Enteric fever presentation

1. Typhoid Fever
2nd Year CHO/CHA-2022
Dr. Brima Bobson Sesay
(MBChB, MPH)
DMO-Bonthe

2. Typhoid
 Definition
 Etiology
 Pathogenesis
 Epidemiology
 Clinical
manifestations
 The laboratory and
other examinations
 Complications
 Diagnosis and
differential
diagnosis
 Prognosis
 Treatment

3. 1.Definition of Typhoid fever
 Acute enteric infectious disease
 caused by Salmonella typhi (S.Typhi).
 prolonged fever, Relative bradycardia, apathetic
facial expressions, roseola, splenomegaly,
hepatomegaly, leukopenia.
 intestinal perforation, intestinal hemorrhage

4. 2. Etiology
 Salmonella typhi
 Gram-negative
 rod
 non-spore
 flagella
 Culture characteristics

5.  Antigens: located in the cell capsule
H (flagellar antigen).
O (Somatic or cell wall antigen).
Vi (polysaccharide virulence)
“widel test”

6. A schematic diagram of a single Salmonella typhi cell
showing the locations of the H (flagellar), 0 (somatic), and
Vi (K envelope) antigens.

7. 3. Epidemiology
 continues to be a global health problem
 areas with a high incidence include Asia,
Africa and Latin America
 affects about 6000000 people with more
than 600000 deaths a year. 80% in Asia .
 sporadic occur usually, sometimes have
epidemic outbreaks.

8. 4. Source of infection
 Cases and chronic carriers
Cases discharge from incubation, more in
2~4 weeks after onset, a few (about 2~5%)
last longer than 3 months
chronic carrier Typhoid Mary

9. 5. Transmission
 fecal-oral route
 close contact with patients or
carriers
 contaminated water and food
 flies and cockroaches.

10. 6. Pathogenesis
 gastrointestinal tract host-
pathogen interactions
 The amount of bacilli infection
(>105baeteria).

11. ingested orally
 Stomach barrier (some Eliminated)
 enters the small intestine
Penetrate the mucus layer
 enter mononuclear phagocytes of ileal peyer's
patches and mesenteric lymph nodes
 proliferate in mononuclear phagocytes
spread to blood. initial bacteremia (Incubation
period).
Pathogenesis

12. Pathogenesis
 enter spleen, liver and bone marrow
(reticulo-endothelial system)
further proliferation occurs
 A lot of bacteria enter blood again.
(second bacteremia).
 Recovery

13. Pathology
 essential lesion:
proliferation of RES (reticulo-endothelial
system )
specific changes in lymphoid tissues
and mesenteric lymph nodes.
"typhoid nodules“
 Most characteristic lesion:
ulceration of mucosa in the region of the
Peyer’s patches of the small intestine

14. Major findings in lower ileum
 Hyperplasia stage(1st week):
swelling of lymphoid tissue and
proliferation of macrophages.
 Necrosis stage(2nd week):
necrosis of swollen lymph nodes
or solitary follicles.

15. Major findings in lower ileum
 Ulceration stage(3rd week):
shedding of necrosis tissue and
formation of ulcer ----- intestinal
hemorrhage, perforation .
 Stage of healing (from 4th week):
healing of ulcer, no cicatrices and no
contraction

16. Clinical manifestations
Incubation period: 3～60 days(7～14).
The initial period (early stage)
 First week.
 Insidious onset.
 Fever up to 39~400C in 5~7 days
 chills、ailment、tired、sore throat、
cough ,abdominal discomfort and
constipation et al.

17. The fastigium satge
 second and third weeks.
 Sustained high fever、partly remittent
fever or irregular fever. Last 10～14 days.
 Gastro-intestinal symptoms: anorexia、
abdominal distension or pain、diarrhea
or constipation
 Neuropsychiatric manifestations:
confusion、blunt respond even delirium
and coma or meningism

18.  Circulation system:
relative bradycardia.
 splenomegaly、hepatomegaly
toxic hepatitis.
 roseola :30%, maculopapular rash
a faint pale color, slightly raised
round or lenticular, fade on pressure
2-4 mm in diameter, less than 10 in number
on the trunk, disappear in 2-3 days.

20. Fatal complications:
 Intestinal hemorrhage
 Intestinal perforation
 Severe toxemia

21. defervescence stage
 fever and most symptoms resolve by
the forth week of infection.
 Fever come down, gradual
improvement in all symptoms and
signs, but still danger.
convalescence stage
 the fifth week. disappearance of all
symptoms, but can relapse

22. Special manifestations
 In children
Often atypical
sudden onset with high fever.
Respiratory symptoms and diarrhea, dominant.
Convulsion common in below 3.
relative bradycardia rare.
Splenomegaly, roseola and leucopenia less common.

23.  In the aged
temperature not high, weakness common.
More complications.high mortality.

24. 7. Laboratory findings.
I. Routine examinations:
white blood cell count is normal or
decreased.
Leukocytopenia(specially eosinophilic
leukocytopenia).
recovery with improvement of diseases
decreased in relapse

25. II. Bacteriological examinations:
 Blood culture:
the most common use
80~90% positive during the first 2 weeks of illness
50% in 3rd week
not easy in 4th week
re-positive when relapse and recrudesce
attention to the use of antibiotics

26. 8. Complications
 Intestinal hemorrhage
 Intestinal perforation
 Toxic hepatitis
 Toxic myocarditis
 Bronchitis, bronchopneumonia

27. Other complications:
 toxic encephalopathy.
 Hemolytic uremic syndrome.
 acute cholecystitis、
 meningitis、
 nephritis et al.

28. 9.Differential diagnosis
 Viral infections
 Malaria
 Leptospirosis
 Tuberculosis
 Septicemia of Gram-negative bacilli

29. 10. Prognosis:
 Case fatality 0.5～1%.
 But high in old ages、infant、and serious
complications
 Have immunity for ever after diseases
 About 3% of patients become fecal
carriers .

30. 11. TREATMENT
General treatment
 Isolation and rest
 good nursing care and supportive
treatment
close observation T,P,R,BP,abdominal
condition and stool .
suitable diet include easy digested food or
half-liquid food.drink more water
intravenous injection to maintain water and
acid-base and electrolyte balance

31.  Symptomatic treatment:
for high fever:
 physical measures firstly
 antipyretic drugs such as aspirin should be
administrated with caution
 delirium,coma or shock,2-4mg
dexamethasone in addition to antibiotics
reduces mortality.

32. Etiologic and special treatment
1.Quinolones:
first choice
it’s highly against S.typhi
penetrate well into macrophages,and achieve high
concentrations in the bowel and bile lumens
 Norfloxacin (0.1～0.2 tid～qid/10～14 days).
 Ofloxacin (0.2 tid 10～14days).
 ciprofloxacin (0.25 tid)
caution: not in children and pregnant

33. 3.Cephalosporines:
Only third generation effective
Cefoperazone and Ceftazidime.
2～4g/day .10~14 days.
4.Treatment of complication.
 Intestinal bleeding:
bed rest, stop diet,close observation T,P,R,BP.
intravenous saline and blood transfusion,and
attention to acid-base balances.
sometimes,operative.

34.  Perforation:
early diagnosis.
stop diet.
decrease down the stomach pressure.
intravenous injection to maintain electrolyte
and acid-base balances.
use of antibiotics.
sometimes operative.

35.  Toxic myocarditis:
bed rest, cardiac muscle protection drugs,
dexamethasone, digoxin.
5.Chronic carrier:
 Ofloxacin 0.2 bid or ciprofloxacin 0.5 bid, 4～6
weeks.
 Ampicillin 3～6g/day tid plus probenecid 1～
1.5g/day. 4～6 weeks.
 TMP+SMZ
2 tabs. Bid. 1～3 months.
 Cholecystitis may require cholecystectomy.