1. ABOUT INFECTION 2. OVERVIEW ABOUT IMMUNITY 3. INFECTION OF GRAM NEGATIVE BACTERIA 4. INFECTION BY SALMONELLA Cause of infection Causative agent Virulence factors Pathogenesis Laboratory Diagnosis Prophylaxis Treatment Preventive measures.

1. INFECTIONAND IMMUNITY
INFECTIONSOF GRAMNEGATIVEBACTERIA
SALMONELLA
Dr. Smita Milind Dharmadhikari
Associate Professor
Department of Microbiology
Government College of Arts and Science,
Aurangabad

2. POINTSTOBEDISCUSS
• 1. ABOUT INFECTION
• 2. OVERVIEW ABOUTIMMUNITY
• 3. INFECTIONOF GRAM NEGATIVEBACTERIA
• 4. INFECTIONBY SALMONELLA
• Cause of infection
• Causative agent
• Virulence factors
• Pathogenesis
• LaboratoryDiagnosis
• Prophylaxis
• Treatment
• Preventive measures.

3. INFECTION
Invasion and growth of
germsin the body
germsmay be bacteria,
viruses,yeast, fungi, or
other microorganisms
Some cancer treatments
can weaken the immune
system, which may lead to
infection.
When the body’s immune
system is strong, it can
often fight the germs and
cure an infection
An infectioncan cause
feverand other health
problems,depending
on where it occurs in
the body

4. Sources
of
Infection

5. Causative Agent
Viruses and related
agents such
as viroids(HIV, R
hinovirus, Lyssaviru
ses such as Rabies
virus, Ebolavirus an
d Severe acute
respiratory
syndrome
coronavirus 2)
Bacteria
Mycobacterium
tuberculosis,
Staphylococcus
aureus,
Escherichia coli,
Clostridium
botulinum, and
Salmonella spp.)
Fungi
yeasts - Candida,
Fungi -
Aspergillus,
Pneumocystis
spp,
and dermatophy
teshuman-
pathogenic
genus
Cryptococcus

6. Causative Agent
Parasites, which are
usually divided into:[5]
• Unicellular organisms
(e.g. malaria, Toxoplasm
a,
• Babesia)
• Macroparasites (worms
or helminths)
including nematodes,
such as parasitic
roundworms
and pinworms, tapewor
ms (cestodes), and
flukes (trematodes, such
as schistosomiasis)
Arthropods such
as ticks, mites, fleas,
and lice, can also
cause human disease,
which conceptually
are similar to
infections, but
invasion of a human
or animal body by
these macroparasites
is usually
termed infestation.
Prions and
other non
microbial
agents-
mutagen,carci
nogen,polluta
nts

7. General Signs and Symptoms of Infection
• Fever (this is sometimes the only sign of an
infection).
• Chills and sweats.
• Change in cough or a new cough.
• Sore throat or new mouth sore.
• Shortness of breath.
• Nasal congestion.
• Stiff neck.
• Burning or pain with urination.

8. WhatisImmunity
• state of protection frominfectious diseases
• Immune Systemhave following functions:
• Defense against invading pathogens (viruses &
bacteria)
• Removal of 'worn-out' cells (e.g., old RBCs) & tissue
debris (e.g., from injury or disease)
• Identification & destruction of abnormal or mutant
cells (primary defense against cancer)
• Rejection of 'foreign' cells (e.g., organ transplant)
• Inappropriate responses:
• Allergies - response to normally harmless substances
• Autoimmune diseases

9. OverviewoftheImmuneSystem
Immune System
Innate
(Nonspecific)
1o line of defense
Adaptive
(Specific)
2o line of defense

10. A typical immune response
INNATE IMMUNITY
Rapid responses to a
broad rangeof microbes
ACQUIRED
IMMUNITY
Slowerresponsesto
specificmicrobes
External defenses Internal defenses
Skin
Mucous membranes
Secretions
Phagocytic cells
Antimicrobial proteins
Inflammatory
response
Natural killer cells
Humoral response
(antibodies)
Cell-mediated
response
(cytotoxic
lymphocytes)
Invading
microbes
(pathogens)
Complement

11. • Hematopoiesis
• Early in hematopoiesis, stem cell
(HSC)differentiates to either
• Lymphoid progenitor cell
• Myeloid progenitor cell
• HematopoieticHomeostasis
• Life Span of RBCs---120days
• Life Span of WBCs - 1 day to 20-30
years

12. Innateimmunesystem:componentsof Blood
Complement proteins
Coagulationproteins
Cytokines
WBCs

14. Monocytes circulate in blood and
then migrate into tissue and
differentiateinto specific
macrophages
 Intestinal macrophages in gut
 Alveolar macrophages in lung
 Histiocytes in connective tissue
 Kupffer cells in the liver
 Mesangial cells in the kidney
 Microglial cells in the brain
 Osteoclastsin bone
 Activated macrophages are
more effective than resting ones
○ Complex antigens are phagocytized, the resulting phagosome fuses with a lysosome
○ The digested antigen is then eliminated through exocytosis
○ Some of it is presented on membrane on MHC
○ Phagocytosis is enhanced when antibody is attached to the antigen
○ Antibody acts as opsonin: molecule that bindsto both antigen and phagocyte

15. Granulocytes – Neutrophils
Multi-lobednucleus, light granules
1st
to arrive at site of inflammation
High #’s is 1st
indication of infection
Phagocytize
Generate antimicrobial agents
Neutrophils are very short livedwhen compared to
macrophages
Granulocytes – Eosinophils
Phagocytize
Play a role in parasitic organisms
Granulocytes – Basophils
Nonphagocytic
Play a role in allergic reactions
Mast cells
Play important role in developmentof allergies

16. CYTOKINES
Small proteins – secreted by cells of the immune system, -
Affect the behaviour of other cells
signalling molecules-Key players in innateand acquired immunity
Cells producing cytokines
Neutrophils – when they encounter a pathogen
Macrophages – when they encounter a pathogen
NK cells – on encounteringa microbe infected cell /tumour cell
Lymphocytes – when they are activated
Examples of cytokines- Interferons, Interleukins, Tumour necrosis factor (TNF)

17. Lymphocytes-
BcellsandTcells
Adaptiveimmunity
Smalllymphocytes
Thosethathavenot
interactedwithantigen
arecallednaïve
Interactionwithantigen
–proliferationinto
effectorcells(i.e.plasma
cells)andmemorycells

18. DIFFERENCESBETWEENTANDBLYMPHOCYTES
S.N. Characteristics B lymphocytes (B cells) T lymphocytes (T cells)
1.
Site of
Maturation
B lymphocytes both originate
and mature in the bone
marrow.
T lymphocytes mature in the thymus
after its originationin the bone
marrow.
2. Position
Mature B cells occur mostly
outside the lymph node.
Mature T cells occur mostly inside the
lymph node.
3. Distribution
Germinal centers of lymph
nodes,spleen,gut, respiratory
tract; also subcapsular and
medullarycords of lymph
nodes.
Parafollicular areas ofcortex in lymph
nodes, periarteriolar in the spleen.
.4. Receptors
The B-cell receptors (BCRs)
constitute ofmembrane
antibodies known as
immunoglobulin surface
receptors.
Surface receptors are called T-cell
receptors (TCRs)and differ from
membrane antibodies.
5. Binds with
Extracellular antigens such as
bacteria,free viruses and
other circulatingfree foreign
material.
The foreign antigen in association
with self-antigen onlysuch as a virus-
infected cell

19. DIFFERENCESBETWEENTANDBLYMPHOCYTES
S.N. Characteristics B lymphocytes (B cells) T lymphocytes (T cells)
6.
The need of
Antigen
Processing
Antigen processingis not
necessary.
Antigen processingis necessary.
7. Connection
They bind directly with the antigens
onthe surface of the invadingvirus
or bacteria.
They canonly bind to antigens on the
outside of infectedcells andnot directly.
8.
C3 complement
receptor
Receptors for C3 complement
present.
Receptors forthe C3 complement are
absent.
9.
Cell Surface
Marker
CD19 is the cell surface markers of
B cells.
CD3 is the cell surface markers of T cells.
10.
Microvilli onthe
cell surface
Present Absent
11.
Types of Active
Cells
They differentiate into plasma cells
and memory cells.
They differentiate into many subsets of T
cells such as Cytotoxic T cells (CD8+ T cells),
Helper T cells (CD4+ T cells)and suppressors
cells alongwith memory cells.

20. DIFFERENCES BETWEEN TAND B LYMPHOCYTES
S.N. Characteristics B lymphocytes (B cells) T lymphocytes (T cells)
12. Abundance
It constitutes about 20% of
lymphocytes inthe blood.
It constitutes about 80% of lymphocytes in
the blood.
13. Secretory Product
Antibodies are the chief secretory
product of B cells.
Cytokines (lymphokines)are the chief
secretory product of T cells.
14. Type of Immunity
Involvedinhumoral (antibody-
mediated)immunity.
Involvedincell-mediatedimmunity.
15. Life Span
They have comparatively a shorter
life span.
They have a comparatively longer life span.
16. Relationship
Since B cells are also Antigen
Presenting cells,they present
antigens to T-cells.
They help to activate B cells andaidin
antibody productionagainst antigens which
are T-dependent.
17. Functions
Help eliminate free foreigninvaders
by enhancing immune responses
against them; provide immunity
against most foreignantigens and
bacteria.
Help lyse virus-infectedcells and tumor
cells; provide immunity against most viruses
and intracellularbacterial pathogens; helpB
cells in antibody production.

21. Primary
Thymus and bone marrow
Place of maturationoflymphocytes
Secondary
Lymph nodes,spleen,mucosa-associated lymphoid
tissues such as gut-associated lymphoid tissues
Mature lymphocytes interact with antigen
Bone marrow
Lymphocytes arise there, T cells go to thymus to
mature,B cells mature here
90% of plasma IgG and IgA comes from B cells in the
bone marrow
Thymus
 T cell development and maturation
 Bilobed organ aboveheart,surrounded by
capsule and divided into lobules
 Outer part of lobule is cortex, inner is medulla
 Network of epithelial cells,dendriticcells,and
macrophages
 Thymus will induce death of those T cells that
can’t: Recognize self-MHC molecules
 Those that interact with MHC molecules too
strongly(could produce autoimmune disorder)
 Function decreases with age

22. DIFFERENCES BETWEEN GramPositiveandGramNegativeBacteria
S.N. Characteristics Gram Positive Gram Negative
1. Gram Reaction
Retaincrystal violet dye andstain
blue orpurple onGram’s staining.
Accept safraninafter decolorization
and stainpink orred onGram’s
staining.
2. Cell wall thickness
Thick (20-80 nm),multi-layered
Peptidoglycan,rigid and less
elastic. Outermembrane present
Thin (8-10 nm),single layered
Peptidoglycan,less rigid and more
elastic. No outermembrane
3.
Aromatic andSulfur-
containingamino acidincell
wall,
periplasmic space
Absent
No
Present
Present
4.
Chemical compositionof
cell wall
High Techoic acidlow Lipidand
LipoproteinContent,
No lipopolysaccharide
Very low Techoic acid,HighLipid and
LipoproteinContent,
Lipopolysaccharide present
5. Morphology
Usually cocci orspore forming
rods (exception: Lactobacillus
and Corynebacterium). Few are
pathogenic.
Usually non-spore formingrods
(Exception: Neisseria). Most are
pathogenic

23. InfectionsofGramNegativeBacteria
Sr.No. Name of Pathogen Morphology Name of Disease
1 Neisseria meningitidis
Neisseria gonorrhoea
G –ve oval or spherical
cocci
Meningococcal meningitis
Gonorrhea
2 Escherichia coli G –ve coccobacillary
rods
UTI,Diarrhea,
3 Klebsiella pneumoniae G –ve capsulated rods Pneumonia,
UTI,Septicemia
4 Shigella dysenteriae G –ve short rods Bacillarydysentery
5 Salmonella typhi G –ve short rods Entericfever
Gastroenteritis
Septicemia
6 Vibrio cholerae G –ve short curved
rods,comma shape
Cholera
7 Pseudomonas aeruginosa G –ve short rods Hospital cross infections

24. InfectionsofGramNegativeBacteria
Sr.No. Name of Pathogen Morphology Name of Disease
8 Yersinia pestis G-ve rods with rounded ends
and convex sides
Plague
9 Haemophillus
influenzae
G –ve shoet
rods,pleomorphic
Meningitis,
Pneumonia,Bronchitis
10 Bordetella pertussis G –ve ovoid coccobacillary
rods
WhoopingCough
11 Brucella abortus G –ve short rods arranged in
chain
Brucellosis
12 Mycobacterium
tuberculosis
G –ve stright or curved rods Tuberculosis

25. • History
• In 1885, pioneeringAmerican veterinary scientist, Daniel E.
Salmon, discovered the first strain of salmonella from the
intestine of a pig. This strain was called Salmonella
choleraesuis.
• In 1880s, the typhoidbacilluswas first discovered by Eberthin
spleen sectionsand mesenteric lymphnodes froma patient
who died fromtyphoid.
• Robert Koch confirmed arelated finding and succeededin
cultivating the bacteriumin 1881.
• Serodiagnosisof typhoid was thus made possibleby 1896.
• Wright and his team preparedheat killed vaccinefromS.typhi
in 1896

26. 1.The best known carrier was "Typhoid Mary“; Mary Mallon was a
cook in Oyster Bay, New York in 1906 who is known to have
infected 53 people, 5 of whom died.
2.Later returned with false name but detained and quarantined after
another typhoid outbreak.
3.She died of pneumonia after 26 years in quarantine.

27. InfectionbyGram NegativeBacterium -Salmonella
• Salmonella is rod-shaped (bacillus) Gram-negative bacteria of the
family Enterobacteriaceae.
• The two species of Salmonella are Salmonella enterica
• and Salmonella bongori.
• S. enterica is the type species and is further divided into six subspecies
that include over 2,600 serotypes.
• Salmonella was named after Daniel Elmer Salmon (1850–1914), an
American veterinary surgeon.
• Salmonella species are non-spore-forming, predominantly motile
enterobacteria with cell diameters between about 0.7 and 1.5 μm,
lengths from 2 to 5 μm, and peritrichous flagella (all around the cell
body).
• They are chemotrophs obtaining their energy from oxidation and
reduction reactions using organic sources.
• They are also facultative anaerobes, capable of generating ATP with
oxygen ("aerobically") when it is available, or when oxygen is not
available, using other electron acceptors or fermentation
("anaerobically").
•

28. Infection By Salmonella spp
• An infectious feverish disease caused by the bacterium
Salmonella typhi(Salmonella enterica Serovar Typhi ) and
less commonly by Salmonella paratyphi.
• The term enteric fever or typhoid fever is a communicable
disease, found only in man and includes both typhoid fever
caused by S.typhi and paratyphoid fever caused by S.
paratyphi A, B and C .
• It is an acute generalized infection of the reticulo
endothelial system, intestinal lymphoid tissue, and the gall
bladder
• The infection always comes from another human, either an
ill person or a healthy carrier of the bacterium. The
bacterium is passed on with water and foods and can
withstand both drying and refrigeration.

29. • Epidemology
• According to the World Health Organization,globally some 16
million cases occurannually resultingin more than 600,000
deaths.
• Morethan 62% of the global cases occur in Asia, of which,7
million occurannually in South East Asia.
• Other countrieswith a high incidenceincludeCentral and
South America, Africa and Papua New Guinea.
• World largest outbreak of typhoid in SANGLI on December
1975 to February1976 . This disease is endemicin India
• 1992 : 3,52,980 cases with 735 deaths
• 1993 : 3,57,452 cases and 888 deaths
• 1994 : 2,78,451 cases and 304 deaths
• Case fatality rate dueto typhoid has been varyingbetween
1.1% to 2.5 % in last few years.

30. AntigensofSalmonella
Sr.
No.
Characteristics O Antigen H Antigen
1. Types SomaticAntigen Flagellarantigen
2. Composition Polysaccharide Proteinacious
3. Antibodyformation Rapid and Early Rapid and Sustained
4. Level Falls off quickly Persists forlonger periods
5. Production Produces granular clumps.
Produces cottony, fluffy
precipitates.
6. Observation
Round bottom Felix tube are
used to see agglutination.
Conical bottom Dreyer’s tube
are used to see agglutination.
7.
Heat and alcohol
sensitivity
heat stable and resistant to
alcohol
heat-labile and sensitive to
alcohol
8. Extraction
Trichloro-aceticacid is used
for extraction
Formaldehyde is used for
extraction
9. Immunogenicity
Less immunogenic-Abs
produce with low titre.
Highly immunogenic-Abs
produced with high titre.

31. AntigensofSalmonella
• Vi antigen
• It is surfacepolysaccharideproducingantigenenvelopingthe
O antigen.
• Invented by Felix and describeas antigen related to virulence
of Salmonella.
• It is heat labile,destroyed by acid and alkali but resistantto
alcohol and formaldehyde.
• Strains of S.typhi showing Vi Ag are more virulent but fail to
agglutinate with O antiserumin widal test.
• It can be identified by phagetyping.
• Polysaccharideact as Virulentfactor inhibiting phagocytosis,
resistingcomplementactivation and bacterial lysis.

32. Virulence factors of Salmonella-Molecular design
Salmonella enterica serovar Typhi (S. Typhi), the etiologic agent of
typhoid fever, is a human restricted pathogen.
The molecular mechanism of Salmonella pathogenicity is complex.
Pathogenic Salmonella spp. shows presence of specific pathogenicity
genes, often organized in so-called pathogenicity islands (PIs).
The type III secretion system (T3SS) proteins encoded by
two Salmonella PIs (SPIs) are associated with the pathogenicity at
molecular level.
The T3SS encoded by SPI-1 contains invasion genes
SPI-2 is responsible for intracellular pathogenesis
(systemic infection)
The understanding of the mechanisms by which Salmonella evade the
host defense system and establish pathogenesis will be important for
proper disease management.

33. Routes of transmission
The disease is transmitted by faeco - oral route or urine – oral routes –
either directly through hands soiled with faeces or urine of cases or
carriers or indirectly by ingestion of contaminated water, milk, food, or
through flies. Contaminated ice, ice-creams, and milk products are a
rich source of infection.

34. Pathogenecity

35. Ingestion of contaminated food or water.
Salmonella invadesmall intestineand enter the bloodstream
Invadesmall intestineand enter the bloodstream
Carried by white blood cells in the liver, spleen,and bone marrow
Multiply and reenterthe bloodstream.
Bacterium invadethe gallbladder, biliary system,and the lymphatic
tissue of the bowel and multiply in high numbers.
Then pass into the intestinal tract and can be identified for
diagnosis in culturesfromthe stool tested in the laboratory.
Salmonella typhi infectingthe body via the Peyer'spatchesof the
small intestine.
The bacteria migrates to mesentericlymph nodesand arrivevia
the blood in the liver and spleen duringthe first exposure.
After multiple replication in the abovelocations,the bacteria
migrates back into the Peyer's patchesof the small intestine for the
secondary exposureand consequently theclinical symptomsare
seen.
Inflammationin the small intestineleads to ulcersand necrosis.

36. 36
Clinical Syndromes of Salmonella
Salmonellosis = Generic term for disease
Enteritis (acute gastroenteritis)
Enteric fever (prototype is typhoid fever and
less severe paratyphoid fever)
Septicemia (particularly S. choleraesuis, S. typhi,
and S. paratyphi)
Asymptomatic carriage (gall bladder is the
reservoir for Salmonella typhi)

37. 1st week
The body temperature rises slowly, and fever fluctuations are seen
with relative bradycardia (Faget sign), malaise, headache, and cough.
A bloody nose (epistaxis) is seen in a quarter of cases, and abdominal
pain is also possible.
A decrease in the number of circulating white blood cells (leukopenia)
occurs with eosinopenia and relative lymphocytosis.
Blood cultures are positive for Salmonella enterica subsp. enterica
serovar Typhi.
The Widal test is usually negative in the first week.
SYMPTOMS

38. SYMPTOMS
2nd week
In the second week,the person is often too tiredto getup, with high fever
in plateauaround 40 °C (104°F) and bradycardia(sphygmothermic
dissociationor Fagetsign), classicallywitha dicroticpulse wave.
Deliriumcan occur, wherethe patient is often calm,but sometimes
becomesagitated.Thisdeliriumhas led to typhoid receiving thenickname
"nervous fever".
Rose spots appear on the lowerchestand abdomenin around a third of
patients.Rhonchi (rattlingbreathingsounds) are heard in the base of the
lungs.
The abdomenis distendedand painful in the right lowerquadrant, where
a rumblingsound can be heard.
Diarrheacan occur in this stage,but constipationis also common.
The spleenand liverare enlarged(hepatosplenomegaly)and tender, and
livertransaminasesareelevated.
The Widaltest is stronglypositive,with antiO and antiH antibodies.(1:640)
Blood culturesare sometimesstillpositiveat this stage.

39. SYMPTOMS
3rd week
In the third weekof typhoid fever,a number of complicationscan
occur:Intestinalhaemorrhagedueto bleedingin congestedPeyer's
patchesoccurs; this can be very serious,but is usually not fatal.
Intestinalperforationin the distal ileumis a very seriouscomplicationand
is frequentlyfatal.It may occurwithout alarmingsymptoms
until septicaemiaor diffuse peritonitissetsin.
Encephalitis
Respiratorydiseasessuchas pneumonia and acute bronchitis
Neuropsychiatricsymptoms (describedas "mutteringdelirium"or "coma
vigil"),with pickingat bedclothesor imaginaryobjects
Metastaticabscesses,cholecystitis,endocarditis,and osteitis
The feveris stillveryhigh and oscillatesverylittleover24 hours.
Dehydrationensues,and the patientis delirious(typhoid state).One-third
of affectedindividualsdevelopa macular rash on the trunk.
Low plateletcount(thrombocytopenia)cansometimesbeseen.[

40. Rose spots High fever
Diarrhea
Typhoid Meningitis
Aches and pains
Chest congestion

41. LaboratoryDiagnosis
• Samples /Specimens-
• Blood, Stool ,Urine
• Cultural Characterization using selective and differential
media.
• Molecular level identification by PCR
• Serological diagnosis by Widal test (Slide and Tube test)
• Antimicrobial susceptibilitytesting.
• Blood cultures are positive in 70-80% of cases during the
1st week.
• Stool and urine cultures are usually positive (45-75%)
during the 2nd-3rd week.
• Bone marrow aspirate cultures give the best confirmation
(85-95%)
• The tracing of carriers in cities by sewer – swab technique

42. • Blood Culture
• A positive blood cultureis diagnostic.
• Bacteremia occursearly in the disease and blood culturesare
positive appro.In 90% cases in first week of fever,75%in 2nd
week and 60% in 3rd week.
• Blood (5-10 ml) is collected in specificblood culturemedia
containingsodiumpolyethanolsulphonate(inhibit bactericidal
action of blood)and 0.5% bile.
• Developmentof pale pink colour coloniesafter overnight
incubation at 370C are further identified and confirmed
biochemically.
• Culture decleared negativeonly after incubation for 10 days.

43. Stool/Urine Culture
Wilson and Blair bismuthsulphite mediumjet black colony
with a metallicsheen

44. Serological diagnosis Widal test
A test involving agglutination of typhoid bacilli when they
are mixed with serum containing typhoid antibodies from
an individual having typhoid fever; used to detect the
presence of Salmonella typhi and S. paratyphi.“
Two types of tubes are used-Dreyer’s tube (conical
tapering bottom for H agglutination and Felix
tubes(round bottom) for O agglutination).
Reaction temp.50-55 0C for two hrs and then overnight
at RT or overall at 37 0C overnight
H agglutination shows loose,cotton-woolyclumps.
O agglutination shows disc like pattern at botton of tube.

45. Standard test tube method
Take four sets of 8 test tubes and label them 1 to 8 for O,H,AH and BH antibody
detection.
Pipette in to the tube No.1 of all sets 1.9 ml of isotonic saline.
To each of the remaining tubes (2 to 8) add 1.0 ml of isotonic saline.
To the tube No. 1 tube in each row add 0.1 ml of the serum sample to be tested and
mix well.
Transfer 1ml of the diluted serum from tube no.1 to tube no.2 and mix well.
Discard the 1ml of the diluted serum from tube no.7 of each set.

46. Tube no.8 in all sets, serves as a saline control. Now the dilution of the serum
sample achieved in each set is as follows:
Tube no. 1 2 3 4 5 6 7 8 (control)
Dilutions 1:20 1:40 1:80 1:160 1:320 1:640 1:1280 –
To all tubes (1 to 8) of each set add one drop of the respective WIDAL TEST
antigen suspension (O,H,AH,BH) from reagent vials and mix well.
Cover the tubes and incubate at 37 C overnight (approx. 18 hrs).
Dislodge the sedimented button gently and observe.

47. Interpretation
• The highest dilution of the patients serum in which
agglutinations occurs is noted, ex. if the dilution is 1 in 160
then the titer is 160.
• Agglutination in dilution up to <1:60 is seen in normal
individuals.
• Agglutination in dilution 1:160 is suggestive of Salmonella
infection.
• Agglutination in dilution of and more than 1:320 is
confirmatory of Enteric fever .

48. • Laboratory Diagnosis
• Polymerase chain reaction (PCR) can be
performed on peripheral mononuclear cells.
The test is more sensitive than blood culture
alone (92% compared with 50-70%) but
requires significant technical expertise.
• Blood clot culture test.
• Bacteriophage typing(Salmonella typhi A and
E phages specific to Vi antigen of S.typhi)

49. RAPID TESTSFORDIAGNOSINGTYPHOID
• Typhidot –this test that detects presence of IgM and
IgG in one hour (sensitivity>95%, Specificity 75%)
• Typhidot-M, that detects IgM only (sensitivity 90%
and specificity 93%) . Produced against
lipopolysaccharide antigens.
• Typhidot rapid (sensitivity 85% and Specificity 99%)
is a rapid 15 minute immunochromatographic test to
detect IgM.
• IgM dipstick test

50. Prophylaxis
THREE TYPES OF VACCINES
1. TAB Vaccine-
• Heat killed typhoid bacillus vaccine
• First develop by Almroth Wright during Boer war in South Africa.
• Vaccine is given in 2 doses of 0.5 ml subcutaneously at an interval of
4-6 weeks.
• Killed vaccines do not provide cell mediated immunity.
2. Live Oral Vaccine
3. Typhoral is live vaccine of stable mutant of S.typhi strain Ty2 1a
lacking the enzyme UDP-galactose-4 epimerase.
4. Vaccine is enteric coated capsule containing 109 viable lyophilised
mutant bacilli,dose is one capsule per day taken 1 hr before food
on day 1,3 and 5.

51. Injectable Typhim –Vi
1. It contain purified Vi polysaccharideantigen(25ugm per
dose) from S. typhi Ty2 1a mutant.
2. This single-dose injectable typhoid vaccine, from the
bacterial capsule of S. typhi strain of Ty21a.
3. This vaccine is recommended for use in children over 2
years of age.
4. Sub-cutaneous or intramuscular injection
5. Efficacy : 64% -72%

52. SIDE EFFECTS.
Injectable Typhim -Vi
The most common adverse reactions are injection
site pain, erythema, and induration, which almost
always resolve within 48 hours of vaccination.
Occasional fever, flu-like episodes, headache,
tremor, abdominal pains, vomiting, diarrhea, and
cervical pains have been reported.
Typhoral
Nausea, abdominal pain and cramps, vomiting,
fever, headache, and rash or urticaria may occur in
some instances but are rare.

53. Indications for Vaccination
1. Travelers going to endemic areas who will be
staying for a prolonged period of time,
2. Persons with intimate exposure to a documented
S. typhi carrier
3. Microbiology laboratory technologists who work
frequently with S. typhi
4.Immigrants
5. Military personnel

54. Treatment
Consultations
• An infectious disease specialist or surgeon should be consulted.
SurgicalCare
• Usually indicated in cases of intestinal perforation.
• Mostsurgeons prefer simple closure of the perforationwith drainage
of the peritoneum.
• Small-bowel resection is indicated for patientswith multiple
perforations.
• If antibiotictreatmentfails to eradicatethe hepatobiliary carriage,the
gallbladder should be resected.
• Cholecystectomyis not always successfulin eradicatingthe carrier
statebecause of persistinghepatic infection.

55. Managementand Treatment of typhoid fever:
Sr.No Name Dose
1 Chloramphenicol The recommended dosage is 50 - 75 mg per kg
per day for 14 days divided into four doses per
day, or for at least five to seven days after
defervescence.
2 Cephalosporin Ceftriaxone: 50-75mg per kg per day one or two
doses.
Cefotaxime:40-80mg per kg per day in two or
three doses.
Cefoperazone:50-100mg per kg per day
3 Amoxicillin (Trimox,Amoxil, Biomox) daily dose of 75-100
mg/kg tid (three times a day) for 14 d.
4 Dexamethasone
(Decadron)
Initial dose of 3 mg/kg by slow i.v. infusion over
30 minutes.
1 mg/kg 6 hourly for 2 days.

56. Diet
• Fluids and electrolytes should be monitored and replaced
diligently.
• Oral nutrition with a soft digestible diet is preferable in the
absence of abdominal distension or ileus.
Activity
• No specific limitations on activity are indicated.
• Rest is helpful, but mobility should be maintained if
tolerable.
• The patient should be encouraged to stay home from work
until recovery.

57. ControlofTyphoidfever
MEASURES DIRECTEDTO RESERVOIR
a) Case detection and treatment
b) Isolation
c)Disinfection of stools and urine
d)Detection & treatment of carriers
MEASURESAT ROUTES OF TRANSMISSION
a)Water sanitation
b) Food sanitation
c) Excreta disposal
d) Fly control
MEASURES FORSUSCEPTIBLES
a)Immunoprophylaxis
b)Health education

58. • MDR is mediatedby plasmid The genes for antibioticresistancein S
typhi and S paratyphiare acquired into a region called an integronfrom
Escherichiacoliand other gram-negativebacteria via plasmids.
• Quinolone resistanceis frequently mediated by single point mutationsin
the quinolone-resistance–determiningregionof the gyrA gene.
• Nalidixic acid resistant:MICof fluoroquinolones for these strainswas 10
times thatfor fully susceptible strains.
Antibiotic resistance

59. • Keep the premises and kitchen utensils
clean. Dispose rubbish properly.
• Keep hands clean and fingernails
trimmed.
• Wash hands properly with soap and
water before eating or handling food,
and after toilet or changing diapers.
• Drinking water should be from the
mains and preferably boiled.
• Purchase freshfoodfrom reliable
sources.Do not patronize illegal
hawkers.
• Avoid high-risk food like shellfish, raw
food or semi-cookedfood.
• Wear clean washable aprons andcaps
during food preparation.
• Clean and wash food thoroughly.
• Scrub and rinse shellfish in clean
water. Immerse them in clean water
for sometime to allow self-purification.
• Store perishable food in refrigerator,
well covered
HEALTH PROMOTION