TYPHOID FEVER
GERALD MUPETA CHONGO
INTRODUCTION
SALMONELLA
• Salmonellosis is a common and widely distributed food-
borne disease.
• Salmonellae live in the intestinal tracts of warm- and cold-
blooded animals. Some species are ubiquitous, whereas
others are specifically adapted to a particular host.
• Salmonella causes 2 clinical syndromes in humans: a
gastroenteritis that is usually self-limited, and typhoid fever
that is a relatively severe systemic illness classically caused
by S. typhi. Nontyphoidal strains of Salmonella can also
cause a severe bacteremic illness in some circumstances.
Nontyphoidal Salmonellosis
ETIOLOGY.
• Salmonellae are motile, nonsporulating, nonencapsulated,
gram-negative rods that grow aerobically and are capable
of facultative anaerobic growth.
• Most serotypes have a broad host spectrum. Typically,
such strains cause gastroenteritis that is often
uncomplicated and does not need treatment, but can be
severe in the young, the elderly, and patients with
weakened immunity. The causes are typically S. Enteritidis
and S. Typhimurium, the 2 most important serotypes for
salmonellosis transmitted from animals to humans.
ENTERIC FEVER (TYPHOID FEVER)
ETIOLOGY.
• Typhoid fever is caused by Salmonella Typhi (S.
Typhi), a gram-negative bacterium. A very similar but
often less severe disease is caused by S. Paratyphi A
and rarely by S. Paratyphi B and S. Paratyphi C.
• Ingestion of foods or water contaminated with S.
Typhi from human feces is the most common mode
of transmission, although water-borne outbreaks
due to poor sanitation or contamination can occur in
developing countries.
PATHOGENESIS
• The disease occurs by the ingestion of the organism, and a
variety of sources of fecal contamination have been reported,
including street foods and contamination of water reservoirs.
• After ingestion, S. Typhi organisms invade the body through the
gut mucosa in the terminal ileum. S. Typhi crosses the intestinal
mucosal barrier after attachment to the microvilli . After passing
through the intestinal mucosa, S. Typhi organisms enter the
mesenteric lymphoid system, and then pass into the
bloodstream via the lymphatics. This primary bacteremia is
usually symptomless, and blood cultures are frequently negative
at this stage of the disease. The blood-borne bacteria are
disseminated throughout the body and are thought to colonize
the organs of the reticulo-endothelial system( liver, spleen, bone
marrow) , where they may replicate within macrophages.
• After a period of bacterial replication, S. Typhi organisms are
shed back into the blood, causing a secondary bacteremia,
which coincides with the onset of clinical symptoms and
marks the end of the incubation period.
• Patients who are infected with HIV are at significantly
increased risk for clinical infection with S. Typhi and S.
Paratyphi. Similarly patients with Helicobacter pylori infection
also have an increased risk for acquiring typhoid fever.
CLINICAL FEATURES.
• Incubation period of typhoid fever is usually 7–14 days . The
clinical presentation varies from a mild illness with low-grade
fever, malaise, and slight dry cough to a severe clinical picture
with abdominal discomfort and multiple complications.
• Many factors influence the severity and overall clinical
outcome of the infection.
• The presentation of typhoid fever may also differ according to
age.
• Diarrhea, toxicity, and complications such as disseminated
intravascular complications are more common in infancy.
However, some of the other features and complications of
typhoid fever seen in adults, such as relative bradycardia,
neurologic manifestations, and gastrointestinal bleeding, are
rare.
• Typhoid fever usually presents with high-grade fever with a wide
variety of associated features such as generalized myalgia,
abdominal pain, hepatosplenomegaly, abdominal pain, and
anorexia . In children, diarrhea may be present in the earlier stages
of the illness and may be followed by constipation. The fever may
rise gradually, but the classic stepladder rise of fever is relatively
rare. In about 25% of cases, a macular or maculopapular rash (rose
spots) may be visible around the 7th–10th day of the illness, and
lesions may appear in crops of 10–15 on the lower chest and
abdomen and last 2–3 days .
• If no complications occur, the symptoms and physical findings
gradually resolve within 2–4 wk; however, the illness may be
associated with malnutrition in a number of affected children.
Although enteric fever caused by S. Paratyphi organisms has been
classically regarded as a milder illness, recent reports of infections
with drug-resistant isolates indicate that paratyphoid fever may also
be severe, with significant morbidity and complications.
Summary of clinical features
High-grade fever Hepatomegaly
Coated tongue Maculopapular rash ( Rose spots )
Anorexia Headache
Jaundice Constipation
Obtundation Splenomegaly
Vomiting
Hepatomegaly
Diarrhea
Toxicity
Abdominal pain
Pallor ( cause ? )
COMPLICATIONS
1. Central nervous system
Encephalopathy, cerebral edema, subdural empyema, cerebral abscess,
meningitis, seizures, Guillain-Barré syndrome, psychosis, peripheral and
optic neuritis, ICP.
2. Cardiovascular system
Endocarditis, myocarditis, pericarditis, congestive heart failure.
3. Pulmonary system
Pneumonia, empyema, bronchopleural fistula, bronchitis.
4. Bone and joint
Osteomyelitis, septic arthritis
5. Hepatobiliary
Cholecystitis, hepatitis, hepatic abscesses, splenic abscess, peritonitis,
paralytic ileus
6. Genitourinary system
Urinary tract infection,pyelonephritis, renal abscess, pelvic
infections, testicular abscess, prostatitis, epididymitis.
7. GIT
Intestinal hemorrhage and perforation ( esp distal ileum ) is
infrequent among children. Intestinal perforation may be preceded
by a marked increase in abdominal pain (usually in the right lower
quadrant), tenderness, vomiting, and features of peritonitis.
Intestinal perforation and peritonitis may be accompanied by a
sudden rise in pulse rate, hypotension, marked abdominal
tenderness and guarding, and subsequent abdominal rigidity.
8. Other reported complications include fatal bone marrow necrosis,
disseminated intravascular coagulation (DIC), hemolytic uremic
syndrome, nephrotic, parotitis, orchitis, and suppurative
lymphadenitis.
INVESTIGATIONS
1. Diagnosis
Blood culture -blood cultures are positive in 40–60% of
the patients seen early in the course of the disease
Stool culture- cultures become positive after the 1st
wk.
Urine culture - cultures become positive after the 1st
wk.
Bone marrow culture- most sensitive method, but are
difficult to obtain and relatively invasive.
2. Other investigations.
Depends on clinical picture.
DIFFERENTIAL DIAGNOSIS.
1. Acute gastroenteritis
2. Bronchitis in early stages
3. Bronchopneumonia.
4. Malaria
5. Sepsis with other bacterial pathogens
6. Viral infections such as acute hepatitis, and
infectious mononucleosis.
TREATMENT
• Adequate rest, and Hydration are important to correct
fluid-electrolyte imbalance.
• Antibiotic therapy is critical to minimize complications.
Chloramphenical 25mg/kg every 6hrs
for 2 weeks.
alternatives where there is high resistance to
chloramphenical- ceftriaxone 50-75 mg/kg daily
- ciprofloxacin
