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Enteric Fever 1

Enteric fever, primarily caused by Salmonella serovars such as S. typhi, is a systemic febrile infection with significant global incidence, particularly in endemic regions. Clinical presentation includes a stepwise fever, abdominal pain, and potential complications like intestinal perforation and meningitis, with untreated mortality rates ranging from 12-30%. Prevention strategies focus on hygiene and vaccination, although current vaccines do not provide complete protection against all serovars.
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0% found this document useful (0 votes)
63 views15 pages

Enteric Fever 1

Enteric fever, primarily caused by Salmonella serovars such as S. typhi, is a systemic febrile infection with significant global incidence, particularly in endemic regions. Clinical presentation includes a stepwise fever, abdominal pain, and potential complications like intestinal perforation and meningitis, with untreated mortality rates ranging from 12-30%. Prevention strategies focus on hygiene and vaccination, although current vaccines do not provide complete protection against all serovars.
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ENTERIC FEVER

Enteric fever
Outline
• Etiology
• Epidemiology
• Pathogenesis
• Clinical presentation
• Complications
• Sequelae
• Labs
• Treatment
• Prevention
• Typhoid and HIV
• Summary
• Questions
Etiology
• An acute systemic febrile infection of
mononuclear phagocytes
• Caused by serovars of salmonella including;
- S. typhi,
- S. paratyphi A, S. paratyphi B and
- S. typhimuriu
Epidemiology
• 13-17million cases world wide
• 200,000 deaths per year
• Infants most susceptible
• Endemic in India, Asia, south and central
America
• About 300 cases reported in the USA per year
• African data scanty
Risk factors for transmission

• Rapid population growth


• Increased urbanization
• Inadequate human waste treatment
• Limited water supply, and
• Overburdened health care systems
Transmission
• Humans only known hosts
• Transmission is through ingestion of contaminated
food or water
Pathogenesis
• Infectious dose usually <10ᶟ CFUs
• Organisms that survive gastric acid cause a mild
often clinically insignificant enteritis
• Organisms invade the submucosa either via the
M cells or via direct penetration into or around
the epithelial cell
• Salmonellae proliferate in the submucosa with
mononuclear cell and lymphocyte proliferation
resulting in hypertrophy of peyers patches
Pathogenesis cont…
• Hypertrophy with resultant surrounding necrosis results
in abdominal symptoms and perforation
• Spread to the RES occurs via lymphatics and blood
• Replication within the RES is responsible for the
clinical features
• Eventually organisms reside in the MQs of the spleen,
liver and BM
• BM acts as a clinical sanctuary for organisms
• Intracellular organisms in these sites are responsible for
relapses and the late pyogenic complications including
pericarditis, visceral abscesses, or osteomyelitis

Clinical presentation
• Incubation period of 5 -21days
• Week 1 - rising ("stepwise") fever and
bacteremia (38.8°C to 40.5°C)
• Week 2 - abdominal pain and rash (rose spots)
• Week 3 - hepatosplenomegaly, intestinal
bleeding and perforation
• Resolution in weeks – months
• Mortality rate of 15% in preantibiotic era, and
1.5% in a NY series of 479 cases (1980 -1990)
Clinical presentation cont…
Symptoms
• Prodrome of non specific symptoms, Chills,
Weakness, Headache, Sore throat, Anorexia,
Dizziness, Cough, Muscle pains
• Variable GI symptoms, abdominal pain,
constipation or diarrheoa
• Epistaxis
Signs
• Relative bradycardia
• Rash (Rose spots)
• Hepatosplenomegaly
• Neuropsychiatric symptoms
Complications
-Intestinal perforation -Meningitis
and/or -Nephritis
-Gastrointestinal -Myocarditis
hemorrhage -Pneumonia
-Pancreatitis -Arthritis
-Hepatic and splenic -Osteomyelitis and
abscesses
-Parotitis
-Endocarditis
-Orchitis
-Pericarditis
-Hepatitis
Sequelae
• Disease lasts for 3-4 weeks if untreated with
mortality rates of 12-30%
• Asymptomatic chronic carriers (1-5%) – shed
bacteria in urine for up to 1year
• Chronic carriage higher among women,
billiary abnormalities (e.g., gallstones,
carcinoma of the gallbladder) and GI
malignancies
Lab tests
• CBC
- Leukopenia (15 – 25%)
- Normal WBC counts(majority)
- Leukocytosis especially in children during first
10days
• Abnormal LFTs
• Culture (gold standard)
- Blood culture, variable yield (90% 1n week 1
to 50% week 5)
Lab tests cont…
- Bone marrow highly sensitive (upto 90% after
5 days of antibiotics)
- Stool cultures positive in 30-40% of patients
- Urine, rose spots and duodenal contents may
be cultured
• Serologic tests, Widal test
- High rates of false positivity and negativity
- Not clinically useful
Treatment
General supportive management
• Bed rest
• Nutrition and hydration
• Antipyretics, if necessary
Specific therapy
• Guided by culture and sensitivity.
• Empiric therapy initiated with;
-Fluoroquinolones: ciprofloxacin (500 mg bid) or
ofloxacin (400 mg bid), orally or IV for 7-10/7.
-Cefalosporins: IV ceftriaxone (2-3 g od) or cefixime (20
to 30 mg/kg/day orally in two divided doses) for 7 to 14
days
-Azithromycin 1g stat then 500mg od for 5-7days
Prevention
• Hygiene
• "boil it, cook it, peel it, or forget it.“
• Vaccines: live oral S. Typhi vaccine strain
TY21a and parenteral Vi polysaccharide
vaccine
- Both vaccines are not fully protective against
s. typhi
- None is protective against paratyphoid fever

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