Salmonella bacteria can cause typhoid fever, which affects over 20 million people annually. The bacteria are transmitted through contaminated food or water. Symptoms include sustained fever, headache, abdominal pain and possible complications like intestinal bleeding or perforation. Diagnosis involves blood or stool cultures. Treatment is usually with antibiotics like ciprofloxacin. Prevention involves vaccination, especially in endemic areas.

1. SalmonellosisSalmonellosis
Typhoid FeverTyphoid Fever

2.  Bacteria of the genus Salmonella are highlyBacteria of the genus Salmonella are highly
adapted for growth in both humans and animalsadapted for growth in both humans and animals
and cause a wide spectrum of disease.and cause a wide spectrum of disease.
 The growth of S. Typhi and S. Paratyphi isThe growth of S. Typhi and S. Paratyphi is
restricted to human hosts, in whom theserestricted to human hosts, in whom these
organisms causeorganisms cause enteric (typhoid) feverenteric (typhoid) fever ..
 The remaining serotypes (The remaining serotypes (non-typhoidalnon-typhoidal
Salmonella or NTSSalmonella or NTS) can colonize the) can colonize the
gastrointestinal tracts of a broad range ofgastrointestinal tracts of a broad range of
animals, including mammals, reptiles, birds andanimals, including mammals, reptiles, birds and
insects.insects.

3. EtiologyEtiology
 Salmonellae are gram negative, non-sporeSalmonellae are gram negative, non-spore
forming, facultatively anaerobic bacilli.forming, facultatively anaerobic bacilli.
 Two speciesTwo species
– S. bongoriS. bongori
– S. entericaS. enterica
(S. Typhimurium)(S. Typhimurium)
 Six subspeciesSix subspecies
 More than 2500 known serovarsMore than 2500 known serovars
– Many zoonotic (non-typhoidal)Many zoonotic (non-typhoidal)

4. EtiologyEtiology
 All salmonellae are grouped based on
the somatic O antigen, the surface
virulence (Vi) antigen (restricted to S.
Typhi and S. Paratyphi) and flagellar H
antigen.

5. EtiologyEtiology
 Somatic or 0 Antigens contain long chain
lipopolysaccharide ( LPS ) cell-wall
components.
 Flagellar or H Antigens are strongly
immunogenic and induces antibody formation
rapidly and in high titers following infection or
immunization.

6. ENTERIC (TYPHOID)ENTERIC (TYPHOID)
FEVERFEVER

7.  Typhoid fever is a systemic diseaseTyphoid fever is a systemic disease
characterized by fever and abdominalcharacterized by fever and abdominal
pain caused by dissemination of S.pain caused by dissemination of S.
Typhi or S. paratyphi.Typhi or S. paratyphi.
 It is associated with enlarged Peyer’sIt is associated with enlarged Peyer’s
patches and mesenteric lymph nodes.patches and mesenteric lymph nodes.

8. HistoryHistory
Antonius MusaAntonius Musa , a Roman physician who, a Roman physician who
achieved fame by treating the Emperorachieved fame by treating the Emperor
Augustus 2,000 year ago, with cold bathsAugustus 2,000 year ago, with cold baths
when he fell ill with typhoid.when he fell ill with typhoid.
Thomas WillisThomas Willis who is credited with thewho is credited with the
first description of typhoid fever in 1659first description of typhoid fever in 1659..

9. HistoryHistory
French physicianFrench physician Pierre CharlesPierre Charles
Alexandre LouisAlexandre Louis first proposedfirst proposed
the namethe name “typhoid fever”“typhoid fever”
William Wood GerhardWilliam Wood Gerhard who waswho was
the firstthe first
to differentiate clearly between typhusto differentiate clearly between typhus
fever and typhoid in 1837.fever and typhoid in 1837.

10. HistoryHistory
Carl Joseph EberthCarl Joseph Eberth whowho
discovered thediscovered the
typhoid bacillus in 1880.typhoid bacillus in 1880.
Georges WidalGeorges Widal who described the who described the
‘‘Widal agglutination reaction’Widal agglutination reaction’
of the blood in 1896.of the blood in 1896.

12. Typhoid fever affects roughly 20 million
people each year and kills an estimated
600,000.

13. EpidemiologyEpidemiology
 S. typhi and S. paratyphi are pathogenic exclusively
in humans.
 The source of infection is sick human or
bacteriocarrier.
 People are typically infected with S . typhi through
food and beverages contaminated by a chronic
stool carrier (fecal-oral route of transmission).
 Less commonly, carriers may shed the bacteria in
urine , saliva and breast milk .
 Typhoid fever is potentially fatal if untreated.

14. Cases
A case is infectious as long as bacilli appears in
stools or urine.
Case may be missed, mild or severe.
Carriers
Temporary/incubatory- excrete bacilli for 6 to 8
weeks
Chronic- excrete bacilli for more than a year,
organism persist in gall bladder/biliary tract. e.g.
“Typhoid Marry” real name Mary Mallon

17. HOST FACTORS
 Age- occur at any age but highest incidence in 5-19
yrs age group.
 Sex- cases more in Males than Female; carrier rate
is more in females.
 Immunity- antibody may be stimulated by infection
or immunization. Antibody against (O) antigen is
higher in patient with the disease and antibody
against (H) antigen is higher in immunized person.

18. ENVIRONMENTAL & SOCIAL
FACTORS
 Typhoid fever regarded as “Index of general sanitation” in
any country.
 Increase incidence in July-September.
 Outside human body bacilli found in
- water- 2 to 7 days
- soil irrigated with sewage- 35 to 70 days
- ice & icecream- over a month food- multiply &
survive for sometime
- milk- grow rapidly without altering its taste
- vegetables grow in sewage plant.

19. PathogenesisPathogenesis
Ingestion of contaminated food or waterIngestion of contaminated food or water
Invade small intestine and enter the bloodstreamInvade small intestine and enter the bloodstream
Carried to the liver, spleen and bone marrowCarried to the liver, spleen and bone marrow
Multiply and reenter the bloodstreamMultiply and reenter the bloodstream

20. PathogenesisPathogenesis
Bacteria invade the gallbladder, biliary system andBacteria invade the gallbladder, biliary system and
the lymphatic tissue of the bowel and multiply inthe lymphatic tissue of the bowel and multiply in
high numbershigh numbers
Then pass into the intestinal tract and can beThen pass into the intestinal tract and can be
identified for diagnosis in cultures from the stoolidentified for diagnosis in cultures from the stool
tested in the laboratorytested in the laboratory

21. Clinicl CourseClinicl Course
Incubation period – averages 10-14 days– averages 10-14 days
(ranges from 3 to 21 days) depending upon(ranges from 3 to 21 days) depending upon
the dose of the bacilli ingested, the host’sthe dose of the bacilli ingested, the host’s
health and immune statushealth and immune status..

22. Clinical CourseClinical Course
 Prolonged (continued) fever (38.8-40.5) for up to 4Prolonged (continued) fever (38.8-40.5) for up to 4
weeks if untreated.weeks if untreated.
 Headache (80%)Headache (80%)
 Chills(35-45%)Chills(35-45%)
 Cough (30%)Cough (30%)
 Sweating (20-25%)Sweating (20-25%)
 Myalgias (20%)Myalgias (20%)
 Malaise (10%)Malaise (10%)
 Arthralgia (2-4%)Arthralgia (2-4%)

23. Gastrointestinal symptoms:Gastrointestinal symptoms:
 Anorexia (55%)Anorexia (55%)
 Abdominal pain (30-40%)Abdominal pain (30-40%)
 Nausea (18-24%)Nausea (18-24%)
 Vomiting (18%)Vomiting (18%)
 Diarrhea (22-28%) more common thanDiarrhea (22-28%) more common than
 Constipation (13-16%)Constipation (13-16%)
 Coated tongue (51-56%)Coated tongue (51-56%)
 Splenomegaly (5-6%)Splenomegaly (5-6%)
 Abdominal tenderness (4-5%)Abdominal tenderness (4-5%)

24. Clinical CourseClinical Course
 First week: Malaise, headache, cough & sore
throat in prodromal stage. The disease classically
presents with step-ladder fashion rise in
temperature (40 - 41°C) over 4 to 5 days,
accompanied by headache, vague abdominal pain,
and constipation or pea soup Diarrhoea.
 Second week: Between the 7th -10th day of
illness, mild hepato- splenomegally occurs in
majority of patients. Relative bradycardia may occur
and rose-spots may be seen.

25. Clinical CourseClinical Course
 Third week: The patient will appear in the "typhoid
state" which is a state of prolonged apathy,
toxemia, delirium, disorientation and/or coma.
Diarrhoea will then become apparent. If left
untreated by this time, there is a high risk of
intestinal hemorrhage and perforation.

26. ComplicationsComplications
 Gastroinestinal bleeding (10-20%)Gastroinestinal bleeding (10-20%)
 Intestinal perforation (1-3%)Intestinal perforation (1-3%)
(Most commonly occur in the third and(Most commonly occur in the third and
fourth weeks of illness and result fromfourth weeks of illness and result from
hyperplasia, ulceration and necrosis ofhyperplasia, ulceration and necrosis of
the ileocecal Peyer’s patches at thethe ileocecal Peyer’s patches at the
initial site of Salmonella infiltration).initial site of Salmonella infiltration).

27. Neurological complicationsNeurological complications
 Neurological complications occur in 2-40% ofNeurological complications occur in 2-40% of
patients .patients .
 MeningitisMeningitis
 Guillain-Barre SyndromeGuillain-Barre Syndrome
 NeuritisNeuritis
 Neuropsychiatric symptomsNeuropsychiatric symptoms

28. Rare complications:
 Hepatitis
 Pneumonia
 Thrombophlebitis
 Myocarditis, Endocarditis, pericarditis
 Cholecystitis
 Nephritis
 Osteomyelitis
 Psychosis.
2-5% patients may become Gall-bladder carriers

29. DiagnosisDiagnosis
 Microbiological procedures
 Serological procedures
 New diagnostic tests

30. Microbiological procedure
 Blood Cultures Bacteremia occurs early in
the disease
 Blood Cultures are positive in
 1st week in 90%
 2nd week in 75%
 3rd week in 50%
 4th week and later in 25%

31. SEROLOGICAL PROCEDURE
FELIX-WIDAL TEST
Significant Titers helps in Diagnosis
• Serum agglutinins raise abruptly during the
2nd or 3rd week
• Following Titers of antibodies against the
antigens are significant when single sample is tested
O > 1 in 160
H > 1 in 320
• Testing a paired sample (7-10 days) for raise
of antibodies carries a greater significance

32.  Polymerase chain reaction and DNAPolymerase chain reaction and DNA
probe assays to detect S. Typhi inprobe assays to detect S. Typhi in
blood are being developed.blood are being developed.

33. TreatmentTreatment
 CiprofloxacinCiprofloxacin (first line) 500mg bid (PO) or(first line) 500mg bid (PO) or
400mg q12h (i/v) – (5-7 days)400mg q12h (i/v) – (5-7 days)
 AmoxicillinAmoxicillin (second line) 1g tid (PO) or 2g q6h(second line) 1g tid (PO) or 2g q6h
(i/v) – (14 days)(i/v) – (14 days)
 ChloramphenicolChloramphenicol 25mg/kg tid (PO or i/v)- (14-2125mg/kg tid (PO or i/v)- (14-21
days)days)
 Trimethoprim-sulfamethoxazoleTrimethoprim-sulfamethoxazole 160/800 mg160/800 mg
bid (PO) – (14 days)bid (PO) – (14 days)

34. PreventionPrevention
Vaccination recommended to
1- those live in endemic area
2- household contacts
3- Group at risk like school children and hospital staff
Two types of vaccines
1. Injectable Typhoid vaccine (Vi CPS)
2. The oral live attenuated vaccine (TY21a)

35. Parenteral vaccine – Vi CPS
 This single-dose injectable typhoid vaccine, consisting
of purified Vi polysaccharide from the bacterial
capsule.
 Given in 1 dose, with a booster every 2 years.
 This vaccine is recommended for use in children over
2 years of age.
 Sub-cutaneous or intramuscular injection
 Efficiency : 55%

36. The oral live attenuated vaccine
(TY21a)
 This is a live-attenuated-bacteria vaccine
manufactured from the Ty21a strain of S. typhi.
 Not recommended for use in children younger than
6 years of age.
 The course consists of one capsule orally, taken an
hour before food with a glass of water or milk on
days 1, 3, 5 and 7 with a booster every 5 years.
 Efficiency: 51%