Typhoid and paratyphoid fever are acute enteric diseases caused by Salmonella bacteria. Typhoid fever is caused by Salmonella Typhi and results in prolonged fever, bradycardia, roseola rash, and possible complications affecting the intestines, liver, and spleen. It is typically diagnosed through blood or bone marrow cultures early in the disease or serological tests later. Treatment involves antibiotics like fluoroquinolones or third generation cephalosporins. Preventive measures center on controlling infection sources, interrupting transmission routes like untreated water/food, and possible vaccination. Paratyphoid fever is caused by other Salmonella serotypes and has similar characteristics but milder symptoms.

1. TYPHOID FEVER
AND
PARATYPHOID FEVER
Dr nawin kumarDr nawin kumar

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

3. 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.

4. • haemorrhage;
• perforation;
• cholecystitis;
• phlebitis;
• genitourinary inflammation;
• arthritis
• osteomyelitis.

5. Etiology
Serotype: Dgroup of Salmonella
Gram-negative
rod
non-spore
flagella
Culture characteristics

6. • Antigens: located in the
cell capsule
H(flagellarantigen).
O (Somatic orcell wall
antigen).
Vi (polysaccharide
virulence)
“widel test”

7. • Endotoxin
• A variety of plasmids
• Resistance: Live 2-3 weeks in water. 1-2
months in stool. Die out quickly in
summer
Resistance to drying and cooling

8. 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 occurusually, sometimes have
epidemic outbreaks.

9. Source of infection
Cases and chronic carriers
Cases discharge fromincubation, more in
2~4 weeks afteronset, a few (about 2~5%)
last longerthan 3 months
chronic carrier TyphoidMary

11. Transmission
• fecal-oral route
• close contact with patients orcarriers
• contaminated waterand food
• flies and cockroaches.

12. Susceptibility and immunity
• all people equally susceptible to infection
• acquired immunity can keep longer,
reinfection are rare
• immunity is not associated with antibody
level of “H”, “O”and “VI”.
• No cross immunity between typhoid and
paratyphoid.

13. Susceptibility and immunity
• All seasons, usually in summerand
autumn.
• Most cases in school-age children and
young adults.
• both sexes equally susceptible.

14. Pathogenesis
• gastrointestinal tract host-
pathogen interactions
• The amount of bacilli infection
(>105
baeteria).

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

16. Pathogenesis
→ enterspleen, liverand bone marrow (reticulo-
endothelial system)
furtherproliferation occurs
→ A lot of bacteria enterblood again.
(second bacteremia).
→ Recovery

17. S.Typhi.
stomach
Lower
ileum
peyer's patches &
mesenteric lymph nodes
thoracic
duct
1st bacteremia
(Incubation stage)
10-14d
(mononmonon
uclearuclear
phagocphagoc
ytesytes )
2nd bacteremia
liver 、 spleen 、 gall 、
BM ,ect
early stage&acme stage
(1-3W ）
LN Proliferate,swell
necrosis
defervescence stage
（ 3-4w ）
Bac. In gall
Bac. In
feces
S.Typhi eliminated
convalvescence stage
(4-5w)
Enterorrhagia,i
ntestinal
perforation

18. Pathology
• essential lesion:
proliferation of RES (reticuloendothelial
system)
specific changes in lymphoid tissues
and mesenteric lymph nodes.
"typhoid nodules“
• Most characteristic lesion:
ulceration of mucous in the region of the
Peyer’s patches of the small intestine

19. (PEYER’S PATCHES)

20. (TYPHOID NODULE)

21. Majorfindings in lowerileum
• Hyperplasia stage(1st week):
swelling lymphoid tissue and
proliferation of macrophages.
• Necrosis stage(2nd week):
necrosis of swelling lymph nodes or
solitary follicles.

22. Majorfindings in lowerileum
• Ulceration stage(3rd week):
shedding of necrosis tissue and formation
of ulcer----- intestinal hemorrhage,
perforation .
• Stage of healing (from4th week):
healing of ulcer, no cicatrices and no
contraction

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

24. The fastigiumsatge
• second and third weeks.
• Sustained high fever、 partly remittent
feverorirregularfever. Last 10～ 14 days.
• Gastro-intestinal symptoms:
anorexia 、 abdominal distension orpain、
diarrhea orconstipation
• Neuropsychiatric manifestations:
confusion、 blunt respond even delirium
and coma ormeningism

25. • Circulation system:
relative bradycardia ordicrotic pulse.
• splenomegaly 、 hepatomegaly
toxic hepatitis.
• roseola :30%, maculopapularrash
a faint pale color, slightly raised
round orlenticular, fade on pressure
2-4 mmin diameter, less than 10 in number
on the trunk, disappearin 2-3 days.

27. • fatal complications:
intestinal hemorrhage
intestinal perforation
severe toxemia

28. defervescence stage
• feverand most symptoms resolve by the
forth weekof infection.
• Fevercome down, gradual improvement
in all symptoms and signs, but still
danger.
convalescence stage
• the fifth week. disappearance of all
symptoms, but can relapse

29. Clinical forms:
• Mild infection:
very common seen recently
symptomand signs mild
good general condition
temperature is 380
C
short period of diseases
recovery expected in 1~3 weeks
seen in early antibiotics users
young children mild more
easy to misdiagnose

30. • Persistent infection:
diseases continue than 5 weeks
• Ambulatory infection:
mild symptoms,early intestinal bleeding or
perforation.

31. • Fulminate infection:
rapid onset, severe toxemia and
septicemia.
High fever,chill,circulation failure,
shock, delirium, coma, myocarditis,
bleeding and othercomplications, DIC

32. 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.

33. • In the aged
temperature not high, weakness common.
More complications.high mortality.

34. • clinical manifestations reappear
• less severe than initial episode
• It’s temperature recrudesce when temperature start
to step down but abnormal in the period of 2-3
weeks and persist 5~7 days then backto normal.
• seen in patients with short therapy of antibiotics.
Recrudescence

35. relapse
• serumpositive of S.typhi after 1～ 3
weeks of temperature down to normal.
• Symptomand signs reappear
• the bacilli have not been completely
removed
• Some cases relapse more than once

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

37. 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

38. • The bone marrow culture
the most sensitive test
specially in patients pretreated with antibiotics.
• Urine and stool cultures
increase the diagnostic yield
positive less frequently
stool culture betterin 3~4 weeks
• The duodenal string test to culture bile
useful forthe diagnosis of carriers.
• Rose spots: Not use routinely

39. Serological tests(Vidal test):
five types of antigens:
somatic antigen(O),flagella(H) antigen, and paratyphoid fever
flagella(A,B,C) antigen.
• Antibody reaction appearduring first week
• 70% positive in 3~4 weeks and can prolong to
several months
• in some cases, antibodies appearslowly, orremain
at a low level,
• some(10~30%) not appearat all.

40. • "O"agglutinin antibody titer≥1:80 and "H" ≥1:160
or"O"4 times highersupports a diagnosis of
typhoid fever
• "O"rises alone, not "H", early of the disease.Only "H"
positive, but "O"negative, often nonspecifically
elevated by immunization orprevious infections or
anamnestic reaction.
• Antibody level maybe lowerwhen have used
antibiotics early.

41. • Some cross reaction between group “D” and “A”.
• False positive in some infectious diseases.
• Some positive in blood culture ,but negative in
vidal test.
• 'Vi" often useful forcarrier(1:40)
molecularbiological tests:
DNA probe orpolymerase chain reaction (PCR)

42. Complications
Intestinal hemorrhage
Commonly appearduring the second-third week of illness
difference between mild and greaterbleeding
often caused by unsuitable food, diarrhea etc
serious bleeding in about 2~8%
a sudden drop in temperature 、 rise in pulse 、 and
signs of shockfollowed by darkorfresh blood in the stool.

43. Intestinal perforation:
• The more serious .Incidence,1-4%
• Commonly appear during 2-3 weeks.
• Take place at the lowerend of ileum.
• Before perforation,abdominal pain or
diarrhea,intestinal bleeding .
• When perforation, abdominal pain, sweating, drop in
temperature, and increase in pulse rate, then, rebound
tenderness when press abdomen,
abdomen muscle entasia, reduce ordisappearin the sonant
extent of liver, leukocytosis .
• Temperature rise .peritonitis appear.
• celiac free airunderx-ray.

44. • Toxic hepatitis:
common,1-3 weeks
hepatomegaly, ALT elevated
get betterwith improvement of diseases in 2~3
weeks
• Toxic myocarditis.
seen in 2-3 weeks, usually severe toxemia.
• Bronchitis, bronchopneumonia.
seen in early stage

45. Othercomplications:
• toxic encephalopathy.
• Hemolytic uremic syndrome.
• acute cholecystitis 、
• meningitis 、
• nephritis et al.

46. Diagnosis
• Epidemiology data
• Typical symptoms and signs
• Laboratory findings.

47. Differential diagnosis
• Viral infections:
such as upperrespiratory tract infection.
abrupt onset with fever, headache, leucopenia, sore
throat, cough, coryza.
no rose spots, no enlargement of liver& spleen. The
course of illness no more than 2 wks.
differential diagnosis depends on typical
manifestations and blood culture.

48. Malaria
history of exposure to malaria.
Paroxysms(often periodic) of sequential
chill,high feverand sweating.
Headache, anorexia, splenomegaly, anemia,
leukopenia
Characteristic parasites in
erythrocytes,identified in thickorthin blood
smears.

49. • Leptospirosis
Endemic area,contacted with urine of mice.
Abrupt fever,chills,severe headache,and myalgias,
especially of the calf muscles.
Leptospires can be isolated fromblood,cerebrospinal
fluid.
Special agglutination titers develop after7 days and
may persist at high levels formany years.

50. Epidemic Louse-Borne typhus
• prodromal of malaise and headache followed by
abrupt chills and fever.
• headaches,prostration,persisting high fever.
• Maculopapularrash appears on the forth to seventh
days on the trunkand in the axillas, spreading to the
rest of the body but sparing the face,palms,and
soles.
• Laboratory confirmation by proteins OX19
agglutination and specific serologic tests.

51. Tuberculosis
• continuous high orlow fever,fatigue,weight
loss,night sweats.
• Mild cough
• pulmonary infiltration on chest radiograph
• positive tuberculin skin test reaction(most cases)
• acid-fast bacilli on smearof sputum
• sputumculture positive formycobacterium
tuberculosis.

52. Septicemia of Gram-negative bacilli
• abrupt onset,high fever,symptomof toxemia.
• Chill,sweats.
• Shock.
• Positive of gram-negative bacilli fromblood
culture.

53. Prognosis:
• Case fatality 0.5～ 1%.
• but high in old ages 、 infant 、 and serious
complications
• Have immunity foreverafterdiseases
• About 3% of patients become fecal carriers .

54. 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 orhalf-
liquid food.drinkmore water
intravenous injection to maintain waterand acid-
base and electrolyte balance

55. • Symptomatic treatment:
forhigh fever:
• physical measures firstly
• antipyretic drugs such as aspirin should be
administrated with caution
• delirium,coma orshock,2-4mg dexamethasone
in addition to antibiotics reduces mortality.

56. 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

57. 2.Chloramphenicol:
• Forcases without multiresistant S.typhi.
• Children in dose of 50～ 60mg/kg/perday.
• adult 1.5～ 2g/day. tid.
• Unable to take oral medication, the same dosage
given introvenously
• afterdefervescence reduced to a half. complete a 10
～ 14 day course.
• But ,drug resistance, a high relapse rate,bone
marrow toxicity.

58. 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.

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

60. • Toxic myocarditis:
bed rest, cardiac muscle protection drugs,
dexamethasone, digoxin.
5.Chronic carrier:
• Ofloxacin 0.2 bid orciprofloxacin 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.

61. • Prophylaxis
1.control source of infection
Isolation and treatment of patients
stool culture one time per5 days.
if negative continued two times ,without isolation.
Control of carriers.
observation of 25 days(15 days in paratyphoid) when
close contact

62. 2. Cut of course of transmission
key way
avoid drinking untreated waterand
food.
3.Vaccination
side-effect more, less use

63. Paratyphoid feverA,B,C
• Caused by Salmonella paratyphoid
A,B,C.respectively.
• in no way different fromtyphoid feverin
epidemiology, pathogenesis,
pathology,clinical manifestations,
diagnosis, treatment and
Prophylaxis

64. Paratyphoid A,B:
• incubation period 2~15days, in genaral,8~10 days.
• milderin severity
• fewerin complications.
• Betterin prognosis,
• relapse more common in Paratyphoid A.
• Treatment same as in typhoid fever.

65. Paratyphoid C:
• Always sudden onset.
• Rapid rise of temperature.
• Presented in different forms-- Septicemia,
Gastroenteritis and Enteric fever
• Complications--arthritis, abscess formation,
cholecystitis, pulmonary complications are
commonly seen.
• Intestinal hemorrhage and perforation not as
common as in typhoid fever.