Rabies is a viral disease that causes acute encephalitis
(inflammation of the brain) in warm blooded animals. Rabies is a zoonotic disease (a disease that is transmitted to humans from animals) that is caused by a virus
Rabies is a viral disease that causes acute encephalitis
(inflammation of the brain) in warm blooded animals. Rabies is a zoonotic disease (a disease that is transmitted to humans from animals) that is caused by a virus
Rabies is entirely preventable, and vaccines,
medicines, tools, and technologies have long
been available to prevent people from dying of
dog-mediated rabies. Nevertheless, rabies still
kills about 60 000 people a year, of whom over
40% are children under 15, mainly in rural areas
of economically disadvantaged countries in Africa
and Asia. Of all human cases, up to 99% are
acquired from the bite of an infected dog.
Poliovirus is a picornaviridae. it has 3 wildtypes, Wildtype 2 has been eradicated from the world. All countries have been declared polio free except Pakistan, Afghanistan and Nigeria. Global Polio Eradication Initiative has been discussed.
Rabies is entirely preventable, and vaccines,
medicines, tools, and technologies have long
been available to prevent people from dying of
dog-mediated rabies. Nevertheless, rabies still
kills about 60 000 people a year, of whom over
40% are children under 15, mainly in rural areas
of economically disadvantaged countries in Africa
and Asia. Of all human cases, up to 99% are
acquired from the bite of an infected dog.
Poliovirus is a picornaviridae. it has 3 wildtypes, Wildtype 2 has been eradicated from the world. All countries have been declared polio free except Pakistan, Afghanistan and Nigeria. Global Polio Eradication Initiative has been discussed.
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
This ppt is About Rabies epidemiology and treatment .
This is done by using Park book 24th edition of PSM .
This presentation is presented in academics of Master of public health in Christian medical college .
One more Important thing is that that zareb regime (intramuscular ) is not practiced . We try to make this ppt lucid. and the statistics is used in the presentation is upto 27 june 2018
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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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.
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.
4. Introduction
• Zoonotic disease of carnivorous animals ; dogs-enzootic
• CNS ( Brain and spinal cord) - Acute fatal encephalomyelitis
• Caused by RNA virus - Lyssavirus - Family : Rhabdovirideae
• Most important viral zoonoses of warm blooded animals
• Variable incubation period, short period of illness and most characteristic feature
is “fear of water” – painful spasms of muscles of deglutition followed by
respiratory paralysis, delirium, asphyxia and death.
8. Etiology
• Caused by a bullet shaped ,single stranded, non segmented, RNAVirus.
• The virus has spikes all over and contain glycoprotein which is the antigenic
substance
9. Pathophysiology
• Neurotropic virus - tendency to affect the CNS
• The spike like projections help the virus to establish
itself in the axoplasm (cytoplasm of the nerve cells)
• In the neurons of the brain, these viral particles are
seen as inclusion bodies , called ‘ Negri Bodies’ which
is pathognomonic of rabies.
• Absence of Negri bodies however does not rule out
rabies.
• Virus are often found in various body fluids like saliva,
milk, urine, lymph of rabid animals,and in saliva,
semen, sweat and tears among affected persons.
10. Characteristics of rabies virus
• Lipid content of the sheath – inactivated by fat solvents like disinfectants such as
Dettol, Savlon ,Tincture Iodine
• Inactivated by UV Rays, heating for 30 seconds , and 40% alcohol.
• The virus is highly resistant against cold, dryness, decay
• Virus remains infectious for weeks in cadavers.
11. STREETVIRUS
• Wild virus in saliva of rabid animals – StreetVirus
• Highly pathogenic – virulent to both man and animals
• Capable of producing Negri Bodies in neurons
• Incubation period: 3 weeks to 3 months
12. FIXEDVIRUS
• Successive passage of the street virus through the brain of lab animals , the street
virus is made to lose it’s pathogenicity and capacity to produce Negri bodies. ,
however retaining its antigenicity.
• Hence the incubation period becomes short and fixed – 5-6 days in lab animal.
• Modified virus is called Fixed virus – avirulent to man
• Antigenicity present, no capacity to invade
• Cannot multiply or produce Negri Bodies.
13. Reservoir of infection
• The principal reservoir of infection are the rabid animals like dogs, wolves, foxes
etc.
• No carriers among humans. Carrier state among animals is not conclusively
established.
• Cases of hydrophobia constitute potential source of infection.
• Vampire bats serve as constant source of infection for humans and wild animals
and enables the virus to be present in nature.
• Dogs are principal reservoirs in India
14. Period of infectivity
• Humans are infectious during period of illness
• Rabid animal infectious during last 3 to 5 days of incubation period and during
entire period of illness 12 to 15 days
• All warm blooded animals are susceptible
• ONLY 15 -20% get the disease as the virus is excreted intermittently through the
saliva of rabid animals.
15. Modes ofTransmission
• Lick of bite of rabid animal.
• Sylvatic cycle in wild animals
• Urban cycle in domestic animals
• And accidentally to human beings from animals
• Human to human transmission does not occur as saliva doesn’t have optimum
number of virus and humans do not have biting tendency. Rabies in man is a ‘dead
end disease’. Can spread through transplantation.
16. Furious Rabies (Mad dog syndrome)
• 80 to 90% of cases
• Dog behaves abnormally – goes to dark corners ,
restless and shows agitation, run amuck
• Bites man and animals without provocation
• Paralysis of lower jaw, protruded tongue, drooling saliva,
paralysis of vocal cord, limbs and trunk.
• Death due to respiratory paralysis and convulsions.
• Mortality is 100 percent.
17. Dumb Rabies ( Paralytic Rabies )
• 10 to 20% of rabies
• Dog becomes silent and withdraws itself
• Death from general paralysis
• HYDROPHOBIA not a feature
18. Clinical Features
• Prodromal stage : Headache, restlessness, Fever,Tingling and numbness at the
site of bite and malaise.
19. Clinical Features
• Stage of convulsions:
• Sensory system – Sensitive to senses of touch , cold, hot – can get convulsions
• Motor system – Increased tone and spasticity of muscles- exaggerated reflexes,
jerks
• Sympathetic system- Excessive perspiration, lacrimation, salivation
• Aerophobia and photophobia
20. Clinical Features
• Stage of paralysis: Difficulty and pain in swallowing food – choking sensation-
painful spasms
21. Lab diagnosis ( Antemortem)
• Nuchal skin biopsy
• Saliva –Virus isolation or RTPCR
• Serum and spinal fluid for antibodies
23. Management of Hydrophobia
• Isolation in quiet room
• Sedatives, antipyretics, analgesics, anti-histaminics and anticonvulsants
• IV rehydration, steroids, osmotic diuretics like mannitol
• Expert nursing care
• Mechanical ventilation of lung
• Medical attendants should receive pre exposure prophylaxis with antirabies
vaccines and are advised to wear glasses, masks, gloves, shoes, plastic apron.
They should avoid contact with saliva, urine, tears of patient.
24.
25. Principles of Post Exposure Prophylaxis
• To reduce viral load
• To neutralise virus at point of entry
• Prevent nerve infection
• To induce systemic immunity
26. Post Exposure Prophylaxis
• Wound treatment
• Observation of the animal
• Antirabies immunization - Antirabies vaccine and Immnunoglobulin
• Advice to patient
27. 1.WoundTreatment (First AidTreatment)
• Thorough washing of wound with soap and running tap water for 10 mins
• Application of virucidal agents like povidone iodine and tincture iodine
• Deep wounds exploration and debridement must be carried out
• Suturing of wounds must be avoided. (If required – only after administering Ig)
• Bandaging must not be done
• Immunisation for tetanus must be carried out
• Analgesics and anti-inflammatory, antibiotics to prevent secondary infection
28. 2. OBSERVETHE BITTENANIMAL FOR
10 DAYS
• CHANGE IN BEHAVIOUR
• WITHDRAWING
• RUNAMUCK
• CHANGE IN BARK
• DEATH
30. Active Immunization
• All anti rabies vaccines are killed vaccines.
• Virus is killed or inactivated by Beta PropionoLactone (BPL)
• They are broadly classified into 3 categories:
NERVETISSUEVACCINES (NTV)
DUCK EMBRYOVACCINE (DEV)
MODERNTISSUE OR CELL CULTUREVACCINES (TCVs OR CCVs)
31. Cell CultureVaccines
• Human diploid cell vaccine (HDCV),
• Purified Vero cell rabies vaccine (PVRV),
• Purified chick-embryo cell vaccine (PCECV)
• Purified duck embryo vaccine (PDEV).
• Higher potency, safe and provide longer immunity
34. Essen Regimen
• First 3 doses should be given on indicated days else vaccine failure
• If animal is healthy, can be stopped after 3 doses
• Immunity developed after 8 to 10 Days
38. Intradermal schedule
• Total of 4 visits, less vaccine required
• Useful in resource limited settings
• However skilled personnel needed
• Not given in immunosuppressed patients
• DO NOT GIVE MIXED SCHEDULES
39. Immunoglobulin
• Rabies Ig : In all category 3 patients
• Immediate protection
• Given on Day 0
• Irrespective of interval between exposure and beginning of treatment
• Serum alone not to be administered
40. Immunoglobulin
• ERIG – Ionorab (Intradermal test needed) – 40 IU /kg bodywt
• HRIG –Rabivax - 20 IU/kg body wt
41. Rabies Immunoglobulin
• As much as possible inject Ig into the depth of the wound and also infiltrated
around the wound.
• Remaining RIG should be administered intramuscularly into the gluteal region in
single dose on day 0 along with active immunisation , followed by complete
course.
• Has local virucidal effect. And prevents virus from entering susceptible nerve
cells.
42. 4. Advice to patient
• Proper follow up and complete treatment
43. What to do in case of reexposure?
• If patient has received complete course of preexposure or post exposure
prophylaxis by IM or ID requires only 2 doses of vaccine
• On day 0 and 3 by IM.
44. PRE EXPOSURE PROPHYLAXIS
• Veterinarians
• Animal handlers
• Lab personnel
• Pet owners
• 3 doses ofTCV on days 0,7 and 28
45. Personal protection against rabies
• Do not touch animal bitten wounds with bare hands
• Do not provoke any animal
• Avoid contact with secretions of hydrophobia patient
• Take pre exposure immunisation if you belong to at risk group
• Vets to wear masks and gloves while examining rabid animals
46. REFERENCES
• ParksTextbook of Public Health 23rd Edition
• Community Medicine with recent advances by AH Suryakantha