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SalmonellosisSalmonellosis
Typhoid FeverTyphoid Fever
 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.
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)
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.
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.
ENTERIC (TYPHOID)ENTERIC (TYPHOID)
FEVERFEVER
 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.
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..
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.
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.
Typhoid fever affects roughly 20 million
people each year and kills an estimated
600,000. 
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.
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
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.
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.
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
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
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..
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%)
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%)
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. 
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.
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).
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
Rare complications:
 Hepatitis
 Pneumonia
 Thrombophlebitis
 Myocarditis, Endocarditis, pericarditis
 Cholecystitis
 Nephritis
 Osteomyelitis
 Psychosis.
2-5% patients may become Gall-bladder carriers
DiagnosisDiagnosis
 Microbiological procedures
 Serological procedures
 New diagnostic tests
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%
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 
 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.
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)
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)
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%
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%

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Typhoid 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.
  • 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.
  • 11.
  • 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
  • 15.
  • 16.
  • 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%

Editor's Notes

  1. Salmonella spp. are members of the family Enterobacteriaceae. They are Gram negative, facultatively anaerobic rods. The genus Salmonella contains two species, S. enterica, the type species, and S. bongori. S. enterica. contains six subspecies: S. enterica subsp. enterica, S. enterica subsp. salamae, S. enterica subsp. arizonae, S. enterica subsp. diarizonae, S. enterica subsp. houtenae and S. enterica subsp. indica. Within each subspecies are serovars; over 2500 serovars are presently known. Most of the isolates that cause disease in humans and other mammals belong to S. enterica subsp. enterica. A few serovars, Salmonella ser. Typhi, Salmonella ser. Paratyphi and Salmonella ser. Hirschfeldii are human pathogens that are transmitted from human to human. The remaining Salmonella serovars, sometimes referred to as non-typhoidal Salmonella, are zoonotic or potentially zoonotic.
  2. Despite having fairly similar names, typhoid and typhus have little in common. One major similarity, and why many have thought them to be the same disease for so long, is the symptoms: Typhus: Abdominal pain, rash, high fever, cough, headache, joint and muscle pain, nausea, chills, confusion and low blood pressure Typhoid: Abdominal tenderness, agitation, bloody stool, chills, confusion, delirium, hallucinations, nose bleeds and fatigue. The few differences in symptoms can make diagnosis problematic. The identification is also, at times, what causes confusion. Both diseases contain the word ‘typhi’ in their official names. Rickettsia typhi is the proper name of typhus and it’s Salmonella typhi for typhoid. Infection vector, treatment and prevention, however, could not be more different: Vector: Typhoid infection is food borne; typhus infection is flea-borne Treatment: Typhoid treatment involves fluids and electrolytes as well as low-grade antibiotics. Typhus treatment requires specific antibiotics and may need intravenous fluids or oxygen. Prevention: Typhoid is preventable through vaccination and avoiding contaminated food and water sources. Typhus prevention is more difficult, requiring repellents and insecticides. Maintaining proper hygiene is a must for preventing both diseases. To find out more about typhoid, see our typhoid vaccination page.
  3. Epidemiology Typhoid fever occur worldwide but primarily in developing nations where sanitary conditions are poor. World map showing incidence of typhoid fever. Strongly endemic; Endemic and Sporadic cases. It is endemic in Asia, Africa, Latin America, the Caribbean, and Oceania.
  4. Up to 10% of untreated patients with typhoid fever excrete S. Typhi in the feces for up to 3 months and 1-4% develop chronic asymptomatic carriage, shedding S. Typhi in either urine or stool for > 1 year. Chronic carriage is more common among women, infants and persons with biliary abnormalities ssociated with the latter conditions presumable allow prolonged colonization.
  5. Later returned with false name but detained and quarantined after another typhoid outbreak.
  6. Public health pioneer Sara Josephine Baker, MD, PhD tracked her down after discovering that she was the common link among many people who had become ill from typhoid fever She was traced to typhoid outbreaks a second time so she was put in prison again where she lived until she died.
  7. Both complications are life-threatening and require immediate fluid resuscitation and surgical intervention, with broadened antibiotic coverage for polymicrobial peritonitis and treatment of gastrointestinal hemorrhages, including bowel resection.
  8. The definitive diagnosis of enteric fever requires the isolation of S. Typhi or from blood, bone marrow, other sterile sites, rose spots, stool or intestinal secretions.
  9. The yield of blood cultures is quite variable. A low yield is related to low numbers of salmonellae (<15 organisms/ml) and/or to recent antibiotic treatment. Unlike blood culture , bone marrow culture remains highly (90%) sensitive despite < 5 days of antibiotic therapy. Culture of intestinal secretions can be positive despite a negative bone marrow culture.
  10. Widal test in not sufficiently sensitive or specific to replace culture-based methods for the diagnosis of enteric fever in developing countires.
  11. Endemic countries are Indian subcontinent, The Philippines or Latin America.