-

Salmonella Infections
Complications
Extra-intestinal
infectious complications
recognition
of these can prevent a delay in diagnosis

can

occur

and

Intestinal
The two most serious complications of enteric fever are intestinal
haemorrhage and perforation, which usually occur when the
sloughs overlying the Peyers patches separate during the late
second or early third week of the illness.
Haemorrhage
Clinical signs of haemorrhage are :
- a sharp fall in body temperature and blood pressure,
- and sudden tachycardia.
- The blood passed per rectum is usually bright red but may
be altered if intestinal stasis is present. Sometimes there
may not be any passage of blood when frank ileus is
present.
Management of haemorrhage is conservative, with sedation and
transfusion unless there is evidence of perforation, when surgery
is indicated.
Perforation
Clinical sign :
- Unlike other causes of intestinal perforation, typhoid
perforation occurs in a patient who already had a vaguely
tender distended abdomen with scanty bowel sounds.
Therefore, recognition of perforation can be diffi cult.
- Usually, pain and tenderness worsen, the pulse rises and
the temperature falls suddenly.

Abdominal rigidity may not be a prominent sign and bowel

sounds may not disappear altogether.
- The discovery of free fluid in the abdomen may be the only
sign of perforation.
- Demonstration of gas under the diaphragm by X-ray is a
valuable aid to diagnosis.
The treatment of choice for typhoid perforation :
- Surgical intervention. Most surgeons prefer simple closure
of perforation with drainage of the peritoneum, and reserve
small-bowel
resection
for
patients
with
multiple
perforations
- conservative management with nasogastric suction,
antibiotic therapy directed against anaerobes and
Enterobacteriaciae, and general supportive care will reduce
the mortality to 30%
- The prognosis is clearly related to the time elapsed
between perforation and surgery.
Liver, gallbladder and pancreas
Mild jaundice may occur in enteric fever and may be due to
hepatitis, cholangitis, cholecystitis or haemolysis. Biochemical
changes indicative of hepatitis are common during the acute
stage. Liver biopsy in such cases often shows cloudy swelling,
balloon degeneration with vacuolation of hepatocytes, moderate
fatty change and focal collection of mononuclear cells typhoid
nodules (Figure 52.2). Intact typhoid bacilli can be seen at these
sites. Pancreatitis has also been reported.
Cardiorespiratory
Toxic myocarditis and endocarditis occur in 15% of cases and
represent a signifcant cause of death in endemic countries. Both
occur in severely ill toxaemic patients and is characterized by
tachycardia, weak pulse and heart sounds, hypotension and
electrocardiographic abnormalities. Respiratory symptoms, such

as cough and mild bronchitis, occur in 1186% of cases and

bronchopneumoniaor lobar consolidation may develop rarely.

Nervous system
A toxic confusional state, characterized by disorientation, delirium
and restlessness, is characteristic of late-stage typhoid but
occasionally these and other neurpsychiatric features may
dominate the clinical picture from an early stage. Facial twitching
or convulsion(s) may be the presenting feature; sometimes,
paranoid psychosis or catatonia may develop during
convalescence.
Meningism is not uncommon but bacterial meningitis caused by
S. Typhi is a rare, but recognized, complication. Encephalomyelitis
may develop and the underlying pathology may be that of
demyelinating leukoencephalopathy.Rarely, transverse myelitis,
polyneuropathy or cranial mononeuropathy may develop.
Haematological and renal
Subclinical disseminated intravascular coagulation occurs
commonly in typhoid fever; this rarely manifests as haemolytic
uraemic syndrome. Haemolysis may also be associated with
glucose 6-phosphate dehydrogenase (G6PD) defi ciency. Immune
complex glomerulitis has been reported and IgM immunoglobulin,
C3 and S. Typhi antigen can be demonstrated in the glomerular
capillary wall. Nephrotic syndrome may complicate chronic S.
Typhi bacteraemia associated with urinary schistosomiasis.
Musculoskeletal and other systems
Skeletal muscle characteristically shows Zenkers degeneration (a
hyaline degeneration of muscle fi bres), particularly affecting the

abdominal wall and thigh muscles; clinically evident polymyositis

may occur.
Localization may occur in almost any organ/system, and
involvement of bones, joints, meninges, endocardium, spleen and
ovary have all been reported, but such cases are rare.

Diagnosis
The definitive diagnosis of enteric fever requires the isolation of S.
Typhi or S. Paratyphi from blood, bone marrow, other sterile sites,
rose spots, stool, or intestinal secretions.. Isolation from stool or
urine provides strong presumptive evidence only in the presence
of a characteristic clinical picture.
Blood and bone marrow culture
The defi nitive diagnosis of typhoid is by the isolation of the
organism from a sterile site. Isolation of the organism from the
stool is useful information but may be a false positive due to
longterm carriage. Thus, in patients with suspected typhoid, blood
or bone marrow cultures should be performed. Modern automated
systems rapidly detect the presence of the organism, but
conventional non-automated methods also have a high diagnostic
yield
Faecal and urine cultures
With modern techniques, faecal cultures are often positive even
during the first week, though the percentage positivity rises
steadily thereafter. Urine cultures are positive less often.
Serology
The traditional Widal test measures antibodies against flagellar
(H) and somatic (O) antigens of the causative organism. In acute
infection, O antibody appears first, rising progressively, later
falling and often disappearing within a few months. H antibody
appears a little later but persists for longer. Rising or high O
antibody titre generally indicates acute infection, whereas raised
H antibody helps to identify the type of enteric fever.
However, the Widal test has many limitations :

Raised antibodies may have resulted from previous typhoid

immunization or earlier infection(s) with salmonellae
sharing common O antigens with S. Typhi or S. Paratyphi.
- In endemic countries, patients have higher H antibody
titres. This is a particular problem in developing countries,
where background antibodies mean that the Widal test
lacks sensitivity.
- Some patients show a poor or negligible antibody response
to active infection.
Vi antibody is often raised during acute infection and persists
afterwards during chronic carriage. However, its use as a
screening test for the carrier state is limited because of the
frequency of false positives and false negatives
Newer Diagnostic Methods
Newer tests that directly detect IgM or IgG antibodies to a wide
range of specific S. typhi antigens have been developed, such as

Typhidot and Tubex. Some of these tests have been adapted to a

simple dipstick technique using whole bacteria antigens to detect
IgM antibody and may be of benefit in situations where a
laboratory is not available. While they compare favourably with
the Widal test, none of them performs as well as blood culture.
Furthermore, antimicrobial susceptibility testing cannot be
performed, nor can molecular epidemiological work. Their use
should currently be confined to outbreak situations, where pretest
probability of typhoid is high. Urinary Vi antigen ELISAs and PCRbased assays are under development,but have not yet reached
the point where they are ready for deployment as rapiddiagnostic tests.
Reference :
- Mansons Tropical Disease 23
- Harrisons Internal Medicine