Foot and mouth disease is a highly contagious viral disease that affects cloven-hooved animals. It causes the formation of vesicles in the mouth and on the feet. The disease is caused by a picornavirus with multiple serotypes. Clinical signs include fever, vesicles in the mouth and on the feet that can rupture and cause lameness. The disease is typically self-limiting but can have severe economic impacts. Diagnosis involves virus detection by tests like PCR. Control relies on vaccination and movement restrictions.
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Vesicular stomatitis in Cattle, Horse and pigsRakshith K, DVM
Caused by Rhabdoviridae family, Vesiculovirus. Development of vesicles on the mouth and feet. The virus, an arbovirus, is spread to cattle, horses, and pigs primarily by sandflies and blackflies. The mechanism of injury in vesicular stomatitis is cell dysfunction and lysis leading to intercellular edema with vesiculation, erosion, and ulceration of mucosae and skin. Pathogenesis of the disease is by the bite of the flies, entry of virus, viral replication in the cell and rupture of the cell, which form intercellular space that is fluid filled to form vesicles. Rupture of this vesicles leads to erosion/ulceration of overlying mucosa or skin.
Malignant catarrhal fever (MCF) is an infectious systemic disease that presents as a variable complex of lesions affecting mainly ruminants and rarely swine. It is principally a disease of domestic cattle, water buffalo, Bali cattle (banteng), American bison, and deer. In addition to these farmed animals, MCF has been described in a variety of captive ruminants in mixed zoologic collections.MCF results from infection by one of several members of a group of closely related ruminant gammaherpesviruses of the Rhadinovirus genus.
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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?
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Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
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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.
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.
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
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
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
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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2. FOOT & MOUTH DISEASE
• Highly contagious febrile infectious viral disease of many
wild and domestic cloven footed mammals.
• Formation of vesicles in the epithelial tissue especially in
squamous epithelium (Stratum spinosum is involved).
• Vesicles are formed in lips,muzzle,tongue,udder, fore-
stomach, interdigital space, coronary band of feet, teats
etc.
• Low mortality, but high morbidity
3. Etiology
• Agent-Picornaviridae family-Aphthous virus genus—
FMDV
• Seven immunologically different serotypes- O,A,C, Asia –I,
SAT- I, SAT-II & SAT-III ( Different antigenic subtypes
under each serotype, no cross protection hence vaccination
failure is common)
• O,A,C, Asia –I – Asian countries SAT- I, SAT-II & SAT-III
• O,A,C, SAT- I, SAT-II & SAT-III – African countries
• Synonyms-Aphthous fever, Panters
• In India after 1995, strain C was absent.
5. Route of infection
1. Ingestion of feed and water contaminated by
infected material like saliva, urine, feces, milk and
discharges from lesions of infected animal.
2. Inhalation as virus will be present in the exhaled air
( Esp. in pigs) and carried as aerosols ( Via dust)
3. Contact with contaminated bedding materials and
other fomites
4. Rapid spread due to small size of virus
6. INCUBATION PERIOD
• OIE recognizes IP as 2-14 days.
• The viral dose, susceptible species, and route of
infection all influence the speed with which signs of
illness appear.
• Also IP varies according to the serotypes.
• OIE List A Disease
7. Pathogenesis
Through inhalation or ingestion, virus get into the body of animal.
Initial replication in the pharyngeal lymphoid tissue or tonsils and they replicate in the
lymph node.
They move to lymphatics and through veins they get into systemic circulation.
Now its viremia stage (Virus in blood).
Since it is epitheliotropic, localization in the regions of epithelial tissues of mouth,
skin and feet and in organs like mammary gland, lymph nodes, thyroid glands,
adrenals etc.
Second phase of replication in areas of localization and forms lesions.
Recovered animals may become panters because thyroid is affected and BMR is
altered.
8. Clinical signs
• Onset of disease is by sharp rise of temperature (104 to 106).
• Anorexia, Sudden drop in milk yield.
• Formation of vesicles- inner lips, cheeks, gums, hard palate,
dental pad, sides and dorsum of tongue, muzzle, external nares,
interdigital cleft, coronary band, teats etc.
• Usually, Blisters produce secondary bacterial infection.
• Smacking of lips, Grinding of teeth, Drooling of saliva,
Kicking of feet etc. (due to blisters)
• Loss of heat control (panters)
9. Clinical signs
• Vesicles in mouth causes excess salivation – Stringy/ ropy salivation.
• Lameness due to foot lesions, hooves may slough off.
• Mastitis will occur if teats are affected.
• Pregnant animals may abort.
• Islets of pancreas can get affected leading to diabetes mellitus.
• High Mortality occurs in pigs.
• Blister are common in snout region for pigs.
• Since vesicles occur at pressure points in pigs-Knuckling.
• In cattle, Milk may have virus up to 3 months
10. Gross lesions
• In the oral cavity, there is buccal hyperemia with development of vesicles
on inner lips, cheeks, gums, hard palate, dental pad, sides and dorsum of
tongue and muzzle.
• Foot lesions are also in the form of vesicles in the interdigital cleft and
coronary band.
• In udder, vesicles may form on teats and they may burst.
• Sometimes the epithelium sloughs off forming ulcers with raw red bases.
• Mottled myocardial lesions.
• Thyroid atrophy.
• Myocardial hemorrhage.
• Fluid presence in myocardium.
11.
12.
13. Gross lesions
• In young animals/ calves, FMD is characterized by grayish
white streaks on the ventricular and papillary musculature and
septal wall especially of left ventricle – TIGROID HEART due
to special pattern in ventricular musculature.
• Cause of Death in Suckling calves-Acute Myocarditis.
14. Microscopic lesions
• Cells of stratum spinosum are affected, virus replicate in the
cytoplasm.
• Ballooning/ Hydropic degeneration, spongiosis, acantholysis,
finally forming vesicles.
• Roof of the vesicle- Stratum granulosum, lucidum and
corneum, Base- Stratum germinativum
• Vesicles coalesce and form bullae.
• Sometimes the epithelium sloughs off forming ulcers.
• Lesions in mouth can be described as vesicular & ulcerative
stomatitis.
15. Microscopic lesions
• In young calves- Hyaline degeneration and necrosis of myocardial
fibers with large numbers of infiltrating lymphocytes and a very few
neutrophils – Mononuclear/lymphocytic and necrotizing myocarditis
• No inclusion body formation.
Microscopic image of calf ’s heart (“tiger-heart”)
from a calf that died from an acute form of
FMD, showing severely affected muscle fibers
with coagulative necrosis), with infiltration of
lymphocytes. (PAS stain, 600x)
16. Diagnosis
• Tentative Diagnosis: History, Clinical Signs, Details from owner.
Laboratory Diagnosis:
1. Swab Test-Swabs from mucosal eruptions and Pharynx are
taken and cultured to check the presence of virus.
2. Complement Fixation Test
3. Virus Neutralization Test
4. PCR,RT-PCR, ELISA, Electron Microscopy.
18. Prevention and Control
• Proper Hygiene measure should be practiced.
• Vaccination should be properly practiced.
• Ring Vaccination is practiced
• Vaccine: Raksha “O”VAC
• Vaccination started at 4 months of age.
19. Special Points
• 1.Most Common strain-O
• 2.Immunogenic viral polypeptide-VP1
• 3.Cause of death in neonates-Acute myocarditis.
• 4.Size of virus-very small (Pico)
• 5. Semen and Urine can also carry virus, so during mating
it can be spread.
• 6.It is a zoonotic disease with very little problems in
human.