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Journal of Clinical Microbiology, July 1999, p. 2381-2382, Vol. 37, No. 7
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Typhoid Fever Due to Salmonella Kapemba
Infection in an Otherwise Healthy Middle-Aged Man
Hans-Eckart
Sarnighausen,1,*
Claus
Benz,1
Martin
Eickenberg,1
J.
Bockemühl,2
H.
Tschäpe,2 and
Jürgen F.
Riemann1
Department of Internal Medicine C, Clinic of
the City of Ludwigshafen, D-67069 Ludwigshafen,1
and Robert Koch-Institut, D-13302
Berlin,2 Germany
Received 23 November 1998/Returned for modification 4 February
1999/Accepted 26 March 1999
 |
ABSTRACT |
We report the case of a patient with a Salmonella
Kapemba infection, who suffered, 3 weeks after a holiday in Israel,
occurrences of high fever and lower back pain for 10 days and icterus
for 2 days before admission. Laboratory findings revealed a slight cholestasis and elevation of acute phase protein levels. In the blood
culture a Salmonella Kapemba-type organism was cultured. The patient was afebrile for 10 days after hospitalization and then
suddenly developed a temperature of 40°C again. At the same time
leukopenia, thrombocytopenia, and a rise of D-dimer levels were
detected. The patient was admitted to the intensive care unit for a few
days, because a disseminated intravascular coagulation was suspected.
With magnetic resonance imaging and bone scintigraphy no osteomyelitis
or abscess formation could be found. A transesophageal ultrasonography
of the heart revealed no signs of endocarditis. In multiple stool
cultures no salmonellas could be detected. After antibiotic treatment
with ciprofloxacin the fever and lower back pain subsided, and the
patient was discharged a fortnight later. This is the first reported
case of typhoid fever due to the bacterium Salmonella Kapemba.
| |
CASE REPORT |
We report the case of a patient who, 3 weeks after a 14-day trip
to Israel, presented with fever up to 40.2°C, icterus, anorexia, weight loss of 4 kg in 2 weeks, and lower back pain. He was not coughing and had no diarrhea. The disease began 10 days before admission to the hospital with lower back pain, nausea, vomiting, and
brown urine. He had taken acetaminophen, metamizole, benzodiazepine, and nonsteroid anti-inflammatory drugs to control pain and fever.
For 10 years the patient had had hypertensive disease, which was drug
treated, and he reported a chemical-toxic hepatitis caused by
carboxychlorids 23 years ago.
The 57-year-old man was in a reduced health status and 184 cm tall,
with a body weight of 85.6 kg and a temperature of 37.9°C. A physical
examination revealed bradycardia (52 beats per min and rhythmic) and a
blood pressure of 160/90 mm of Hg, and the liver was palpable at a
position 5 to 6 cm medioclavicular below the right rib bow. No heart
murmur was found, pulmonary, renal, and spleen findings were normal, no
clinical signs of meningitis or other neurological abnormalities were
found, and lymph nodes were not palpable. Pressure caused pain at the
lumbar part of the spine.
Laboratory studies showed slightly elevated levels of cholestatic
enzymes and transaminases. Screening for hepatitis, tuberculosis, and
malaria was negative.
An X ray of the lumbar spine revealed lumbarization of the first sacral
segment with failure of fusion of the laminae of the neural arch. In
ultrasonography a splenomegaly (140 by 55 mm) and two renal cysts
smaller than 5 cm in the left upper kidney were found. Endoscopy and
magnetic resonance imaging findings of the upper gastrointestinal tract
and biliary system were normal. The magnetic resonance imaging of the
spine revealed a slightly increased intensity of the T2 sequence and
decreased intensity of the T1 sequence between L2 and L3, giving a hint
of an initial spondylitis with a minimal increased level of
radioactivity in the bone scan. The transthoracic and transesophageal
ultrasound of the heart showed a left ventricular hypertrophy without
valvular failure in the sense of endocarditis.
Initially no focus of the infection could be found: a chest X ray, a
urine sample, and stool samples were normal or negative. In the
anaerobe blood tube a Salmonella serovar, Kapemba, was cultured. As the patient was without fever on the third day of hospitalization and the lower back pain was treated sufficiently with
analgetics, no antibiotic treatment was initiated. Suddenly, 14 days
after admission, he became very sick again with shivering and fever up
to 40°C. Three blood cultures revealed the same bacterium as before
in both the aerobe and anaerobe tubes: Salmonella Kapemba. It is a salmonella of type D in the Kauffmann-White classification (4) and its O antigen is identical with that of
Salmonella enteritidis. It is serologically classified with
the formula 9,12:1,v:1,7 (somatic antigen [O]:flagellar antigen [H]
phase I:phase II).
We began antibiotic treatment with 400 mg of the gyrase inhibitor
ciprofloxacin intravenously twice a day. A decrease in all three blood
cell line levels (leukocytes, 3.8/nl; hemoglobin, 13.5 g/dl; and
thrombocytes, 131/nl) in combination with bradycardia and high body
temperature led us to the presumptive diagnosis of a salmonella sepsis
with initial disseminated intravascular coagulation. This suspicion was
heightened by the finding of slightly increased amounts of D-dimers
(1.0 mg/liter). As a result the patient was transferred to the
intensive care unit. A transesophageal echocardiography did not show
signs of endocarditis, and a colonoscopy did not reveal signs of
infection. Three days later the patient was retransferred, and he
recovered under further antibiotic treatment. The intravenous
administration was changed to an oral administration after 14 days, and
the patient was dismissed with the recommendation to take the
antibiotic for the whole of the next month.
Four months later the patient was well and had nearly no back pain, and
the fever did not return.
Discussion.
Typhoid fever is a distinctive acute systemic
febrile infection of the mononuclear phagocytes usually caused by
Salmonella typhi, S. paratyphi A and B, and
occasionally S. typhimurium. Due to improvements in
environmental sanitation in the United States the incidence of typhoid
cases dropped to 0.2 per population of 100,000 in the last 50 years. At
the same time the infections acquired abroad increased over 60%. The
bacterium is endemic to Mexico, Peru, Chile, India, Pakistan, Egypt,
and Indonesia (6).
The most common infection route of the almost always human-adapted
salmonella is contaminated water or food ingestion of more than 100,000 bacteria. The organisms invade the upper small bowel and produce a
transient bacteremia before they are phagocytized by mononuclear cells
and multiply intracellularly. The incubation period varies from 3 to 60 days and depends on the number of ingested bacteria and the patient's
immune status.
The disease usually begins with a gradual rise of body temperature to
40 to 41°C and is associated with headache and malaise. It is
characterized by a prolonged fever of 4 to 8 weeks if untreated. Typical findings are bradycardia, leukopenia, and sometimes
pancytopenia, along with "rose spots" on the chest and abdomen. In
severe cases it is complicated by disseminated intravascular
coagulation, encephalomeningitis, necrotizing cholecystitis, intestinal
bleeding and perforation, osteomyelitis, nephritis, and infections of
other parenchymatous organs. The outcome is lethal in 2% of cases.
Three to five percent of patients, some of whom never have symptoms,
become long-term carriers.
The patient mentioned above did not suffer from abdominal cramping or
diarrhea, and in several stool samples no bacterium
could be cultured.
Because of the initial fever and the slightly
elevated level of
bilirubin, it was first suggested to be a spontaneous
loss of a gall
stone. The choledochus duct could not be visualized
by two retrograde
endoscopic cholangiopancreatographies, and a
gall culture for a
microbiological investigation was not taken,
because the patient was
afebrile at that time. The bile system
was shown to be absolutely
normal with the magnetic resonance
cholangiopancreatography. Because of
the transient icterus, the
positive blood cultures, and the return of
the fever without any
positive stool culture for salmonellae, the
source of the bacterium
was thought to be the biliary
system.
This was actually the first time that this
Salmonella
serovar has been isolated in Ludwigshafen. A review of the existing
literature showed very few studies of this organism after its
first
description in 1954 by Kauffmann et al. (
3,
4). In
the
existing literature this serovar has been associated with
gastroenteric
symptoms in
humans.
The available literature does not provide much information. Horvath in
1976 described a cerebral and cerebrocortical necrosis
caused by a
Salmonella Kapemba infection in a newborn (
2).
Ketyi et al., also Hungarians, found in 1979 that the heat-labile
enterotoxin of
Salmonella Kapemba fails to exert a
biological
effect, although it is antigenically related to the
heat-labile
enterotoxin of
Escherichia coli (
5).
A Spanish group found
that
Salmonella Kapemba is one of the
most commonly isolated serotypes
in irrigation waters and crops. In
humans,
S. typhimurium and
S. enteritidis were
found to be the most common (
1).
According to our national reference center for salmonella and enteritis
infections
Salmonella Kapemba is a seldom-encountered
but
universal strain without any endemic preference. Most of the
infections
with this bacterium are accompanied by gastroenteritis
with typhoid
symptoms in only very few cases. It is not known
as an exceptionally
virulent strain. Israel is not known to be
a region where this type is
endemic. We are not sure that this
case of typhoid fever is due to the
virulence of the bacterium
alone, and we do not know if there is a
special disposition for
this reaction in our
patient.
This is the first reported case of a patient with typhoid fever due to
Salmonella Kapemba without any gastroenteric
symptoms.
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FOOTNOTES |
*
Corresponding author. Present address: An den
Mühlwegen 34, D-55129 Mainz, Germany. Phone: 49-6131-58 23-54, Fax: 49-6131-58 23-59. E-mail:
sarnigha{at}mail.uni-mainz.de.
| |
REFERENCES |
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Journal of Clinical Microbiology, July 1999, p. 2381-2382, Vol. 37, No. 7
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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Abstract
Case Report
