HIPPOCRATES

Father of Medicine (460 B.C. 377 B.C.)

Rejected evil spirits

and superstitions as a
cause of diseases.
Importance of Clinical
History & Examination
Described Fever

Thanks
Monsoon
to Mania
AAFP

S
U
R
I
V
U
R
I
V

E
C
L AN

VE

S
R
O
T
C

E
U
G
A
V

MEDI-NEWS

MEDI-NEWS

MEDI-NEWS

MEDI-NEWS

MEDI-NEWS

After 26th July 2005..

MEDI-NEWS

Fever, Fever, Everywhere!

LEPTOSPIROSIS

CHIKUNGUNYA

What is fever ?
Fever is an elevation of

body temperature that

exceeds the normal daily
variation, in conjunction
with an increase in
hypothalamic set point
A Diagnostic Clue
Essential host defense
mechanism
With or without localizing
signs
Infection, Inflammation or
Neoplasm

Range

Hypothermia

<36

Normal

37

Mild

38.2-39

Moderate

39 40

High-Grade

40 41.5

Severe

> 41.5

Effects of Fever
For each 1 C elevation of body temp:
Metabolic

rate increases

10-15%

Insensible
300

O2

water loss increase

to 500ml/m2/day

consumption increase 13%

Heart rate increase 10-15/min

Patterns of Temperature
Continuous fever
Constantly elevated above the normal level

Remittent fever
Fluctuates daily, constantly above normal

Intermittent fever
Daily fluctuation, going below the normal 37C

Relapsing fever
Normal temperature alternate with fever

Problem Oriented Medical Record

S OAP
Provisional DAY 1

DAY 2

Subjective

Fever, N V

Fever, Cough Fever, Expt

Objective

101 F

Assessment

Liver +

100 F
Continuous
Liver ++

100 F
Reduced
Liver / Spleen

Plan

CBC MP
Antipyretics

Leucopenia
Cefixime

Blood Culture
Cefixime

DAY 3

Common Clues from Symptoms

Respiratory - URTI , LRTI, Tuberculosis,
Urinary - UTI, APN, Cystitis
Abdominal Typhoid, Appendicitis
Bone & Joint - RA, SLE, AS
Multi system - Viral, Typhoid, Autoimmune

Acute

Sub-acute
Chronic

Travel History
Malaria Endemic areas
Dengue fever - eg. Singapore
Epidemic areas
Viral fevers
Typhoid
Schistosomiasis
Tuberculosis hospitals, contact history

Fever with Myalgia

Viral fevers Leuco & thrombocytopenia
Influenza URTI symptoms
Polymyositis
Proximal muscle weakness,
Muscle pain & tenderness, CPK high
Meningococcal infection

With rash, CNS symptoms

Sepsis

Fever with Night Sweats

Tuberculosis
Lymphoma
Abscess
Brucellosis
Infective Endocarditis
Alcohol withdrawal syndrome

Fever with Brady, Tachycardia

BRADYCARDIA

TACHYCARDIA

Typhoid fever
Malaria

All fevers
Anemia

Meningitis

Thyrotoxicosis

Leptospirosis

Toxins

Viral
Drug fever

Fever with Jaundice

Hepatitis- Viral, Drugs (AKT)
Alcoholic Hepatitis
Cirrhosis of Liver
Hepatoma
Viral fevers
Malaria
Leptospirosis + Renal failure

Generalised Lymphadenopathy
Leukaemia - ALL , CLL
Lymphoma Mediastinal Nodes
HIV Oral Candidiasis
Hepatosplenomegaly
Toxoplasma,

Rubella
Disseminated TB
Epitrochlear Nodes
Milliary TB, Lymphoma
HIV, Syphilis

Fever with Hepato-splenomegaly

Malaria
Typhoid
Lymphoma
Leukemia
Disseminated TB
Infective Endocarditis
Brucellosis
Kala azar

Fever & Eyes

Eye pain Temporal Arteritis
Watery eyes- Peri Arteritis Nodosa
Dry eyes SLE,RA
Subcutaneus hage S/A bacterial endocarditis
Conjunctivitis TB,SLE
Conjunctival suffusion- Leptospirosis
Uveitis- TB,SLE, Sarcoidosis

Skin Lesions with Fever

Measles Chickenpox Mumps

Boil

Abscess Carbuncle

Skin Lesions with Fever

Herpes zooster

Oral Cavity and fever

Fever with Mental Confusion

Meningitis viral / bacterial / TB
Meningism Typhoid / TB
Hiv Opportunistic Infection
Brucellosis
CNS Neoplasms

It is more important to know

what sort of person has a disease,
than to know what sort of disease a
person has. - Hippocrates

I will try to be more

Viral Fever A Casual Diagnosis

Air-borne, Water Borne or Sexually

Transmitted
Show generalised symptoms
But may target specific organs.
Fatigue, Malaise, Headaches, body
aches and a skin rash with Upper
respiratory symptoms
Require only symptomatic treatment
Some are highly contagious

Virus A Non living Organism

Who gets Viral Diseases?

Mammals and Birds
Amphibians, Reptiles
Fish
Plants and Fungi
Insects
Bacteria

Viral Diseases

Viral Rash

Treatment and Prognosis

Purely symptomatic with antipyretic and

analgesic drugs.
Bed rest and adequate fluid intake
Nasal decongestants

Steroids are not advised as it may

lead to bacterial super-infection.
Antibiotics are NOT routinely
advised for prophylaxis

Influenza Virus Strains

Type A
Moderate

to severe illness
All age groups
Humans and other animals
Type B
Changes

less rapidly
Milder epidemics
Humans only
Primarily affects children

Influenza Type A Subtypes

H

Determined by Hemagglutinin (H) and

Neuraminidase (N). Antibodies are specific to

different types of surface antigens
Changes in H and N allow virus to evade
previously developed immune responses

H1N1

Different species shelter

different strains of flu virus

H1N1

Swine Flu - H1N1

Swine influenza is a respiratory disease

of pigs caused by a virus

Influenza A, H1N1 swine flu has moved
from pigs to humans and can be
transmitted from human to human.
Mainly from person to person when an
infected person coughs or sneezes and
spreads tiny particles into the air

Signs and Symptoms

Fever, cough, sore throat,

body aches, headache,

chills and fatigue
Diarrhea and vomiting
Serious symptoms in

individuals with chronic

medical conditions
Pneumonia, respiratory

failure, and deaths have

been reported.

Virology or serology?
Virus detection using

Superior to antibody
Rapid virus isolation
determination for
Antigen staining
diagnosis.
Molecular biological
techniques
Detecting Specific
Complementary tool
antibodies
to confirm the
IgG,
diagnosis
IgM
retrospectively.

Anti-viral Treatment
Tamiflu and Relenza, seem to be

effective.
However, the drugs must be
administered at an early stage to be
effective. (Within 2 days)
? Availability, Cost
Swine flu vaccine is developed,
Not yet available with us.

BIRD FLU - H5N1

Viral disease affecting respiratory,

enteric or nervous system of many kinds

of poultry and birds.
Most virulent is the acute, generalized
disease with short course and extremely
high mortality.
In 2000-2002, H5N1 avian viruses
reappeared in the poultry markets of
Hong Kong, although they have not
infected humans.

Influenza vaccines
Live Vaccine Not preferred
0.25 ml of the Reconstituted Vaccine
in each nostril.
Inactivate vaccine Best Results
0.5 ml intramuscular
0.25ml for a child (6months to 3
years)
One dose above 9 years
Get vaccinated each year with the

prevalent strains of the last year.

SARS
2003 epidemic of SARS - Corona virus family
The SARS virus may live for up to 6 hours in

droplets and up to 3 hours after the droplets

have dried.
Symptoms of URTI with fever
May cause Ac Respiratory failure
Rx - Antivirals, Antibiotics, Steroids

Since 2004, no cases of SARS

reported anywhere in the world.

To do nothing
is sometimes a good remedy
Hippocrates

u
f
n
o
C
l
l
i
t

?
g
n
i
s

Dengue fever
Most important arbovirus in terms of morbidity,

mortality and economic cost

Primary infection with dengue usually results
in a febrile, self limiting disease
Secondary infection may result in severe
complications such as dengue shock
syndrome (DSS) or dengue haemorrhagic
fever (DHF).
Characteristic antibody responses to the
disease enable serological diagnosis and
differentiation between primary and secondary
dengue.

Pathogenesis Dengue Virus

DEN 1 18%
DEN 2 62%
DEN 3 14%
DEN 4 6%
DEN 2 SE
Asian Strain
Most Virulent

RNA virus of family

Flaviviridae

Serotypes DEN 1, 2, 3 and 4

Different strains within each

serotype

Transmitted by Aedes

aegypti mosquito

Incubation period ranges

from 3 to 10 days

The Vector
Aedes Egypti
Fresh & clean water breeder
Strong fliers, Day Biter
Their bites are painful
Meal time
8-13

hrs
15 to 17 hrs.
Voracious

appetite

Mosquito Bite
Mosquito inserts its

proboscis into a small

vessel. Its saliva contains
anticoagulant proteins.
It sucks your blood into
their abdomen.
Saliva evoke an immune
response of Histamine.
Histamine causes nerve
irritation (itching) and
vasodilatation (redness)

Breeding Places -AEDES

BREEDS IN PERIDOMESTIC
CONTAINERS MOSTLY
BLACK IN COLOUR

Dengue - Pathophysiology
Vasculopathy
Increased capillary permeability
High Hematocrit
Abnormal Homeostasis
Thrombocytopenia

You Bleed,
If They Breed

Dengue Illness
DSS
DHF
CLASSICAL DENGUE
BREAKBONE FEVER

UNDIFFERENTIATED
FEBRILE ILLNESS
* With Rash

* With Respiratory symptoms

* Both
* With none

Clinical features
Primary Infection
Acute febrile illness of sudden onset
Fever lasting 3 to 5 days
Headache, myalgia, arthralgia or muscular
pain, retro-orbital pain, anorexia
Fine maculopapular rash on extremities
Recovery associated with fatigue and
depression
Children usually have milder disease than
adults

40
39
38
Temperature
37

Course of Events

120
Blood Pressure
60
Platelets

224 140 70 35 38 135

Polyserositis

Packed cell volume

1

38
5

45 52
6

35
9

10

Clinical features
Secondary Infection
90% of cases of DHF and DSS occur in
patients previously infected with the virus
Symptoms are similar to primary infection,
although after a period of 3 to 7 days the
patient has haemorrhagic symptoms
Bleeding, particularly in skin (petechiae),
occasionally in gums and nose
Increased vascular permeability resulting in
leakage of plasma into extravascular spaces
which leads to hypovolaemia

Dengue Presentation

Dengue Presentation
Positive
Tourniquet test

Dengue Presentation

Dengue Presentation

Dengue Presentation

Dengue Presentation

Dengue Presentation

Risk Markers
Very Low Platelet counts
Reduced blood pressure
Vascular changes and coagulopathy
Presence of blood in stools, vomitus,

urine
Circulatory shock
Vomiting and abdominal pain
Lymphadenopathy and hepatomegaly

Primary Infection
Antibodie Appear
s
IgM
5 days
IgG
14 days

Rise

Till

1-3 wks

6 mths
Life

Primary Infection results in lifelong

immunity to that serotype, but only

temporary immunity to other serotypes

Secondary Infection
Antibodi
es
IgM
IgG

Appear Rise

Titers

May
not
2 days

Very Low

Slow
rise

Higher Titers

Secondary Infection may be more

severe with complications.
It may require Hospitalization

Treatment of Dengue
No Specific treatment for primary dengue

Secondary Infection
Intravenous fluid replacement and
Use of plasma expanders
Oxygen therapy
Blood transfusions in cases of severe
bleeding

Chikungunya - CHIKV Fever

2006 Epidemic after 33 years was the

largest Hydrabad, Karnataka, MS

African word - to bend or twist
Caused by RNA - Arbovirus
Vector for Transmission Aedes aegypti
Aedes albopictus (Tiger mosquito).
Self-limiting and rarely fatal.
The symptoms like dengue: but there is
no DHS or DSS

Chikungunya Symptoms
Incubation 2 to 12 days
Symptoms can persist for several wks.
High fever which can reach 39C, lasts

for two days and abruptly comes down

Nausea, Vomiting, Headache,
conjunctival injection, photophobia
Myalgia, Arthralgia or arthritis affecting
multiple joints
Rash - Petechial or maculopapular rash
usually involving the limbs and trunk

Diagnosis
1. Four fold rise of HI Antibody
2. IgM capture ELISA - Pune
3. IIFT - Indirect Immuno

Flourescence Test
4. Virus Isolation - Vero BHK21 cell lines
5. Nucleic acid amplification by
PCR & RT- PCR

Differential Diagnosis
Feature

CHIKV

DENGUE

Presentation

A+F mild rash

A+F+Rash

Arthralgia

Moderate

Severe

Arthritis

Not common

Frequent

Bone pains

None

Break bone fever

Thrombocytopenia

Mild (Not < 1lac)

May be severe

Hemorrhage

None

May be present

Shock syndrome

Never

May occur

Immunity (IgG)

Life long

2nd attack fatality

Management
No specific treatment for Chikungunya.
Chloroquine and HCQS - possible

treatment for the symptoms

Aspirin is contraindicated - By CDC
Ibuprofen, Naproxen and other NSAIDs
are recommended for arthritic pain and
fever.
No untoward effects on pregnancy is
noticed following the infection.

Leptospirosis
Mud / Swamp fever
Japanese 7 day fever
Rice Field Fever
Spirochete Jaundice
Canicola Fever
Leptospiral Jaundice
Autumn Fever
Swineherds Disease

The Causative Bacterium

Order Spirochaetales
Treponema, Borrelia, Leptospira
Family Leptospiraceae,
- Susceptible to heat, Chlorine, acid
Genus Leptospira,
26 serogroups, 250 serovars
Corkscrew shaped, Delicate,

Gram -ve

Long & Thick, coiled, flagellate, Actively motile

Epidemiology
Difficult to pinpoint the source of infection
Any person can get infected
Rainfall; Water logging
Inadequate drainage facilities
Rodents, cattle & stray dogs
Walking/ working bare foot

Reservoirs of Infection
Leptospira are excreted in the urine
Direct contact - with urine - Through skin

abrasions, intact mucus membrane

Indirect contact - Broken skin with
infected soil, water or vegetation and
Ingestion of contaminated food & water
Droplet infection - Inhalation of droplets
of infected urine

Leptospirosis

Pathogenesis of Severe Disease

Leptospira

Damage
to small
blood vessels

Migration of fluid from Intravascular

to interstitial compartment

Vasculitis

Direct cytotoxic injury

Immunological injury

Renal dysfunction, Vascular Injury

Clinical Presentation
Types

Anicteric (common - 95% recover)

Icteric ( Weils Syndrome) (Rare, Fatal)
Hepato-Renal syndrome
Hemorrhagic syndrome with ARF
Atypical Pneumonia syndrome
Aseptic Meningo-encephalitis
Myocarditis, Chronic Uveitis

Clinical Presentation

Common, Mild
< 2% Mortality

Rare, Severe
15% Mortality

1
0
%

Icteric

o
f
C
a
s
e
s

Anicteric

o
f
C
a
s
e
s
9
0
%

PathogenesisIncubation : 7~13 days

Early Stage - 1-2 Days
Three toxic symptoms:
Fever,
Myalgia,
Fatigue
Middle Stage
3-10 Days
Severe toxic symptoms

Convalescent stage
After fever
Immunopathological

Three signs:
Conjunctival Suffusion
Muscle tenderness
Large lymphonodes
Influenza form
Pneumo-haerrhagic form
Ictero-hemorrhagic form
Meningo-encephalitis
Renal failure form
Sequele of eyes;
Reactive meningitis;
Cerebro arteritis obliterans.

Anicteric Presentation
Leptospiremic Phase
Initial

Immune Phase
Subsequent

Fever, Myalgia

Mild fever

Severe head ache

Meningism

Conjunctival suffusion

Uveitis

Abd. pain, Epistaxis

I.P: 5 to 14 days

Icteric Presentation
Jaundice in 4 to 6 days
Serum Bilirubin increased markedly
SGOT & SGPT Mildly elevated
Hepatocellular Necrosis
Intrahepatic cholestasis
Death Not due to Liver Disease

Renal Leptospirosis
KIDNEYS Mild to Severe
Urinalysis : Hematuria / Pyuria / Proteinuria
Renal Failure: Pre renal azotemia, ATN / AIN
Oliguric / Non Oliguric

Mechanism
Nephrotoxicity
Bacterial

Endotoxin, (Direct )

migration, Toxic Metabolites

Hypoperfusion Hypotension, Fluid loss/ shift
G.I. Bleed, Myocarditis

Hemorrhagic Manifestations
Hemorrhagic Fever - Vascular injury
Respiratory, Alimentary, Renal & Genital tracts
More common in Icteric & with Renal Failure

Hemorrhagic Pneumonitis
Hemoptysis / Respiratory failure
CXR : Single/ Multiple ill defined opacities
Occurs in 2nd week (as early as 24-48 hours)

Laboratory Tests
TC / DC / ESR / Hb / Platelet count
Serum Bilirubin / SGOT/ SGPT
Blood Urea, Creatinine & Electrolytes
Chest X-Ray; ECG
Tests for diagnosis of Leptospirosis

Culture for Leptospira: Positive

MAT; Sero conversion or 4 fold rise
ELISA / MSAT : positive
MAT: Microscopic agglutination test
(M)SAT: Microscopic slide agglutination Test

Interpretation of Tests

MAT

Antibody IgM titers of >1/80 or IgG 1/400

titers indicate current infection
Declining titers indicate past infection
To confirm, second sample is essential

ELISA
SAT

Valuable for Dx of current infection

IgM antibodies alone are useful

Interpretation of Tests
ELISA/SAT

MAT

Interpretation

Positive

Positive

Current Infection

Positive

Negative

Current Infection

Negative

Positive

Past Infection

Negative

Negative

R/o Leptospirosis

Not available

Rising titers

Current Infection

Score of 25 or more Presumptive Diagnosis

Score of 20 to 25 Possible case of leptospirosis

Alb, creatinine

Headache

Rain fall

Fever

Contaminate H20

Temp > 39 F

Animal contact

Conjn. suffusion

15

ELISA IgM + ve

Meningism

15

SAT positive

Muscle pain

15

MAT high titer

Jaundice

25

MAT rising titer

Definite

Culture positive

WHO Guide - Faines Criteria

Treatment
Mild CasesStart Rx. early

Severe CasesStart intensive Rx.

Oral Rx 7 to 10 day

IV Rx 5 to 7 days

Doxycycline 100 mg b.i.d

Benzyl Penicillin 20L q.i.d

Amoxicillin 500 mg q.i.d

Ampicillin 1G q.i.d

Ampicillin 500 mg q.i.d

Ceftriaxone 1G od

Supportive treatment

Cefotaxime 1G t.i.d

Prevention
Difficult due to wild animal infection
Good sanitation, Immunization of live stock
Personal hygiene, PPE, Water treatment
Human vaccines Not Useful
Doxycycline 200 mg weekly for at risk groups

Carry Home
Message

Dos for the Monsoon

Do nots for the Monsoon

For all of us
Monsoon fevers need extra care
Keep proper clinical assessment (SOAP)
Judicious use of Investigations
Virus Late Diagnosis , Early Treatment?
Choice, Dose, Duration of Antibiotics
Prompt Hospitalization for Risky cases

For all of us
To Avoid Patient Doctor Transmission
To Use Gloves, Masks, Disinfectants
To Discuss with colleagues, be prepared
To Report Infectious Diseases - BMC
To be aware of Antibiotic Resistance

Cure sometimes,
Treat often,
Comfort always - Hippocrates

Mo

y
o
j
En

e
c
i
t
c
a
r
P
n
o
o
ns

Drug fever

DRUG FEVER
All drugs can produce Drug INDUCED fever

except DIGOXIN
Bradycardia, hypotension, Skin rash,
Pruritus, Eosinophilia
Commonest - Pencillin, Sulpha, AKT
Causes
Contamination of the drug
Pharmacologic action of the drug itself
Allergic reaction to the drug

DRUG FEVER
Fever out of proportion to clinical picture
Associated findings:

Rigor 43%, Myalgia 25%,

Rash 18%, Headache 18%,
Leukocytosis 22%, Eosinophilia 22%,
Serum sickness, Proteinuria, Abnormal LFT

Onset and duration:

Onset: 1-3 weeks after the start of therapy

Duration: remits 2-3 days after therapy is
stopped

History of Typhoid
Antonius Musa :
A Roman physician who achieved
fame by treating the Emperor
Augustus 2,000 year ago, with cold
baths when he fell ill with typhoid.

Typhoid Mary
She was the accuse of severe
typhoid outbreaks. Since Mary was
the first Healthy Carrier" of typhoid
fever in the United States.

Typhoid fever
A case of typhoid fever may present as a
disease clinically indistinguishable from
malaria, progress to a bacillary dysentery,
mimic a case of acute bronchitis, simulate
a fully fledged lobar pneumonia, cause an
acute abdomen with perforation, and then
finally in convalescence, with its evil spent,
linger on as an orchitis, a myocarditis or a
peripheral neuritis.
Ronald L. Huckstep, CMG, Hon MD, MA, MD, FRCS, FRACS, FTSE

Bacteriology
Salmonella typhi, Paratyphi A, B, C
Family Enterobacteriaciae ,
70 phage types
Motile gram-negative rods
Antigens

O antigen (Somatic) - Group specific.

Vi antigen (Virulence) - Detection of carriers.
H antigen (Flagellae) - Differ from one another.

Source of infection
No animal host ,
Source of infection Patient
Carriers : 3 types :

convalescent carrier : Excrete 6 months after an

attack
chronic fecal carrier : Excrete intermittently at
least one year after infection. Located in Gall
Bladder
chronic urinary carrier : Renal pelvis infected &
bacilli pass in urine

Salmonella
Typhi

2nd Bacteremia
Leucopenia
Pancytopenia

Liver, Spleen,
Gall Bl. BM ,ect
Early acme stage
(1-3Wks
Bacteria In
Gall bladder

IMMUNE
ACTIVATION

LN Proliferate,
Swelling, Necrosis
Intestinal Perforation

Mononuclear
Phagocytes
Peyer's Patches &
Mesenteric Lymph Nodes

In feces

1st Bacteremia
(Incubation stage)
10-14days
All Symptoms
Signs

Defervescence stage
3-4wks
S.Typhi eliminated
Convalescence stage
(4-5wks)

Pathological changes in typhoid

Payer's patches - hyperplasia and ulceration to

ulceration and perforation.

Liver - Enlarged with fatty changes.
Skin collections of bacilli - Rose Spots
Infected gall stones - Cholecystitis
Spleen - Enlarged and soft.
Mesenteric glands - Enlarged.
Kidneys - Cloudy swelling with albuminuria.
Bronchitis with diffuse rles and rhonchi.
Heart - Enlarged with fatty degeneration.
Deep vein thrombosis in the lower limb

Classical Typhoid Case

High Grade Step Ladder Fever
Pulse Slow, Dicrotic
Respiration Less than 30/min
Toxic face, Coated tongue, Rose spots,
Bronchitic chest, Enlarged spleen,
Tender doughy abdomen, mentally confused,
Blood culture 1st week, Widal 2nd week,
Stool, Urine culture 3rd week,
Leucopenia, Urine Diazo Test positive

Main Symptoms.
Insidious onset of Generalized

malaise, headache, anorexia and

lassitude
Vague abdominal discomfort,
Vomiting, Constipation
Joint pains, backache, dry cough
Non-specific symptoms

General signs.
Dull expressionless, lethargic face
Flushed cheeks, bright eyes, Toxic look
Rose spots - on the abdomen and chest,

slightly raised and fade on pressure

Fever - Step ladder rise in the first wk,
with an evening rise and a morning fall.
Pulse rate may be disproportionately low

Specific signs.
Respiratory rate - 20-30/min.
Bronchitic chest is a common finding. Vary from

a few rhonchi to a frank acute bronchitis.

Bradycardia
Tongue may be dry and coated
Upper abdominal tenderness in the liver and
spleen with distension
Meningism, neck retraction, photophobia, and
severe headache

Diagnosis of Typhoid Fever

Suspected
Fever
Headache
Abd Distress
Toxic Look
Bronchitis
Abd Distension
Palpable spleen

Positive widal > 160

after one week
Probable case

Positive Bl Culture
Rising Widal Titer
Confirmed case

Laboratory Investigations
Normochromic Anemia
WBCs Normal or Reduced
Mild Thrombocytopenia, Subclinical DIC
LFT Mildly elevated
Blood Culture 40 - 90% Positive

1st Wk 90%, 2nd Wk 60%, 3rd Wk 45%

Positive even after 72hrs of antibiotics

Bone Marrow Culture 75 95%

Widal Test Not so Helpful

Delayed elevation Peak 3-5 wks
Wide Laboratory differences
O Titer Specific but less sensitive
H Titer Sensitive but less specific
O antibodies appear on days 6-8 and
H antibodies on days 10-12
Single Titer Difficult to interpret
4 Fold Rise Highly suggestive, but false +ve

Widal Test Not so Helpful

1:160 in Non-endemic area
1:640 in Endemic area
Negative in up to 30% of culture-proven cases
False-positive results with

other Salmonella, Malaria, Typhus, Bacteraemia

caused by other organisms and Cirrhosis

New serological tests

IDL Tubex
Typhidot - Better, High negative predictive value
Dipstick test

Typhi dot Test

After 4 days of Suspected Fever
Interpretation

IgM

IgG

Interpretation

Positive

Negative

Ac. Infection

Positive

Positive

Recent Infection

Negative

Positive

Past / Ac Infection

DIAZO TEST OF URINE

In developing countries, many patients
with typhoid fever attend for treatment
late.
Their need for chloramphenicol is often
immediate, and they cannot await the
delay of obtaining a positive blood culture.
In addition a blood culture will often become
negative within two hours of the
administration of chloramphenicol.

DIAZO TEST OF URINE

It is known that the putrefaction of

protein in the intestine of patients
with typhoid fever results in a
breakdown product which is
excreted in urine as a phenol ring
compound. This can be detected by
the Diazo test.

DIAZO TEST OF URINE

The diazo test, which is positive in about 80-90%
of typhoid cases, is particularly valuable:
as a practical diagnostic test in countries where
laboratories are primitive.
when a quick and practical test is required.
where the blood has been sterilized by previous
chloramphenicol.
when the Widal reaction has been invalidated by
previous TAB vaccine administration.

Treatment - Uncomplicated Typhoid

Susceptibility
Fully
Susceptible
Multi-drug
Resistant
Quinolone
Resistance

First Line

Second Line

Chloramphenicol
Fluoroquinolone
Amoxacillin
TMP-SMX
Fluoroquinolone
Azithromycin

Azithromycin
Cefixime
Cefixime

Treatment - Severe Typhoid

Susceptibility
Fully
Susceptible

First Line

Second Line

Chloramphenicol
Fluoroquinolone
Amoxacillin
TMP-SMX

Multi-drug
Resistant

Fluoroquinolone

Ceftrioxone
Cefotaxime

Quinolone
Resistance

Ceftrioxone
Cefotaxime

Fluoroquinolone

Dexamethasone Therapy
Short-term, high-dose Corticosteroid

treatment, combined with specific antibiotics

and supportive care, clearly reduced mortality
in critically ill patients.
Indication :

Shock
Altered Sensorium, Delirium, Coma

3mg/kg Loading Dose,

1mg/kg every 6 hrs for 48 hrs.

Vaccination
Vi polysaccharide, is given in a single dose
Protection begins seven days after injection,
Maximum protection being reached 28 days

after injection.
Protective efficacy was 72% one and half
years after vaccination and was still 55%
three years after a single dose.

Live oral vaccine Ty2la

three doses two days apart on an empty

stomach.
Protection as from 10-14 days after the third
dose.
> 5 years.
Protective efficacy of the enteric-coated capsule
formulation seven years after the last dose is still
62% in areas where the disease is endemic;
Antibiotics should be avoided for seven days
before or after the immunization

Mo

y
o
j
En

e
c
i
t
c
a
r
P
n
o
nso