks in 14 percent
of children [42,43]. In one of these studies, children ages 4 to 17 years were assigned to
seven days of therapy with either azithromycin (10 mg/kg per day; maximum 500 mg) or
ceftriaxone (75 mg/kg per day, maximum 2.5 g per day) [42]. There were four relapses with
ceftriaxone compared with none with azithromycin (14 versus 0 percent).
· Among the third generation cephalosporins, ceftriaxone may be superior to cefotaxime [44].
Oral cefixime is probably comparable to ceftriaxone for uncomplicated typhoid, although the
two drugs have not been extensively studied head-to-head [45,46].
Based upon these observations, ceftriaxone or cefixime is probably best given for 10 to 14 days to
minimize risk of relapse [42,43,45,46].
OTHER TREATMENT CONSIDERATIONS
Corticosteroids — Early studies with chloramphenicol suggested that concomitant corticosteroid
therapy might be beneficial in patients with typhoid fever. In a randomized, prospective, double blind study performed in Indonesia in the early 1980s, the administration of 3 mg/kg of dexamethasone as an initial dose with chloramphenicol was associated with a substantially lower
mortality in critically ill patients (shock, obtundation) with typhoid fever compared with those who
received chloramphenicol alone (10 versus 55 percent) [47]. Whether these findings will be
confirmed in the "post-chloramphenicol era" and in different clinical settings is uncertain, but severe
typhoid fever remains one of the few indications among acute bacterial infections for corticosteroid
therapy infections [48]. Dose in adults and children with severe disease (delirium, obtundation,
stupor, coma, or shock) consists of an initial dose of 3 mg/kg followed by 1 mg/kg every six hours
for a total of 48 hours.
Ileal perforation — Typhoid ileal perforation usually occurs in the third week of febrile illness and is
due to necrosis of the Peyer's patches in the antimesenteric bowel wall [49]. Affected patients
present with increasing abdominal pain, distension, peritonitis, and sometimes secondary
bacteremia with enteric aerobic and anaerobic microorganisms.
Prompt surgical intervention is usually indicated, as is wider antimicrobial coverage to cover fecal
peritonitis. The extent of surgical intervention remains controversial; the best surgical procedure
appears to be segmental resection of the involved intestine, when possible [50,51].
In a retrospective review from West Africa including 112 patients undergoing laparotomy for typhoid perforation, most of the perforations were single (80 percent) and in the terminal ileum [52]. Primary repair was successful in 84 percent of cases, although reoperative management was required in some patients who did not respond immediately. Even with surgery, mortality rates of 14, 16, and 34 percent have been reported in series from Nigeria, Togo, and the Ivory Coast.
Relapse — Relapse of typhoid fever after clinical cure can occur in immunocompetent individuals;
in such cases, it typically occurs two to three weeks after resolution of fever. Earlier studies in which the bacteriostatic agent chloramphenicol was the standard drug used noted relapse rates of 10 to 25 percent [55,56]. Most recent studies, which include multidrug resistant S. typhi infections and
newer antibiotics, have noted lower relapse rates of 1 to 6 percent. Thus, the fluoroquinolones may reduce relapse rates when the organisms are fully sensitive. An additional course of therapy with a drug to which the organism is clearly sensitive is indicated for relapsing illness. Longer treatment courses with third generation cephalosporins are also reasonable.
Chronic carriage — Chronic carriage of Salmonellae is defined as excretion of the organism in
stool for more than 12 months after the acute infection. Chronic carriage rates after S. typhi
infection range from 1 to 6 percent; rates are higher in patients with cholelithiasis or other biliary
tract abnormalities [58]. Chronic carriage occurs much more frequently with typhoidal strains than
nontyphoidal strains. (See "Approach to the patient with nontyphoidal Salmonella in a stool
culture".)
Chronic carriers do not develop recurrent symptomatic disease. They appear to have reached an
immunologic equilibrium in which they are chronically colonized, and may excrete large numbers of
organisms, but have high levels of systemic immunity and do not develop clinical disease. However,
chronic carriers represent an infectious risk to others, particularly if involved in food preparation. For this reason, eradication of carriage is usually attempted once such individuals are identified.
In the past, high dose ampicillin (4 to 6 g/day), sometimes in combination with cholecystectomy,
was frequently employed but not always successful for eradication of chronic carriage [59,60]. The
fluoroquinolones appear to be much more effective and better tolerated than ampicillin for
eradication of chronic carriage. In one study of 23 carriers, for example, the cure rate
with norfloxacin (400 mg orally twice daily for 28 days) was 86 percent in those with normal
gallbladders and 75 percent in those with gallstones [61]. Several smaller studies, evaluating 10 to
12 patients each, have found that ciprofloxacin (500 or 750 mg orally twice daily) for 14 to 28 days
eliminated carriage in 90 to 93 percent of cases [62].
Thus, attempted eradication with four weeks of fluoroquinolone therapy (eg, ciprofloxacin 500 to
750 mg orally twice daily or ofloxacin 400 mg orally twice daily) is a reasonable approach, with
subsequent consideration of additional therapy and cholecystectomy, if needed and appropriate.
Chronic urinary carriage of S. typhi is rare. It is usually associated with abnormalities of the urinary
tract such as urolithiasis or prostatic hypertrophy [63], or concurrent infection with Schistosoma
haematobium [64,65].
PREVENTION — Typhoid fever results from the ingestion of contaminated food or water. For
travelers, the main mechanism of transmission is ingestion of the local cuisine in areas where
sanitation and personal hygiene may be poor. The inoculum in food is likely higher than that in
contaminated water. (See "Travel advice", section on 'Food and water'.)
Typhoid vaccines — There are two vaccines available for protection against S. typhi: live oral S.
Typhi vaccine strain TY21a and parenteral Vi polysaccharide vaccine. Neither is completely
effective against S. typhi and neither provides protection against paratyphoid fever.
For travelers to high-risk areas such as the Indian subcontinent, typhoid vaccination may provide
protection at very little risk. In a review of laboratory-confirmed cases reported to the Centers for
Disease Control and Prevention (CDC) between 1994 and 1999, 75 percent of cases were
associated with travel; only 4 percent of these travelers had been vaccinated [66].
(See "Immunizations for travel", section on 'Typhoid vaccine'.)
In endemic areas, prevention of enteric fever would require implementing immunization for young
children. In a study including more than 37,000 children two to five years of age, the parenteral Vi
polysaccharide vaccine was useful for inducing both direct and indirect protection (overall protection was 57 percent). These data should inform further efforts in prevention of typhoid in endemic areas. Natural infection does not provide complete protection against recurrent illness (which is not the same as relapsed infection). One study suggests early treatment of natural infection may blunt humoral responses to capsular antigens [68]. Vaccination may be considered even after clinical illness, particularly in those not living in endemic areas, if re-exposure is expected. The optimal timing for vaccination following clinical illness is not known.
Experimental vaccines — Research is ongoing for alternative vaccines for the prevention of
typhoid due to the inconvenience of the oral vaccine and the frequent need for reimmunization with
both the oral and injectable formulations [69].
One vaccine far along in development follows the model of other polysaccharide-protein conjugate
vaccines (eg, Haemophilus influenzae and Streptococcus pneumoniae vaccines) by conjugating the
Vi capsular polysaccharide of S. typhi to a nontoxic recombinant Pseudomonas aeruginosa
exotoxin A. The vaccine was tested for safety, immunogenicity, and efficacy in a randomized
controlled trial in Vietnamese children ages two to five years [70]. S. typhi was isolated from 4 of
5525 children receiving two doses of vaccine compared with 47 of 5566 injected with placebo for a
91.5 percent efficacy over the subsequent 27 months. This efficacy persisted at 89 percent over 19
additional months of passive surveillance [71]. Although not yet available, this vaccine holds
promise for the immunization of individuals ≥2 years of age.
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Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on “patient info” and the keyword(s) of interest.)
· Basics topics (see "Patient information: Typhoid fever (The Basics)")
SUMMARY AND RECOMMENDATIONS
· Treatment of typhoid fever has been complicated by the development and rapid
dissemination of typhoidal organisms resistant to ampicillin, trimethoprim-sulfamethoxazole,
and chloramphenicol. In recent years, development of creeping resistance to
fluoroquinolones has resulted in more challenges. (See 'Multidrug-resistant strains' above.)
· Fluoroquinolone-resistant organisms have become a major problem worldwide. Laboratory
breakpoints for fluoroquinolone sensitivity have been decreased such that previously
nonresistant organisms may now be designated as resistant. Nalidixic acid resistance is still
a reasonable marker for decreased sensitivity to fluoroquinolones, but laboratories are
moving to direct testing for ciprofloxacin andofloxacin sensitivity. Nalidixic acid-resistant
organisms are less effectively treated with fluoroquinolones, especially "short courses" of
three to five days (such courses are very effective when used against organisms
susceptible to nalidixic acid and fluoroquinolones). (See 'Fluoroquinolone-resistant
organisms' above.)
· For treatment of severe systemic illness, we recommend antibiotic therapy
with ceftriaxone (Grade 1B). For treatment of uncomplicated illness in the absence of
known or suspected antimicrobial resistance, we suggest antibiotic therapy
with ciprofloxacin (Grade 2B). In general, fluoroquinolones should NOT be used as a firstline
treatment for typhoid fever in patients from South Asia or other regions with high rates
of fluoroquinolone resistance unless antibiotic susceptibility data demonstrate
fluoroquinolone or nalidixic acid sensitivity. For treatment of uncomplicated typhoid due to a
known or suspected quinolone-resistant isolate, we suggest antibiotic therapy
with azithromycin (Grade 2B); ceftriaxone may also be used. Antibiotics can be adjusted if
and when formal sensitivities are available. (See'Antimicrobial regimens' above.)
· For treatment of severe systemic illness with shock or coma, dexamethasone (3 mg/kg
followed by 1 mg/kg every six hours for a total of 48 hours) should be considered in addition
to antibiotic therapy. (See'Corticosteroids' above.)
· Treatment of ileal perforation requires surgical therapy in addition to antibiotic therapy.
(See 'Ileal perforation' above.)
· Relapse of typhoid fever after clinical cure can occur two to three weeks after resolution of
illness. Relapse should be treated with an additional course of antimicrobial therapy with a
drug to which the organism is known to be susceptible (See 'Relapse' above.)
· Chronic Salmonella carriage is defined as excretion of the organism in stool >12 months
after acute infection. Chronic carriers represent an infectious risk to others, particularly in
the setting of food preparation. We suggest treatment of chronic carriers with four weeks of
fluoroquinolone therapy for eradication of carriage (Grade 2C). (See 'Chronic
carriage' above.)
· Typhoid fever results from the ingestion of contaminated food or water; attention to
behavioral precautions is important for travelers to regions where sanitation and personal
hygiene may be poor. There are two vaccines available for protection against S. typhi: live
oral S. Typhi vaccine strain TY21a and parenteral Vi polysaccharide vaccine.
(See 'Prevention' above and "Immunizations for travel", section on 'Typhoid vaccine'.)
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