This document provides information about enteric (typhoid) fever, including:
- It is caused by the bacterium Salmonella enterica and is a global public health problem affecting millions annually.
- Clinical features include prolonged high fever, abdominal discomfort, diarrhea or constipation, and potential complications like intestinal perforation.
- Diagnosis involves blood, stool, or bone marrow cultures and serologic tests. Ceftriaxone is the treatment of choice for multidrug-resistant cases. Early diagnosis and appropriate antibiotic treatment are important to prevent complications.
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.
is an upper respiratory tract bacterial infection associated with a characteristic rash, which is caused by an infection with pyrogenic exotoxin (erythrogenic toxin) -producing GAS in individuals who do not have antitoxin antibodies In the past.
scarlet fever was thought to reflect infection of an individual lacking toxin-specific immunity with a toxin-producing strain of GAS.
Subsequent studies have suggested that development of the scarlet fever rash may reflect a hypersensitivity reaction requiring prior exposure to the toxin.
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.
is an upper respiratory tract bacterial infection associated with a characteristic rash, which is caused by an infection with pyrogenic exotoxin (erythrogenic toxin) -producing GAS in individuals who do not have antitoxin antibodies In the past.
scarlet fever was thought to reflect infection of an individual lacking toxin-specific immunity with a toxin-producing strain of GAS.
Subsequent studies have suggested that development of the scarlet fever rash may reflect a hypersensitivity reaction requiring prior exposure to the toxin.
Tetanus Presentation
77 slides
Including drip rates of muscle relaxants
PDF : http://www.mediafire.com/download/k00ciibf73d7y6p/
For more, visit www.medicalgeek.com
This is a series of lectures on microbiology, useful for both undergraduate and post graduate medical and paramedical students... This lecture covers cholera, typhoid, diarrhoea and dysentry
Brief and easily understandable description on measles along with images for undergraduate students. this presentation would help in picturising what measles is.
Tetanus Presentation
77 slides
Including drip rates of muscle relaxants
PDF : http://www.mediafire.com/download/k00ciibf73d7y6p/
For more, visit www.medicalgeek.com
This is a series of lectures on microbiology, useful for both undergraduate and post graduate medical and paramedical students... This lecture covers cholera, typhoid, diarrhoea and dysentry
Brief and easily understandable description on measles along with images for undergraduate students. this presentation would help in picturising what measles is.
Parvo virus infection in dog - preventive medicinerajboy19
Canine parvovirus is a highly contagious infection of dogs caused by a Parvovirus. This slide include virology,transmission,pathogenesis,clinical sign and symptoms,diagnosis, differential diagnosis,treatment, prevention and control.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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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.
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
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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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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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Typhoid fever (Enteric fever)
1. - Dr. Lokanadha Reddy M V
Consultant Paediatrician
Sreenika children’s clinic
Bangalore
ENTERIC
FEVER/TYPHOID
FEVER
2. Salmonellosis - Why?
• Common and widely distributed
• Global major public health problem
• Affecting millions
• Food borne disease
• Significant mortality
3. ETIOLOGY
• Salmonella enterica serovars (Gm -ve)
• Typhi (S.Typhi) - Most common
• Paratyphi - very similar but less severe
• A
• B (Schotmulleri)
• C (Hirschfeldii)
• Disease ratio 10:1 (Typhi : Paratyphi)
4. EPIDEMIOLOGY
• 26.9 Million typhoid cases/year worldwide (80%)
• 1% mortality MC in Asia
• 5.4 Million paratyphoid cases/year (20%)
• 12 Million DALY
• More in children < 5 years, of incidence,
complications and hospitalisation
5. • Gram-Negative Facultative Rods
• Family - Enterobacteriaceae, like E.Coli
• Habitat - Intestinal tract of warm and cold blooded
animals
• Causes 2 diseases
• Enteric fever - Bloodstream infection
• AGE - Food-borne infection
MICROBIOLOGY
8. Somatic (O) /
Cell wall antigens
Surface
(Envelope)
antigens
Flagellar (H)
antigens
Heat stable
Alcohol resistant
May mask O
antigens
Heat labile
Used for
serological studies
Vi antigen occurs
in only 3 servers
Used for
serological studies
Typhi, Paratyphi C
and Dublin
Antigenic structure
10. • Exotoxins: Enterotoxin, Cytotoxin have role in
diarrhoeal symptoms
• Genetics: Plasmids in salmonella code for antibiotic
resistance
• Most specific gene products - Vi (virulence)
polysaccharide capsule, seen in 90% of S.Typhi and
has protective effect against bactericidal action of
serum of infected patients
• Antibiotic susceptibility: Resistance to Ampicillin,
streptomycin, chloramphenicol, sulphonamides.
Colistin resistance is not yet observed.
• DOC till 1972 was chloramphenicol. In 1972
chloramphenicol-resistant strains emerged.
11. EPIDEMIOLOGY
• Resistant to Ampicillin, chloramphenicol &
Cotrimoxazole
• Increased resistance to Nalidixic acid (Quinolone) and
Fluoroquinolones
• Mode of transmission: Ingestion of foods or water
contaminated with human feces, seafoods
contaminated with sewage water
• Risk factors : Antacids, PPI, H2 blockers - reduce
infective dose
12. PATHOGENESIS
Infective dose
105 -109
Gut mucosa -
terminal ileum
Street food
contaminated
water
M cells, Enterocytes
Paracellular route
Attaches to
microvilli & stays
in payers patches
Mesenteric lymph
nodes
Blood
(1o Bacteremia)
Asymptomatic, B/C -ve
Reticuloendothelial
system - replicates in
macrophages
Liver,
spleen,
GB,BM
Blood
(2o Bacteremia)
Clinical symptoms
End of Inc. Period
(4-14 days)
Down regulates host
inflammatory response
Re-exp. of PP via Bile
Pro-inflam. ck (IL-6,IL-1B,TNF-a) —> Fever
Enterotoxin, cytotoxin —> Diarrhoea
Host Risk factors : HIV, H.pylori
13.
14. PATHOLOGICAL
CHANGES
INTESTINE:
• Hyperplasia of payers patches —> subsequent
necrosis and sloughing of overlying epithelium —>
Ulcers —>heal without scarring or stricture
• Occasionally ulcer may penetrate muscularis and
serosa causing intestinal perforation
MLN, LIVER, SPLEEN: Hyperaemic with focal necrosis
BM: Mononuclear response with focal necrosis
15. CLINICAL FEATURES
• IP : 7-14 days (3-30 days)
• Mild illness : Low-grade fever, malaise, slight dry cough
• Severe illness : Abdominal discomfort and complications
• Factors influencing severity : Duration of illness before initiating
correct therapy, choice of antibiotics, age, previous exposure or
vaccine, virulence of strain, infective dose, host immune factors
• More dramatic presentation & complications in < 5 years
• Infancy : Diarrhoea, toxicity, DIC, more fatality
• Rare in children : Relative bradycardia, neurologic
manifestations, GI bleeding (common in adults)
17. CLINICAL FEATURES
• Fever : Prolonged High grade (up to 105’F) with chills and rigors,
Initially low-grade at onset and rises gradually, classic step ladder
pattern is rare. Child is not active during inter-febrile period.
Unlike viral fever which peaks at the onset of fever.
• Rash : 25% have macular or maculopapular rash (rose spots) -
7th-10th day (2nd week), in crops of 10-15 on lower chest and
abdomen, lasting 2-3 days
• Hepatosplenomegaly : seen in 35% cases and 15% cases
respectively
• Malaise, dull headache, anorexia, nausea, abdominal discomfort,
coated tongue
• Bronchitis like picture in early days with rhonchi and crepitations
18. CLINICAL FEATURES
• Diarrhoea: With fever is a common presentation, classical
pea soup diarrhoea seen in early days.
• Later constipation ensues with mild abdominal distension,
diffuse tenderness and paralytic ileus. Early constipation may
be due to obstruction of hypertrophied payer’s patches.
• Atypical presentation in malaria endemic areas
• Multidrug-resistant Typhoid : more severe, more toxicity,
complications and mortality
• Usually resolves in 2-4 weeks
• Drug-resistant Paratyphoid also can be severe
19. COMPLICATIONS
• LIVER: Altered liver function is seen in many but
clinically significant jaundice, hepatitis and cholecystitis
are rare and a/w adverse outcomes
• INTESTINE: Hemorrhage (<1%) and perforation (0.5-
1%) are rare in children. Seen in 2nd-3rd week
• Perforation -> markedly increased abdominal
pain(RLQ), tenderness, vomiting, peritonitis features
like Tachycardia, hypotension, rigidity, guarding.
Rising TLC, left shift and free air in AXR are seen.
• TOXIC MYOCARDITIS: Rare, a/w arrhythmias,
Sinoatrial block, cariogenic shock
20. COMPLICATIONS
• CNS: uncommon in children. Delirium, psychosis,
raised ICT, Acute cerebellar ataxia, chorea, deafness,
GBS. Mortality is more(50%) but recovery is complete
with no sequelae. Called severe or complicated enteric
fever.
• OTHERS: Fatal BM necrosis, DIC, HUS,
pyelonephritis, nephrotic syndrome, meningitis,
endocarditis, parotitis, orchitis, suppurative
lymphadenitis
• CARRIER: Chronic carrier rates lower in children
21.
22. DIAGNOSIS
• BLOOD CULTURE: Gold standard, positive in 40-
60% cases in 1st week. Sensitivity 90% in 1st week
to 40% in 4th week. Bile-broth media/BACTEC.
Sufficient blood 10ml in adults/5ml in children in 1:5
ratio of blood: media to be collected
• STOOL CULTURE: Positive after 1st week.
Occasionally positive in incubation period
• URINE CULTURE : Positive after 1st week
• BONE MARROW CULTURE: More sensitive but
invasive, may help in PUO evaluation
23. DIAGNOSIS
• CBC:
• TLC: Frequently low in relation to fever and toxicity like 4000-
5000 cells/uL, but a wide range is seen. In younger children
leukocytosis is common up to 20,000-25,000 cells/uL
• Eosinopenia, Neutrophilic predominance can be there
• PLT : Usually normal. Thrombocytopenia + Anemia is a marker
of severe illness and a/w DIC
• CRP : High, vs Low in dengue/viral fevers
• LFT : may be deranged but significant hepatic
dysfunction/jaundice is rare. AST/ALT may rise to 2-3 times
24. DIAGNOSIS
• WIDAL TEST : Measures antibodies against O and H antigens. Becomes
positive after 5 days of fever
• Lacks sensitivity and specificity in endemic areas
• Many false-positive and false-negatives occur
• Diagnosis of typhoid on widal alone is prone to error
• O titres - 1:160 -> acute enteric fever (appears early)
• H titres - 1: 160 -> Past infection/immunised(positive in recovery)
• Rising titres to four-fold are significant but its time-consuming process
• Positive results may represent previous infection
• Widal does not access Vi Antigens, so its not false positive for newer
vaccines but may be for classical TA vaccine.
25. DIAGNOSIS
• TYPHIDOT:
• A dot ELISA kit that detects IgM and IgG antibodies to OMP-
outer membrane protein
• Becomes positive in 2-3 days
• Sensitivity - 100% and specificity - 80%
• Limitation: Only Qualitative not quantitative like widal test
IgM IgG Interpretation
+ + Acute enteric fever
+ - Early acute infection
- + Past infection
26. DIAGNOSIS
• Newer tests using MABs directly detect S.Typhi
specific antigens in serum or Vi Ag in urine.
These are not proved efficient.
• Nested PCR using H1-d primers is promising and
provides rapid diagnosis.
• “BASU” - Blood culture, Agglutination (widal) test,
Stool culture and Urine culture in 1st, 2nd, 3rd
and 4th weeks.
28. TREATMENT
• Early diagnosis and appropriate treatment
• Vast majority can be managed at home with oral
antibiotics and close follow-up for complications or
failure of response to Rx
• Hospitalisation and IV antibiotics : Persistent
vomiting, severe diarrhoea, abdominal distension
• Adequate Rest, Hydration and correction of fluid
and electrolyte imbalance.
29. TREATMENT
• ISOLATION : should be nursed with precautions
• ANTIPYRETICS : Paracetamol 10-15mg/kg PO every 4-6
Hours. Ibuprofen can be used. Salicylates are
contraindicated - shock.
• DIET : Soft, easily digestible diet except in abdominal
distension or ileus
• ANTIBIOTICS : Critical to minimise complications
• STEROIDS: Dexa 3mg/kg ->1mg/kg Q6H x 48 hrs only in
cases of severely ill with shock, (CNS signs) obtundation,
stupor or coma. May mask abdominal signs.
30.
31. TREATMENT
• CEFTRIAXONE :
• DOC for MDR typhoid as it is common
• Start 75-100 mg/kg/day OD/BD x 5-7 days
• Once afebrile, change to oral Cefixime x 10
days
• Superior to Cefotaxime because of its biliary
excretion (kills bacteria in GB)
32. TREATMENT
• CEFIXIME :
• 20 mg/kg/day in two doses orally x 10-14 days
for mild cases
• Can be used as follow up Rx for IV Ceftriaxone
• As a rule 1st/2nd gen. cephalosporins and
aminoglycosides are not useful in treatment
33. TREATMENT
• CHLORAMPHENICOL :
• 50 mg/kg/day orally x 14 days in areas without resistant bacteria
• IV is given only if oral intake is not possible as 75mg/kg/day
• SE: Bone marrow suppression rarely. Undetectable reticulocytes
gives the clue. “Gray baby syndrome”.
• Afebrile within 7 days of Rx
• If no response then unlikely to respond to Ampicillin, Amoxicillin,
Cotrimoxazole
• Used apart from Aztreonam/Cotrimoxazole, in patients with
penicillin or ceftriaxone allergy.
34. TREATMENT
• CIPROFLOXACIN :
• DOC for Adults and Children >12 years
• < 12 years can be given if ceftriaxone fails or in life-threatening cases
• Dosage: IV 20 mg/kg/day Q8-12H x 7-10 days
• Relatively safe in children
• If culture shows sensitivity to be downgraded to cipro because of lower
relapse rates
• AZITHROMYCIN :
• 20 mg/kg/day (double dose) x 5 days
35. PRACTICAL TIPS
• As a general rule treatment (Ceftraixone) is until 5-7
days after defervescence
• For any Rx response is slow and takes 3-7 days
• Do not give laxatives or enema for constipation -can
cause perforation
• Add Metronidazole and Aminoglycoside if perforation
or peritonitis is suspected
• Osteomyelitis or Meningitis - Rx for 4-6 weeks
36. PRACTICAL TIPS
• If eosinophils appear which were absent earlier, indicates
recovery
• Recovery signs : Subjective improvement, less toxic, improved
appetite, general feeling better, improved feel of abdomen - soft
and not distended, increasing interval between fever spikes, fever
responding better and faster to antipyretics, lower fever spikes
than earlier.
• If two antibiotics fail consider MDR typhoid. Stop the antibiotic
and observe for 2-3 days if child is not toxic and ill.
• Repeat physical examination, CBC, CXR may help in difficult
cases
37. PROGNOSIS
• Depends on age, early diagnosis and appropriate Rx, general
health, nutrition salmonella serotype and complications
• RELAPSE: Despite App. Rx 5-15% may have relapse after initial
clinical response. Milder illness. More with cephalosporins than
with Fluoroquinolones/Azithromycin
• Chronic Carriers : who excrete S.Typhi > 3 mo. <2% in children
and increases with age.
• Rx : Amoxicillin (100 mg/kg/day) with probenecid (30 mg/ kg/day)
or cotrimoxazole (10 mg/kg/day) for 6-12 weeks is recommended.
If the strain is nalidixic acid sensitive, quinolones for 28 days is
better
• A chronic urinary carrier is seen in schistosomiasis
38. • REFERENCES
• Nelson’s Textbook of pediatrics - 20th Edition
• OP Ghai Textbook of pediatrics - 8th Edition
• Santosh kumar manual of pediatric practice -
4th Edition
• Amdekar Lessons from grand rounds 2
• Todar’s textbook of bacteriology - online edition