Typhoid fever overview

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Differentiating Typhoid fever from other Diseases

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

Causes

Typhoid fever is caused by Salmonella enterica serotype Typhi (Salmonella Typhi).[16][17][18][19][20][21] 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.[22]

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.[23][24][5][25][26]

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.[27][28] Worldwide, typhoid fever is most prevalent in overcrowded areas that 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 the individuals who are infected will develop a chronic infection in the gall bladder[29][30]. Worldwide, the incidence of typhoid fever varies in different parts of world[31][26][32]. Age, race, gender and certain environmental factors affect the distribution of disease among these groups[33][34][35].

Risk factors

Common risk factors in the development of typhoid fever are travel to endemic areas, poor hygiene habits, poor sanitation conditions, flying insects feeding on feces, contact with person recently suffered typhoid fever, recent use of antibiotics, achlorhydria, immunosuppressive illnesses such as AIDS, crowded housing, usage of raw fruits and vegetables contaminated with sewage, prolonged illness, health care workers exposed to typhoid infection, clinical microbiologists handling salmonella typhi, childhood period. [36][37][38][39][40][41]. Presence of C282 mutation and CFTR polymorphism may confer protection against typhoid fever. [42][43][44]

Screening

There are no screening guidelines for typhoid fever. However, chronic carriers can be screened using elisa detecting antibodies against Vi antigen.[45][30]

Natural history and complications

The symptoms of typhoid fever usually develop after 5 to 21 days of ingestion of causative organism. If left untreated, patient develops complications in second or third week of illness such as intestinal hemorrhage, bleeding and other life threatening illnesses.[46] Without therapy, the illness may last for 3 to 4 weeks and death rates range between 12% and 30%. Common complications of typhoid fever include intestinal perforation, intestinal hemorrhage, typhoid encephalopathy, meningitis, disseminated intravascular coagulation, miscarriage and relapse.[47][48][49][50][51][52][53][54][55][56][57] Prognosis of typhoid fever varies depending on the incidence rate. The mortality rate of typhoid fever in endemic areas is 1-4% with treatment.[28] However, the mortality rate in the areas with low incidence of typhoid fever is less than 1% with treatment.[26]

Diagnosis

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

History and Symptoms

Obtaining history is the most important aspect of making a diagnosis of typhoid fever. Obtaining history is the most important aspect of making a diagnosis of typhoid fever. It provides insight into cause, risk factors, and associated comorbid conditions. Common symptoms of typhoid fever include stepledder increase in temperature initially and than sustained fever as high as 40°C (104°F)[58], profuse sweating, influenza-like symptoms with chills, malaise, headache[49], poorly localised abdominal pain[59], diarrhea[60], constipation, loss of apatite, nausea[59] and vomiting.

Physical Examination

Physical examination findings are described according to the timing of presentation. These include stepwise increase in temperature, bradycardia,[61] abdominal tenderness, hepatosplenomegaly initially. In the third week of illness patient may present with signs showing complications.[5][62]

Laboratory Findings

Nonspecific laboratory abnormalities associated with typhoid fever include decrease heamoglobin, decreased or increased leukocyte count, elevated CPR, and abnormal liver function tests.[63][5][64][65][66]

X ray

X ray findings may help 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 scan is commonly reserved for patients with complications of typhoid fever such as intestinal perforation, bleeding and abcess formation. It may also help in differentiating typhoid fever from other diseases.[81]

MRI

MRI may help diagnose complications of typhoid fever such as neurological complications, liver and splenic abcesses, osteomyelitis and typhoid spine.[82][83]

Ultrasound

Ultrasonography may help in diagnosing complications of typhoid fever and differentiate it from other diseases presenting with similar symptomatology.[84][68][69][24]

Other Imaging Findings

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

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 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.
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  15. ↑ Keuter, Monique, et al. "Patterns of proinflammatory cytokines and inhibitors during typhoid fever." Journal of Infectious Diseases 169.6 (1994): 1306-1311.
  16. ↑ 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.
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  19. ↑ 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.
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  21. ↑ http://www.cdc.gov/typhoid-fever/health-professional.html
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  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.
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  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.

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