- Foot and mouth disease is caused by an aphthous virus from the picornaviridae family. There are 7 major serotypes that cause disease, with serotype O responsible for 80% of cases in India.
- The disease is highly contagious and affects cloven-hoofed animals like cattle, pigs, sheep, and goats. It is transmitted through inhalation or ingestion of the virus.
- Clinical signs include fever, painful sores or vesicles in the mouth and on the feet. This causes decreased milk production and weight loss. Young animals are more severely affected.
- Diagnosis is through virus isolation from lesions, immunological tests, and microscopic examination.
Foot-and-mouth disease (FMD) is an infectious and sometimes fatal viral disease that affects cloven-hoofed animals, including domestic and wild bovids. The virus causes a high fever lasting two to six days, followed by blisters inside the mouth and near the hoof that may rupture and cause lameness.
FMD has very severe implications for animal farming, since it is highly infectious and can be spread by infected animals comparatively easily through contact with contaminated farming equipment, vehicles, clothing, and feed, and by domestic and wild predators.Its containment demands considerable efforts in vaccination, strict monitoring, trade restrictions, quarantines, and the culling of both infected and healthy (uninfected) animals.
Foot-and-mouth disease (FMD) is an infectious and sometimes fatal viral disease that affects cloven-hoofed animals, including domestic and wild bovids. The virus causes a high fever lasting two to six days, followed by blisters inside the mouth and near the hoof that may rupture and cause lameness.
FMD has very severe implications for animal farming, since it is highly infectious and can be spread by infected animals comparatively easily through contact with contaminated farming equipment, vehicles, clothing, and feed, and by domestic and wild predators.Its containment demands considerable efforts in vaccination, strict monitoring, trade restrictions, quarantines, and the culling of both infected and healthy (uninfected) animals.
Arthropods form a major group of disease vectors with mosquitoes, flies, sand flies, lice, fleas, ticks and mites transmitting a huge number of diseases.
FMD is serious , acute and highly contagious animal disease.
Affecting all cloven hoofed animals(hoof split in to two toes)
High morbidity and low mortality.
FMD is disease of animals not humans and affecting livestock in every part of the world.
Animals include cattle , buffaloes, goats , sheep, swine and many wild animals including deer.
Presentation by Dr Mohamed Hassan of the Ministry of Agriculture, Kingdom of Saudi Arabia, at the Enhancing Safe Inter-regional Livestock Trade held at Dubai, UAE, 13-16 June 2011.
Learning objectives
At the end of this unit, the students will be able to know about:
Epidemiological aspects of blood, and tissue sporozoan
Life cycle and pathogenesis of each blood, and tissue sporozoan
Necessary laboratory procedures for the detection and identification of blood, and tissue Sporozoa.
The preliquisite for high economic returns is raising a healthy pig herd.
Unfortunately, today’s pig farmer does it as a by the way; keeps the pig under very unhygienic environment, a fertile ground for diseases .
Economic losses due to diseases arise as mortality and reduced growth rate.
Arthropods form a major group of disease vectors with mosquitoes, flies, sand flies, lice, fleas, ticks and mites transmitting a huge number of diseases.
FMD is serious , acute and highly contagious animal disease.
Affecting all cloven hoofed animals(hoof split in to two toes)
High morbidity and low mortality.
FMD is disease of animals not humans and affecting livestock in every part of the world.
Animals include cattle , buffaloes, goats , sheep, swine and many wild animals including deer.
Presentation by Dr Mohamed Hassan of the Ministry of Agriculture, Kingdom of Saudi Arabia, at the Enhancing Safe Inter-regional Livestock Trade held at Dubai, UAE, 13-16 June 2011.
Learning objectives
At the end of this unit, the students will be able to know about:
Epidemiological aspects of blood, and tissue sporozoan
Life cycle and pathogenesis of each blood, and tissue sporozoan
Necessary laboratory procedures for the detection and identification of blood, and tissue Sporozoa.
The preliquisite for high economic returns is raising a healthy pig herd.
Unfortunately, today’s pig farmer does it as a by the way; keeps the pig under very unhygienic environment, a fertile ground for diseases .
Economic losses due to diseases arise as mortality and reduced growth rate.
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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FMD.pdf
1. FOOT AND MOUTH DISEASE
APHTHOUS FEVER
Dr. Joice P. Joseph
2.
3. ETIOLOGY
• Aphthous virus
• Family: Picorna viridae
• 7 major serotypes: O, A, C, Asia 1, SAT1, SAT2 & SAT3 (SAT=
Southern African Territories)
• Three serotypes of FMD virus (O, A and Asia1) are prevalent.
• Serotype O is responsible for 80 % of the confirmed cases.
• Serotype C has not been encountered in India since 1995.
• Each serotype has multiple subtype with varying antigenicity and
degrees of virulence
• No cross immunity between serotypes
• Change in antigenicity in developing serotypes
• Capsid protein (VP1, VP2 & VP3) determines ability of virus.
4. EPIDEMIOLOGY
• Highly contagious disease
• Asia is endemic
• Disease free : Newzealand, Australia, USA, UK etc.
• Affect cattle, pig, sheep, goat and all cloven hoofed ruminants
• Transmission: Inhalation/ingestion
• Disinfectant: Sodium hydroxide (2%) / sodium carbonate (4%)/ citric
acid (0.2%)/ acetic acid (2%)/ sodium hypochlorite (3%)/ potassium
peroxymonosulfate / sodium chloride (1%)/ chlorine dioxide.
• Spread by direct contact
• Virus can in atmosphere in aerosol form for long periods in
temperate & subtropical condition
• Spread more in dawn or dusk
• Wind can transmit disease to 250 kms
• Amplifying host: Pig (more potent excretor of virus)
• Reservoir host: Wild fauna
• Reservoir host in Africa: Wild Buffalo (Syncerus caffer)
5. EPIDEMIOLOGY
• Virus is transmitted by animal transport, inanimate objects &
equipment
• Human is also a vehicle of transmission
• After 12 hrs of contact, if attending person changes dress,
transmission can be reduced
• Virus remain for 1 yr in infected premise
• Uncooked food is infective
• Sunlight and boiling destroy virus
• Damage economy
• Mild zoonotic importance also
• Morbidity ---- 100 %
• CFR (Case fatality rate) ---- 2 %
• Fatal in young ones (CFR --- 20 %)
• Causes severe production loss (after recovering also, animal
becomes weak & debilitated)
7. PATHOGENESIS
Stages:
(i) Pre‐viraemic phase: characterized by infection and
replication at the primary replication site
(ii) Viremic phase: with generalization and vesiculation at
secondary infection sites
(iii)Post‐viraemia/convalescet stage: including resolution of
clinical disease that may result in long‐term persistent
infection
First site of infection & rapid multiplication (nasal mucosa) ----
---Pharynx-----------blood-----------Different body region----------
Different epidermal site-----------virus appears in milk & saliva-
---------Vesicle in mouth
8. PATHOGENESIS
• Young animal develops myocarditis
• FMD virus shows cellular tropism for infecting prickle cells in
the stratum spinosum.
• Vesiculation in the tongue originated from the necrosis of
individual prickle cells in the middle to bottom layer of the
stratum spinosum along the midline of the dorsal epithelium.
• Dysregulated metabolic functions of thyroid gland will be
exhibited as heat intolerance (HI) (panting) in recovered
animals.
9. CLINICAL SIGNS
• I.P---1-7 days
• Reduced milk production
• Fever (104-1060F)
• Acute painful stomatitis
• Salivation
• Ropy salivation (hanging in long, ropelike string)
• Smacking of lip
• Vesicle & Bulla on Buccal mucosa, dental pad, tongue------
may rupture after 24 hrs
• Vesicles or blisters can be on the tongue, dental pad, gums,
cheek, hard and soft palate, lips, nostrils, muzzle, coronary
bands, teats, udder, snout of pigs, corium of dewclaws and
interdigital spaces.
10. CLINICAL SIGNS
• Ulcer heals by 1 week
• Vesicle on Feet, cleft & coronet
• Secondary bacterial infection in FMD results non-healing
ulcer
• Pregnant may abort
• Young animal may die
• Endocrine damage can cause: Dyspnea, anemia,
overgrowth of hair, lack of heat intolerance (“Hairy
panter”)
• Vesicular lesions on the snout and dry lesions on the tongue
may occur in pigs
• Sheep and goats: Less lesions compared to cattle
11.
12.
13.
14.
15.
16.
17. DIAGNOSIS
• Sample to be collected: Fresh vesicular fluid & surrounding
epithelial tissue. Transport in phosphate buffered saline.
• Virus Isolation
• Immunology – ELISA, CFT, Virus neutralization
• Experimental transmission – White mice & intradermal
inoculation to Guinea pig plantar pad
• Electron microscopic examination of lesion material
18. D.D
• Vesicular stomatitis
• Vesicular exanthema
• Swine vesicular disease
• Blue tongue
• BVD/MD
• Rinder pest
• Malignant cattarhal fever
• Lumpy skin disease
• Pox
• Ingestion of caustic material
19. NECROPSY FINDINGS
• Erosions on rumen pillars
• Tiger heart appearance: Gray or yellow streaking in the heart
due to degeneration and necrosis of the myocardium in young
animals of all species
20. PREVENTION
• Stamping out (slaughter of all infected and in contact animals)
• Vaccination
• Movement restriction
• Public awareness campaign
• Isolation and containment of affected animals
• If outbreak, it should be reported to state animal husbandry
(as per the act ‘Prevention and control of infectious &
contagious diseases in animals’)
• Each and every outbreak should be investigated to know the
epidemiology of the disease with forward and backward linkage.
• Ring vaccination (5-10 Km) radius around the affected
village/area to cover all the susceptible animals including sheep,
goats, pigs etc.
• Disinfection and implementation of bio-security measures
21. VACCINATION
• Since 2003, a trivalent vaccine incorporating only three strains
(O, A, and Asia 1 serotypes) is used in India.
• Better to produce vaccine from locally isolated strains.
• Vaccination‐based FMD Control Programme (FMDCP) was
launched in India in 2003–2004 (10th 5yr plan)
• Ring Vaccination: To contain out break - The vaccination of all
susceptible animals in a prescribed area around an outbreak of
an infectious disease. It forms a buffer of immune individuals to
prevent the spread of the disease.
• Frontier vaccination: To produce a buffer area between infected
and free countries - Vaccination of susceptible animals along a
country's frontier (border) to a given depth. This is practiced in
countries which doesn’t have a natural barrier. One type of it is
practiced around forests also to control FMD spread.
• Some vaccinated animals can be carriers for 6 month
• Some vaccinated animals show anaphylaxis
22. Killed vaccine
• Inactivation of virus is done with formalin/Binary ethylene
immine
• Immunity: 6 to 8 months
Oil adjuvant vaccine:
It has long immunity (1Yr)
Annual revaccination in adult cattle
Biannual revaccination in young stock
Revaccination at 4 to 6 months interval in pig
Immunity occurs 7 to 20 days after vaccination
Calves should be vaccinated as :
If dam is vaccinated, 6 months followed by 10 month age
If dam is not vaccinated, 4 months followed by 8 month age
23. Attenuated live virus vaccine
• More potent
• Narrow margin between loss of virulence and
loss of immunogenicity
24. COMMON VACCINE
• Raksha - Ovac Trivalent (FMD Oil Adjuvant vaccine)
contains tissue culture virus strains, O, A, Asia-1, and
inactivated with Aziridine compound. Mineral oil is added
as an adjuvant
Dosage:
• Cattle, Buffaloes, Calves and Pigs : 2 ml
• Sheep and Goats : 1 ml
Vaccination Schedule:
• Primary vaccination : 4 months of age (Cattle, Buffaloes,
Sheep and Goats).
• Primary vaccination : 2 months of age (Pigs).
• Booster : 9 months after primary vaccination
(Cattle/buffaloes/Sheep and Goats).
• Revaccination : Every 12 months thereafter (Cattle,
Buffaloes, Sheep and Goats).
• Revaccination : Every 6 months thereafter (Pigs).
