eMedicine Specialties > Infectious Diseases > Bacterial Infections

Typhoid Fever

Author: John L Brusch, MD, FACP, Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance
Coauthor(s): Thomas Garvey, MD, JD, Chief, Medical Affiliated Services, Department of Medicine, Lemuel Shattuck Hospital; Attending Physician, Chest Clinic, Lawrence Memorial Hospital; Co-chair, Medical Advisory Committee for the Elimination of Tuberculosis; Roberto Corales, DO, Medical Director, Principal Investigator, AIDS Community Health Center; Steven K Schmitt, MD, Co-director of Infectious Disease Fellowship Program, Department of Infectious Disease, The Cleveland Clinic Foundation
Contributor Information and Disclosures

Updated: Dec 3, 2008

Introduction

Background

Typhoid fever, also known as enteric fever, is a potentially fatal multisystemic illness caused primarily by Salmonella typhi. The protean manifestations of typhoid fever make this disease a true diagnostic challenge. The classic presentation includes fever, malaise, diffuse abdominal pain, and constipation. Untreated, typhoid fever is a grueling illness that may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death within one month of onset. Survivors may be left with long-term or permanent neuropsychiatric complications.

S typhi has been a major human pathogen for thousands of years, thriving in conditions of poor sanitation, crowding, and social chaos. It may have responsible for the Great Plague of Athens at the end of the Pelopennesian War.1 The name S typhi is derived from the ancient Greek typhos, an ethereal smoke or cloud that was believed to cause disease and madness. In the advanced stages of typhoid fever, the patient's level of consciousness is truly clouded. Although antibiotics have markedly reduced the frequency of typhoid fever in the developed world, it remains endemic in developing countries.2

Transmission

S typhi has no nonhuman vectors. The following are modes of transmission:

  • Oral transmission via food or beverages handled by an individual who chronically sheds the bacteria through stool or, less commonly, urine
  • Hand-to-mouth transmission after using a contaminated toilet and neglecting hand hygiene
  • Oral transmission via sewage-contaminated water or shellfish (especially in the developing world)3

An inoculum as small as 100,000 organisms causes infection in more than 50% of healthy volunteers.4

Pathophysiology

All pathogenic Salmonella species are engulfed by phagocytic cells, which then pass them through the mucosa and present them to the macrophages in the lamina propria. Nontyphoidal salmonellae are phagocytized throughout the distal ilium and colon. With toll-like receptor (TLR)–5 and TLR-4/MD2/CD-14 complex, macrophages recognize pathogen-associated molecular patterns (PAMPs) such as flagella and lipopolysaccharides. Macrophages and intestinal epithelial cells then attract T cells and neutrophils with interleukin 8 (IL-8), causing inflammation and suppressing the infection.5,6

In contrast to the nontyphoidal salmonellae, S typhi enters the host's system primarily through the distal ilium. S typhi has specialized fimbriae that adhere to the epithelium over clusters of lymphoid tissue in the ilium (Peyer patches), the main relay point for macrophages traveling from the gut into the lymphatic system. S typhi has a Vi capsular antigen that masks PAMPs, avoiding neutrophil-based inflammation. The bacteria then induce their host macrophages to attract more macrophages.5

It co-opts the macrophages' cellular machinery for their own reproduction7 as it is carried through the mesenteric lymph nodes to the thoracic duct and the lymphatics and then through to the reticuloendothelial tissues of the liver, spleen, bone marrow, and lymph nodes. Once there, the S typhi bacteria pause and continue to multiply until some critical density is reached. Afterward, the bacteria induce macrophage apoptosis, breaking out into the bloodstream to invade the rest of the body.6

The gallbladder is then infected via either bacteremia or direct extension of S typhi –infected bile. The result is that the organism re-enters the gastrointestinal tract in the bile and reinfects Peyer patches. Bacteria that do not reinfect the host are typically shed in the stool and are then available to infect other hosts.6,2

Life cycle of <EM>Salmonella typhi</EM>.

Life cycle of Salmonella typhi.

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Life cycle of <EM>Salmonella typhi</EM>.

Life cycle of Salmonella typhi.


Risk factors

S typhi are able to survive a stomach pH as low as 1.5. Antacids, histamine-2 receptor antagonists (H2 blockers), proton pump inhibitors, gastrectomy, and achlorhydria decrease stomach acidity and facilitate S typhi infection.6

HIV/AIDS is clearly associated with an increased risk of nontyphoidal Salmonella infection; however, the data and opinions in the literature as to whether this is true for S typhi infection are conflicting. If an association exists, it is probably minor.8,9,10,11

Other risk factors for clinical S typhi infection include various genetic polymorphisms. These risk factors often also predispose to other intracellular pathogens. For instance, PARK2 and PACGR code for a protein aggregate that is essential for breaking down the bacterial signaling molecules that dampen the macrophage response. Polymorphisms in their shared regulatory region are found disproportionately in persons infected with Mycobacterium leprae and S typhi.12

On the other hand, protective host mutations also exist. The fimbriae of S typhi bind in vitro to cystic fibrosis transmembrane conductance receptor (CFTR), which is expressed on the gut membrane. Two to 5% of white persons are heterozygous for the CFTR mutation F508del, which is associated with a decreased susceptibility to typhoid fever, as well as to cholera and tuberculosis. The homozygous F508del mutation in CFTR is associated with cystic fibrosis. Thus, typhoid fever may contribute to evolutionary pressure that maintains a steady occurrence of cystic fibrosis, just as malaria maintains sickle cell disease in Africa.13,14

Environmental and behavioral risk factors that are independently associated with typhoid fever include eating food from street vendors, living in the same household with someone who has new case of typhoid fever, washing the hands inadequately, sharing food from the same plate, drinking unpurified water, and living in a household that does not have a toilet.15,12 As the middle class in south Asia grows, some hospitals there are seeing a large number of typhoid fever cases among relatively well-off university students who live in group households with poor hygeine.16 American clinicians should keep this in mind, as members of this cohort often come to the United States for higher degrees.

Frequency

United States

Since 1900, improved sanitation and successful antibiotic treatment have steadily decreased the incidence of typhoid fever in the United States. In 1920, 35,994 cases of typhoid fever were reported. Currently, 200-400 cases of typhoid fever are reported per year in the United States, 75% of which occur in international travelers (mostly to the Indian subcontinent and Latin America)17 within 30 days of entry. The rare outbreaks of typhoid fever due to S typhi transmission within the United States are generally traceable to imported food or to a food handler from an endemic region.2

International

Typhoid fever occurs worldwide, primarily in developing nations whose sanitary conditions are poor. Typhoid fever is endemic in Asia, Africa, Latin America, the Caribbean, and Oceania. Typhoid fever infects roughly 21.6 million people and kills an estimated 200,000 people every year.18

Mortality/Morbidity

With prompt and appropriate antibiotic therapy, typhoid fever is typically a short-term febrile illness with a negligible risk of mortality. Untreated typhoid fever is a life-threatening illness of several weeks' duration with long-term morbidity. The case fatality rate in the United States in the pre-antibiotic era was 9-13%.19

Race

Typhoid fever has no racial predilection.

Sex

Typhoid fever has no sexual predilection.

Age

Most documented typhoid fever cases involve school-aged children and young adults. However, the true incidence among very young children and infants is thought to be higher. The presentations in these age groups may be atypical, ranging from a mild febrile illness to severe convulsions, and the S typhi infection may go unrecognized. This may account for conflicting reports in the literature that this group has either a very high or a very low rate of morbidity and mortality.16,20

Clinical

History

A severe nonspecific febrile illness in a patient who has been exposed to S typhi should always raise the diagnostic possibility of typhoid fever (enteric fever).

Classic typhoid fever syndrome

Typhoid fever begins 7-14 days after ingestion of S typhi. The fever pattern is stepwise, characterized by a rising temperature over the course of each day that drops by the subsequent morning. The peaks and troughs rise progressively over time.

Over the course of the first week of illness, the notorious gastrointestinal manifestations of the disease develop. These include diffuse abdominal pain and tenderness and, in some cases, fierce colicky right upper quadrant pain. Monocytic infiltration inflames Peyer patches and narrows the bowel lumen, causing constipation that lasts the duration of the illness. The individual then develops a dry cough, dull frontal headache, delirium, and an increasingly stuporous malaise.2

At approximately the end of the first week of illness, the fever plateaus at 103-104°F (39-40°C). The patient develops rose spots, which are salmon-colored, blanching, truncal, maculopapules usually 1-4 cm wide and fewer than 5 in number; these generally resolve within 2-5 days.2 These are bacterial emboli to the dermis and occasionally develop in persons with shigellosis or nontyphoidal salmonellosis.21

During the second week of illness, the signs and symptoms listed above progress. The abdomen becomes distended, and soft splenomegaly is common. Relative bradycardia and dicrotic pulse (double beat, the second beat weaker than the first) may develop.

In the third week, the still febrile individual grows more toxic and anorexic with significant weight loss. The conjunctivae are infected, and the patient is tachypneic with a thready pulse and crackles over the lung bases. Abdominal distension is severe. Some patients experience foul, green-yellow, liquid diarrhea (pea soup diarrhea). The individual may descend into the typhoid state, which is characterized by apathy, confusion, and even psychosis. Necrotic Peyer patches may cause bowel perforation and peritonitis. This complication is often unheralded and may be masked by corticosteroids. At this point, overwhelming toxemia, myocarditis, or intestinal hemorrhage may cause death.

If the individual survives to the fourth week, the fever, mental state, and abdominal distension slowly improve over a few days. Intestinal and neurologic complications may still occur in surviving untreated individuals. Weight loss and debilitating weakness last months. Some survivors become asymptomatic S typhi carriers and have the potential to transmit the bacteria indefinitely.16,22,23,2,6

Various presentations of typhoid fever

The clinical course of a given individual with typhoid fever may deviate from the above description of classic disease. The timing of the symptoms and host response may vary based on geographic region, race factors, and the infecting bacterial strain. The stepladder fever pattern that was once the hallmark of typhoid fever now occurs in as few as 12% of cases. In most contemporary presentations of typhoid fever, the fever has a steady insidious onset.

Young children, individuals with AIDS, and one third of immunocompetent adults who develop typhoid fever develop diarrhea rather than constipation. In addition, in some localities, typhoid fever is generally more apt to cause diarrhea than constipation.

Atypical manifestations of typhoid fever include isolated severe headaches that may mimic meningitis, acute lobar pneumonia, isolated arthralgias, urinary symptoms, severe jaundice, or fever alone. Some patients, especially in India and Africa, present primarily with neurologic manifestations such as delirium or, in extremely rare cases, parkinsonian symptoms or Guillain-Barré syndrome. Other unusual complications include pancreatitis,24 meningitis, orchitis, osteomyelitis, and abscesses anywhere on the body.2

Table 1. Incidence and Timing of Various Manifestations of Untreated Typhoid Fever2,25,26,27,28

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Table
 
Incubation
Week 1
Week 2
Week 3
Week 4
Post
Systemic
Recovery phase or death (15% of untreated cases)
10-20% relapse; 3-4% chronic carriers;
long-term neurologic sequelae (extremely rare);
gallbladder cancer (RR=167; carriers)
Stepladder fever pattern or insidious onset fever
 
Very commona
Very common
Acute high fever
 
Very rareb
 
 
Chills
 
Almost allc
Rigors
 
Uncommon
Anorexia
 
Almost all
Diaphoresis
 
Very common
Neurologic
Malaise
 
Almost all
Almost all
Typhoid state (common)
Insomnia
 
 
Very common
Confusion/delirium
 
Commond
Very common
Psychosis
 
Very rare
Common
 
Catatonia
 
Very rare
 
 
Frontal headache
(usually mild)
 
Very common
 
 
Meningeal signs
 
Raree
Rare
 
Parkinsonism
 
Very rare
 
 
Ear, nose, and throat
Coated tongue
 
Very common
 
 
Sore throatf
 
 
 
 
Pulmonary
Mild cough
 
Common
 
 
Bronchitic cough
 
Uncommon
 
 
Rales
 
Common
 
 
Pneumonia
 
Rare (lobar)
Rare
Common
(basal)
Cardiovascular
Dicrotic pulse
 
Rare
Common
Myocarditis
 
Rare
 
 
Pericarditis
 
Extremely rareg
 
 
Thrombophlebitis
 
 
 
Very rare
Gastrointestinal
Constipation
 
Very common
Common
Diarrhea
 
Rare
Common (pea soup)
Bloating
 
Very common
 
 
 
Diffuse mild abdominal pain
 
Very common
 
 
 
Sharp right lower quadrant pain
 
Rare
 
 
 
Gastrointestinal hemorrhage
 
Very rare; usually trace
Very common
intestinal perforation
 
 
 
Rare
Hepatosplenomegaly
 
Common
Jaundice
 
Common
Gallbladder pain
 
Very rare
Urogenital
Urinary retention
 
Common
Hematuria
 
Rare
Renal pain
 
Rare
Musculoskeletal
Myalgias
Very rare
Arthralgias
Very rare
Rheumatologic
Arthritis (large joint)
Extremely rare
Dermatologic
Rose spots
 
Rare
Miscellaneous
Abscess (anywhere)
 
Extremely rare
Extremely rare
Extremely rare
 
Incubation
Week 1
Week 2
Week 3
Week 4
Post
Systemic
Recovery phase or death (15% of untreated cases)
10-20% relapse; 3-4% chronic carriers;
long-term neurologic sequelae (extremely rare);
gallbladder cancer (RR=167; carriers)
Stepladder fever pattern or insidious onset fever
 
Very commona
Very common
Acute high fever
 
Very rareb
 
 
Chills
 
Almost allc
Rigors
 
Uncommon
Anorexia
 
Almost all
Diaphoresis
 
Very common
Neurologic
Malaise
 
Almost all
Almost all
Typhoid state (common)
Insomnia
 
 
Very common
Confusion/delirium
 
Commond
Very common
Psychosis
 
Very rare
Common
 
Catatonia
 
Very rare
 
 
Frontal headache
(usually mild)
 
Very common
 
 
Meningeal signs
 
Raree
Rare
 
Parkinsonism
 
Very rare
 
 
Ear, nose, and throat
Coated tongue
 
Very common
 
 
Sore throatf
 
 
 
 
Pulmonary
Mild cough
 
Common
 
 
Bronchitic cough
 
Uncommon
 
 
Rales
 
Common
 
 
Pneumonia
 
Rare (lobar)
Rare
Common
(basal)
Cardiovascular
Dicrotic pulse
 
Rare
Common
Myocarditis
 
Rare
 
 
Pericarditis
 
Extremely rareg
 
 
Thrombophlebitis
 
 
 
Very rare
Gastrointestinal
Constipation
 
Very common
Common
Diarrhea
 
Rare
Common (pea soup)
Bloating
 
Very common
 
 
 
Diffuse mild abdominal pain
 
Very common
 
 
 
Sharp right lower quadrant pain
 
Rare
 
 
 
Gastrointestinal hemorrhage
 
Very rare; usually trace
Very common
intestinal perforation
 
 
 
Rare
Hepatosplenomegaly
 
Common
Jaundice
 
Common
Gallbladder pain
 
Very rare
Urogenital
Urinary retention
 
Common
Hematuria
 
Rare
Renal pain
 
Rare
Musculoskeletal
Myalgias
Very rare
Arthralgias
Very rare
Rheumatologic
Arthritis (large joint)
Extremely rare
Dermatologic
Rose spots
 
Rare
Miscellaneous
Abscess (anywhere)
 
Extremely rare
Extremely rare
Extremely rare

a Very common: Symptoms occur in well over half of cases (approximately 65%-95%).
b Very rare: Symptoms occur in less than 5% of cases.
c Almost all: Symptoms occur in almost all cases.
d Common: Symptoms occur in 35-65% of cases.
e Rare: Symptoms occur in 5-35% of cases.
f Blank cells: No mention of the symptom at that phase was found in the literature.
g Extremely rare: Symptoms have been described in occasional case reports.

Treated typhoid Fever
If appropriate treatment is initiated within the first few days of full-blown illness, the disease begins to remit after about 2 days, and the patient's condition markedly improves within 4-5 days. Any delay in treatment increases the likelihood of complications and recovery time.

Physical

See History.

Causes

S typhi and Salmonella paratyphi cause typhoid fever.

More on Typhoid Fever

Overview: Typhoid Fever
Differential Diagnoses & Workup: Typhoid Fever
Treatment & Medication: Typhoid Fever
Follow-up: Typhoid Fever
Multimedia: Typhoid Fever
References
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Further Reading

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Keywords

typhoid fever, enteric fever, Eberth disease, Salmonella typhi, S typhi, Salmonella choleraesuis, S choleraesuis, Salmonella enterica, S enterica, Enterobacteriaceae, paratyphoid fever, rose spots, typhoid state, Widal test, pneumotyphoid, typhoid cystitis

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Contributor Information and Disclosures

Author

John L Brusch, MD, FACP, Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance
John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Coauthor(s)

Thomas Garvey, MD, JD, Chief, Medical Affiliated Services, Department of Medicine, Lemuel Shattuck Hospital; Attending Physician, Chest Clinic, Lawrence Memorial Hospital; Co-chair, Medical Advisory Committee for the Elimination of Tuberculosis
Thomas Garvey, MD, JD is a member of the following medical societies: American College of Legal Medicine, American College of Physicians, American Society of Law Medicine and Ethics, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Roberto Corales, DO, Medical Director, Principal Investigator, AIDS Community Health Center
Roberto Corales, DO is a member of the following medical societies: American Medical Association, American Osteopathic Association, and International AIDS Society
Disclosure: Nothing to disclose.

Steven K Schmitt, MD, Co-director of Infectious Disease Fellowship Program, Department of Infectious Disease, The Cleveland Clinic Foundation
Steven K Schmitt, MD is a member of the following medical societies: Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Medical Editor

Martin J Wood, MD †, Former Consulting Staff, Department of Infection and Tropical Medicine, Birmingham Heartlands Hospital, UK
Martin J Wood, MD † is a member of the following medical societies: Alliance for the Prudent Use of Antibiotics, American Society for Microbiology, Infectious Diseases Society of America, International Society for Infectious Diseases, and Royal College of Physicians
Disclosure: Nothing to disclose.

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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Richard B Brown, MD, FACP, Chief, Division of Infectious Diseases, Baystate Medical Center; Professor, Department of Internal Medicine, Tufts University School of Medicine
Richard B Brown, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
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