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Enteric Fever: A Review of Ninety Cases

Bienvenido D. Alora, M.D., D.T.M. & H.* and Pamela Lloren,M.D.**


(*Associate Professor and Chief, Section of Infectious Diseases, Department of Medicine, Faculty of Medicine and
Surgery; **Senior Resident, Dept. of Medicine, STUH)
SUMMARY
Ninety cases of enteric fever admitted in tile Santo Tomas University Hospital, Clinical Division from 1973
to 1977 were reviewed. Fifty five percent were males and the majority was in the first and second decades of life.
The clinical and physical features were discussed. Fever, toxemia, and relative bradycardia were the most
common symptoms.
The different laboratory findings, complications, and management were presented. [Phil J Microbiol Infect
Dis 1980; 9(2):118-128]
Key Words: enteric fever, Salmonella typhi, Salmonella paratyphi, salmonellosis
INTRODUCTION
Enteric fever is essentially a human infection and the invariable source is either a patient
suffering from a mild form, or a chronic carrier. Salmonella typhi, the most serious cause of
enteric fever, affects mainly the lower part of the ileum where it enters the lymphoid follicles.
These undergo necrosis and ulceration, the mesenteric lymph nodes become infected and the
salmonella invades the bloodstream via the thoracic duct. Bacteremia begins during the first week
and may continue up to the fourth week. During this phase, the bone marrow, spleen, kidney,
liver, and gallbladder may become infected. The gallbladder may re-infect the intestines causing
further acute infla mmation of the lymphoid follicles. Salmonella paratyphi may produce
ulceration lower down in the intestines and these organisms pass through the feces resulting in
contamination of the water and food supply by carriers or flies which are the usual transmission
of infection.(Figure 1)
Figure 1. Pathophysiology of Enteric Fever
Medical history attests that enteric fever has existed for several centuries. Willis made the
first description of the epidemic typhoid in 1659. Gerhard, in 1837, was the first to clearly
differentiate typhoid from typhus fever. In 1880, Eberth discovered the typhoid agglutinins and
its diagnostic application. In 1896, Archard and Bensaude were the first to isolate S. paratyphi
and other salmonella. In 1948, Woodward et al first used Chloramphenicol against typhoid fever
(Table 1).
Table 1. Historical Background
Willis (1659) first description of epidemic typhoid
Gerhard (1837) first distinct differentiation of typhoid from typhus fever
Eberth (1880) discoverer of typhoid bacillus
Widal (1895) discoverer of typhoid agglutinins and its diagnostic applications
Archard and Bensaude (1896) discoverer of paratyphoid bacillus and other salmonellae
Woodward et al first used chloramphenicol vs. typhoid fever
Enteric fever is still one of the major health problems in the Philippines today. A total of
150 cases admitted at the STUH-CD were diagnosed as enteric fever. Ninety of the eases were
selected for this review upon fulfilling the following criteria: first, clinical features of prolonged
pyrexia of more than one week duration, toxemia, or pulse fever disproportion, second, positive
Widal test, or positive bacteriologic culture in the blood, urine or stool or a histologic picture
compatible with enteric fever, and third, favorable response to treatment against enteric fever
(Table 2)
It is the objective of this paper to determine the incidence the clinical and laboratory
features, complications and management of enteric fever in our hospital.
Table 2. Criteria
Clinical features
a. Prolonged pyrexia (more than one week duration)
b. Toxemia
c. Pulse and fever disproportion
d. Splenomegaly and/or hepatomegaly
e. Rose spots
Laboratory Features
a. Positive Wida1 Test
b. Positive bacteriologic culture in the blood, stoo1, or urine
c. Histopathologic picture
Favorable response to medications against enteric fever
Table 3 shows the age and sex distribution. 55% were males and the majority was in the
first and second decades of life.
Table 3. Age and Sex Distribution
Age Male Female Total
10 - 19 18 16 34 (38%)
20 - 29 19 15 34 (38%)
30 - 39 7 4 11 (12%)
40 - 49 5 4 9 (10%)
50 - above 1 1 2 (2%)
Total 50 (55%) 40 (45%) 90 (100%)
Table 4 illustrates the different clinical manifestations. Fever was the most constant
symptom in our series, Headaches and chills were present hi 53%, abdominal pain 48%, anorexia
in 44%, malaise in 33%, vomiting in31%, diarrhea in 29%. Jaundice was seen in 15.5% of the
patients as corn-pared to the 50% reported by Perez et al in 1973. Constipation and nausea were
seen in 12% and disorientation in 3%.
Table 4. Clinical Manifestations
No. Percent
Fever 90 100%
Headache 48 53%
Chills 48 53%
Abdominal Pain 43 48%
Anorexia 40 44%
Malaise 30 33%
Vomiting 28 31%
Diarrhea 26 29%
Jaundice 14 15.5%
Constipation 11 12%
Nausea 11 12%
Disorientation 3 3%
Table 5 presents the various physical features in our series. Pyrexia was present in all.
The type, severity, and duration of pyrexia were not helpful in the diagnosis. The temperature was
usually high (39.5OC) but it was sometimes moderate (37.7OC) to (39OC) or even subnormal (less
than 37.7°C).
Toxemia was seen in 88% of the cases. Foreign authors reported a lower incidence of 34-
45.6%. Relative bradycardia was present in 73%. Development of tachycardia in some patients
indicated complications such as hemorrhage or other associated infections. Abdominal tenderness
was present in 46.6%; Lucindo et al reported a similar incidence while Perez showed a higher
incidence of 59%. Hepatomegaly was present in 26.6% and splenomegaly, in 12% as compared
to Perez with a higher incidence of 31% and 27%. Congested throat was seen in 11%; CVA
tenderness in 3%, rose spots and stupor in 2% each. Lucindo reported a lower incidence of rose
spots, 0.9%.
Table 5. Physical Features
No. Percent
Fever 90 1,00%
Toxemia 79 88%
Relative bradycardia 66 73%
Abdominal tenderness 41 46.6%
Hepatomegaly 24 26.6%
Splenomegaly 11 12%
Congested throat 10 11,%
CVA tenderness 3 3%
Rose spots 2 2%
Stupor 2 2%
Table 7 shows the results of laboratory examination and procedures in this series. Widal
test was positive in 63% of cases at 1:160 level adequate for diagnosis of enteric fever. There
were some patients where the Widal test was not done. Blood culture was positive in only one
case. Liver biopsy done in two patients showed granulomatous necrosis of parenchymal
degeneration compatible with enteric fever. Hb level of less than 10 gms was noted in 28 patients
or 31%. Sixty four percent showed normal wbc, 26.7% had leukocytosis, and 4% showed
leukopenia. Lymphocytosis was noted in 65.5% and thrombocytopenia in 3% or 3 patients. The
liver function tests showed varying degrees of bilirubin levels, in 16 patients it was over 2 mgs,
more of the direct type. The serum transaminases done in 10-20% of the cases were not
considerab1y elevated as compared to viral hepatitis with levels beyond 500 units. Urinary
findings showed mild pyuria and cylindruria in 3% respectively and bacteriuria in 1%.
Table 6. Laboratory Features
No. Percent
A. Widal test
Positive 57 64%
Negative 12 36%
B. Bacteriologic Studies
Blood culture
Positive 1
Negative 10
Stool culture Negative 11 100%
Urine culture Negative 4 100%
C. Liver biopsy Positive 4 100%
D. Blood test
Hemoglobin (less than 10 gms) 28 31%
WBC
Normal 58 64 %
Leucocytosis (more than 10,000/cu mm) 24 26%
Leucopenia (less than 5,000/cu mm) 4 4%
Lymphocytosis (more than 30%) 59 65.5%
Thrombocytopenia (less than 160,000/cu mm) 3 3%
D. Liver Function Tests
S. Bilirubin (above 2 mg%) 16 18%
SGOT (above 50 units) 13 14.4%
SGPT (above 50 units) 9 10%
F. Urinary Findings
Pyuria (more than 4 cells/HPF) 3 3%
Cylindruria 3 3%
Bacteriuria 1 1%
Table 7 discloses the different complications encountered in the series. Hemorrhage
occurred in 25.5% mostly affecting the GI tract. Pangan reported a similar incidence of 26% in
1971 while Perez showed a lower incidence of 21% in 1973. Pneumonitis was noted in 18
patients or 21%, ileus and mechanical obstruction 1% each. Perforation developed in one case
with detection of pneumoperitoneum by x-ray. This patient eventually succumbed and
postmortem showed hyperplasia of Peyer's patches with enlarged mesenteric pericolic,
portohepatic lymph nodes. Pangan reported a 28% mortality rate in patients with perforation. One
patient developed psychosis and another had an abortion during the course of the illness.
Table 7. Complications
No. Percent
Intestinal Hemorrhage 23 25.5%
Pneumonitis 18 2.1%
Ileus 1 1%
Mechanical Obstruction 1 1%
Perforation 1 1%
Psychosis 1 1%
Abortion 1 1%
Table 8 presents the treatment of enteric fever. All of the patients were managed
medically. Twenty four or 26.6% responded to cotrimoxazole, 17 or 19% to chloramphenicol
alone, 15 or 17% to a combination of chloramphenicol and cotrimoxazole, 14 or 16% to
chloramphenicol + cotrimoxazole with steroids. The rest responded with either chloramphenicol
or cotrimoxazole together with other antibiotics or steroids, General supportive management of
the patient supplemented antibiotic therapy. Bed rest extending to early convalescence was
essential. All patients were hydrated and only 8 or 9% received blood transfusion. Laxatives and
promiscuous use of enemas were avoided because of the danger of perforation or hemorrhage of
the intestinal lesions. Ambulation was initiated gradually to avoid undue fatigue and exertion.
Table 8. Management
No. Percent
A. Antibiotics
Cotrimoxazole 24 26.6%
Chloramphenicol 17 19%
Chloramphenicol + Cotrimoxazole 15 17%
Chloramphenicol + Cotrimoxazole + Steroids 5 5.5%
Chloramphenicol + Other Antibiotics 5
Cotrimoxazole + Steroids 5
Cotrimoxazole + Other Antibiotics 5
Chloramphenicol + Cotrimoxazole + Other Antibiotics 2
Ampicillin 1
B. Supportive
Blood transfusion 8 9%
REFERENCES
1. Castillo R, Pangan J. et al. Intestinal hemorrhage in typhoid fever. Santo Tomas J Med 1971; 26:310.
2. Lucindo et al. A review of typhoid fever in San Lazaro Hospital. PJMID.
3. Perez J, et al. Typhoid fever at Santo Tomes University Hospital Clinical Division. Santo Tomas J Med 1972; 27:145.
4. Stuart BM, Pullin RL. Typhoid clinical analysis of 360 cases. Arch Intern Med 1946; 78:629.
5. Butler T, et al. Typhoid fever. Arch Intern Med 1978; 138:407.
6. Gamboa EL. Observations on typhoid fever, Santo Tomas J Med 1952; 7:142.
7. Studies in typhoid fever, Nos. I, III and III. Johns Hopkins Hospital, Baltimore: The Johns Hopkins Press, 1901.
8. Typhoid Fever Co nsidered as a Problem of Scientific Medicine. Semi-centennial Publications of the University of California. pp.
1968-1918
9. Cecil, Loeb, Beeson, McDermott. Textbook of Medicine, 13th ed., 1971.
10. Current Diagnosis and Treatment. Kruff, Chatton, Margen (eds). Lange Medical Library II, 1971.
11. Barglow D. Typhoid fever. Practice of Medicine. Tice-Sloan, W.F. Prior, Co., Inc., 4:459-565; 1959.
12. Paulson M. Acute Diarrhea. Gastroenterologic Medicine. Philadelphia: Lea and Febiger 1969. pp. 860-871,
13. Kolmer JA, et al. Approved laboratory technique, Ed. 5. New York: Appleton-Century-Croft, Inc., 1951.
14. Woodward T, et al. Management of typhoid fever and its complications. Ann Intern Med 1964; 60:144.

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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: Apr 8, 2010

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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 Salmonella typhi.
[ CLOSE WINDOW ]
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. In 2006, there were 314.
Between 1999 and 2006, 79% of typhoid fever cases occurred in patients who had been outside
of the country within the preceding 30 days. Two thirds of these individuals had just journeyed
from the Indian subcontinent. The 3 known outbreaks of typhoid fever within the United States
were traced to imported food or to a food handler from an endemic region. Remarkably, only
17% of cases acquired domestically were traced to a carrier.17
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, but
80% of cases come from Bangladesh, China, India, Indonesia, Laos, Nepal, Pakistan, or
Vietnam.18 Within those countries, typhoid fever is most common in underdeveloped areas.
Typhoid fever infects roughly 21.6 million people (incidence of 3.6 per 1,000 population) and
kills an estimated 200,000 people every year.19
In the United States, most cases of typhoid fever arise in international travelers. The average
yearly incidence of typhoid fever per million travelers from 1999-2006 by county or region of
departure was as follows:17
• Canada - 0
• Western Hemisphere outside Canada/United States - 1.3
• Africa - 7.6
• Asia - 10.5
• India - 89 (122 in 2006)
• Total (for all countries except Canada/United States) - 2.2
Mortality/Morbidity
With prompt and appropriate antibiotic therapy, typhoid fever is typically a short-term febrile
illness requiring a median of 6 days of hospitalization. Treated, it has few long-term sequelae
and a 0.2% risk of mortality.17 Untreated typhoid fever is a life-threatening illness of several
weeks' duration with long-term morbidity often involving the central nervous system. The case
fatality rate in the United States in the pre-antibiotic era was 9%-13%.20
Race
Typhoid fever has no racial predilection.
Sex
Fifty-four percent of typhoid fever cases in the United States reported between 1999 and 2006
involved males.17
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.16,21
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.22
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.16,23,24,2,6
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,25 meningitis, orchitis,
osteomyelitis, and abscesses anywhere on the body.2
Table 1. Incidence and Timing of Various Manifestations of Untreated Typhoid Fever2,26,27,28,29,30
Open table in new window
[ CLOSE WINDOW ]
Table

Incubation Week 1 Week 2 Week 3 Week 4 Post

Systemic Recovery 10%-20%


phase or relapse; 3%-
Stepladder fever Very Very common death (15% 4% chronic
pattern or insidious commona of untreated carriers;
onset fever cases) long-term
neurologic
Acute high fever Very rareb sequelae
(extremely
Chills Almost allc rare);
gallbladder
Rigors Uncommon
cancer
Anorexia Almost all (RR=167;
carriers)
Diaphoresis Very common

Neurologic

Malaise Almost all Almost all Typhoid


state
Insomnia Very (common)
common

Confusion/delirium Commond Very


common

Psychosis Very rare Common

Catatonia Very rare

Frontal headache Very


(usually mild) common

Meningeal signs Raree Rare

Parkinsonism Very rare

Ear, nose, and throat

Coated tongue Very


common

Sore throatf

Pulmonary

Mild cough Common


Bronchitic cough Common

Rales Common

Pneumonia Rare Rare Common


(lobar) (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 with tympany Very


common
(84%) 30

Diffuse mild Very


abdominal pain common

Sharp right lower Rare


quadrant pain

Gastrointestinal Very rare; Very common


hemorrhage usually
trace

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 Extremely Extremely


rare rare rare

Incubation Week 1 Week 2 Week 3 Week 4 Post

Systemic Recovery 10%-20%


phase or relapse; 3%-
Stepladder fever Very Very common death (15% 4% chronic
pattern or insidious commona of untreated carriers;
onset fever cases) long-term
neurologic
Acute high fever Very rareb sequelae
(extremely
Chills Almost allc rare);
gallbladder
Rigors Uncommon
cancer
Anorexia Almost all (RR=167;
carriers)
Diaphoresis Very common

Neurologic

Malaise Almost all Almost all Typhoid


state
Insomnia Very (common)
common

Confusion/delirium Commond Very


common
Psychosis Very rare Common

Catatonia Very rare

Frontal headache Very


(usually mild) common

Meningeal signs Raree Rare

Parkinsonism Very rare

Ear, nose, and throat

Coated tongue Very


common

Sore throatf

Pulmonary

Mild cough Common

Bronchitic cough Common

Rales Common

Pneumonia Rare Rare Common


(lobar) (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 with tympany Very


common
(84%) 30
Diffuse mild Very
abdominal pain common

Sharp right lower Rare


quadrant pain

Gastrointestinal Very rare; Very common


hemorrhage usually
trace

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 Extremely Extremely


rare rare 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.