MyEClinic
MyEClinic
Health Dictionary Find a Doctor

Typhoid fever

This page is about clinical aspects of the disease.  For microbiologic aspects of the causative organism(s), see Salmonella typhi.

For patient information click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Aslam, M.B.B.S[2]

Synonyms and keywords: Enteric fever

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Aslam, M.B.B.S[2]

Overview

Typhoid fever, also known as enteric fever and Salmonella typhi infection,[1] is an illness caused by the bacterium Salmonella enterica serovar typhi. Common worldwide, it is transmitted through the fecal-oral route—the ingestion of food or water contaminated with feces from an infected person.[2] The bacteria then multiply in the bloodstream of the infected person and are absorbed into the digestive tract and eliminated as waste.

Historical perspective

Around 430–426 B.C., a devastating plague, which some believe to have been typhoid fever, killed one-third of the population of Athens, including Pericles, the state’s leader. A 2006 study detected DNA sequences similar to those of the bacterium responsible for typhoid fever in a DNA sample dating back to the time of the epidemic.[3] Other scientists have disputed the findings, citing serious methodologic flaws in the dental pulp-derived DNA study.[4]

The most notorious carrier of typhoid fever—though by no means the most destructive—was Mary Mallon, also known as Typhoid Mary. In 1907, Mallon became the first American carrier to be identified and traced. She was a cook in New York who was believed to be the source of infection for several hundred people. She is closely associated with forty-seven cases of the illness and three deaths.

In 1897, Almroth Edward Wright developed an effective vaccine for typhoid fever. Antibiotics were introduced in clinical practice in 1942, greatly reducing mortality.

Classification

There is no established classification system for typhoid fever. However, typhoid fever may be informally classified based on duration of illness, serologic type, severity of illness, and virulence factors.[5]

Pathophysiology

The sequence of events in the pathogenesis of typhoid fever include innoculation, gastrointestinal infection, systemic involvement, and chronic carrier state.[5][6][7][8][9][10][11][12][13][14][15] The presence of the C282Y mutation and CFTR polymorphisms may confer protection against typhoid fever. [16][17][18]

Causes

Typhoid fever is caused by Salmonella enterica serotype Typhi (Salmonella Typhi).[19][20][21][22][23][24] Salmonella Typhi is a flagellated, facultatively anaerobic, gram negative bacillus that belongs to the Enterobacteriaceae family and contains three important antigens: O, H, and Vi.[25]

Differentiating typhoid fever from other diseases

Typhoid fever must be differentiated from other diseases that cause fever, diarrhea, and dehydration, such as Ebola, Shigellosis, Malaria, Lassa fever, Brucellosis, Viral hepatitis, leptospirosis, rheumatic fever, typhus, appendicitis, dengue fever, toxoplasmosis, rickettsial diseases, leishmaniasis, tuberculosis, and mononucleosis.[26][27][5][28][29]

Epidemiology and Demographics

  • An estimated 16-33 million cases of typhoid result in 500,000 to 600,000 deaths annually. In 2000, typhoid fever caused an estimated 21.7 million illnesses and 217,000 deaths.[30][31]
  • Worldwide, typhoid fever is most prevalent in overcrowded areas with poor hygiene and sanitation. Typhoid fever remains common in the developing world, where it affects about 21.5 million people each year. 1-6% of infected individuals will develop a chronic infection in the gall bladder.[32][33]
  • The incidence of typhoid fever varies in different parts of world.[34][29][35] Age, race, gender, and certain environmental factors affect the distribution of disease among different groups.[36][37][38]

Risk factors

Common risk factors in the development of typhoid fever are:[39][40][41][42][43][44]

  • travel to endemic areas
  • poor hygiene habits
  • poor sanitation conditions
  • contact with recently infected person
  • recent use of antibiotics
  • achlorhydria

Screening

There are no screening guidelines for typhoid fever. However, chronic carriers can be screened using ELISA to detect antibodies against the Vi antigen.[45][33]

Natural history, complications and prognosis

Diagnosis

The diagnosis of typhoid fever is based on history, physical examination, labortary findings, and other diagnostic tests and imaging studies.

History and Symptoms

Physical Examination

Physical examination findings are dependent upon the timing of presentation. Common physical examination findings for a patient presenting early in the course of the disease include stepwise increase in temperature, bradycardia, abdominal tenderness, and hepatosplenomegaly.[61] In the third week of illness or later, a patient may present with signs of complications.[5][62]

Laboratory Findings

Laboratory findings consistent with the diagnosis of typhoid fever include:[63][5][64][65][66]

X ray

X ray findings may be helpful in diagnosing complications of typhoid fever such as lobar pneumonia, intestinal perforation and osteomyelitis.[67][68][69][70][71]

Other diagnostic tests

Other diagnostic studies associated with typhoid fever include microbial culture, serology and PCR. However, microbial culture is the gold standard tests for diagnosing typhoid fever.[5][64][72][73][72][74][75][73][76][72][75][77][78][79][80]

CT

CT scans are commonly reserved for patients with complications of typhoid fever such as intestinal perforation, bleeding, and abscess formation. CT scans may be helpful in differentiating typhoid fever from other diseases.[81]

MRI

MRI may be helpful in diagnosing complications of typhoid fever such as neurological complications, liver and splenic abscesses, osteomyelitis, and typhoid spine.[82][83]

Ultrasound

Ultrasonography may be helpful in diagnosing complications of typhoid fever and differentiating it from other diseases presenting with similar symptomatology.[84][68][69][27]

Other Imaging Findings

Other imaging findings which may be helpful in diagnosing complications of typhoid fever and differentiaing it from other conditions presenting with similar symptoms include barium enema, upper endoscopy, echocardiography, and ECG.[85][86][87][88][89]

Treatment

Medical Therapy

The mainstay of therapy for typhoid fever is antimicrobial therapy. Patients with uncomplicated typhoid fever are treated with either Azithromycin or a fluoroquinolone, whereas patients with severe or complicated forms of the disease are treated with either Ceftriaxone, Cefotaxime, or a fluoroquinolone.

Primary Prevention

Effective measures for the primary prevention of typhoid fever include vaccination, improving personal hygiene and sanitation,[90] ensuring proper sewage disposal, avoiding overcrowding, and avoiding close contact or sharing utensils with people already suffering from typhoid.[91][92][93][94][5][28][95][96][28]

Secondary Prevention

There are no established guidelines for secondary prevention of typhoid fever. However, early diagnosis and prompt and adequate treatment—including the administration of antibiotics, good nursing care, maintenance of fluid electrolyte balance, adequate nutrition,[97] steroids in severe cases,[49] and cholecystectomy—may help prevent development of the chronic carrier state.[98]

References

  1. ↑ Kotton C. Typhoid fever. MedlinePlus. URL: http://www.nlm.nih.gov/medlineplus/ency/article/001332.htm. Accessed on: May 4, 2007.
  2. ↑ Giannella RA (1996). “Salmonella”. Baron’s Medical Microbiology (Baron S et al, eds.) (4th ed. ed.). Univ of Texas Medical Branch. ISBN 0-9631172-1-1.
  3. ↑ Papagrigorakis MJ, Yapijakis C, Synodinos PN, Baziotopoulou-Valavani E (2006). “DNA examination of ancient dental pulp incriminates typhoid fever as a probable cause of the Plague of Athens”. Int J Infect Dis. 10 (3): 206–14. PMID 16412683}.
  4. ↑ Shapiro B, Rambaut A, Gilbert M (2006). “No proof that typhoid caused the Plague of Athens (a reply to Papagrigorakis et al.)”. Int J Infect Dis. 10 (4): 334–5, author reply 335–6. PMID 16730469.
  5. ↑ 5.0 5.1 5.2 5.3 5.4 5.5 5.6 Parry CM, Hien TT, Dougan G, White NJ, Farrar JJ (2002). “Typhoid fever”. N Engl J Med. 347 (22): 1770–82. doi:10.1056/NEJMra020201. PMID 12456854.
  6. ↑ McCormick BA, Miller SI, Carnes D, Madara JL (1995). “Transepithelial signaling to neutrophils by salmonellae: a novel virulence mechanism for gastroenteritis”. Infect Immun. 63 (6): 2302–9. PMC 173301. PMID 7768613.
  7. ↑ Kohbata S, Yokoyama H, Yabuuchi E (1986). “Cytopathogenic effect of Salmonella typhi GIFU 10007 on M cells of murine ileal Peyer’s patches in ligated ileal loops: an ultrastructural study”. Microbiol Immunol. 30 (12): 1225–37. PMID 3553868.
  8. ↑ Kops SK, Lowe DK, Bement WM, West AB (1996). “Migration of Salmonella typhi through intestinal epithelial monolayers: an in vitro study”. Microbiol Immunol. 40 (11): 799–811. PMID 8985935.
  9. ↑ Mills SD, Finlay BB (1994). “Comparison of Salmonella typhi and Salmonella typhimurium invasion, intracellular growth and localization in cultured human epithelial cells”. Microb Pathog. 17 (6): 409–23. doi:10.1006/mpat.1994.1086. PMID 7752882.
  10. ↑ Tartera C, Metcalf ES (1993). “Osmolarity and growth phase overlap in regulation of Salmonella typhi adherence to and invasion of human intestinal cells”. Infect Immun. 61 (7): 3084–9. PMC 280966. PMID 8514418.
  11. ↑ Hornick RB, Greisman SE, Woodward TE, DuPont HL, Dawkins AT, Snyder MJ (1970). “Typhoid fever: pathogenesis and immunologic control”. N Engl J Med. 283 (13): 686–91. doi:10.1056/NEJM197009242831306. PMID 4916913.
  12. ↑ Fields PI, Swanson RV, Haidaris CG, Heffron F (1986). “Mutants of Salmonella typhimurium that cannot survive within the macrophage are avirulent”. Proc Natl Acad Sci U S A. 83 (14): 5189–93. PMC 323916. PMID 3523484.
  13. ↑ Groisman EA, Chiao E, Lipps CJ, Heffron F (1989). “Salmonella typhimurium phoP virulence gene is a transcriptional regulator”. Proc Natl Acad Sci U S A. 86 (18): 7077–81. PMC 297997. PMID 2674945.
  14. ↑ Lai CW, Chan RC, Cheng AF, Sung JY, Leung JW (1992). “Common bile duct stones: a cause of chronic salmonellosis”. Am J Gastroenterol. 87 (9): 1198–9. PMID 1519582.
  15. ↑ Keuter, Monique, et al. “Patterns of proinflammatory cytokines and inhibitors during typhoid fever.” Journal of Infectious Diseases 169.6 (1994): 1306-1311.
  16. ↑ Weinberg ED (2008). “Survival advantage of the hemochromatosis C282Y mutation”. Perspect Biol Med. 51 (1): 98–102. doi:10.1353/pbm.2008.0001. PMID 18192769.
  17. ↑ Moalem S, Weinberg ED, Percy ME (2004). “Hemochromatosis and the enigma of misplaced iron: implications for infectious disease and survival”. Biometals. 17 (2): 135–9. PMID 15088940.
  18. ↑ van de Vosse E, de Visser AW, Al-Attar S, Vossen R, Ali S, van Dissel JT (2010). “Distribution of CFTR variations in an Indonesian enteric fever cohort”. Clin Infect Dis. 50 (9): 1231–7. doi:10.1086/651598. PMID 20233062.
  19. ↑ Arndt MB, Mosites EM, Tian M, Forouzanfar MH, Mokhdad AH, Meller M; et al. (2014). “Estimating the burden of paratyphoid a in Asia and Africa”. PLoS Negl Trop Dis. 8 (6): e2925. doi:10.1371/journal.pntd.0002925. PMC 4046978. PMID 24901439.
  20. ↑ Maskey AP, Day JN, Phung QT, Thwaites GE, Campbell JI, Zimmerman M; et al. (2006). “Salmonella enterica serovar Paratyphi A and S. enterica serovar Typhi cause indistinguishable clinical syndromes in Kathmandu, Nepal”. Clin Infect Dis. 42 (9): 1247–53. doi:10.1086/503033. PMID 16586383.
  21. ↑ Oboegbulam SI, Oguike JU, Gugnani HC (1995). “Microbiological studies on cases diagnosed as typhoid/enteric fever in south-east Nigeria”. J Commun Dis. 27 (2): 97–100. PMID 7499779.
  22. ↑ Vollaard AM, Ali S, Widjaja S, Asten HA, Visser LG, Surjadi C; et al. (2005). “Identification of typhoid fever and paratyphoid fever cases at presentation in outpatient clinics in Jakarta, Indonesia”. Trans R Soc Trop Med Hyg. 99 (6): 440–50. doi:10.1016/j.trstmh.2004.09.012. PMID 15837356.
  23. ↑ Wain J, Hendriksen RS, Mikoleit ML, Keddy KH, Ochiai RL (2015). “Typhoid fever”. Lancet. 385 (9973): 1136–45. PMID [//www.ncbi.nlm.nih.gov/pubmed/25458731 doi=10.1016/S0140-6736(13)62708-7 25458731 doi=10.1016/S0140-6736(13)62708-7] Check |pmid= value (help). line feed character in |pmid= at position 9 (help)
  24. ↑ http://www.cdc.gov/typhoid-fever/health-professional.html
  25. ↑ Fàbrega, Anna, and Jordi Vila. “Salmonella enterica serovar Typhimurium skills to succeed in the host: virulence and regulation.” Clinical microbiology reviews 26.2 (2013): 308-341.
  26. ↑ “CDC Typhoid Fever”. Center for Disease Control. 2005-10-25. Retrieved 2007-10-02.
  27. ↑ 27.0 27.1 “Reorganized text”. JAMA Otolaryngol Head Neck Surg. 141 (5): 428. 2015. doi:10.1001/jamaoto.2015.0540. PMID 25996397.
  28. ↑ 28.0 28.1 28.2 MacFadden DR, Bogoch II, Andrews JR (2016). “Advances in diagnosis, treatment, and prevention of invasive Salmonella infections”. Curr Opin Infect Dis. 29 (5): 453–458. doi:10.1097/QCO.0000000000000302. PMID 27479027.
  29. ↑ 29.0 29.1 29.2 Lynch MF, Blanton EM, Bulens S, Polyak C, Vojdani J, Stevenson J; et al. (2009). “Typhoid fever in the United States, 1999-2006”. JAMA. 302 (8): 859–65. doi:10.1001/jama.2009.1229. PMID 19706859.
  30. ↑ Crump, J. A., & Mintz, E. D (2010). “Global trends in typhoid and paratyphoid fever”. Clinical Infectious Diseases. 50 (2): 241–246. doi:10.1086/649541. PMID 20014951.
  31. ↑ 31.0 31.1 Daul CB, deShazo RD, Andes WA, Pankey GA (1986). “Immunologic studies in homosexual and hemophiliac subjects with persistent generalized lymphadenopathy: a comparative analysis”. J Allergy Clin Immunol. 77 (2): 295–301. PMID 3484760.
  32. ↑ Schmoldt A, Benthe HF, Haberland G (1975). “Digitoxin metabolism by rat liver microsomes”. Biochem Pharmacol. 24 (17): 1639–41. PMID doi:10.1093/infdis/146.6.724 Check |pmid= value (help).
  33. ↑ 33.0 33.1 Lanata CF, Levine MM, Ristori C, Black RE, Jimenez L, Salcedo M; et al. (1983). “Vi serology in detection of chronic Salmonella typhi carriers in an endemic area”. Lancet. 2 (8347): 441–3. PMID 6192305.
  34. ↑ Crump JA, Luby SP, Mintz ED (2004). “The global burden of typhoid fever”. Bull World Health Organ. 82 (5): 346–53. PMC 2622843. PMID 15298225.
  35. ↑ Jensenius M, Han PV, Schlagenhauf P, Schwartz E, Parola P, Castelli F; et al. (2013). “Acute and potentially life-threatening tropical diseases in western travelers–a GeoSentinel multicenter study, 1996-2011”. Am J Trop Med Hyg. 88 (2): 397–404. doi:10.4269/ajtmh.12-0551. PMC 3583336. PMID 23324216.
  36. ↑ “Typhoid Fever”. World Health Organisation. Retrieved 2007-08-28. Check date values in: |accessdate= (help)
  37. ↑ Dewan AM, Corner R, Hashizume M, Ongee ET (2013). “Typhoid Fever and its association with environmental factors in the Dhaka Metropolitan Area of Bangladesh: a spatial and time-series approach”. PLoS Negl Trop Dis. 7 (1): e1998. doi:10.1371/journal.pntd.0001998. PMC 3554574. PMID 23359825.
  38. ↑ Schmoldt A, Benthe HF, Haberland G (1975). “Digitoxin metabolism by rat liver microsomes”. Biochem Pharmacol. 24 (17): 1639–41. PMID http://dx.doi.org/10.1016/S0140-6736(98)09 Check |pmid= value (help).
  39. ↑ Luby SP, Faizan MK, Fisher-Hoch SP, Syed A, Mintz ED, Bhutta ZA; et al. (1998). “Risk factors for typhoid fever in an endemic setting, Karachi, Pakistan”. Epidemiol Infect. 120 (2): 129–38. PMC 2809381. PMID 9593481.
  40. ↑ Marshall E, Howells RE (1986). “Turnover of the surface proteins of adult and third and fourth stage larval Brugia pahangi”. Mol Biochem Parasitol. 18 (1): 17–24. PMID 2870432.
  41. ↑ Srikantiah P, Vafokulov S, Luby SP, Ishmail T, Earhart K, Khodjaev N; et al. (2007). “Epidemiology and risk factors for endemic typhoid fever in Uzbekistan”. Trop Med Int Health. 12 (7): 838–47. doi:10.1111/j.1365-3156.2007.01853.x. PMID 17596250.
  42. ↑ Mermin, Jonathan H., et al. “A massive epidemic of multidrug-resistant typhoid fever in Tajikistan associated with consumption of municipal water.” Journal of Infectious Diseases 179.6 (1999): 1416-1422.
  43. ↑ Black, Robert E., et al. “Case—control study to identify risk factors for paediatric endemic typhoid fever in Santiago, Chile.” Bulletin of the World Health Organization 63.5 (1985): 899.
  44. ↑ Parry CM, Thompson C, Vinh H, Chinh NT, Phuong le T, Ho VA; et al. (2014). “Risk factors for the development of severe typhoid fever in Vietnam”. BMC Infect Dis. 14: 73. doi:10.1186/1471-2334-14-73. PMC 3923984. PMID 24512443.
  45. ↑ http://www.uspreventiveservicestaskforce.org/
  46. ↑ Neil KP, Sodha SV, Lukwago L, O-Tipo S, Mikoleit M, Simington SD; et al. (2012). “A large outbreak of typhoid fever associated with a high rate of intestinal perforation in Kasese District, Uganda, 2008-2009”. Clin Infect Dis. 54 (8): 1091–9. doi:10.1093/cid/cis025. PMID 22357703.
  47. ↑ Bitar, Roger, and John Tarpley. “Intestinal perforation in typhoid fever: a historical and state-of-the-art review.” Review of Infectious Diseases 7.2 (1985): 257-271.
  48. ↑ van Basten JP, Stockenbrügger R (1994). “Typhoid perforation. A review of the literature since 1960”. Trop Geogr Med. 46 (6): 336–9. PMID 7892698.
  49. ↑ 49.0 49.1 49.2 Hoffman SL, Punjabi NH, Kumala S, Moechtar MA, Pulungsih SP, Rivai AR; et al. (1984). “Reduction of mortality in chloramphenicol-treated severe typhoid fever by high-dose dexamethasone”. N Engl J Med. 310 (2): 82–8. doi:10.1056/NEJM198401123100203. PMID 6361558.
  50. ↑ Punjabi NH, Hoffman SL, Edman DC, Sukri N, Laughlin LW, Pulungsih SP; et al. (1988). “Treatment of severe typhoid fever in children with high dose dexamethasone”. Pediatr Infect Dis J. 7 (8): 598–600. PMID 3050856.
  51. ↑ Seoud M, Saade G, Uwaydah M, Azoury R (1988). “Typhoid fever in pregnancy”. Obstet Gynecol. 71 (5): 711–4. PMID 3357660.
  52. ↑ Reed RP, Klugman KP (1994). “Neonatal typhoid fever”. Pediatr Infect Dis J. 13 (9): 774–7. PMID 7808844.
  53. ↑ Wain J, Hien TT, Connerton P, Ali T, Parry CM, Chinh NT; et al. (1999). “Molecular typing of multiple-antibiotic-resistant Salmonella enterica serovar Typhi from Vietnam: application to acute and relapse cases of typhoid fever”. J Clin Microbiol. 37 (8): 2466–72. PMC 85257. PMID 10405386.
  54. ↑ Levine, Myron M., Robert E. Black, and Claudio Lanata. “Precise estimation of the numbers of chronic carriers of Salmonella typhi in Santiago, Chile, an endemic area.” Journal of Infectious Diseases 146.6 (1982): 724-726.
  55. ↑ Gupta SP, Gupta MS, Bhardwaj S, Chugh TD (1985). “Current clinical patterns of typhoid fever: a prospective study”. J Trop Med Hyg. 88 (6): 377–81. PMID 3837121.
  56. ↑ Huang DB, DuPont HL (2005). “Problem pathogens: extra-intestinal complications of Salmonella enterica serotype Typhi infection”. Lancet Infect Dis. 5 (6): 341–8. doi:10.1016/S1473-3099(05)70138-9. PMID 15919620.
  57. ↑ Lutterloh E, Likaka A, Sejvar J, Manda R, Naiene J, Monroe SS; et al. (2012). “Multidrug-resistant typhoid fever with neurologic findings on the Malawi-Mozambique border”. Clin Infect Dis. 54 (8): 1100–6. doi:10.1093/cid/cis012. PMID 22357702.
  58. ↑ STUART BM, PULLEN RL (1946). “Typhoid; clinical analysis of 360 cases”. Arch Intern Med (Chic). 78 (6): 629–61. PMID 20278487.
  59. ↑ 59.0 59.1 Pohan HT (2004). “Clinical and laboratory manifestations of typhoid fever at Persahabatan Hospital, Jakarta”. Acta Med Indones. 36 (2): 78–83. PMID 15673941.
  60. ↑ Butler, Thomas, et al. “Patterns of Morbidity and Mortality in Typhoid Fever Dependent on Age and Gender: Review of 552 Hopitalized Patients with Diarrhea.” Review of Infectious Diseases 13.1 (1991): 85-90.
  61. ↑ Ostergaard L, Huniche B, Andersen PL (1996). “Relative bradycardia in infectious diseases”. J Infect. 33 (3): 185–91. PMID 8945708.
  62. ↑ Azmatullah A, Qamar FN, Thaver D, Zaidi AK, Bhutta ZA (2015). “Systematic review of the global epidemiology, clinical and laboratory profile of enteric fever”. J Glob Health. 5 (2): 020407. doi:10.7189/jogh.05.020407. PMC 4672836. PMID 26649174.
  63. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett’s principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  64. ↑ 64.0 64.1 Wain J, Diep TS, Ho VA, Walsh AM, Nguyen TT, Parry CM; et al. (1998). “Quantitation of bacteria in blood of typhoid fever patients and relationship between counts and clinical features, transmissibility, and antibiotic resistance”. J Clin Microbiol. 36 (6): 1683–7. PMC 104900. PMID 9620400.
  65. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett’s principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  66. ↑ Cooper EC, Ratnam I, Mohebbi M, Leder K (2014). “Laboratory features of common causes of fever in returned travelers”. J Travel Med. 21 (4): 235–9. doi:10.1111/jtm.12122. PMID 24754384.
  67. ↑ Valderhaug J (1974). “A histologic study of experimentally induced periapical inflammation in primary teeth in monkeys”. Int J Oral Surg. 3 (3): 111–23. PMID 4209424.
  68. ↑ 68.0 68.1 Schiff GM (1986). “Wither we goest? Notes of a society watcher plus other comments and thoughts”. J Lab Clin Med. 108 (1): 3–6. PMID 3711723.
  69. ↑ 69.0 69.1 Bomanji J, Garner A, Prasad J, Albert DM, Hungerford JL, Granowska M; et al. (1987). “Characterisation of ocular melanoma with cutaneous melanoma antibodies”. Br J Ophthalmol. 71 (9): 647–50. PMC 1041267. PMID 3311140.
  70. ↑ Giaccai, L., and H. Idriss. “Osteomyelitis due to Salmonella infection.” The Journal of pediatrics 41.1 (1952): 73-78.
  71. ↑ Neu, Carmen Ortiz, et al. “Bone and joint infections due to Salmonella.” Journal of Infectious Diseases 138.6 (1978): 820-828.
  72. ↑ 72.0 72.1 72.2 Vallenas C, Hernandez H, Kay B, Black R, Gotuzzo E (1985). “Efficacy of bone marrow, blood, stool and duodenal contents cultures for bacteriologic confirmation of typhoid fever in children”. Pediatr Infect Dis. 4 (5): 496–8. PMID 3900945.
  73. ↑ 73.0 73.1 Gasem MH, Dolmans WM, Isbandrio BB, Wahyono H, Keuter M, Djokomoeljanto R (1995). “Culture of Salmonella typhi and Salmonella paratyphi from blood and bone marrow in suspected typhoid fever”. Trop Geogr Med. 47 (4): 164–7. PMID 8560588.
  74. ↑ Hoffman SL, Edman DC, Punjabi NH, Lesmana M, Cholid A, Sundah S; et al. (1986). “Bone marrow aspirate culture superior to streptokinase clot culture and 8 ml 1:10 blood-to-broth ratio blood culture for diagnosis of typhoid fever”. Am J Trop Med Hyg. 35 (4): 836–9. PMID 3089041.
  75. ↑ 75.0 75.1 Hoffman SL, Punjabi NH, Rockhill RC, Sutomo A, Rivai AR, Pulungsih SP (1984). “Duodenal string-capsule culture compared with bone-marrow, blood, and rectal-swab cultures for diagnosing typhoid and paratyphoid fever”. J Infect Dis. 149 (2): 157–61. PMID 6421940 PMID: 6421940 Check |pmid= value (help).
  76. ↑ Gilman RH, Terminel M, Levine MM, Hernandez-Mendoza P, Hornick RB (1975). “Relative efficacy of blood, urine, rectal swab, bone-marrow, and rose-spot cultures for recovery of Salmonella typhi in typhoid fever”. Lancet. 1 (7918): 1211–3. PMID 48834.
  77. ↑ Shukla S, Patel B, Chitnis DS (1997). “100 years of Widal test & its reappraisal in an endemic area”. Indian J Med Res. 105: 53–7. PMID 9055495.
  78. ↑ Bhutta, Zulfiqar Ahmed, and Naseem Mansurali. “Rapid serologic diagnosis of pediatric typhoid fever in an endemic area: a prospective comparative evaluation of two dot-enzyme immunoassays and the Widal test.” The American journal of tropical medicine and hygiene 61.4 (1999): 654-657.
  79. ↑ House D, Wain J, Ho VA, Diep TS, Chinh NT, Bay PV; et al. (2001). “Serology of typhoid fever in an area of endemicity and its relevance to diagnosis”. J Clin Microbiol. 39 (3): 1002–7. doi:10.1128/JCM.39.3.1002-1007.2001. PMC 87864. PMID 11230418.
  80. ↑ Song JH, Cho H, Park MY, Na DS, Moon HB, Pai CH (1993). “Detection of Salmonella typhi in the blood of patients with typhoid fever by polymerase chain reaction”. J Clin Microbiol. 31 (6): 1439–43. PMC 265558. PMID 8314983.
  81. ↑ Hennedige T, Bindl DS, Bhasin A, Venkatesh SK (2012). “Computed tomography features in enteric fever”. Ann Acad Med Singapore. 41 (7): 281–6. PMID 22892604.
  82. ↑ Sejvar J, Lutterloh E, Naiene J, Likaka A, Manda R, Nygren B; et al. (2012). “Neurologic manifestations associated with an outbreak of typhoid fever, Malawi–Mozambique, 2009: an epidemiologic investigation”. PLoS One. 7 (12): e46099. doi:10.1371/journal.pone.0046099. PMC 3513310. PMID 23226492.
  83. ↑ Ahmed, Munawwar, et al. “Magnetic resonance imaging findings in a fatal case of Salmonella typhi-associated encephalopathy: A case report and literature review.” Neurology India 59.2 (2011): 270.
  84. ↑ George P, Ahmed A, Maroli R, Tauro LF (2012). “Peritonitis secondary to ruptured splenic abscess: a grave complication of typhoid fever”. Asian Pac J Trop Med. 5 (12): 1004–6. doi:10.1016/S1995-7645(12)60191-6. PMID 23199723.
  85. ↑ http://appliedradiology.com/articles/imaging-infection-and-inflammation-of-the-terminal-ileocecal-region-emphasis-on-typhoid
  86. ↑ Lynch JJ, Beneventano TC (1980). “Typhoid fever. An unusual radiographic presentation with appendicitis”. Am J Gastroenterol. 73 (2): 168–73. PMID 7395845.
  87. ↑ Débat Zoguéreh D, Dubau A, Badiaga S (1998). “[Calcified splenic abscess, colonic fistula and ascites in a chronic carrier of Salmonella typhi]”. Gastroenterol Clin Biol. 22 (12): 1102–5. PMID 10051988.
  88. ↑ Shaikhani MA, Husein HA, Karbuli TA, Mohamed MA (2013). “Colonoscopic findings and management of patients with outbreak typhoid fever presenting with lower gastrointestinal bleeding”. Indian J Gastroenterol. 32 (5): 335–40. doi:10.1007/s12664-013-0337-y. PMID 23703658.
  89. ↑ Prabha A, Pereira P, Raghuveer CV (1995). “Myocarditis in enteric fever”. Indian J Med Sci. 49 (2): 28–31. PMID 7558213.
  90. ↑ Ivanoff, Bernard. “Typhoid fever: global situation and WHO recommendations.” Southeast Asian Journal of Tropical Medicine and Public Health 26 (1995): 1-6.
  91. ↑ Schmoldt A, Benthe HF, Haberland G (1975). “Digitoxin metabolism by rat liver microsomes”. Biochem Pharmacol. 24 (17): 1639–41. PMID http://dx.doi.org/10.1136/bmj.316.7125.110 Check |pmid= value (help).
  92. ↑ Wahdan, M. H., et al. “A controlled field trial of live Salmonella typhi strain Ty 21a oral vaccine against typhoid: three-year results.” Journal of Infectious Diseases 145.3 (1982): 292-295.
  93. ↑ Acharya IL, Lowe CU, Thapa R, Gurubacharya VL, Shrestha MB, Cadoz M; et al. (1987). “Prevention of typhoid fever in Nepal with the Vi capsular polysaccharide of Salmonella typhi. A preliminary report”. N Engl J Med. 317 (18): 1101–4. doi:10.1056/NEJM198710293171801. PMID 3657877.
  94. ↑ Lin FY, Ho VA, Khiem HB, Trach DD, Bay PV, Thanh TC; et al. (2001). “The efficacy of a Salmonella typhi Vi conjugate vaccine in two-to-five-year-old children”. N Engl J Med. 344 (17): 1263–9. doi:10.1056/NEJM200104263441701. PMID 11320385.
  95. ↑ http://wwwnc.cdc.gov/travel/diseases/typhoid
  96. ↑ Hainsworth T (2002). “Travel vaccines: a guide to appropriate use”. Nurs Times. 98 (25): 40–2. PMID 12168224.
  97. ↑ van de Vosse E, Hoeve MA, Ottenhoff TH (2004). “Human genetics of intracellular infectious diseases: molecular and cellular immunity against mycobacteria and salmonellae”. Lancet Infect Dis. 4 (12): 739–49. doi:10.1016/S1473-3099(04)01203-4. PMID 15567123.
  98. ↑ Münnich D, Békési S (1979). “Curing of typhoid carriers by cholecystectomy combined with amoxycillin plus probenecid treatment”. Chemotherapy. 25 (6): 362–6. PMID 520079.

Template:WH Template:WS

Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Aslam, M.B.B.S[2]

Overview

Around 430–426 B.C., a devastating plague, which some believe to have been typhoid fever, killed one-third of the population of Athens, including Pericles, the state’s leader. A 2006 study detected DNA sequences similar to those of the bacterium responsible for typhoid fever in a DNA sample dating back to the time of the epidemic.[1] Other scientists have disputed the findings, citing serious methodologic flaws in the dental pulp-derived DNA study.[2]

The most notorious carrier of typhoid fever—though by no means the most destructive—was Mary Mallon, also known as Typhoid Mary. In 1907, Mallon became the first American carrier to be identified and traced. She was a cook in New York who was believed to be the source of infection for several hundred people. She is closely associated with forty-seven cases of the illness and three deaths.

In 1897, Almroth Edward Wright developed an effective vaccine for typhoid fever. Antibiotics were introduced in clinical practice in 1942, greatly reducing mortality.

Historical Perspective

  • Around 430–426 B.C., a devastating plague, which some believe to have been typhoid fever, killed one-third of the population of Athens, including Pericles, the state’s leader. This enabled the balance of power in the region to shift from Athens to Sparta, ending the Golden Age of Pericles that had marked Athenian dominance in the ancient world.
  • Ancient historian Thucydides also contracted the disease, but he survived to write about the plague. His writings are the primary source of information about this outbreak.
  • The cause of the plague has long been disputed, with modern academics and medical scientists considering epidemic typhus the most likely cause. However, a 2006 study detected DNA sequences similar to those of the bacterium responsible for typhoid fever.[1]
    • Other scientists have disputed the findings, citing serious methodologic flaws in the dental pulp-derived DNA study.[2] The disease is most commonly transmitted through poor hygiene habits and public sanitation conditions; during the period in question, the whole population of Attica was besieged within the Long Walls and lived in tents.
  • In the late 19th century, typhoid fever mortality rate in Chicago averaged 65 per 100,000 people a year. The worst year was 1891, when the typhoid death rate was 174 per 100,000 persons.[3]
  • The most notorious carrier of typhoid fever—though by no means the most destructive—was Mary Mallon, also known as Typhoid Mary. In 1907, she became the first American carrier to be identified and traced. She was a cook in New York and the source of infection for several hundred people. She is closely associated with forty-seven cases and three deaths.[4] Public health authorities told Mary to give up working as a cook or have her gall bladder removed. Mary quit her job but returned later under a false name. She was detained and quarantined after another typhoid outbreak. She died of pneumonia after 26 years in quarantine.
  • In 1897, Almroth Edward Wright developed an effective vaccine.
  • Most developed countries saw declining rates of typhoid fever throughout first half of 20th century due to vaccinations and advances in public sanitation and hygiene. Antibiotics were introduced in clinical practice in 1942, greatly reducing mortality. At the present time, incidence of typhoid fever in developed countries is around 0.5 cases per 100,000 people per year.
  • An outbreak in the Democratic Republic of Congo in 2004-05 recorded more than 42,000 cases and 214 deaths.[5]

References

  1. ↑ 1.0 1.1 Papagrigorakis MJ, Yapijakis C, Synodinos PN, Baziotopoulou-Valavani E (2006). “DNA examination of ancient dental pulp incriminates typhoid fever as a probable cause of the Plague of Athens”. Int J Infect Dis. 10 (3): 206–14. PMID 16412683}.
  2. ↑ 2.0 2.1 Shapiro B, Rambaut A, Gilbert M (2006). “No proof that typhoid caused the Plague of Athens (a reply to Papagrigorakis et al.)”. Int J Infect Dis. 10 (4): 334–5, author reply 335–6. PMID 16730469.
  3. ↑ “1900 Flow of Chicago River Reversed”. Chicago Timeline. Chicago Public Library. Retrieved 2007-02-08.
  4. ↑ “Nova: The Most Dangerous Woman in America”.
  5. ↑ “Typhoid Fever”. World Health Organisation. Retrieved 2007-08-28. Check date values in: |accessdate= (help)

Template:WH Template:WS

Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Aslam, M.B.B.S[2]

Overview

There is no established classification system for typhoid fever. Typhoid fever may be classified informally based on duration of illness, serologic type, severity of illness, and virulence factors.[1]

Classification

There is no established classification system for typhoid fever. However, typhoid fever may be classified informally as follows.[1]

Duration of illness

Acute disease [2][3][4]

  • Sudden-onset
  • Severe in nature
  • Lasts < 12 months
  • Mostly symptomatic

Chronic disease [2][3][4]

  • Lasts > 12 months
  • Less severe
  • Asymptomatic
  • Spread infection to others

Severity of illness

Mild disease[5][6]

Moderate to severe disease[7][6]

Virulence factors

High virulence factors[8][9][1]

  • PhoP/phoQ genes
  • CdtB protein
  • Vi antigen-positive strains

Low virulence factors[3][10][11]

  • Absence of above factors
  • Presence of following host factors
  • C282 mutation
  • CFTR mutation

References

  1. ↑ 1.0 1.1 1.2 Parry CM, Hien TT, Dougan G, White NJ, Farrar JJ (2002). “Typhoid fever”. N Engl J Med. 347 (22): 1770–82. doi:10.1056/NEJMra020201. PMID 12456854.
  2. ↑ 2.0 2.1 Lai CW, Chan RC, Cheng AF, Sung JY, Leung JW (1992). “Common bile duct stones: a cause of chronic salmonellosis”. Am J Gastroenterol. 87 (9): 1198–9. PMID 1519582.
  3. ↑ 3.0 3.1 3.2 Hofmann E, Chianale J, Rollán A, Pereira J, Ferrecio C, Sotomayor V (1993). “Blood group antigen secretion and gallstone disease in the Salmonella typhi chronic carrier state”. J Infect Dis. 167 (4): 993–4. PMID 8450268.
  4. ↑ 4.0 4.1 Dham SK, Thompson RA (1982). “Humoral and cell-mediated immune responses in chronic typhoid carriers”. Clin Exp Immunol. 50 (1): 34–40. PMC 1536860. PMID 7172510.
  5. ↑ Bhutta, Zulfiqar Ahmed. “Impact of age and drug resistance on mortality in typhoid fever.” Archives of disease in childhood 75.3 (1996): 214-217.
  6. ↑ 6.0 6.1 Hoffman SL, Punjabi NH, Kumala S, Moechtar MA, Pulungsih SP, Rivai AR; et al. (1984). “Reduction of mortality in chloramphenicol-treated severe typhoid fever by high-dose dexamethasone”. N Engl J Med. 310 (2): 82–8. doi:10.1056/NEJM198401123100203. PMID 6361558.
  7. ↑ Bhutta, Zulfiqar Ahmed. “Impact of age and drug resistance on mortality in typhoid fever.” Archives of disease in childhood 75.3 (1996): 214-217.
  8. ↑ Hohmann EL, Oletta CA, Killeen KP, Miller SI (1996). “phoP/phoQ-deleted Salmonella typhi (Ty800) is a safe and immunogenic single-dose typhoid fever vaccine in volunteers”. J Infect Dis. 173 (6): 1408–14. PMID 8648213.
  9. ↑ Spanò S, Ugalde JE, Galán JE (2008). “Delivery of a Salmonella Typhi exotoxin from a host intracellular compartment”. Cell Host Microbe. 3 (1): 30–8. doi:10.1016/j.chom.2007.11.001. PMID 18191792.
  10. ↑ Darton TC, Blohmke CJ, Giannoulatou E, Waddington CS, Jones C, Sturges P; et al. (2015). “Rapidly Escalating Hepcidin and Associated Serum Iron Starvation Are Features of the Acute Response to Typhoid Infection in Humans”. PLoS Negl Trop Dis. 9 (9): e0004029. doi:10.1371/journal.pntd.0004029. PMC 4578949. PMID 26394303.
  11. ↑ Weinberg ED (2008). “Survival advantage of the hemochromatosis C282Y mutation”. Perspect Biol Med. 51 (1): 98–102. doi:10.1353/pbm.2008.0001. PMID 18192769.


Template:WH Template:WS

Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Aslam, M.B.B.S[2]

Overview

The sequence of events in the pathogenesis of typhoid fever include inoculation, gastrointestinal infection, systemic involvement, and chronic carrier state.[1][2][3][4][5][6][7][8][9][10][11]

Pathogenesis

The pathogenesis of typhoid fever consists of the following sequence of events.[1][2][3][4][5][6][7][8][9][10][11]

Innoculation

  • Orofecal transmission
  • Infective dose: 1000 to 1 million organisms

Gastrointestinal Infection

Stomach

  • Bacterium enters stomach
  • Can survive a pH as low as 1.5

Small intestine

  • Bacterium enters mucosa of the small intestine via M cells or direct penetration
  • Adherence to the mucosal cells via special proteins
  • Invade mucosal M cells overlying peyer’s patches
  • Internalisation in M cells of ileum
  • Translocation to underlying lymphoid tissue and draining lymph nodes

Systemic spread

Chronic carrier state

  • Resides and multiplies in gall bladder
  • Excretion in urine and stool may infect other individuals

References

  1. ↑ 1.0 1.1 Parry CM, Hien TT, Dougan G, White NJ, Farrar JJ (2002). “Typhoid fever”. N Engl J Med. 347 (22): 1770–82. doi:10.1056/NEJMra020201. PMID 12456854.
  2. ↑ 2.0 2.1 McCormick BA, Miller SI, Carnes D, Madara JL (1995). “Transepithelial signaling to neutrophils by salmonellae: a novel virulence mechanism for gastroenteritis”. Infect Immun. 63 (6): 2302–9. PMC 173301. PMID 7768613.
  3. ↑ 3.0 3.1 Kohbata S, Yokoyama H, Yabuuchi E (1986). “Cytopathogenic effect of Salmonella typhi GIFU 10007 on M cells of murine ileal Peyer’s patches in ligated ileal loops: an ultrastructural study”. Microbiol Immunol. 30 (12): 1225–37. PMID 3553868.
  4. ↑ 4.0 4.1 Kops SK, Lowe DK, Bement WM, West AB (1996). “Migration of Salmonella typhi through intestinal epithelial monolayers: an in vitro study”. Microbiol Immunol. 40 (11): 799–811. PMID 8985935.
  5. ↑ 5.0 5.1 Mills SD, Finlay BB (1994). “Comparison of Salmonella typhi and Salmonella typhimurium invasion, intracellular growth and localization in cultured human epithelial cells”. Microb Pathog. 17 (6): 409–23. doi:10.1006/mpat.1994.1086. PMID 7752882.
  6. ↑ 6.0 6.1 Tartera C, Metcalf ES (1993). “Osmolarity and growth phase overlap in regulation of Salmonella typhi adherence to and invasion of human intestinal cells”. Infect Immun. 61 (7): 3084–9. PMC 280966. PMID 8514418.
  7. ↑ 7.0 7.1 Hornick RB, Greisman SE, Woodward TE, DuPont HL, Dawkins AT, Snyder MJ (1970). “Typhoid fever: pathogenesis and immunologic control”. N Engl J Med. 283 (13): 686–91. doi:10.1056/NEJM197009242831306. PMID 4916913.
  8. ↑ 8.0 8.1 Fields PI, Swanson RV, Haidaris CG, Heffron F (1986). “Mutants of Salmonella typhimurium that cannot survive within the macrophage are avirulent”. Proc Natl Acad Sci U S A. 83 (14): 5189–93. PMC 323916. PMID 3523484.
  9. ↑ 9.0 9.1 Groisman EA, Chiao E, Lipps CJ, Heffron F (1989). “Salmonella typhimurium phoP virulence gene is a transcriptional regulator”. Proc Natl Acad Sci U S A. 86 (18): 7077–81. PMC 297997. PMID 2674945.
  10. ↑ 10.0 10.1 Lai CW, Chan RC, Cheng AF, Sung JY, Leung JW (1992). “Common bile duct stones: a cause of chronic salmonellosis”. Am J Gastroenterol. 87 (9): 1198–9. PMID 1519582.
  11. ↑ 11.0 11.1 Keuter, Monique, et al. “Patterns of proinflammatory cytokines and inhibitors during typhoid fever.” Journal of Infectious Diseases 169.6 (1994): 1306-1311.

Template:WH Template:WS

Causes

Causes

Salmonella Typhi – Public Domain, https://commons.wikimedia.org/w/index.php?curid=450281

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Aslam, M.B.B.S[2]

Overview

Causes

Serovars

Other Salmonellae which may cause similar symptoms include:

  • Salmonella Paratyphi A
  • Salmonella Paratyphi B
  • Salmonella Paratyphi C
  • Salmonella choleraesuis

Features of Salmonella Typhi[9][10][11]

  • O polysaccharide antigen
  • H flagellar antigen
  • Vi outer capsular polysaccharide antigen

References

  1. ↑ 1.0 1.1 Arndt MB, Mosites EM, Tian M, Forouzanfar MH, Mokhdad AH, Meller M; et al. (2014). “Estimating the burden of paratyphoid a in Asia and Africa”. PLoS Negl Trop Dis. 8 (6): e2925. doi:10.1371/journal.pntd.0002925. PMC 4046978. PMID 24901439.
  2. ↑ 2.0 2.1 Maskey AP, Day JN, Phung QT, Thwaites GE, Campbell JI, Zimmerman M; et al. (2006). “Salmonella enterica serovar Paratyphi A and S. enterica serovar Typhi cause indistinguishable clinical syndromes in Kathmandu, Nepal”. Clin Infect Dis. 42 (9): 1247–53. doi:10.1086/503033. PMID 16586383.
  3. ↑ 3.0 3.1 Oboegbulam SI, Oguike JU, Gugnani HC (1995). “Microbiological studies on cases diagnosed as typhoid/enteric fever in south-east Nigeria”. J Commun Dis. 27 (2): 97–100. PMID 7499779.
  4. ↑ 4.0 4.1 Vollaard AM, Ali S, Widjaja S, Asten HA, Visser LG, Surjadi C; et al. (2005). “Identification of typhoid fever and paratyphoid fever cases at presentation in outpatient clinics in Jakarta, Indonesia”. Trans R Soc Trop Med Hyg. 99 (6): 440–50. doi:10.1016/j.trstmh.2004.09.012. PMID 15837356.
  5. ↑ 5.0 5.1 Wain J, Hendriksen RS, Mikoleit ML, Keddy KH, Ochiai RL (2015). “Typhoid fever”. Lancet. 385 (9973): 1136–45. PMID [//www.ncbi.nlm.nih.gov/pubmed/25458731 doi=10.1016/S0140-6736(13)62708-7 25458731 doi=10.1016/S0140-6736(13)62708-7] Check |pmid= value (help). line feed character in |pmid= at position 9 (help)
  6. ↑ http://www.cdc.gov/typhoid-fever/health-professional.html
  7. ↑ Fàbrega, Anna, and Jordi Vila. “Salmonella enterica serovar Typhimurium skills to succeed in the host: virulence and regulation.” Clinical microbiology reviews 26.2 (2013): 308-341.
  8. ↑ http://www.cdc.gov/typhoid-fever/health-professional.html
  9. ↑ Fàbrega, Anna, and Jordi Vila. “Salmonella enterica serovar Typhimurium skills to succeed in the host: virulence and regulation.” Clinical microbiology reviews 26.2 (2013): 308-341.
  10. ↑ Grossman, Daniel A., et al. “Flagellar serotypes of Salmonella typhi in Indonesia: relationships among motility, invasiveness, and clinical illness.” Journal of Infectious Diseases 171.1 (1995): 212-216.
  11. ↑ Schmoldt A, Benthe HF, Haberland G (1975). “Digitoxin metabolism by rat liver microsomes”. Biochem Pharmacol. 24 (17): 1639–41. PMID 10.1056/NEJMra020201 DOI: 10.1056/NEJMra020201 Check |pmid= value (help).

Template:WH Template:WS

Differentiating Typhoid fever from other Diseases

Differentiating Typhoid fever from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2], Aysha Aslam, M.B.B.S[3]

Overview

Typhoid fever must be differentiated from other diseases that cause fever, diarrhea, and dehydration, such as Ebola, Shigellosis, malaria, and Lassa fever.

Differentiating Typhoid fever from other Diseases

The table below summarizes the findings that differentiate Typhoid fever from other conditions that cause fever, diarrhea, dehydration, and non-specific abdominal symptoms.[1][2][3][4][5][6][7][8]

Disease Findings
Typhoid fever-like syndrome Caused by Salmonella Paratyphi A, B, C or Choleraesuis. Presents with fever, chills, vomiting, abdominal pain, generalized pain or malaise following an incubation period of 5-21 days.
Ebola Presents with fever, chills, vomiting, diarrhea, generalized pain or malaise, and sometimes internal and external bleeding following an incubation period of 2-21 days.
Shigellosis & other bacterial enteric infections Presents with diarrhea, possibly bloody, accompanied by fever, nausea, and sometimes toxemia, vomiting, cramps, and tenesmus. Stools contain blood and mucous in a typical case. A search for possible sites of bacterial infection, together with cultures and blood smears, should be made. Presence of leukocytosis distinguishes bacterial infections from viral infections.
Malaria Presents with acute fever, headache, and sometimes diarrhea (in children). A blood smear must be examined for malaria parasites. The presence of parasites does not exclude concurrent viral infection. An antimalarial should be prescribed as an empiric therapy.
Lassa fever Disease onset is usually gradual, with fever, sore throat, cough, pharyngitis, and facial edema in the later stages. Inflammation and exudation of the pharynx and conjunctiva are common.
Yellow fever and other Flaviviridae Present with hemorrhagic complications. Epidemiological investigation may reveal a pattern of disease transmission by an insect vector. Virus isolation and serological investigation are helpful for distinguishing these viruses. Confirmed history of previous yellow fever vaccination will rule out yellow fever.
Abdominal abscess (e.g., ameobic hepatic abcess) May present with abdominal pain, fever, loss of appetite, nausea, vomiting, diarrhea, constipation. H/o surgery, presence of a mass on physical examination, ultrasound or CT scan may help rule out abdominal abscess in such cases.
Brucellosis Presents with recurrent fevers, acute abdominal pain, and other symptoms resembling typhoid fever. History of exposure to infected animals, including work in a slaughterhouse or as a veterinarian, may help differentiate brucellosis from typhoid fever.
Others Viral hepatitis, leptospirosis, rheumatic fever, typhus, appendicitis, dengue fever,toxoplasmosis, rickettsial diseases, leishmaniasis, tuberculosis, and mononucleosis can produce signs and symptoms that may be confused with typhoid fever in the early stages of infection.
Differentiating diagnosis of Typhoid fever Symptoms Signs Diagnosis Additional Findings
Fever Rash Diarrhea Abdominal pain Weight loss Painful lymphadenopathy Hepatosplenomegaly Arthritis Lab Findings
Brucellosis ✔ ✔ ✘ ✔ ✔ ✔ ✔ ✔ Relative lymphocytosis Night sweats, often with characteristic smell, likened to wet hay
Typhoid fever ✔ ✔ ✘ ✔ ✘ ✘ ✔ ✔ Decreased hemoglobin Incremental increase in temperature initially and than sustained fever as high as 40°C (104°F)
Malaria ✔ ✘ ✔ ✔ ✘ ✘ ✔ ✔ Microcytosis,

elevated LDH

“Tertian” fever: paroxysms occur every second day
Tuberculosis ✔ ✔ ✘ ✔ ✔ ✔ ✔ ✔ Mild normocytic anemia, hyponatremia, and

hypercalcemia

Night sweats, constant fatigue
Lymphoma ✔ ✘ ✘ ✔ ✔ ✘ ✔ ✘ Increase ESR, increased LDH Night sweats, constant fatigue
Mumps ✔ ✘ ✘ ✘ ✘ ✔ ✘ ✘ Relative lymphocytosis, serum amylase elevated Parotid swelling/tenderness
Rheumatoid arthritis ✘ ✔ ✘ ✘ ✘ ✘ ✘ ✔ ESR and CRP elevated, positive rheumatoid factor Morning stiffness
SLE ✘ ✔ ✘ ✔ ✔ ✘ ✘ ✔ ESR and CRP elevated, positive ANA Fatigue
HIV ✘ ✘ ✘ ✔ ✔ ✔ ✘ ✔ Constant fatigue

References

  1. ↑ “CDC Typhoid Fever”. Center for Disease Control. 2005-10-25. Retrieved 2007-10-02.
  2. ↑ “Reorganized text”. JAMA Otolaryngol Head Neck Surg. 141 (5): 428. 2015. doi:10.1001/jamaoto.2015.0540. PMID 25996397.
  3. ↑ Parry CM, Hien TT, Dougan G, White NJ, Farrar JJ (2002). “Typhoid fever”. N Engl J Med. 347 (22): 1770–82. doi:10.1056/NEJMra020201. PMID 12456854.
  4. ↑ MacFadden DR, Bogoch II, Andrews JR (2016). “Advances in diagnosis, treatment, and prevention of invasive Salmonella infections”. Curr Opin Infect Dis. 29 (5): 453–458. doi:10.1097/QCO.0000000000000302. PMID 27479027.
  5. ↑ Lynch MF, Blanton EM, Bulens S, Polyak C, Vojdani J, Stevenson J; et al. (2009). “Typhoid fever in the United States, 1999-2006”. JAMA. 302 (8): 859–65. doi:10.1001/jama.2009.1229. PMID 19706859.
  6. ↑ Güleşen R, Levent B, Üvey M, Bayrak H, Akgeyik M (2016). “[Serotype distribution and antimicrobial susceptibilities of Salmonella strains recovered from environmental samples between 2008-2014]”. Mikrobiyol Bul. 50 (3): 371–81. PMID 27525393.
  7. ↑ SAPHRA I, WASSERMANN M (1954). “Salmonella cholerae suis: a clinical and epidemiological evaluation of 329 infections identified between 1940 and 1954 in the New York Salmonella Center”. Am J Med Sci. 228 (5): 525–33. PMID 13207112.
  8. ↑ Göke M, Neurath M, Braunstein S, Daniello S, Knolle P, Dippold W; et al. (1993). “Brucellosis: differential diagnosis of acute abdominal pain”. Z Gastroenterol. 31 (11): 671–4. PMID 8291280.

Template:WH Template:WS

Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Aslam, M.B.B.S[2]

Overview

An estimated 16-33 million cases of typhoid result in 500,000 to 600,000 deaths annually. In 2000, typhoid fever caused an estimated 21.7 million illnesses and 217,000 deaths.[1][2] Worldwide, typhoid fever is most prevalent in overcrowded areas with poor hygiene and sanitation. Typhoid fever is still common in the developing world, where it affects about 21.5 million people each year. 1-6% of the individuals who are infected will develop a chronic infection of the gall bladder.[3] The incidence of typhoid fever varies in different parts of world.[4][5][6] Age, race, gender and certain environmental factors affect the distribution of disease among these groups.[7][8][9]

Epidemiology

  • An estimated 16-33 million cases of typhoid result in 500,000 to 600,000 deaths annually.
  • In 2000, typhoid fever caused an estimated 21.7 million illnesses and 217,000 deaths.[1][2]
  • In 2013, typhoid fever resulted in about 161,000 deaths as compared to 181,000 in 1990.[10][11]

Prevalance

  • Worldwide, typhoid fever is most prevalent in overcrowded areas with poor hygiene and sanitation.
  • In endemic areas, the World Health Organisation identifies typhoid as a serious public health problem.
  • Typhoid fever is still common in the developing world, where it affects about 21.5 million people each year.
  • Typhoid fever is common in the most parts of the world except in the industrialized regions such as the United States, Canada, Western Europe, Australia, and Japan.
  • 1-6% of the individuals who are infected will develop a chronic infection of the gall bladder.[12][3]

Incidence

The incidence of typhoid fever varies in different parts of world.[4][5][6]

  • Areas with the highest incidence of typhoid fever (>100/100,000 cases/year) include south-central Asia and south-east Asia.[13].
  • Areas with the medium incidence (10-100/100,000 cases/year) include the rest of Asia, Africa, Latin America and the Caribbean, and Oceania, except for Australia and New Zealand[13]
  • Areas with the low incidence (<10/100,000 cases/year) include Europe, North America, and the rest of the world.[13]
  • The incidence of typhoid fever is estimated to be less than 400 cases per year in the United States and 75% of these are acquired while travelling internationally.[14]

Case fatality rate

  • The case fatality rate for typhoid fever is 1%.[15]
Death rates for Typhoid Fever in the U.S. 1906-1960 – Source: https://www.cdc.gov/

Demographics

The following demographic factors may affect the incidence and prevalence of typhoid fever.

Age

The incidence of typhoid fever is highest in children between the ages of 5 and 19 years.[7][8][9]

Race

There is no racial predilection for typhoid fever.

Gender

Males are more commonly affected with the typhoid fever than females. The male to female ratio is approximately 1.36 to 1.[8]

Environmental factors

The incidence of typhoid fever increases with an increase in temperature and rainfall.[8]

Developed countries

Typhoid fever is sporadic in developed countries but may be seen in travellers returning from endemic areas. The incidence of typhoid fever in the United States has been stable at about 200-300 cases in 2013.[16]

Developing countries

The incidence and prevalence of typhoid fever is highest in developing countries.[8][2][17][9] The incidence of typhoid fever in the Mekong Delta region of Vietnam and Delhi in India is approximately 198 per 100,000 and 980 per 100,000 per year, respectively, based on recent reports.[18][19]

References

  1. ↑ 1.0 1.1 Crump, J. A., & Mintz, E. D (2010). “Global trends in typhoid and paratyphoid fever”. Clinical Infectious Diseases. 50 (2): 241–246. doi:10.1086/649541. PMID 20014951.
  2. ↑ 2.0 2.1 2.2 Daul CB, deShazo RD, Andes WA, Pankey GA (1986). “Immunologic studies in homosexual and hemophiliac subjects with persistent generalized lymphadenopathy: a comparative analysis”. J Allergy Clin Immunol. 77 (2): 295–301. PMID 3484760.
  3. ↑ 3.0 3.1 Lanata CF, Levine MM, Ristori C, Black RE, Jimenez L, Salcedo M; et al. (1983). “Vi serology in detection of chronic Salmonella typhi carriers in an endemic area”. Lancet. 2 (8347): 441–3. PMID 6192305.
  4. ↑ 4.0 4.1 Crump JA, Luby SP, Mintz ED (2004). “The global burden of typhoid fever”. Bull World Health Organ. 82 (5): 346–53. PMC 2622843. PMID 15298225.
  5. ↑ 5.0 5.1 Lynch MF, Blanton EM, Bulens S, Polyak C, Vojdani J, Stevenson J; et al. (2009). “Typhoid fever in the United States, 1999-2006”. JAMA. 302 (8): 859–65. doi:10.1001/jama.2009.1229. PMID 19706859.
  6. ↑ 6.0 6.1 Jensenius M, Han PV, Schlagenhauf P, Schwartz E, Parola P, Castelli F; et al. (2013). “Acute and potentially life-threatening tropical diseases in western travelers–a GeoSentinel multicenter study, 1996-2011”. Am J Trop Med Hyg. 88 (2): 397–404. doi:10.4269/ajtmh.12-0551. PMC 3583336. PMID 23324216.
  7. ↑ 7.0 7.1 “Typhoid Fever”. World Health Organisation. Retrieved 2007-08-28. Check date values in: |accessdate= (help)
  8. ↑ 8.0 8.1 8.2 8.3 8.4 Dewan AM, Corner R, Hashizume M, Ongee ET (2013). “Typhoid Fever and its association with environmental factors in the Dhaka Metropolitan Area of Bangladesh: a spatial and time-series approach”. PLoS Negl Trop Dis. 7 (1): e1998. doi:10.1371/journal.pntd.0001998. PMC 3554574. PMID 23359825.
  9. ↑ 9.0 9.1 9.2 Schmoldt A, Benthe HF, Haberland G (1975). “Digitoxin metabolism by rat liver microsomes”. Biochem Pharmacol. 24 (17): 1639–41. PMID http://dx.doi.org/10.1016/S0140-6736(98)09 Check |pmid= value (help).
  10. ↑ Infants, children, and adolescents in south-central and Southeast Asia experience the greatest burden of illness.
  11. ↑ Crump JA, Luby SP, Mintz ED (2004). “The global burden of typhoid fever”. Bull World Health Organ. 82: 346–353.
  12. ↑ Schmoldt A, Benthe HF, Haberland G (1975). “Digitoxin metabolism by rat liver microsomes”. Biochem Pharmacol. 24 (17): 1639–41. PMID doi:10.1093/infdis/146.6.724 Check |pmid= value (help).
  13. ↑ 13.0 13.1 13.2 Schmoldt A, Benthe HF, Haberland G (1975). “Digitoxin metabolism by rat liver microsomes”. Biochem Pharmacol. 24 (17): 1639–41. PMID doi:10.1128/jb.00581-12 . doi:10.1128/jb.00581-12 Check |pmid= value (help).
  14. ↑ Imanishi M, Newton AE, Vieira AR, Gonzalez-Aviles G, Kendall Scott ME, Manikonda K; et al. (2015). “Typhoid fever acquired in the United States, 1999-2010: epidemiology, microbiology, and use of a space-time scan statistic for outbreak detection”. Epidemiol Infect. 143 (11): 2343–54. doi:10.1017/S0950268814003021. PMID 25427666.
  15. ↑ Heymann, David L., ed. (2008), Control of Communicable Diseases Manual, Washington, D.C.: American Public Health Association, pg 665. ISBN 978-0-87553-189-2.
  16. ↑ Center for Disease Control United States http://wwwnc.cdc.gov/travel/yellowbook/2016/infectious-diseases-related-to-travel/typhoid-paratyphoid-fever. Accessed on September 12, 2016.
  17. ↑ Baddam R, Kumar N, Thong KL, Ngoi ST, Teh CS, Yap KP; et al. (2012). “Genetic fine structure of a Salmonella enterica serovar Typhi strain associated with the 2005 outbreak of typhoid fever in Kelantan, Malaysia”. J Bacteriol. 194 (13): 3565–6. doi:10.1128/JB.00581-12. PMC 3434757. PMID 22689247.
  18. ↑ Parry CM, Hien TT, Dougan G, White NJ, Farrar JJ (2002). “Typhoid fever”. N Engl J Med. 347 (22): 1770–82. doi:10.1056/NEJMra020201. PMID 12456854.
  19. ↑ Chau TT, Campbell JI, Galindo CM, Van Minh Hoang N, Diep TS, Nga TT; et al. (2007). “Antimicrobial drug resistance of Salmonella enterica serovar typhi in asia and molecular mechanism of reduced susceptibility to the fluoroquinolones”. Antimicrob Agents Chemother. 51 (12): 4315–23. doi:10.1128/AAC.00294-07. PMC 2167998. PMID 17908946.

Template:WH Template:WS

Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Aslam, M.B.B.S[2]

Overview

Common risk factors in the development of typhoid fever are travel to endemic areas, poor hygiene habits, poor sanitation conditions, proximity to flying insects feeding on feces, contact with someone who recently suffered from typhoid fever, recent use of antibiotics, achlorhydria, immunosuppressive illnesses such as AIDS, crowded housing, consumption of raw fruits and vegetables contaminated with sewage, and childhood.[1][2][3][4][5][6] The presence of the C282Y mutation and CFTR polymorphism may confer protection against typhoid fever. [7][8][9]

Risk factors

Common risk factors in the development of typhoid fever are:[1][2][3][10][11][6]

  • Travel to endemic areas
  • Poor hygiene habits
  • Poor sanitation conditions
  • Proximity to flying insects feeding on feces
  • Contact with someone who recently suffered from typhoid fever
  • Recent use of antibiotics
  • Achlorhydria
  • Immunosuppressive illnesses such as AIDS
  • Crowded housing
  • Consumption of raw fruits and vegetables contaminated with sewage
  • Prolonged illness
  • Being a health care worker
  • Being a clinical microbiologists who handles salmonella typhi
  • Childhood

Protective factors

Presence of certain biological characteristics may confer protection against typhoid fever.

C282Y mutation causing hemochromatosis

Hemochromatosis results in depletion of intracellular iron in macrophages, which is required for growth of salmonella typhi.[7][8]

CFTR polymorphism

CFTR protein enables the translocation of salmonella typhi in the intestine if mutated, thereby conferring relative protection against typhoid fever.[9]

References

  1. ↑ 1.0 1.1 Luby SP, Faizan MK, Fisher-Hoch SP, Syed A, Mintz ED, Bhutta ZA; et al. (1998). “Risk factors for typhoid fever in an endemic setting, Karachi, Pakistan”. Epidemiol Infect. 120 (2): 129–38. PMC 2809381. PMID 9593481.
  2. ↑ 2.0 2.1 Marshall E, Howells RE (1986). “Turnover of the surface proteins of adult and third and fourth stage larval Brugia pahangi”. Mol Biochem Parasitol. 18 (1): 17–24. PMID 2870432.
  3. ↑ 3.0 3.1 Srikantiah P, Vafokulov S, Luby SP, Ishmail T, Earhart K, Khodjaev N; et al. (2007). “Epidemiology and risk factors for endemic typhoid fever in Uzbekistan”. Trop Med Int Health. 12 (7): 838–47. doi:10.1111/j.1365-3156.2007.01853.x. PMID 17596250.
  4. ↑ Mermin, Jonathan H., et al. “A massive epidemic of multidrug-resistant typhoid fever in Tajikistan associated with consumption of municipal water.” Journal of Infectious Diseases 179.6 (1999): 1416-1422.
  5. ↑ Black, Robert E., et al. “Case—control study to identify risk factors for paediatric endemic typhoid fever in Santiago, Chile.” Bulletin of the World Health Organization 63.5 (1985): 899.
  6. ↑ 6.0 6.1 Parry CM, Thompson C, Vinh H, Chinh NT, Phuong le T, Ho VA; et al. (2014). “Risk factors for the development of severe typhoid fever in Vietnam”. BMC Infect Dis. 14: 73. doi:10.1186/1471-2334-14-73. PMC 3923984. PMID 24512443.
  7. ↑ 7.0 7.1 Weinberg ED (2008). “Survival advantage of the hemochromatosis C282Y mutation”. Perspect Biol Med. 51 (1): 98–102. doi:10.1353/pbm.2008.0001. PMID 18192769.
  8. ↑ 8.0 8.1 Moalem S, Weinberg ED, Percy ME (2004). “Hemochromatosis and the enigma of misplaced iron: implications for infectious disease and survival”. Biometals. 17 (2): 135–9. PMID 15088940.
  9. ↑ 9.0 9.1 van de Vosse E, de Visser AW, Al-Attar S, Vossen R, Ali S, van Dissel JT (2010). “Distribution of CFTR variations in an Indonesian enteric fever cohort”. Clin Infect Dis. 50 (9): 1231–7. doi:10.1086/651598. PMID 20233062.
  10. ↑ Mermin, Jonathan H., et al. “A massive epidemic of multidrug-resistant typhoid fever in Tajikistan associated with consumption of municipal water.” Journal of Infectious Diseases 179.6 (1999): 1416-1422.
  11. ↑ Black, Robert E., et al. “Case—control study to identify risk factors for paediatric endemic typhoid fever in Santiago, Chile.” Bulletin of the World Health Organization 63.5 (1985): 899.

Template:WH

Template:WS

Screening

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Aslam, M.B.B.S[2]

Overview

There are no screening guidelines for typhoid fever. However, chronic carriers can be screened using ELISA to detect antibodies against the Vi antigen.[1][2]

Screening

There are no screening guidelines for typhoid fever. However, chronic carriers can be screened using ELISA to detect antibodies against the Vi antigen.[2]

References

  1. ↑ http://www.uspreventiveservicestaskforce.org/
  2. ↑ 2.0 2.1 Lanata CF, Levine MM, Ristori C, Black RE, Jimenez L, Salcedo M; et al. (1983). “Vi serology in detection of chronic Salmonella typhi carriers in an endemic area”. Lancet. 2 (8347): 441–3. PMID 6192305.


Template:WH

Template:WS

Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Aslam, M.B.B.S[2]

Overview

Symptoms of typhoid fever, which usually begin to develop 5 to 21 days after ingestion of the causative organism, include fever, headache, malaise, and bradycardia. If left untreated, the patient will develop complications in the second or third week of illness such as intestinal perforation, intestinal hemorrhage, typhoid encephalopathy, meningitis, disseminated intravascular coagulation, miscarriage, or relapse.[1][2][3][4][5][6][7][8][9][10][11][12] Without therapy, the illness may last for 3 to 4 weeks and mortality rates range between 12% and 30%. The prognosis of typhoid fever varies depending on the local incidence rate. The mortality rate of typhoid fever in endemic areas is 1-4% with treatment, while it is less than 1% with treatment in areas with low incidence of typhoid fever.[13][14]

Natural history

The symptoms of typhoid fever usually develop 5 to 21 days after ingestion of the causative organism.[12][15][16][17][18]

First Week Second Week[12] Third Week Fourth Week[16][19]
  • Prostration
  • High grade fever which plateaus around 40°C
  • Bradycardia (Sphygmo-thermic dissociation), classically with a dicrotic pulse wave
  • Delirium or agitation (nervous fever)
  • Rose spots on the lower chest and abdomen (1/3 patients)
  • Rhonchi in lung bases
  • Abdominal pain (right lower quadrant)
  • Diarrhea (six to eight stools/day), green with a characteristic smell, comparable to pea-soup[20]
  • Constipation
  • Resolution
  • Chronic carrier state[14]
  • Death

Complications

Common complications of typhoid fever include:[2][3][4][5][6][7][9][10][11][21][22]

Gastrointestinal

Neurologiocal

Cardiovascular

Respiratory

Heamatologic

Other

Prognosis

Worldwide, the prognosis of typhoid fever varies depending on the local incidence rate. The mortality rate of typhoid fever in endemic areas is 1-4% with treatment as compared to 10-30% without treatment.[13] However, the mortality rate in the areas with low incidence of typhoid fever is less than 1% with treatment.[14]

  • Favorable prognostic factors:
  • Early diagnosis and treatment[25]
  • Susceptibility to drugs[26]
  • Less virulent strain[27]
  • Good compliance
  • Poor prognostic factors:

References

  1. ↑ Bitar, Roger, and John Tarpley. “Intestinal perforation in typhoid fever: a historical and state-of-the-art review.” Review of Infectious Diseases 7.2 (1985): 257-271.
  2. ↑ 2.0 2.1 van Basten JP, Stockenbrügger R (1994). “Typhoid perforation. A review of the literature since 1960”. Trop Geogr Med. 46 (6): 336–9. PMID 7892698.
  3. ↑ 3.0 3.1 3.2 Hoffman SL, Punjabi NH, Kumala S, Moechtar MA, Pulungsih SP, Rivai AR; et al. (1984). “Reduction of mortality in chloramphenicol-treated severe typhoid fever by high-dose dexamethasone”. N Engl J Med. 310 (2): 82–8. doi:10.1056/NEJM198401123100203. PMID 6361558.
  4. ↑ 4.0 4.1 Punjabi NH, Hoffman SL, Edman DC, Sukri N, Laughlin LW, Pulungsih SP; et al. (1988). “Treatment of severe typhoid fever in children with high dose dexamethasone”. Pediatr Infect Dis J. 7 (8): 598–600. PMID 3050856.
  5. ↑ 5.0 5.1 5.2 Seoud M, Saade G, Uwaydah M, Azoury R (1988). “Typhoid fever in pregnancy”. Obstet Gynecol. 71 (5): 711–4. PMID 3357660.
  6. ↑ 6.0 6.1 Reed RP, Klugman KP (1994). “Neonatal typhoid fever”. Pediatr Infect Dis J. 13 (9): 774–7. PMID 7808844.
  7. ↑ 7.0 7.1 7.2 Wain J, Hien TT, Connerton P, Ali T, Parry CM, Chinh NT; et al. (1999). “Molecular typing of multiple-antibiotic-resistant Salmonella enterica serovar Typhi from Vietnam: application to acute and relapse cases of typhoid fever”. J Clin Microbiol. 37 (8): 2466–72. PMC 85257. PMID 10405386.
  8. ↑ Levine, Myron M., Robert E. Black, and Claudio Lanata. “Precise estimation of the numbers of chronic carriers of Salmonella typhi in Santiago, Chile, an endemic area.” Journal of Infectious Diseases 146.6 (1982): 724-726.
  9. ↑ 9.0 9.1 9.2 Gupta SP, Gupta MS, Bhardwaj S, Chugh TD (1985). “Current clinical patterns of typhoid fever: a prospective study”. J Trop Med Hyg. 88 (6): 377–81. PMID 3837121.
  10. ↑ 10.0 10.1 10.2 Huang DB, DuPont HL (2005). “Problem pathogens: extra-intestinal complications of Salmonella enterica serotype Typhi infection”. Lancet Infect Dis. 5 (6): 341–8. doi:10.1016/S1473-3099(05)70138-9. PMID 15919620.
  11. ↑ 11.0 11.1 Lutterloh E, Likaka A, Sejvar J, Manda R, Naiene J, Monroe SS; et al. (2012). “Multidrug-resistant typhoid fever with neurologic findings on the Malawi-Mozambique border”. Clin Infect Dis. 54 (8): 1100–6. doi:10.1093/cid/cis012. PMID 22357702.
  12. ↑ 12.0 12.1 12.2 12.3 Neil KP, Sodha SV, Lukwago L, O-Tipo S, Mikoleit M, Simington SD; et al. (2012). “A large outbreak of typhoid fever associated with a high rate of intestinal perforation in Kasese District, Uganda, 2008-2009”. Clin Infect Dis. 54 (8): 1091–9. doi:10.1093/cid/cis025. PMID 22357703.
  13. ↑ 13.0 13.1 Daul CB, deShazo RD, Andes WA, Pankey GA (1986). “Immunologic studies in homosexual and hemophiliac subjects with persistent generalized lymphadenopathy: a comparative analysis”. J Allergy Clin Immunol. 77 (2): 295–301. PMID 3484760.
  14. ↑ 14.0 14.1 14.2 Lynch MF, Blanton EM, Bulens S, Polyak C, Vojdani J, Stevenson J; et al. (2009). “Typhoid fever in the United States, 1999-2006”. JAMA. 302 (8): 859–65. doi:10.1001/jama.2009.1229. PMID 19706859.
  15. ↑ Schmoldt A, Benthe HF, Haberland G (1975). “Digitoxin metabolism by rat liver microsomes”. Biochem Pharmacol. 24 (17): 1639–41. PMID http://dx.doi.org/10.1016/S0140-6736(98)09 Check |pmid= value (help).
  16. ↑ 16.0 16.1 Crump JA, Luby SP, Mintz ED (2004). “The global burden of typhoid fever”. Bull World Health Organ. 82 (5): 346–53. PMC 2622843. PMID 15298225.
  17. ↑ Khanam F, Sayeed MA, Choudhury FK, Sheikh A, Ahmed D, Goswami D; et al. (2015). “Typhoid fever in young children in Bangladesh: clinical findings, antibiotic susceptibility pattern and immune responses”. PLoS Negl Trop Dis. 9 (4): e0003619. doi:10.1371/journal.pntd.0003619. PMC 4388457. PMID 25849611.
  18. ↑ Bose KS, Sarma RH (1975). “Delineation of the intimate details of the backbone conformation of pyridine nucleotide coenzymes in aqueous solution”. Biochem Biophys Res Commun. 66 (4): 1173–9. PMID Epidemiology, clinical presentation, labo result2 Epidemiology, clinical presentation, labo Check |pmid= value (help).
  19. ↑ http://www.cdc.gov/typhoid-fever/symptoms.html
  20. ↑ Gotuzzo E, Frisancho O, Sanchez J, Liendo G, Carrillo C, Black RE; et al. (1991). “Association between the acquired immunodeficiency syndrome and infection with Salmonella typhi or Salmonella paratyphi in an endemic typhoid area”. Arch Intern Med. 151 (2): 381–2. PMID 1899554.
  21. ↑ Levine, Myron M., Robert E. Black, and Claudio Lanata. “Precise estimation of the numbers of chronic carriers of Salmonella typhi in Santiago, Chile, an endemic area.” Journal of Infectious Diseases 146.6 (1982): 724-726.
  22. ↑ Bitar, Roger, and John Tarpley. “Intestinal perforation in typhoid fever: a historical and state-of-the-art review.” Review of Infectious Diseases 7.2 (1985): 257-271.
  23. ↑ Bitar, Roger, and John Tarpley. “Intestinal perforation in typhoid fever: a historical and state-of-the-art review.” Review of Infectious Diseases 7.2 (1985): 257-271.
  24. ↑ Ali G, Rashid S, Kamli MA, Shah PA, Allaqaband GQ (1997). “Spectrum of neuropsychiatric complications in 791 cases of typhoid fever”. Trop Med Int Health. 2 (4): 314–8. PMID 9171838.
  25. ↑ Swan SK, Gilbert DN, Kohlhepp SJ, Leggett JE, Kohnen PW, Bennett WM (1992). “Duration of the protective effect of polyaspartic acid on experimental gentamicin nephrotoxicity”. Antimicrob Agents Chemother. 36 (11): 2556–8. PMC 284375. PMID 1489205.
  26. ↑ Bhutta, Zulfiqar A., and Husein Lalji Dewraj. “Current concepts in the diagnosis and treatment of typhoid fever.” British Medical Journal 7558 (2006): 78.
  27. ↑ Wain J, Hendriksen RS, Mikoleit ML, Keddy KH, Ochiai RL (2015). “Typhoid fever”. Lancet. 385 (9973): 1136–45. doi:10.1016/S0140-6736(13)62708-7. PMID 25458731.
  28. ↑ Schmoldt A, Benthe HF, Haberland G (1975). “Digitoxin metabolism by rat liver microsomes”. Biochem Pharmacol. 24 (17): 1639–41. PMID :10.1136/adc.75.3.214 Check |pmid= value (help).
  29. ↑ Butler, Thomas, et al. “Patterns of Morbidity and Mortality in Typhoid Fever Dependent on Age and Gender: Review of 552 Hopitalized Patients with Diarrhea.” Review of Infectious Diseases 13.1 (1991): 85-90.
  30. ↑ Chalya PL, Mabula JB, Koy M, Kataraihya JB, Jaka H, Mshana SE; et al. (2012). “Typhoid intestinal perforations at a University teaching hospital in Northwestern Tanzania: A surgical experience of 104 cases in a resource-limited setting”. World J Emerg Surg. 7: 4. doi:10.1186/1749-7922-7-4. PMC 3311140. PMID 22401289.
  31. ↑ 31.0 31.1 Parry CM, Hien TT, Dougan G, White NJ, Farrar JJ (2002). “Typhoid fever”. N Engl J Med. 347 (22): 1770–82. doi:10.1056/NEJMra020201. PMID 12456854.
  32. ↑ Van Belle H, Goossens F, Wynants J (1987). “Formation and release of purine catabolites during hypoperfusion, anoxia, and ischemia”. Am J Physiol. 252 (5 Pt 2): H886–93. PMID 3578539.
  33. ↑ Bhutta ZA (1996). “Impact of age and drug resistance on mortality in typhoid fever”. Arch Dis Child. 75 (3): 214–7. PMC 1511710. PMID 8976660.

Template:WH

Template:WS

Diagnosis

Diagnosis

History and Symptoms | | Physical Examination |Surgical therapy | Laboratory Findings | Other diagnostic tests | X ray | CT | MRI | Ultrasound | Other Imaging Findings

Treatment

Treatment

Medical Therapy | Primary Prevention | Secondary Prevention | Cost Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

Related Chapters
For a similar disease with a similar name, see typhus.
For a related disease which is caused by a different bacterium, see Paratyphoid fever.
External links

Template:Bacterial diseases


Template:WikiDoc Sources

Looking for the patient version?

Back to the patient-friendly article

Imprint

Privacy Policy

Terms and Conditions

© 2026 MyEClinic – IFTM Institut für Telematik in der Medizin GmbH