Pertussis : Highly contagious respiratory infection caused by Bordetella pertussis
Outbreaks first described in 16th century
Bordetella pertussis isolated in 1906
Estimated >300,000 deaths annually worldwide
Before the availability of pertussis vaccine in the 1940s, public health experts reported more than 200,000 cases of pertussis annually.
Since widespread use of the vaccine began, incidence has decreased more than 75% compared with the pre-vaccine era.
In 2012, the last peak year, CDC reported 48,277 cases of pertussis.
Extremely contagious-attack rate 100%
Immunity is never complete
Protection begins to wane in 3-5 yrs after vaccination
Scrub typhus, also known as bush typhus, is a disease caused by a bacteria called ORIENTIA TSUTSUGAMUSHI.
Scrub typhus is spread to people through bites of infected chiggers (larval mites).
Most cases of scrub typhus occur in rural areas of Southeast Asia, Indonesia, China, Japan, India, and northern Australia. Anyone living in or travelling to areas where scrub typhus is found could get infected
Scrub typhus is not transmitted directly from person to person; it is only transmitted by the bites of vectors
Chiggers are abundant in locales with high relative humidity (60%–85%), low temperature (20°C–30°C), low incidence of sunlight, and a dense substrate-vegetative canopy.
Occupational risk is higher in farmers (aged 50–69 years), females.
Pertussis : Highly contagious respiratory infection caused by Bordetella pertussis
Outbreaks first described in 16th century
Bordetella pertussis isolated in 1906
Estimated >300,000 deaths annually worldwide
Before the availability of pertussis vaccine in the 1940s, public health experts reported more than 200,000 cases of pertussis annually.
Since widespread use of the vaccine began, incidence has decreased more than 75% compared with the pre-vaccine era.
In 2012, the last peak year, CDC reported 48,277 cases of pertussis.
Extremely contagious-attack rate 100%
Immunity is never complete
Protection begins to wane in 3-5 yrs after vaccination
Scrub typhus, also known as bush typhus, is a disease caused by a bacteria called ORIENTIA TSUTSUGAMUSHI.
Scrub typhus is spread to people through bites of infected chiggers (larval mites).
Most cases of scrub typhus occur in rural areas of Southeast Asia, Indonesia, China, Japan, India, and northern Australia. Anyone living in or travelling to areas where scrub typhus is found could get infected
Scrub typhus is not transmitted directly from person to person; it is only transmitted by the bites of vectors
Chiggers are abundant in locales with high relative humidity (60%–85%), low temperature (20°C–30°C), low incidence of sunlight, and a dense substrate-vegetative canopy.
Occupational risk is higher in farmers (aged 50–69 years), females.
Tetanus Presentation
77 slides
Including drip rates of muscle relaxants
PDF : http://www.mediafire.com/download/k00ciibf73d7y6p/
For more, visit www.medicalgeek.com
all about rabies
epidemiology of rabies,
pathogenesis of rabies,
clinical features of rabies,
treatment of rabies,
prevention of rabies,
rabies virus,
post exposure prophylaxis,
rabies in dogs
The lecture gives concise review about the main four groups of viruses causing hemorrhagic fever i.e. Flavivirues, Filoviruses, Arenaviruses and Bunyaviruses.
Tetanus Presentation
77 slides
Including drip rates of muscle relaxants
PDF : http://www.mediafire.com/download/k00ciibf73d7y6p/
For more, visit www.medicalgeek.com
all about rabies
epidemiology of rabies,
pathogenesis of rabies,
clinical features of rabies,
treatment of rabies,
prevention of rabies,
rabies virus,
post exposure prophylaxis,
rabies in dogs
The lecture gives concise review about the main four groups of viruses causing hemorrhagic fever i.e. Flavivirues, Filoviruses, Arenaviruses and Bunyaviruses.
Typhoid fever, also known as enteric fever, is a potentially fatal multisystemic illness caused primarily by Salmonella enterica, subspecies enterica serovar typhi and, to a lesser extent, related serovars paratyphi A, B, and C.
The protean manifestations of typhoid fever make this disease a true diagnostic challenge. The classic presentation includes fever, malaise, diffuse abdominal pain, and constipation. Untreated, typhoid fever is a grueling illness that may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death within 1 month of onset. Survivors may be left with long-term or permanent neuropsychiatric complications.
Typhoid Fever is an acute bacterial infection characterized by high fever caused by ingesting the food or water contaminated with faeces from an infected person.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
2. Overview
• History
• Epidemiology
• Etiology
• Pathogenesis
• Clinical Features
• Complications
• Diagnosis
• Differential Diagnosis
• Treatment
• Prevention and Vaccination
• References
3. History
Thomas Willis: In 1659 credited with the first
description of Typhoid fever
Evidence of cases of Typhoid Fever dates back to 430 BC, when a devastating
illness killed one-third of the population of Athens. In 2006, a study detected
DNA sequences similar to Salmonella in dental pulp extracted from a burial pit
dated to the time of the outbreak.
Until the nineteenth century Typhoid Fever and
Typhus were considered the same. John Huxam
in 1739 first described the difference between the
two.
Thomas Willis
4. In 1880, Karl Joseph Eberth described a
typhoid bacillus. In 1884, pathologist Georg
Theodor August Gaffky confirmed Eberth's
findings, and the organism was given names
such as Eberth's bacillus, Eberthella typhi, and
Gaffky-Eberth bacillus.
French physician Pierre Charles Alexandre Louis
in 1829 first proposed the name “Typhoid Fever”-
meaning to resemble typhus.
In 1837 William Wood Gerhard was the first to
differentiate clearly between typhus fever and
typhoid
William Budd in 1856 described the feco-oral
method of transmission of Typhoid fever
Pierre Charles Alexandre
Louis
Karl Joseph Eberth
5. Georges-Fernand-Isidor
Widal
In 1896 Georges-Fernand-Isidor Widal described the
‘Widal agglutination reaction’ and called it “Sero-
Diagnosis”
In the same year Sir Almroth Edward Wright
developed an injectable heat killed whole cell vaccine for
Typhoid.
S. Paratyphi isolated in 1902 by H. Kayser
Mary Mallon, also known as Typhoid Mary. In 1907, she
became the first American carrier to be identified and
traced. She was a cook in New York and was associated
with 53 cases and 3 deaths. Health authorities told Mary
to give up working as a cook or have her gall bladder
removed. She was detained and quarantined after
another typhoid outbreak. She died of pneumonia after
26 years in quarantine.
6. Epidemiology
• Over 21.6 million cases of Typhoid annually
worldwide
• Over 2,00,000 deaths annually due to Typhoid
• Additional 5.4 million cases of Paratyphoid annually
• Indian subcontinent has the highest incidence of
the disease worldwide.
• Enteric Fever is endemic in India
• In India the incidence is 214.2/1,00,000/yr
• Age-Specific studies show that incidence in younger
children are higher (0-4y:2,730; 5-19y:1,170; 20-
40y:110 /1,00,000 per year)
7.
8. Enteric Fever
is a collective term used for
Typhoid and Paratyphoid fevers.
9. • Typhoid fever is caused by Samonella enterica sub-
species enterica serovar Typhi (S. Typhi)
• Paratyphoid fever is caused by Samonella enterica sub-
species enterica serovar Paratyphi A, Paratyphi B (also
called S. schottmuelleri), Paratyphi C (also called S.
hirschfeldii)
• Belong to Enterobacteriaceae family
• Gram Negetive, Rod-shaped, non-spore-forming,
predominantly motile bacteria with and
peritrichous flagella
• Are chemoorganotrophs and facultative anaerobes.
Etiology
10. Antigenic Structure
• Salmonella posses following antigens on which
they are classified and identified:
1. Flagellar or H Antigen: present on the flagella
and is dual core heat labile protein. Strongly
Immunogenic. Agglutinate rapidly with antisera.
(Large, loose, fluffy clumps)
2. Somatic or O Antigen: phospholipid-protein-
polysaccharide complex. Integral part of cell wall.
Endotoxin. Heat Stable. Slow agglutination with
antisera (Compact, chalky, granular clumps)
3. Surface, Capsule or Vi Antigen: surface
polysaccharide antigen enveloping O antigen.
Heat labile. Act as Virulence factor. Poorly
immunogenic
11.
12. Gram Staining of S. Typhi
S. Typhi showing
peritrichous flagella
13. Pathogenesis
• Humans are the only reservoir of S. Typhi and S.
Paratyphi A.
• S. Paratyphi B, and S. Paratyphi C also infect
dogs, cattle and poultry and can also transmit by
eggs or poorly cooked meat.
• Mode of Transmission : Feco-Oral Route (Most
Common). Less commonly urine of infected
person.
• Infectious Dose : 105 – 109 organisms.
• Incubation Period : usually 7 – 14 days (can be
upto 3 – 30 days depending upon the infecting
dose)
14. Ingestion of contaminated food or water
S. typhi reaches terminal ileum and invades gut mucosa
through specialized antigen-sampling cells known as M cells (Microform cells).
Within the Peyer patches in the terminal ileum. S. typhi is phagocytosed by
macrophages.
These macrophages then enter the mesenteric lymphoid system and then pass into
the blood stream via the lymphatics.
These bacteria are disseminated throughout the body and colonize the organs of
the reticuloendothelial system
They replicate within macrophages and are shed back into the blood, causing a
secondary bacteremia.
15.
16. • The surface Vi polysaccharide capsular antigen found in
S. Typhi interferes with phagocytosis and an virulence
trait encoded by the PhoP regulon gives ability to survive
within macrophages after phagocytosis
• S. typhi avoids triggering of an early inflammatory
response in the gut and instead colonize deeper tissues
and organ systems.
• Produces an inflammatory response in the deeper
mucosal layers and underlying lymphoid tissue causing
hyperplasia of Peyer patches and subsequent necrosis
and sloughing of overlying epithelium.
17. • These ulcers can bleed but usually heal
without scarring or stricture formation.
• Inflammatory lesion may occasionally
penetrate the muscularis and serosa of the
intestine and produce perforation.
• The mesenteric lymph nodes, liver, and
spleen are hyperemic and generally have
areas of focal necrosis as well.
• A mononuclear response may be seen in the
bone marrow in association with areas of
focal necrosis.
18. Carriers
• The propensity to become a carrier follows the epidemiology
of gallbladder disease.
• Increasing with patient age and the antibiotic resistance of the
prevalent strains.
• Carriage are generally lower in children than adults.
• Types of Carriers:
– Convalescent carrier: passes bacilli in the excreta form
3weeks-3months after clinical cure of typhoid.
– Temporary carrier: passes bacilli in the excreta form 3months-
1year after clinical cure of typhoid
– Chronic faecal carrier: continues to pass bacilli intermittently in
the excreta at least one year after infection.
– Chronic urinary carrier: the renal pelvis is infected & bacilli
pass in urine
19. Clinical Features
• Mean age of onset in India is 10yrs.
• Onset is insidious and varies from a mild
illness with low-grade fever, malaise, and
slight, dry cough to a severe clinical picture
with abdominal discomfort and multiple
complications
• Presentation of typhoid may be more
dramatic in children younger than 5 yrs of
age, with comparatively higher rates of
complications and hospitalization.
20. Features of 1st week of illness
• Rising Step ladder type of fever, with chills but
rigors are rare
• Relative Bradycardia
• Dull, expressionless and toxic facies
• Dry skin with little sweating
• Coated tongue
• Musty, damp hay-like/baked bread like odour
• Vomiting
• Tender, doughy abdomen with slight guarding
• Constipation / Diarrhea (Pea Soup diarrhea)
• Occasionally minimal, non-productive cough
• Meningismus may occur early.
22. Features of 2nd week of illness
• Continuous High grade fever (39.5-40.5 C)
• Worsening of cough may occur
• Rose Spots
• Abdominal Pain and tenderness
• Soft tender splenomegaly
• Soft tender hepatomegaly
23. Rose Spots
• Faint salmon coloured macules on the trunk and
abdomen
• Appear in crops of 10-15
• First seen after 7-10 days of illness
• Last for upto 2-3 days
• Fades on pressure
• Difficult to see in dark-skinned children.
24. Features of 3rd week of illness
• Hepatosplenomegaly
• Intestinal bleeding or perforation
• Features of peritonitis
• Septic Shock
• Altered Sensorium
• In absence of acute complications or death,
symptoms gradually resolve over 2-4 weeks,
however, the illness may be associated with
malnutrition in a number of affected children
25.
26.
27. • Enteric fever caused by S. Paratyphi
organisms classically have a milder
course.
• However, there have been several
outbreaks of infection with drug-resistant
S. paratyphi A, suggesting that
paratyphoid fever may also be severe,
with significant morbidity and
complications
31. Diagnosis
• Bacteriological diagnosis of enteric fever
consists of:
1. Isolation of the bacilli from patient (Culture)
2. Demonstration of antibodies in serum
(Serological)
3. Demonstration of typhoid antigen in serum or
urine (Serological)
32. Blood Culture
• Bacteremia occurs early in the disease
• Blood culture is positive in about
90% cases in 1st week
75% cases in 2nd week
60% cases in 3rd week
25% thereafter till subsidence of pyrexia
• Blood cultures rapidly becomes negative
on treatment with antibiotics.
Isolation of the bacilli from patient
33. Method of Blood Culture
• 5-10 ml of blood is collected and inoculated into a
culture bottle containing 50-100 ml of 0.5% bile broth.
• After incubation overnight at 37 oC, the bile broth is
sub cultured on MacConkey agar.
• Pale, non-lactose fermenting colonies that grow are
further subjected to biochemical tests.
• Salmonella will be motile, indole and urease negative
and ferment glucose, mannitol and maltose but not
lactose or sucrose.
• Typhoid bacillus will be anaerogenic while Paratyphoid
bacilli will form acid and gas from sugar.
• Further confirmation is done by slide agglutination of
the colonies
• Cultures should be declared negative only after the
broth is sub cultured every day for ten days.
35. S. Typhi
Does not
fermet sugar to
produce acid
and gas
S.Paratyphi
Fermet sugar to
produce acid
and gas
36. • Other samples which can be cultured
1. Bone Marrow
2. Blood Clot
3. Feces
4. Urine
5. Bile
6. CSF
7. Pus from suppurative lesions
8. Sputum
9. Rose Spots
38. Demonstration of antibodies in serum
Widal Test
• This is a test for the measurement of H
and O agglutinins for typhoid and
paratyphoid bacilli in the patients sera.
• The antigens used in the test are the H
and O antigens of S. typhi and H antigens
of S. paratyphi A and B.
• Readymade Widal kits of stained antigen
are now available commercially for use
39. Interpreting the Widal Test
1. The agglutination titre will depend upon the stage of
the disease. Agglutinins usually appear by the end of
the first week and increases steadily till the third or
the fourth week, after which it declines gradually.
2. Demonstrating of a rise in titre of antibodies, by
testing two or more serum samples, is more
meaningful than a single test.
3. The result of a single test should be interpreted with
caution. It is difficult to lay down levels of significance
though it is generally stated that titres of 1/100 or
more of O agglutinins and 1/200 or more for H
agglutinins are significant.
40. 4. Agglutinins may be present on account of prior
disease, inapparent infection or immunization.
Therefore the mere presence of agglutinin in the
Widal test should not be taken as proof of typhoid
fever
5. Persons who have had a prior infection or
immunization may develop an anamnestic response
during an unrelated fever. This may be differentiated
by repetition of the test after a week. The anamnestic
response shows only a transient rise, while in entric
fever the rise is sustained.
6. Bacterial suspensions used as antigens should be
free form fimbria. False positive results may
otherwise occur.
7. Cases treated early with chloramphenicol may show
a poor agglutinin response.
41. Other test to detect circulating antibodies:
1. ELISA – e.g. Typhidot
Typhidot consists of a dot ELISA kit that detects IgM and IgG
antibodies against the outer membrane protein of S. typhi. The
typhidot test becomes positive within 2–3 days of infection and
separately identifies IgM and IgG antibodies. The most
important limitation of this test is that it is not quantitative and
result is only positive or negative.
2. Counterimmunoelectrophoresis(CIE)
3. Indirect Hemeagglutination
42. Demonstration of antigen in
serum/urine
1. Sensitized Staphylococcal coagglutination test.
2. PCR
Other investigations
• Results of other laboratory investigations are
nonspecific.
• CBC:
– Leukocytopenia in relation to the fever and toxicity. In younger
children leukocytosis is common and may reach 20,000-25,000
cells/μL.
– Thrombocytopenia: may be a marker of severe illness and
may accompany disseminated intravascular coagulopathy
• Liver function test results may be deranged, but
significant hepatic dysfunction is rare.
43. Differential Diagnosis
O t h e r S a l m o n e l l a I n f e c t i o n GIT symptoms (V&D) are more
acute than the general
manifestations
Pyrexia much lower and of shorter
duration
M a l a r i a History of previous attacks
More rapid onset
Shivering and sweating
High early pyrexia
Relative infrequent abdominal
symptoms and signs
Positive blood smear
I n f l u e n z a More rapid onset
High temperature,
Severe sore throat and cough
Absence of a palpable spleen and
rose spots.
44. B a c i l l a r y d y s e n t e r y Acute onset
Severe bloody diarrhea
The signs and symptoms in
dysentery are usually abdominal
Typhus a n d o t h e r
r i c k e t t s i a l i n f e c t i o n s
Acute onset
High temperature at an early stage.
Rigors are common
Prostration is rapid.
Rash is brownish red in colour, and
much more profuse and does not
fade on pressure.
Leukocytosis
Weil-Felix test becomes
significantly positive at about the
tenth day
Tu b e r c u l o s i s
( Ab d o m i n a l / P u l m o n a r y )
The pyrexia and vague symptoms
and signs may be very similar.
A chest X-ray, or laboratory
confirmation of typhoid, may be the
only sure method of diagnosis.
B r u c e l l o s i s Onset tends to be more insidious.
Painful joint is frequently present.
45. Treatment
• Majority of children with typhoid fever can be managed at home with oral
antibiotics and close medical follow-up for complications or failure of
response to therapy.
• Patients with persistent vomiting, severe diarrhea, and abdominal distention
may require hospitalization and parenteral antibiotic therapy.
• General Measure
– Adequate rest
– Adequate hydration
– correct fluid and electrolyte imbalance.
– Antipyretic therapy (Paracetamol 10-15 mg/kgevery 4-6 hr PO) should be
provided as required.
– Soft, easily digestible diet should be continued unless the patient has abdominal
distention or ileus.
46. Antimicrobials
• Traditional therapy with chloramphenicol or amoxicillin is
associated with relapse rates of 5-15% and 4-8%,
respectively
• Use of the quinolones and third generation cephalosporins is
associated with higher cure rates.
• The antibiotic treatment of typhoid fever is also influenced by
the prevalence of antimicrobial resistance. Emergence of
multidrug-resistant strains of S. Typhi (i.e., isolates fully
resistant to amoxicillin, trimethoprim-sulfamethoxazole, and
chloramphenicol) has necessitated treatment with
fluoroquinolones with cephalosporins as an alternative.
• The emergence of resistance to quinolones places
tremendous pressure on public health systems because
alternative therapeutic options are limited.
• Azithromycin may be an alternative antibiotic for children with
uncomplicated typhoid fever.
48. Dexamethasone (3 mg/kg for the initial dose, followed by 1 mg/kg every 6 hr
for 48 hr) is recommended for severely ill patients with shock, obtundation,
stupor, or coma;
49. Fluoroquinolones : A dilemma!!!
• The fluoroquinolone drugs are generally very well tolerated.
However, in some countries the use of fluoroquinolones is
relatively contraindicated in children because of concerns that
they may cause articular damage.
• There is now extensive experience in the use of these drugs
in large numbers of children with long term follow-up. Their
considerable benefits, particularly in areas where there
are no affordable oral alternatives, outweigh the putative
risk.
• The only known articular side effect is Achilles tendon rupture
in patients who are also taking corticosteroids, and this has
been reported only rarely.
• A Cochrane systematic review of the treatment of typhoid
fever also indicates that there is little evidence to support the
carte blanche administration of fluoroquinolones in all cases
of typhoid fever
50. Why Fluoroquinolones???
• High drug levels are achieved within the GI lumen
after oral administration no need of isolation
• The MIC for most salmonella is extremely low
(<0.1mcg/ml)
• Bactericidal against Salmonella low relapse
• Good Intracellular penetration rapid onset and
high cure rate
• Ciprofloxacin is concentrated in the biliary tract, a
known site of persistent infection during chronic
carriage of salmonella prevention of carrier
• Oral form and IV form are available cheap
51. Treatment of Carriers
Drugs Duration Cure Rate
Amoxicillin or Ampicillin (100 mg/kg/d)
PLUS
probenecid (1 g orally or 23 mg/kg)
OR
TMP-SMZ (160- 800 mg twice daily)
6 weeks 60%
Ciprofloxacin (750mg twice daily)
OR
Norfloxacin (400mg twice daily)
28 days 80%
Cholecytectomy may be required in chronic cases not treated by
the above regimens and carriers with cholelithiasis
Guidelines for management of typhoid fever. WHO. July 2011
56. Vaccination
• Typhoid vaccination was part of India’s
national immunization program till 1985
• Types of Typhoid Vaccines
1. Whole cell inactivated typhoid/ paratyphoid
(TAB) Vaccine
2. Vi-capsular polysaccharide (Vi-PS) vaccine
3. live oral vaccine
57. Whole cell inactivated typhoid/ paratyphoid (TAB) Vaccine
• Type of Vaccine: Heat-inactivated phenol-
preserved whole-cell
• Protective Efficacy: 51-88%
• Age of vaccination: >6 mths of age
• Vaccination Schedule: 2 doses s.c 4 weeks apart
• Revaccination: 2 yrs
Discontinued due to side effects like fever, malaise,
local pain
58. Vi-capsular polysaccharide (Vi-PS) vaccine
• Type of Vaccine: Highly purified antigenic fraction of Vi antigen of
S. typhi
• Protective Efficacy: 55-72%
• Age of vaccination: >2 yrs of age
• Vaccination Schedule: single dose (25mcg of antigen) s.c. or i.m.
• Revaccination: 3yrs
The vaccine is stable for 6 mths at 37ºC and for 2 yrs at 22ºC.
It is not immunogenic in below 2 years of age and has no
immune memory
Protection begins seven days after injection and maximum
reached at 28 days after injection
59. Live oral vaccine
• Type of Vaccine: live attenuated vaccine of Ty21a strain
• Protective Efficacy: 50-60%
• Age of vaccination: >6 yrs.
• Vaccination Schedule: 3 doses of enteric coated capsule(2-6
million bacteria) given on alternated days
• Revaccination:3yrs
Antibiotics should not be given 3 days before and 7 days after
vaccination
Protection starts from 10-14 days after 3rd dose.
Also provides Herd Immunity
Contraindicated in immunodeficiency
60. Newer Vaccines
• Vi-capsular polysaccharide conjugated with
Pseudomonas aeruginosa exotoxin A (Vi-rEPA)
• Vi-PS Conjugate Vaccine Conjugated with Tetanus
Toxoid (Pedatyph®) by Bio-Med Pvt. Ltd.
• Vi-polysaccharide conjugate vaccine conjugated
with Tetanus Toxoid from Bharat Biotech (Typbar-
TCV®)
• S. paratyphi A vaccine composed of the surface
O-specific polysaccharide conjugated with
tetanus toxoid
61. References
1. Ananthnarayan and Panikarys textbook of microbiology 7th
edition
2. Atul Kothari, Amit Pruthi, Tulsi D. Chugh. The Burden of
Enteric Fever. J Infect Developing Countries 2008; 2(4): 253-
259.
3. Background document: The diagnosis, treatment and
prevention of typhoid fever. World Health Organization. May-
2003
4. Crump JA, Luby SP, Mintz ED (2004) The global burden of
typhoid fever. Bull World Health Organ 82:346-353.
5. Ghai Essential Pediatrics 8th Edition
6. Guidelines for managemet of typhoid fever. WHO. July 2011
7. Huang DB, DuPont HL: Problem pathogens: extra-intestinal
complications of Salmonella enterica serotype Typhi
infection, Lancet Infect Dis 5:341–348, 2005
8. K. D. Moudgil M.D., B. S. Narang M.D., Pathogenesis of
typhoid fever. The Indian Journal of Pediatrics July 1985,
Volume 52, Issue 4, pp 371-378
62. 9. IAP guidebook on immunization 2013-2014
10. IAP Task Force Report: Management of Enteric Fever in Children.
Indian Pediatrics. Vol 43 Oct 2006
11. Manuela Raffatellu, R. Paul Wilson et al. Clinical pathogenesis of
typhoid fever. J Infect Developing Countries 2008; 2(4): 260-266.
12. Nelson Text of Pediatrics 19th Edition
13. Ochiai RL, Acosta CJ, Danovaro-Holliday MC et al. (2008) A study
of typhoid fever in five Asian countries: disease burden and
implications for control. Bull World Health Organ 86(4):260-68.
14. PG textbook of Pediatrics
15. Sinha A, Sazawal S, Kumar R et al. (1999) Typhoid fever in
children aged less than 5 years. Lancet 354:734-737
16. Victor Vaughan: A Biography of the pioneering Bacteriologist,
1851-1929 By Richard Adler
17. YK Joshi. SYMPOSIUM : TYPHOID FEVER. Journal Indian
Academy of Clinical Medicine, Vol. 2, No. 1 and 2 , January-June
2001
Evidence of typhoid fever dates back to 430 BC. It was first described by Thomas willis of "Circle of Willis” fame on 1659.
In 1829 the term “typhoid fever” was coined and in 1880 the organism was described by karl joseph eberth
5400000
peritrichous flagella: flagella that are all around the cell body
Chemoorganotrophs: obtaining their energy from oxidation and reduction reactions using organic sources
facultative anaerobes: organism that makes ATP by aerobic respiration if oxygen is present, but is capable of anaerobic respiration if oxygen is absent.
H antigen: induces antibody formation rapidly and in high titres
O antigen: less immunogenic than h antigen. Low titer of antibody.
Virulence factor : Inhibits phagocytosis, resisting complement activation and bacterial lysis by alternative pathway and peroxidase mediate killing.
Strains found to possess Vi antigen were found to cause clinical disease more consistently
Poorly immunogenic: very low titres of antibody formed.
Exotoxins are toxic substances secreted by bacteria and released outside the cell.
Endotoxins are bacterial toxins consisting of lipids that are located within a cell.
Gram negative so pink in colour
Thus a direct contact with an infected person is a prerequisite for typhoid fever
Pass stomach: so any condition of reduced acidity will be risk factor. Like antacid use, achlorhydra
This primary bacteremia is usually asymptomatic, and blood culture results are frequently negative at this stage of the disease.
secondary bacteremia that coincides with the onset of clinical symptoms and marks the end of the incubation period
2-4% become chronic fecal carrier
Classic untreated cases.
The fever may rise gradually, but the classic stepladder rise of fever is relatively rare.
Relative bradycardia is also rare in children
Constipation and diarrhea occur with equal frequency. Diarrhea is more common in younger children. Stools are small in volume, resemble pea-soup, contains erythrocytes but are not grossly bloody.
Rose spots: faint salmon coloured macules on the trunk and abdomen lesions may appear in crops of 10-15 on the lower chest and
abdomen and last 2-3 days (Fig. 198-5). These lesions may be difficult to see in dark-skinned children.
Blood contains growth inhibitory substance hence its essential that sufficient quantity of broth be taken
Lac+ bacteria such as Escherichia coli, Enterobacter and Klebsiella
Non-Lactose fermenting bacteria such as Salmonella, Proteus species, Yersinia, Pseudomonas aeruginosa and Shigella
Bone Marrow: cultures are positive in most cases even if blood culture is negetive.
Blood clot: blood collected is allowed to clot. Serum pipetted out and used for serological tests. Clot broken and added to bile broth with streptokinase. Has higher rate of isolation
Feces: almost as valuable as blood culture. organism is shed in feces throughout the course of disease and even in convalescence with varying frequency. Also positive in carrier. Valuable in patients on antibiotics as antibiotics act late in bacilli in the gut. Has to be culture in selctive media like Wilson-blair bismuth sulphate agar.
Urine: Positive only in the 2nd and 3rd week and thereafter only in 25% cases. Very irregulary positive
Bile: duodenal aspiration. Employed mostly to detect carriers
S.Typhi forms large black colonies with a metallic sheen – rabbit eye colonies.
S. Paratyphi A produces green colonies due to absence of H2S production
The paratyphoid O antigens are not used as they cross react with the typhoid O antigen due to their sharing of factor 12
So that blood taken earlier than 1 week may give a negative result.
If the first sample is taken late in the disease, a rise may not be demonstrated. Instead a fall may be seen in some cases.
. It is necessary to obtain information on the distribution of agglutinin levels in ‘’normal sera” in different areas
4. H agglutinins persists longer than O agglutinins. Individuals with TAB Vaccination will generally have antibodies to S. typhi, s. paratyphi A and B, while in case of infection antibodies will be seen only against infecting species
1. Staph aureus which contain protein A, is stabilised and coated with s. typhi antibody. When such cells are mixed with serum of a patient it shows agglutination reaction within 2 minutes. This test is rapid sensitive and specific but is not positive after the first week of disease.
Bloddy diarrhea is rare in typhoid
corticosteroids should be administered only under strict controlled conditions and supervision, because their use may mask signs of abdominal complications.
Floroquinilones which are the antimicrobial drug of choice for treatment of salmonellosis in adults,