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Enteric fever
Eghan BA
24/2/2005
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Salmonella infections
Genus: Salmonella
Named after : Pathologist, Salmon
Family: enterobacteriacae
2300 serotypes
Grouped: O antigen (somatic)
Further serotyed:Flagella (H) and surface virulence(Vi) antigen
Most of which originating in animals eg poultry andtransmitted to man either directly or in food
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Based on DNA studies, all salmonellae are
now considered a single species (Scholeraesuis),
separated into 7 distinct subgroups.
By convention, these subgroups are often
referred to as separate species (eg, S typhiinstead ofS choleraesuis subgroup typhi)
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Mode of transmission
Ingestion of food derived from infected
animals contaminated with faeces of infectedindividual
Raw milk and raw milk products
Undercooked or raw eggs and egg products
Meat and meat products Contaminated water
Shellfish from water polluted by raw sewage.
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The bacteria must survive the pH in stomach
and colonize the small intestines. Attach and penetrate the intestinal mucosa
resulting in diarrhoea from direct mucosal
damage or by action of bacterial toxins.
Also invasion of the lymphoid tissue withinthe GI tract and multiplication within
macrophages leading to bacteraemia
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Factors predisposing an individual to
infection include
Studies suggest that infection may be inoculum-dependent. In healthyindividuals previously,ingestion of
105 organisms: clinical disease in 25% of volunteers
10
7
organisms: caused disease in 50% of volunteers 109 organisms caused disease in 95% of volunteers.
As the number of organisms increased, the incubation period decreased.
A gastric pH of less than 1.5 kills most salmonellae. Patients who continually ingest antacids
have had a gastrectomy
have achlorhydria due to aging
or other factors eg. Inflammatory bowel disease, malignancy
require lower numbers of organisms to produce clinical disease.
Possession of Vi antigen by S typhiis linked with increased pathogenicity.
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Syndromes of Salmonella infections
Gastroenteritis ( the most frequent manifestation)
Typhoid and paratyphoid fever (enteric fever)
Enterocolitis
Septicaemia
Metastastic lesions (complicating septicaemia) Osteomyelitis, septic arthritis, liver abscess, brain abscess
meningitis, pneumonia, endocarditis, arteritis, septicarthritis, splenic and hepatic abscesses, and soft tissueabscesses.
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Gastroenteritis
Incubation period; 8-48 hours
Presentation:
Nausea, vomiting progressing to abdominal cramping and
diarrhoea which may be bloody
Physical findings:
Fever > 38C
Abdominal tenderness or signs consistent to peritonitis
Gross or occult blood may be found on rectal examination.
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Typhoid fever or enteric fever
History
Incubation period: varies with the size of the infecting dose.
a median dose of one million to one billion organismsnecessary to produce symptoms
Typhoid fever: averages 10-20 (range 3-56) days.
In paratyphoid fever: 1-10 days.
The duration of illness in an untreated individual is usually four
weeks. In the incubation period, 10-20% of patients have transient
diarrhea.
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As bacteremia develops, Fever; 39-40C (Rising remittent fever as high as (39-40C.
Step-wise fashion over 2-3 days.) headaches.
malaise,.
Constipation
anorexia
myalgia,
cough,
sore throat
After 1 week if untreated patients condition worsen leadingmental confusion
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Physical findings
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First week
Rose spots: Crops of 2-4 mm diameter pink
papules which fades with pressure developon the upper abdomen and lower chest
between the 7th and 12th days. Caused by
bacterial embolization, and culture results of
skin snips of the spots may be positive. Relative bradycardia
Dicrotic pulse are also common at this time.
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Second week
Toxic appearance
Apathetic Fever sustained.
Abdomen distention
Splenomegaly
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Third week
Toxicity increases
Weight loss Fever persists
Delirious state (typhoid state or typhoidpsychosis ) emerges.
Pronounced abdominal distension liquid, foul, green-yellow diarrhea (pea soup
diarrhea).
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Third week (contd)
Patient is weak
thready pulse
Tachypnoic
Crackles may develop over the lung bases.
Death may occur at this stage from overwhelming
Toxemia. Myocarditis.
Intestinal hemorrhage.
Perforation.
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Fourth week
In patients surviving into the fourth week, the
fever, mental state, and abdominaldistension slowly improve over a few days,
but intestinal complications may still occur.
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Differentials
Abdominal abscess
Amoebic hepatic abscess
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Investigation
Complete blood count moderate anemia
Raised ESR
Thrombocytopenia relative lymphopenia
WBC increases with perforation
Sometimes a slightly raised prothrombin time (PT) and activated partialthromboplastin time, decreased fibrinogen levels, and circulating fibrindegradation products.
Liver Transaminases: Raised (2X or more) Raised serum bilirubin.
Electrolytes hyponatraemia
hypokalaemia.
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Clinical diagnosis is suggested by:
assays that identify Salmonella antibodies, antigens, or DNA
But definitive diagnosis of typhoid fever requires isolation of theorganism from blood or bone marrow
the most sensitive method of isolating S typhi and paratyphiisobtaining a bone marrow aspirate (BMA) culture.
S typhican be isolated from BMA even if patients have been takingantibiotics for several days
regardless of how long they have been ill. This test may be indicated in patients whose initial blood
culture results are negative, presumably because of priorantibiotic therapy.
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If BMA cannot be performed,
blood, intestinal secretions, and stool culture findings are usually positive in approximately 85-90% of patients
with typhoid fever during the first week, declining to 20-30%later in the course of the disease.
A sensitivity of 63% has also been reported from culturingskin snips of rose spots.
A single rectal swab: sensitivity 30-40%.
S typhihas been isolated from the cerebrospinalfluid, peritoneal fluid, mesenteric lymph nodes,resected intestine, pharynx, tonsils, abscess, bone,and urine.
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Serology
Widal test ( traditional serologic test)
It measures agglutinating antibodies against flagellar
(H) and somatic (O) antigens ofS typhi.
In acute infection, O antibody appears first, rising
progressively, later falling, and often disappearing within a
few months.
H antibody appears slightly later but persists longer. Rising or high O antibody titers generally indicate acute
infection, whereas elevations of H antibody help to identify
the type of enteric fever.
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Numerous studies have shown that the sensitivity,
specificity, and predictive values of this test vary
dramatically among laboratories, rendering the test'svalue to the clinician questionable.
Wide variation is caused by differences in patient
population, antigens, and techniques.
The Widal reaction is indicative of typhoid fever inonly 40-60% of patients at the time of admission.
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New innovations
Indirect hemagglutination, indirect fluorescent Vi
antibody, and indirect enzyme-linked immunosorbent
assay for immunoglobulin M (IgM) andimmunoglobulin G antibodies to S typhi
polysaccharide are available.
Monoclonal antibodies against S typhiflagellin
DNA probes are also available.
Polymerase chain reaction
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Treatment
Medical Care
Nurses and doctors:
adequate hand washing and safe disposal of feces andurine.
Antibiotic therapy is essential and should beginempirically if the clinical evidence is strong.
Antimicrobials:
shorten the course, reduce the rate of complications if begun early
reduce the case-fatality rate.
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Surgical Care
Consultation with a surgeon is advised when typhoid fever is
complicated by gastrointestinal perforation.Surgical intervention for intestinal perforation
simple closure of a perforation
small bowel resection for patients with multiple perforations.
Early diagnosis is key to lower mortality.
Cholecystectomy not always successful because of persisting hepatic infection.
indicated for gallbladder disease but not for the purpose oferadicating the carrier state.
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Medication
Goal is to:
1. eradicate the infection2. reduce morbidity
3. prevent complications.
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antibiotics
Ciprofloxacin (250-500 mg bid for 7-14 d)
Levofloxacin (Levaquin) (250-500mg bid for7days)
Cefotaxime (2 g IV q6h )
Ceftriaxone (Rocephin) 1-2 g IV dly or bid
Chloramphenicol
Amoxicillin Trimethoprim and sulfamethoxazole
Azithromycin (Zithromax)
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Corticosteroids
Reduce mortality in severely ill patients with
depressed levels of consciousness or shock.
Dexamethasone
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Further management
Management of long-term carriers is as follows:
Prolonged courses of amoxicillin or co-trimoxazole. Failure
rate is high if the patient has chronic gallbladder disease.
Ciprofloxacin (750 mg bid) and norfloxacin (400 mg bid)
have been much more effective, with cure rates of 78% and
83%, respectively.
Long-term urinary carriers should be assessed for urinary
tract abnormalities, including schistosomiasis.
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Complications
Intestinal manifestations
intestinal hemorrhage perforation (3-4.6% of hospitalized patients).
Hepatobiliary manifestations
cholangitis, cholecystitis, or hemolysis.
Pancreatitis
Acute renal failure and hepatitis with
hepatomegaly
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Toxic myocarditis:
tachycardia, weak pulse and heart sounds,hypotension, and electrocardiographic
abnormalities.
Pericarditis
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Neuropsychiatric manifestations A toxic confusional state, characterized by disorientation, delirium,
and restlessness, is characteristic of late-stage typhoid.
Facial twitching or convulsions. paranoid psychosis or catatonia may develop during
convalescence.
Meningismus
Encephalomyelitis may develop, and the underlying pathology maybe that of demyelinating leukoencephalopathy.
Rarely transverse myelitis, polyneuropathy, or cranialmononeuropathy may develop.
spastic paraplegia, peripheral or cranial neuritis, Guillain-Barrsyndrome, schizophrenialike illness, mania, and depression.
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Hematologic manifestations
Subclinical disseminated intravascular
coagulation occurs commonly in persons
with typhoid fever.
Hemolytic-uremic syndrome is rare.
Haemolysis may also be associated with
glucose-6-phosphate dehydrogenasedeficiency.
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Genitourinary manifestations
Approximately 25% of patients excrete S typhiin
their urine at some point during their illness.
Immune complex glomerulonephritis and proteinuria
have been reported, and IgM, C3 antigen, and S
typhiantigen can be demonstrated in the glomerular
capillary wall.
Nephritic syndrome may complicate chronic S typhibacteremia associated with urinary schistosomiasis.
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Musculoskeletal manifestations
Skeletal muscle - shows Zenker
degeneration, particularly affecting the
abdominal wall and thigh muscles.
Polymyositis .
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CNS manifestations
Focal intracranial infections are uncommon.
Recently, multiple brain abscesses have been
reported.