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Antibiotic therapy for Shigella dysentery

  1. Prince Christopher1,*,
  2. Kirubah V David2,
  3. Sushil M John2,
  4. Venkatesan Sankarapandian2

Editorial Group: Cochrane Infectious Diseases Group

Published Online: 8 JUL 2009

DOI: 10.1002/14651858.CD006784

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Christopher P, David KV, John SM, Sankarapandian V. Antibiotic therapy for Shigella dysentery (Protocol). Cochrane Database of Systematic Reviews 2007, Issue 4. Art. No.: CD006784. DOI: 10.1002/14651858.CD006784.

Author Information

  1. 1

    Christian Medical College, Family Medicine, Vellore, Tamilnadu, India

  2. 2

    Christian Medical College, LCECU, Vellore, Tamil Nadu, India

*Prince Christopher, Family Medicine, Christian Medical College, Vellore, Tamilnadu, 632004, India. prince.christopher@gmail.com.

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  1. Publication Status: Unchanged
  2. Published Online: 8 JUL 2009

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Background

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. What's new
  8. History
  9. Contributions of authors
  10. Declarations of interest
  11. Sources of support

Shigellosis is a bacterial infection of the colon that causes diarrhoea and can lead to death. Dysentery (frequent mucoid or bloody stools) when caused by Shigella is called Shigella dysentery. Of the estimated 164.7 million Shigella diarrhoeal episodes occurring globally every year, most occur in developing countries (99%) and mainly in children (69%) (WHO 2006). Of the 1.1 million deaths due to Shigella, 69% are in children aged less than five years (Kotloff 1999; WHO 2006).

 

Microbiology and mode of spread

Shigella dysenteriae, S. flexneri, S. sonnei, and S. boydii are the four species of these small, Gram-negative, non-motile bacilli that cause shigellosis, and all but S. sonnei have more than one genetically distinct subtype (serotype) (von Seidlein 2006). The species distribution varies globally; for example, S. flexneri was reported to be most prevalent in India (58%, Dutta 2002) and Rwanda (68%, Bogaerts 1983), while S. sonnei was most frequently detected species in Thailand (85%, von Seidlein 2006), Israel (48.8%, Mates 2000), and the USA (75%, Gupta 2004; Shiferaw 2004).

Shigellae are transmitted by the faeco-oral route, via direct person-to-person contact, and via food, water, and inanimate objects. Only a small number of ingested bacteria are required to produce illness. The disease is communicable as long as an infected person excretes the organism in the stool, which can extend up to four weeks from the onset of illness. Secondary attack rates, the number of exposed persons developing the disease within one to four days following exposure to the primary case (Park 2005), can be as high as 40% among household contacts (Sur 2004)

Shigellosis occurs predominantly in developing countries and is most common where overcrowding and poor sanitation exists. It occurs in densely populated areas and institutions where populations are in close contact with each other, such as day-care centres, cruise ships, institutions for people with mental or psychological problems, and military barracks (Shane 2003; Gupta 2004).

 

Relapse

Clinical relapse can occur. This manifests as an initial clinical improvement or apparent cure with the treatment, followed by the recurrence of diarrhoea after the course of drug treatment is completed. In some instances people have sought the continued presence of Shigella in cultures of stool after the treatment, irrespective of apparent clinical recovery and have documented these as bacteriological failures (Martin 2000), indicative of the potential for relapse. Relapse is an important indicator of treatment failure, though it is clinically difficult to differentiate a relapse of infection with the same species or serotype of Shigella without additional testing for Shigella DNA using polymerase chain reaction (PCR) analysis (von Seidlein 2006).

 

Shigella and HIV infection

Human immunodeficiency virus (HIV) infection may be an important risk factor for Shigella infection. Particularly in HIV-positive people, shigellosis is associated with extensive illness, including Shigella septicaemia, and increased health-care expenditures; the diagnosis of shigellosis in an otherwise healthy adult person could serve as a marker for HIV infection (Huebner 1993; Baer 1999).

 

Mortality

The case-fatality rate is estimated to be less than 1% among those with mild illness, which is usually self-limiting, and those affected are usually treated as outpatients. However, case fatality is as high as 15% among patients with S. dysenteriae type 1 who require hospitalization; this rate is increased by delayed arrival and treatment with ineffective antibiotics. Infants, non-breastfed children, children recovering from measles, malnourished children, and adults older than 50 years have a more severe illness and a greater risk of death (WHO 2005a).

 

Clinical features

The clinical manifestation of shigellosis ranges from an asymptomatic illness to bacteraemia and sepsis. Symptoms include fever, diarrhoea and/or dysentery with abdominal cramps and ineffectual and painful straining at stool or in urinating (Niyogi 2005). Shigellosis may be associated with mild to life-threatening complications, such as rectal prolapse, arthralgia (painful joints), arthritis, intestinal perforation, and toxic mega colon (extreme inflammation and distension of the colon), central nervous disorders, convulsions, enteropathy (protein-losing disease of the intestines), electrolyte imbalance of salts, and sepsis (Sur 2004; WHO 2005b). About 3% of those infected with S. flexneri and who are genetically predisposed can develop Reiter's syndrome (pains in their joints, irritation of the eyes, and painful urination) that can lead to a difficult-to-treat chronic arthritis (CDC 2005). Haemolytic uraemic syndrome (a complication resulting in kidney failure, bleeding, and anaemia) and leukemoid reaction (blood findings resembling leukaemia) complicate infection due to S. dysenteriae type 1 and may be fatal (Sinha 1987). S. dysenteriae type 1 is the only Shigella species with chromosomal genes encoding the protein known as Shiga toxin (Thorpe 2001).

 

Diagnosis

The clinical features of fever, blood, and/or mucus diarrhoea associated with abdominal pain suggest that the aetiology of diarrhoea is Shigella. Routine microscopy of fresh stool is a simple screening test that is cheap, rapid, and easy to perform; and visualization of numerous polymorphonucleocytes suggests a bacterial aetiology. Definite diagnosis of shigellosis can only be made by stool culture (WHO 2005a). However, Shigella species die rapidly in unfavourable environments and stool culture should ideally be supplemented by attempts to identify Shigella DNA using polymerase chain reaction (von Seidlein 2006).

 

Treatment

When an effective antibiotic is given, clinical improvement is seen in 48 hours in the form of fewer stools, less blood in the stools, less fever, and improved appetite (WHO 2005a). This lessens the risk of serious complications and death, shortens the duration of symptoms, and hastens the elimination of Shigella (WHO 2005a). The World Health Organization (WHO) recommends that all suspected cases of shigellosis based on clinical features be treated with effective antimicrobials. The choice of antimicrobial drug has changed over the years as resistance to antibiotics has occurred, with different patterns of resistance being reported around the world. The following antibiotics were recommended for use against Shigella dysentery: nalidixic acid, ampicillin, chloramphenicol, co-trimoxazole, tetracycline, first- and second-generation cephalosporins, and amoxicillin. But the WHO guidelines list them as ineffective against Shigella. (WHO 2005a). The WHO now recommends that clinically diagnosed cases be treated with ciprofloxacin (a quinolone) as first-line treatment and pivmecillinam, ceftriaxone, or azithromycin as second-line treatment (WHO 2005a). However, resistance to quinolones has also been observed since the late 1990s (Datta 2003; Sarkar 2003; Sur 2003; Pazhani 2004; Talukder 2004).

Since the antibiotics used for treating shigellosis can have adverse effects (Appendix 1), some life-threatening, the clinician is faced with a dilemma in choosing an appropriate drug to treat shigellosis. This drug must be effective, locally available at affordable costs, and be associated with minimum adverse effects. We undertook this review in the hope of identifying such a drug or group of drugs.

 

Objectives

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. What's new
  8. History
  9. Contributions of authors
  10. Declarations of interest
  11. Sources of support

To evaluate the efficacy and safety of antibiotics for treating Shigella dysentery.

 

Methods

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. What's new
  8. History
  9. Contributions of authors
  10. Declarations of interest
  11. Sources of support
 

Criteria for considering studies for this review

 

Types of studies

Randomized controlled trials.

 

Types of participants

Adults and children with clinical symptoms suggestive of Shigella dysentery. Both hospitalized and non-hospitalized participants will be included.

 

Types of interventions

 

Intervention

Antibiotics, irrespective of the dose or route of administration.

 

Control

Other antibiotic (irrespective of the dose or route of administration), placebo, or no drug.

We will include trials that used additional interventions if the interventions were used in all treatment arms.

 

Types of outcome measures

 

Primary

  • Diarrhoea at follow up.
  • Relapse, defined as the reappearance of diarrhoea associated with Shigella in the stool or dysentery during follow up.

 

Secondary

  • Fever at follow up: defined as body's temperature above 37.0 ºC or 98.6 ºF.
  • Time to cessation of fever.
  • Time to cessation of diarrhoea.
  • Time to cessation of blood in stools.
  • Total number of stools per day.
  • Bacteriological cure: defined as a negative stool culture at the end of a specified time period after treatment.
  • Duration of hospital stay.
  • Development of severe complications.
  • Death.

 

Adverse events

  • Serious adverse events (ie those that are life-threatening or require hospitalization).
  • Those that lead to discontinuation of treatment.
  • Other types of adverse events.

 

Search methods for identification of studies

We will attempt to identify all relevant trials regardless of language or publication status (published, unpublished, in press, and in progress).

We will search the following databases using the strategies and search terms in Appendix 2: Cochrane Infectious Disease Group Specialized Register; Cochrane Central Register of Controlled Trials (CENTRAL), published in The Cochrane Library; MEDLINE; EMBASE; and LILACS. We will also search the metaRegister of Controlled Trials (mRCT) using 'shigell*' as the search term.

We will search the following conference proceedings listed in Appendix 3 for relevant abstracts, contact individual researchers working in the field and the organizations in Appendix 3 to help identify unpublished and ongoing trials, and contact pharmaceutical companies including those listed in Appendix 3 to help identify unpublished and ongoing trials.

We will also check the reference lists of all studies identified by the above methods.

 

Data collection and analysis

 

Selection of studies

The authors will work in pairs (PC and KVD as one pair, and SMJ and VS as the second pair). Each pair of authors will independently assess the results of the literature search to determine whether the title or abstract of each trial cited is a randomized controlled trial. We will retrieve the full reports of all trials considered by one or both pairs of authors as potentially relevant as well as those that are unclear. Each pair will use a standard eligibility form based on the inclusion and exclusion criteria to assess the trials. We will resolve disagreements through discussion. If eligibility is unclear due to unclear or inadequate information, we will attempt to contact the trial authors for clarification. The reason for excluding studies will be noted. Each trial report will be scrutinized to ensure that multiple publications from the same trial are included only once, and all reports will be linked to the original trial report in the reference list of included studies.

 

Data extraction and management

The pairs of authors will independently extract data from the trials using pre-tested data extraction forms. We will extract data such as the inclusion and exclusion criteria for the participants, treatment/intervention given, total number randomized, number of participants in each group for all outcomes, dropouts and withdrawals and numbers experiencing each outcome. For every outcome, we will extract the number analysed and the number randomized in each treatment group to allow for the assessment of losses to follow up. Any disagreements about data extracted will be resolved by referring to the trial report and by discussion. Where data are insufficient or missing, attempts will be made to contact the trial authors.

Where possible, we will extract data to allow an intention-to-treat analysis in which all randomized participants will be analysed in the groups to which they were originally assigned. If there is discrepancy in the number randomized and the numbers analysed in each treatment group, we will calculate the percentage loss to follow up in each group and report this information. For dichotomous outcomes, we will record the number of participants experiencing the event and the number analysed in each treatment group. We will assign those lost to follow up the worse outcome, except for the outcome of death.

For continuous outcomes, we will aim to extract the arithmetic mean values, standard deviations, and number of participants on whom the outcome was assessed in each of the two groups. We will note whether the numbers assessed in the trial were the number of participants that completed the trial or the number randomized. If medians have been reported we will aim to extract ranges, or interquartile ranges.

If outcomes are reported both at baseline and at a follow up or at trial endpoints, we will extract both the mean change from baseline and the standard deviation of this mean for each treatment group. We will also extract the means and standard deviation at baseline and follow up in each treatment group. If the data have been reported using geometric means, we will record this information and extract a standard deviation on the log scale.

For count data, we will aim to extract the total number of events in each group and the total amount of person-time at risk in each group. We will also record the total number of participants in each group. If this information is not available, we extract alternative summary statistics such as rate ratios and confidence intervals if available.

If count data are presented as dichotomous outcomes, we will extract the number of participants in each intervention group and the number of participants in each intervention group who experience at least one event. If count data are presented continuous outcomes or as a time-to-event outcomes, we will extract the same information are outlined for continuous and time-to-event outcomes.

For time-to-event outcomes, we will aim to extract estimates of the log hazard ratio and its standard error. If standard errors are not available we will extract alternative statistics such as confidence intervals or P values.

 

Assessment of risk of bias in included studies

The pairs of authors will independently assess the generation of allocation sequence and allocation concealment as adequate, inadequate, or unclear according to Jüni 2001. We will describe who was blinded to the intervention (eg patients, providers, and/or assessors). We will record follow up to be adequate if more than 90% of the randomized participants were included in the final analysis, inadequate if less than or equal to 90%, or unclear if this information is not available from the report or trial authors. We will present the results of the quality assessment in tables, and, should there be sufficient trials, use the assessment to perform a sensitivity analysis based on methodological quality. When details of the methodological quality are unclear we will contact the trial authors for clarification. We will resolve differences by discussion and if needed by contacting an Editor with the Cochrane Infectious Diseases Review Group.

 

Assessment of reporting biases

If there are sufficient trials, we will look for asymmetry in a funnel plot of the standard error plotted against the risk ratio measured on a logarithmic scale for primary outcomes as an indication of publication bias. Asymmetry in the funnel plot may indicate publication bias, heterogeneity, and poor methodological quality of smaller studies.

 

Data synthesis

The first two authors will enter data into Review Manager 5 using double-data entry. PC will synthesize the data, which the co-authors will check. All results will be presented with 95% confidence intervals.

The main comparisons will be between any antibiotic drug and placebo, and any antibiotic drug and another antibiotic drug. Due to the variety of combinations of different treatments and different comparators, it may not be possible to combine all included trials in a single meta-analysis. When there is more than one trial comparing similar interventions and comparison groups, we will prepare separate meta-analyses for each combination: (1) an antibiotic drug versus another antibiotic drug belonging to the same or different drug class; (2) antibiotic drugs grouped by drug class versus other antibiotic drugs belonging to a different drug class; and (3) monotherapy with any antibiotic drug versus combination drug therapy with two or more different drugs given together or sequentially.

We will synthesize dichotomous data using pooled and weighted risk ratios. Continuous data summarized by arithmetic means and standard deviations data will be combined using the mean differences. Where continuous data are summarized using geometric means, we will combine them on the log scale using the generic inverse variance method and report them on the natural scale. Medians and ranges will be reported in a table. Count data will be compared using rate ratios when the total number of events in each group and the total amount of person-time at risk in each group are available, or by risk ratios or mean difference when the data have been presented in dichotomous or continuous forms respectively. Hazard ratios from survival data will be combined on the log scale using the inverse variance method and presented on the natural scale.

 

Subgroup analysis and investigation of heterogeneity

We will determine the presence of statistical heterogeneity among the same interventions by examining the forest plot and by performing the chi-squared test for heterogeneity using a P value of 0.10 to determine statistical significance. The I2 test will also be used to quantify inconsistency across trials and a value greater than 50% will be considered as substantial heterogeneity (Deeks 2005). When there is significant statistical heterogeneity, we will aim explore the possible sources of heterogeneity using the following subgroup analyses: participant age (adults versus children); and percentage of participants with confirmed Shigella infection.

 

Sensitivity analysis

We will perform sensitivity analyses for primary outcomes to assess the robustness of the meta-analysis among the same interventions by calculating the results using all trials and then excluding trials of a lower methodological quality (ie trials with inadequate generation of allocation sequence and allocation concealment, trials that were not double blind, and trials where less than or equal to 90% of randomized participants were analysed).

 

Acknowledgements

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. What's new
  8. History
  9. Contributions of authors
  10. Declarations of interest
  11. Sources of support

We acknowledge the support of Sara Bhattcharjee, Prathap Tharyan, Gagandeep Kang, and Thambu David Sudarsanam. This protocol was developed after attendance at a protocol development workshop funded by the Effective Health Care Research Programme Consortium (with funds from the Department for International Development (DFID), UK) of which Prathap Tharyan is a Programme Partner. The views expressed are not necessarily those of DFID.

 

Appendices

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. What's new
  8. History
  9. Contributions of authors
  10. Declarations of interest
  11. Sources of support
 

Appendix 1. Known adverse effects of antibiotics used to treat Shigella dysenterya

AntibioticLife-threateningDiscontinuationbOther
TetracyclineAnaphylaxisOesophageal irritation, antibiotic-associated colitis, headache and visual disturbancesIn children under 12 years of age causes dental hypoplasia and staining, benign intracranial hypertension
ChloramphenicolBlood disorders, peripheral and optic neuritis, erythema multiformeDyspepsia—
AmpicillinHypersensitivity reactionsDiarrhoea—
Co-trimoxazole or trimethoprim-sulfamethoxazoleStevens-Johnson syndromeDiarrhoea, rash—
QuinolonesHypersensitivityDyspepsia, headache, hypotensionPruritis, tachycardia
Norfloxacin—Dyspepsia, headache, hypotensionEuphoria, tinnitus, polyneuropathy
Ciprofloxacin—Dyspepsia, headache, hypotensionHot flushes, sweating, tenosynovitis
Ofloxacin—Dyspepsia, headache, hypotensionAnxiety, unsteady gait
AzithromycinHypersensitivityDyspepsia, flatulence, headache—
CeftriaxoneHypersensitivity reactionsDiarrhoea, headache, abdominal discomfort—
Nalidixic acid—Same as in quinolonesToxic psychosis, increased intracranial tension, cranial nerve palsy
RifaximinAllergic reactionsFlatulence, headache, abdominal pain, defecation urgency, nausea, constipation, pyrexia, vomiting—
CefiximeHypersensitivity reactionsDiarrhoea, headache, abdominal discomfort—
Pivmecillinam—Same as ampicillin, dyspepsia—


aSource: BNF 2007.
bCan result in discontinuation of treatment.

 

Appendix 2. Search methods: detailed search strategies

Search setCIDG SRaCENTRALMEDLINEbEMBASEbLILACSb
1shigell*shigell*shigell*shigell$shigell*
2dysenteryDYSENTERY, BACILLARYDYSENTERY, BACILLARYSHIGELLOSISdysentery
31 or 21 or 21 or 2DYSENTERY1 or 2
4antibiotic*ANTI-BACTERIAL AGENTS/THERAPEUTIC USEANTI-BACTERIAL AGENTS/THERAPEUTIC USE1 or 2 or 3antibiotic*
5tetracycline*ANTI-INFECTIVE AGENTS/THERAPEUTIC USEANTI-INFECTIVE AGENTS/THERAPEUTIC USEtetracycline$tetracycline*
6chloramphenicolantibiotic*antibiotic*chloramphenicolchloramphenicol
7ampicillin*tetracycline*tetracycline*ampicillinampicillin
8co-trimoxazolechloramphenicolchloramphenicolco-trimoxazoleco-trimoxazole
9fluoroquinolone*ampicillinampicillinfluoroquinolone$fluoroquinolone*
10quinolone*co-trimoxazoleco-trimoxazolequinolone$quinolone*
11norfloxacinfluoroquinolone*fluoroquinolone*norfloxacinnorfloxacin
12ciprofloxacinquinolone*quinolone*ciprofloxacinciprofloxacin
13ofloxacinnorfloxacinnorfloxacinofloxacinofloxacin
14azithromycinciprofloxacinciprofloxacinazithromycinazithromycin
15ceftriaxoneofloxacinofloxacinceftriaxoneceftriaxone
16nalidixic acidazithromycinazithromycinnalidixic acidnalidixic acid
17pivmecillinamceftriaxoneceftriaxonerifaximinrifaximin
184-17/ornalidixic acidnalidixic acidcefiximecefixime
193 and 18rifaximinrifaximintrimethoprim-sulfamethoxazoletrimethoprim-sulfamethoxazole
20—cefiximecefiximeantibiotic$pivmecillinam
21—trimethoprim-sulfamethoxazoletrimethoprim-sulfamethoxazolepivmecillinam4-20/or
22—pivmecillinampivmecillinam5-21/or3 and 21
23—4-22/or4-22/orLimit 22 to human—
24—3 and 233 and 23——
25——Limit 24 to human——


aCochrane Infectious Diseases Group Specialized Register.
bSearch terms used in combination with the search strategy for retrieving trials developed by The Cochrane Collaboration (Higgins 2006); upper case: MeSH or EMTREE heading; lower case: free text term.

 

Appendix 3. Search methods: conference proceedings, organizations, and pharmaceutical companies

TypeDetail
Conference proceeding- Commonwealth Congress on Diarrhoea and Malnutrition: 8th, Dhaka, Bangladesh, 6 to 8 February 2006
- Asian Conference on Diarrhoeal Diseases and Nutrition: 10th, Dhaka, Bangladesh, 7 to 9 December 2003
- Annual Scientific Conference: 10th Dhaka, Bangladesh, 11 to 13 June 2002
- Annual Meeting of Infectious Disease Society of America: 44th, Toronto, Ontario, Canada, 12 to 15 October 2006; 43rd, San Francisco, California, 6 to 9 October 2005; 42nd, Boston, Massachusetts, USA, 30 September to 3 October 2004
- Interscience Conference on Antimicrobial Agents and Chemotherapy: 46th, San Francisco, California, 27 to 30 September 2006; 45th, Washington DC, USA, 16 to 19 December 2005; 44th, Washington DC, USA, 30 October to 2 November, 2004
- European Congress of Clinical Microbiology and Infectious Diseases: 16th, Nice, France, 1 to 4 April 2006; 15th, 2 to 5 April 2005
- International Congress on Infectious Diseases: 12th, Lisbon, Portugal, 15 to 18 June 2006; 11th, Cancun, Mexico, 4 to 7 March 2004
- Annual Meeting of The European Society for Paediatric Infectious Disease: 24th, Basel, Switzerland, 3 to 5 May 2006
- Western Pacific Congress of Chemotherapy and Infectious Diseases: 10th, Fukuoka, Japan, 3 to 6 December 2006
- European Congress of Chemotherapy and Infection: 8th, Budapest, Hungary, 25 to 28 October 2006
Organizations- Liverpool School of Tropical Medicine
- World Health Organization
- American Society of Tropical Medicine and Hygiene
- International Society of Tropical Pediatrics
- South East Asian Ministers Education Organization (SEAMEO) TROPMED Network
- International Center for Diarrhoeal Disease Research in Bangladesh
Pharmaceutical companies- Goldshield Pharmaceuticals Ltd (tetracycline, Deteclo; chloramphenicol, Chloromycetin)
- Chemidex (ampicillin, Penbritin)
- GlaxoSmithKline (co-trimoxazole, Septrin)
- Merck Sharp & Dohme Ltd (norfloxacin, Utinor)
- Bayer (ciprofloxacin, Ciproxin)
- Aventis Pharma (ofloxacin, Tarivid)
- Pfizer (azithromycin, Zithromax)
- Roche (ceftriaxone, Rocephin)
- Rosemont Pharmaceuticals Ltd (nalidixic acid, Uriben)
- Salix Pharmaceuticals (rifaximin, Xifaxan)
- Rhone-Poulenc Rorer (cefixime, Suprax)
- LEO pharma (pivmecillinam, Selexid)


 

What's new

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. What's new
  8. History
  9. Contributions of authors
  10. Declarations of interest
  11. Sources of support

DateEventDescription
11 November 2008AmendedConverted to new review format with minor editing.


 

History

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. What's new
  8. History
  9. Contributions of authors
  10. Declarations of interest
  11. Sources of support

Protocol first published: Issue 4, 2007

 

Contributions of authors

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. What's new
  8. History
  9. Contributions of authors
  10. Declarations of interest
  11. Sources of support

PC conceived the review and drafted the protocol. KVD, SMJ, and VS helped develop the protocol.

 

Declarations of interest

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. What's new
  8. History
  9. Contributions of authors
  10. Declarations of interest
  11. Sources of support

None known.

 

Sources of support

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. What's new
  8. History
  9. Contributions of authors
  10. Declarations of interest
  11. Sources of support
 

Internal sources

  • Low Cost Effective Care Unit, Christian Medical College, Vellore, India.
  • South Asian Cochrane Network, India.

 

External sources

  • Department for International Development (DFID), UK.

References

Additional references

  1. Top of page
  2. Abstract
  3. Background
  4. Objectives
  5. Methods
  6. Acknowledgements
  7. Appendices
  8. What's new
  9. History
  10. Contributions of authors
  11. Declarations of interest
  12. Sources of support
  13. Additional references
Baer 1999
  • Baer JT, Vugia DJ, Reingold AL, Aragon T, Angulo FJ, Bradford WZ. HIV infection as a risk factor for shigellosis. Emerging Infectious Diseases 1999;5(6):820-3.
BNF 2007
  • British National Formulary (BNF 53). www.bnf.org/bnf/ March 2007 (accessed 13 June 2007).
Bogaerts 1983
  • Bogaerts J, Verhaegen J, Munyabikali JP, Mukantabana B, Lemmens P, Vandeven J, et al. Antimicrobial resistance and serotypes of Shigella isolates in Kigali, Rwanda (1983 to 1993): increasing frequency of multiple resistance. Diagnostic Microbiology and Infectious Disease 1997;28(4):165-71.
CDC 2005
  • Center for Disease Control and Prevention, Division of Bacterial and Mycotic Diseases. Shigellosis. www.cdc.gov/node.do/id/0900f3ec8000755c 13 October 2005 (accessed 13 June 2007).
Datta 2003
  • Datta D, Bhattacharya MK, Dutta S, Daatta A, Sarkar D, Bhandra B. Emergence of multidrug resistant Shigella dysenteriae type 1 causing sporadic outbreak in and around Kolkata, India. Journal of Health, Population, and Nutrition 2003;21(1):79-80.
Deeks 2005
  • Deeks JJ, Higgins, JPT, Altman DG, editors. Analysing and presenting results. In: Higgins JPT, Green S, editors. Cochrane Handbook for Systematic Reviews of Interventions 4.2.5 [updated May 2005]; Section 8. www.cochrane.org/resources/handbook/hbook.htm (accessed 31 May 2005).
Dutta 2002
  • Dutta S, Rajendran K, Roy S, Chatterjee A, DuttaP, Nair GB, et al. Shifting serotypes, plasmid profile analysis and antimicrobial resistance pattern of shigellae strains isolated from Kolkata, India during 1995-2000. Epidemiology and Infection 2002;129(2):235-43.
Gupta 2004
  • Gupta A, Polyak CS, Bishop RD, Sobel J, Mintz ED. Laboratory-confirmed shigellosis in the United States, 1989-2002: epidemiologic trends and patterns. Clinical Infectious Diseases 2004;38(10):1372-7.
Higgins 2006
  • Higgins JPT, Green S, editors. Highly sensitive search strategies for identifying reports of randomized controlled trials in MEDLINE. Cochrane Handbook for Systematic Reviews of Interventions 4.2.6 [updated September 2006]; Appendix 5b. www.cochrane.org/resources/handbook/hbook.htm (accessed 1 February 2007).
Huebner 1993
  • Huebner J, Czerwenka W, Gruner E, von Graevenitz A. Shigellemia in AIDS patients: case report and review of the literature. Infection 1993;21(2):122-4.
Jüni 2001
  • Jüni P, Altman DG, Egger M. Systematic reviews in health care: Assessing the quality of controlled clinical trials. BMJ 2001;323(7303):42-6.
Kotloff 1999
  • Kotloff KL, Winickoff JP, Ivanoff B, Clemens JD, Swerdlow DL, Sansonetti PJ, et al. Global burden of Shigella infections: implications for vaccine development and implementation of control strategies. Bulletin of the World Health Organization 1999;77(8):651-66.
Martin 2000
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