1. Typhoid Fever Medication

6/19/2014 Typhoid Fever Medication

http://emedicine.medscape.com/article/231135-medication#showall 1/17

Typhoid Fever Medication

Author: John L Brusch, MD, FACP; Chief Editor: Michael Stuart Bronze, MD more...

Updated: Apr 1, 2014

Antibiotics

Class Summary

Definitive treatment of typhoid fever (enteric fever) is based on susceptibility. As a general principle of antimicrobialtreatment, intermediate susceptibility should be regarded as equivalent to resistance. Between 1999 and 2006,13% of S typhi isolates collected in the United States were multidrug resistant.

Until susceptibilities are determined, antibiotics should be empiric, for which there are various recommendations.The authors of this article consider the 2003 World Health Organization (WHO) guidelines to be outdated. Theserecommend fluoroquinolone treatment for both complicated and uncomplicated cases of typhoid fever, but 38% ofS typhi isolates taken in the United States in 2006 were fluoroquinolone resistant (nalidixic acidresistant S typhi[NARST]), and the rate of multidrug resistance was 13%. (Multidrug-resistant S typhi is, by definition, resistant tothe original first-line agents, ampicillin, chloramphenicol, and trimethoprim-sulfamethoxazole.)

The particular sensitivity pattern of the organism in its area of acquisition should be the major basis of empiricantibiotic choice. It may soon become necessary to treat all cases presumptively for multidrug resistance untilsensitivities are obtained.

Note that nalidixic acid is a nontherapeutic drug that is used outside of the United States as a stand-in for

fluoroquinolones in sensitivity assays. In the United States, it is still used specifically for S typhi infection.[44, 22]

History of antibiotic resistance

Chloramphenicol was used universally to treat typhoid fever from 1948 until the 1970s, when widespreadresistance occurred. Ampicillin and trimethoprim-sulfamethoxazole (TMP-SMZ) then became treatments of choice.However, in the late 1980s, some S typhi and S paratyphi strains (multidrug resistant [MDR] S typhi or Sparatyphi) developed simultaneous plasmid-mediated resistance to all three of these agents.

Fluoroquinolones are now recommended by most authorities for the treatment of typhoid fever. They are highlyeffective against susceptible organisms, yielding a better cure rate than cephalosporins. Unfortunately, resistanceto first-generation fluoroquinolones is widespread in many parts of Asia.

In recent years, third-generation cephalosporins have been used in regions with high fluoroquinolone resistancerates, particularly in south Asia and Vietnam. Unfortunately, sporadic resistance has been reported, so it is

expected that these will become less useful over time.[44]

Mechanisms of antibiotic resistance

The genes for antibiotic resistance in S typhi and S paratyphi are acquired from Escherichia coli and other gram-negative bacteria via plasmids. The plasmids contain cassettes of resistance genes that are incorporated into aregion of the Salmonella genome called an integron. Some plasmids carry multiple cassettes and immediatelyconfer resistance to multiple classes of antibiotics. This explains the sudden appearance of MDR strains of S typhi

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and S paratyphi, often without intermediate strains that have less-extensive resistance.

The initial strains of antibiotic-resistant S typhi and S paratyphi carried chloramphenicol acetyltransferase type I,which encodes an enzyme that inactivates chloramphenicol via acetylation. MDR strains may carry dihydrofolatereductase type VII, which confers resistance to trimethoprim. Interestingly, in areas where these drugs have fallen

out of use, S typhi has reverted to wild type, and they are often more effective than newer agents.[45, 46, 47, 35]

Resistance to fluoroquinolones is evolving in an ominous direction. Fluoroquinolones target DNA gyrase andtopoisomerase IV, bacterial enzymes that are part of a complex that uncoils and recoils bacterial DNA for

transcription.[48] S typhi most commonly develops fluoroquinolone resistance through specific mutations in gyrAand parC, which code for the binding region of DNA gyrase and topoisomerase IV, respectively.

A single point mutation gyrA confers partial resistance. If a second gyrA point mutation is added, the resistanceincreases somewhat. However, a mutation in parC added to a single gyrA mutation confers full in vitro resistanceto first-generation fluoroquinolones. Clinically, these resistant strains show a 36% failure rate when treated with a

first-generation fluoroquinolone such as ciprofloxacin.[49] The risk of relapse after bacterial clearance is higher in

both partially and fully resistant strains than in fully susceptible strains.[23]

The third-generation fluoroquinolone gatifloxacin appears to be highly effective against all known clinical strains ofS typhi both in vitro and in vivo. due to its unique interface with gyrA. It achieves better results than cephalosporinseven among strains that are considered fluoroquinolone resistant. However, gatifloxacin is no longer on the market

in the United States, and its use cannot be generalized to any other member of the class.[50, 51]

In any case, as gatifloxacin replaces older fluoroquinolones in high-prevalence resistance is bound to emerge. Anytwo of a number of gyrA mutations, when added to the parC mutation, confer full in vitro resistance. Although sucha combination has yet to be discovered in vivo, all of these mutations exist in various clinic strains, and it seemshighly likely that a gatifloxacin-resistant one will be encountered clinically if selective pressure with

fluoroquinolones continues to be exerted.[49]

Geography of resistance

Among S typhi isolates obtained in the United States between 1999 and 2006, 43% were resistant to at least oneantibiotic.

Nearly half of S typhi isolates found in the United States now come from travelers to the Indian subcontinent,where fluoroquinolone resistance is endemic (see Table 3). The rate of fluoroquinolone resistance in south andSoutheast Asia and, to some extent, in East Asia is generally high and rising (see Table 3). Susceptibility tochloramphenicol, TMP-SMZ, and ampicillin in South Asia is rebounding. In Southeast Asia, MDR strains remainpredominant, and some acquired resistance to fluoroquinolones by the early 2000s.

The most recent professional guideline for the treatment of typhoid fever in south Asia was issued by the IndianAssociation of Pediatrics (IAP) in October 2006. Although these guidelines were published for pediatric typhoidfever, the authors feel that they are also applicable to adult cases. For empiric treatment of uncomplicated typhoidfever, the IAP recommends cefixime and, as a second-line agent, azithromycin. For complicated typhoid fever,

they recommend ceftriaxone. Aztreonam and imipenem are second-line agents for complicated cases.[52] Theauthors believe that the IAP recommendations have more validity than the WHO recommendations for empirictreatments of typhoid fever in both adults and children.

In high-prevalence areas outside the areas discussed above, the rate of intermediate sensitivity or resistance tofluoroquinolones is 3.7% in the Americas (P =.132), 4.7% (P =.144) in sub-Saharan Africa, and 10.8% (P =.706) inthe Middle East. Therefore, for strains that originate outside of south or Southeast Asia, the WHOrecommendations may still be validthat uncomplicated disease should be treated empirically with oral

ciprofloxacin and complicated typhoid fever from these regions should be treated with intravenous ciprofloxacin.[44,

47, 53, 24, 54]

Antibiotic resistance is a moving target. Reports are quickly outdated, and surveys of resistance may have limitedgeographic scope. Therefore, any recommendation regarding antibiotic treatment must be taken with a grain ofsalt. In the authors' opinion, if the origin of the infection is unknown, the combination of a first-generationfluoroquinolone and a third-generation cephalosporin should be used.

Table 3. Antibiotic Recommendations by Origin and Severity (Open Table in a new window)



Location Severity First-LineAntibiotics

Second-LineAntibiotics

South Asia, East Asia[52]

[55, 45]

Uncomplicated Cefixime PO Azithromycin PO

Complicated Ceftriaxone IVor

Cefotaxime IV

Aztreonam IV or

Imipenem IV

Eastern Europe, Middle East, sub-Saharan Africa, SouthAmerica[53, 56]

Uncomplicated CiprofloxacinPO or

Ofloxacin PO

Cefixime PO or

Amoxicillin PO or

TMP-SMZ PO

or Azithromycin PO

Complicated Ciprofloxacin IVor

Ofloxacin IV

Ceftriaxone IV or

Cefotaxime IV or

Ampicillin IV

or

TMP-SMZ IV

Unknown geographic origin or Southeast Asia[57, 52]

[55, 45, 53, 56]

Uncomplicated Cefixime POplus

CiprofloxacinPO or

Ofloxacin PO

Azithromycin PO*



Complicated Ceftriaxone IVor

Cefotaxime IV,plus

Ciprofloxacin IVor

Ofloxacin IV

Aztreonam IV or

Imipenem IV, plus

Ciprofloxacin IV

or

Ofloxacin IV

*Note that the combination of azithromycin and fluoroquinolones is not recommended because it may cause QTprolongation and is relatively contraindicated.

Future directions

A meta-analysis found that azithromycin appeared to be superior to fluoroquinolones and ceftriaxone with lowerrates of clinical failure and relapse respectively. Although the data did not permit firm conclusions, if further studies

confirm the trend, azithromycin could become a first-line treatment.[58]

View full drug information

Chloramphenicol (Chloromycetin)

Binds to 50S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Effectiveagainst gram-negative and gram-positive bacteria. Since its introduction in 1948, has proven to be remarkablyeffective for enteric fever worldwide. For sensitive strains, still most widely used antibiotic to treat typhoid fever. Inthe 1960s, S typh i strains with plasmid-mediated resistance to chloramphenicol began to appear and laterbecame widespread in many endemic countries of the Americas and Southeast Asia, highlighting need foralternative agents.

Produces rapid improvement in patient's general condition, followed by defervescence in 3-5 d. Reducedpreantibiotic-era case-fatality rates from 10%-15% to 1%-4%. Cures approximately 90% of patients. AdministeredPO unless patient is nauseous or experiencing diarrhea; in such cases, IV route should be used initially. IM routeshould be avoided because it may result in unsatisfactory blood levels, delaying defervescence.


Amoxicillin (Trimox, Amoxil, Biomox)

Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activityagainst susceptible bacteria. At least as effective as chloramphenicol in rapidity of defervescence and relapse rate.Convalescence carriage occurs less commonly than with other agents when organisms are fully susceptible.Usually given PO with a daily dose of 75-100 mg/kg tid for 14 d.


Trimethoprim and sulfamethoxazole (Bactrim DS, Septra)



Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Antibacterial activity of TMP-SMZ includescommon urinary tract pathogens, except Pseudomonas aeruginosa. As effective as chloramphenicol indefervescence and relapse rate. Trimethoprim alone has been effective in small groups of patients.


Ciprofloxacin (Cipro)

Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, Staphylococcus epidermidis, and mostgram-negative organisms but no activity against anaerobes. Inhibits bacterial DNA synthesis and, consequently,growth. Continue treatment for at least 2 d (7-14 d typical) after signs and symptoms have disappeared. Proven tobe highly effective for typhoid and paratyphoid fevers. Defervescence occurs in 3-5 d, and convalescent carriageand relapses are rare. Other quinolones (eg, ofloxacin, norfloxacin, pefloxacin) usually are effective. If vomiting ordiarrhea is present, should be given IV. Fluoroquinolones are highly effective against multiresistant strains andhave intracellular antibacterial activity.

Not currently recommended for use in children and pregnant women because of observed potential for causingcartilage damage in growing animals. However, arthropathy has not been reported in children following use ofnalidixic acid (an earlier quinolone known to produce similar joint damage in young animals) or in children withcystic fibrosis, despite high-dose treatment.

Cefotaxime (Claforan)

Arrests bacterial cell wall synthesis, which inhibits bacterial growth. Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms. Excellent in vitro activity against S typhi andother salmonellae and has acceptable efficacy in typhoid fever. Only IV formulations are available. Recently,emergence of domestically acquired ceftriaxone-resistant Salmonella infections has been described.


Azithromycin (Zithromax)

Treats mild to moderate microbial infections. Administered PO at 10 mg/kg/d (not exceeding 500 mg), appears tobe effective to treat uncomplicated typhoid fever in children 4-17 y. Confirmation of these results could provide analternative for treatment of typhoid fever in children in developing countries, where medical resources are scarce.


Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad-spectrum gram-negative activity against gram-positive organisms;Excellent in vitro activity against S typhi and other salmonellae.

Cefoperazone (Cefobid)

Discontinued in the United States. Third-generation cephalosporin with gram-negative spectrum. Lower efficacyagainst gram-positive organisms.


Ofloxacin (Floxin)

A pyridine carboxylic acid derivative with broad-spectrum bactericidal effect.


Levofloxacin (Levaquin)

For pseudomonal infections and infections due to multidrug-resistant gram-negative organisms.

Corticosteroids



Class Summary

Dexamethasone may decrease the likelihood of mortality in severe typhoid fever cases complicated by delirium,obtundation, stupor, coma, or shock if bacterial meningitis has been definitively ruled out by cerebrospinal fluidstudies. To date, the most systematic trial of this has been a randomized controlled study in patients aged 3-56years with severe typhoid fever who were receiving chloramphenicol therapy. This study compared outcomes in 18patients given placebo with outcomes in 20 patients given dexamethasone 3 mg/kg IV over 30 minutes followed bydexamethasone 1 mg/kg every 6 hours for 8 doses. The fatality rate in the dexamethasone arm was 10% versus

55.6% in the placebo arm (P =.003).[59]

Nonetheless, this point is still debated. A 2003 WHO statement endorsed the use of steroids as described above,

but reviews by eminent authors in the New England Journal of Medicine (2002)[4] and the British Medical Journal

(2006)[60] do not refer to steroids at all. A 1991 trial compared patients treated with 12 doses of dexamethasone400 mg or 100 mg to a retrospective cohort in whom steroids were not administered. This trial found no difference

in outcomes among the groups.[61]

The data are sparse, but the authors of this article agree with the WHO that dexamethasone should be used incases of severe typhoid fever.


Dexamethasone (Decadron)

Prompt administration of high-dose dexamethasone reduces mortality in patients with severe typhoid fever withoutincreasing incidence of complications, carrier states, or relapse among survivors.

Contributor Information and DisclosuresAuthorJohn L Brusch, MD, FACP Assistant Professor of Medicine, Harvard Medical School; Consulting Staff,Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians andInfectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)Thomas Garvey, MD, JD Primary Care Physician, Burlington Medical Associates; Co-chair, Medical AdvisoryCommittee for the Elimination of Tuberculosis

Thomas Garvey, MD, JD is a member of the following medical societies: American College of Legal Medicine,American College of Physicians, and American Society of Law, Medicine & Ethics


Roberto Corales, DO Vice President, Chief Medical Officer and Principal Investigator, AIDS Care

Roberto Corales, DO is a member of the following medical societies: American Medical Association, AmericanOsteopathic Association, and International AIDS Society


Steven K Schmitt, MD Staff Physician, Department of Infectious Disease, Cleveland Clinic

Steven K Schmitt, MD is a member of the following medical societies: Infectious Diseases Society of America


Specialty Editor BoardFrancisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical CenterCollege of Pharmacy; Editor-in-Chief, Medscape Drug Reference



Disclosure: Medscape Salary Employment

Richard B Brown, MD, FACP Chief, Division of Infectious Diseases, Baystate Medical Center; Professor,Department of Internal Medicine, Tufts University School of Medicine

Richard B Brown, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, AmericanCollege of Chest Physicians, American College of Physicians, American Medical Association, AmericanSociety for Microbiology, Infectious Diseases Society of America, and Massachusetts Medical Society


Chief EditorMichael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart GWolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health ScienceCenter

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, AmericanCollege of Physicians, American Medical Association, Association of Professors of Medicine, InfectiousDiseases Society of America, Oklahoma State Medical Association, and Southern Society for ClinicalInvestigation


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