This document discusses several bacterial zoonoses that can affect the nervous system. It focuses on tetanus, botulism, and tuberculosis. For tetanus, it describes the causative agent (Clostridium tetani), pathogenesis, clinical signs in humans and various animals, diagnosis, prevention including vaccination, and control. For botulism, it discusses the seven neurotoxins produced by Clostridium botulinum, clinical signs in humans and different species, and prevention in livestock. Finally, it provides background on Mycobacterium tuberculosis complex as the cause of tuberculosis, its epidemiology, and the diseases it can cause in cattle and humans.
introduction and terminologies of preventive vet medicine, ,preventive medicine ,disinfection ,sterilization ,treatment principals ,disease control and eradication ,levels of disease prevention ,etiology and factor based disease types
introduction and terminologies of preventive vet medicine, ,preventive medicine ,disinfection ,sterilization ,treatment principals ,disease control and eradication ,levels of disease prevention ,etiology and factor based disease types
Zoonoses :- derived from the Greek words
Zoon- Animal & Noson – Disease
Zoonoses was coined and first used by Rudolf Virchow who defined it for communicable diseases.
Diseases and infections which are naturally transmitted between vertebrate animals and humans - WHO 1959
Of the 1415 microbial diseases affecting humans, 61% are zoonotic with 13% species regarded as emerging or reemerging
Link b/w human & animals with their surrounding are very close especially in developing countries
Describes factors that are responsible for emergence of zoonoses at the interface. Besides it also includes current scenario of food borne out-breaks, emergence of AMR.
Zoonoses :- derived from the Greek words
Zoon- Animal & Noson – Disease
Zoonoses was coined and first used by Rudolf Virchow who defined it for communicable diseases.
Diseases and infections which are naturally transmitted between vertebrate animals and humans - WHO 1959
Of the 1415 microbial diseases affecting humans, 61% are zoonotic with 13% species regarded as emerging or reemerging
Link b/w human & animals with their surrounding are very close especially in developing countries
Describes factors that are responsible for emergence of zoonoses at the interface. Besides it also includes current scenario of food borne out-breaks, emergence of AMR.
Genus Yersinia&Pasteurella.pptx these are gram negatives non motile bacteriajaphetPeter1
Plague is caused by the bacteria Yersinia pestis, a zoonotic bacteria usually found in small mammals and their fleas.
People infected with Y. pestis often develop symptoms after an incubation period of one to seven days.
There are two main clinical forms of plague infection: bubonic and pneumonic. Bubonic plague is the most common form and is characterized by painful swollen lymph nodes or 'buboes'.
Plague is transmitted between animals and humans by the bite of infected fleas, direct contact with infected tissues, and inhalation of infected respiratory droplets.
Plague can be a very severe disease in people, with a case-fatality ratio of 30% to 60% for the bubonic type, and is always fatal for the pneumonic kind when left untreated.
Antibiotic treatment is effective against plague bacteria, so early diagnosis and early treatment can save lives.
Currently, the three most endemic countries are the Democratic Republic of the Congo, Madagascar, and Peru.
Y. pestis survives and produces F1 and V antigens within blood cells such as monocytes, but not in neutrophils.
Natural or induced Immunity is achieved by the production of specific antibodies against F1 and V antigens
Antibodies against F1 and V induce phagocytosis by neutrophils
Y.pestis causes plague ( a zoonotic diseases which is transmitted fron rats and rodents to humans by infected fleas)
Fleas-blood sucking wingless insect of the order Siphonaptera
Occasionally the infection occurs by inhaling the organism in the airborne droplets or
By handling the infected rodents or domestic animals (e.g cats and dogs) that harbour infected fleas
Bubonic plague
Flea (bite) to humans
Pneumonic plague
Human to human after inhalation and>lungs though blood stream
Septicaemic plague
Plague-Zoonotic disease
Spread from domestic rats to man by bite of rat flea
Plague-greatest killer in history of mankind
Severe epidemics
In India-out break in 1994 (Maharashtra, Gujarat, UP, MP, Karnataka)
In 2002-outbreak in Shimla
Scattered natural foci still exist:kolar,Bead-Lathur belt in Maharashtra, Shimla and Uttaranchal
Self limiting gastroenteritis in young children
Mesenteric adenitis and inflammatory terminal ileitis in older children
Systemic disease seem in aduld:bacteremia,meningitis arthlgia,erythema nodosum
Pathogen of rodents, particularly guinea pigs
Septicemia with mesenteric lymphadenitis similar to appendicitis
Motile at 22 degree centigrade
Pasteurella species are spherical, ovoid or rod-shaped cells 0.3-1.0µm in diameter and 1.0-2.0µm in length
Cells are Gram negative, and occur singly, or in pairs or short chains
Bipolar staining may be seen
Capsules may be present
All species are non-motile
Facultative anaerobic
Microscopy
Gram-negative coccobacilli measuring 1 to 2 μm in length.
Many pathogenic isolates are encapsulated
Cultural characteristics
Primary isolation media
Blood agar incubated in 5-10% CO2 at 35-37°C for 16–48hr ,Colonies are grey and viscous but rough irregular colonies occur
Toxoplasmosis is considered one of the neglected parasitic infections of the United States, a group of five parasitic diseases that have been targeted by CDC for public health action.Q fever is a disease caused by the bacteria Coxiella burnetii. This bacteria naturally infects some animals, such as goats, sheep, and cattle. C. burnetii bacteria are found in the birth products (i.e. placenta, amniotic fluid), urine, feces, and milk of infected animals.
The presentation discusses in detail the efficacy and multipurpose use of an environmentally controlled poultry house and.It basically determines the efficacy of each section of the EC poultry house.
Kerala state is having abundant water source and people are really proud of it and lavishly wastes water.But due to the uprising scarcity of good potable drinking water we should think about conserving water before polluting the sources.This presentation is a description about the water scenario in India briefly and describes about the major water pollution and the main regions that are being affected severely.
Alternative means of communication during a disaster a presentation on the various alternatives when all communication breaks down during a disaster and how social media is also helping.
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
3. BRUCELLOSIS
It is one of the major bacterial zoonotic disease and in humans is also known as
undulent fever ,malta fever or mediterranean fever.
it is caused by different species of brucella group of organisms
6. HOST
All mammals
HUMANS and HORSES are most sensitive
Dogs are relatively resistant
Cats are more resistant
6
7. EPIDEMIOLOGY
World wide
Live in all anaerobic habitat-soil ,faeces & intestinal tracts of
various animals
Especially in hot, damp climate with heavily manured soils
More in developing and under developing countries
IMPORTANT ENDEMIC INFECTION IN INDIA
7
8. EPIDEMIOLOGY ( cont…)
The incubation period of tetanus may be up to
several months, but is usually about eight days.
In general, the injury site is for from the central
nervous system, the longer the incubation period.
The near the C.N.S incubation period IP is short, the
more severe the symptoms.
8
9. Mode of transmission
Contaminated WOUNDS
Tissue injury – surgery, animal bites,
parturation , (dystocia), deep puncture
wounds
Naval infection –Tetanus neonatale
In neonatal tetanus, symptoms usually
appear from 4 to 14 days after birth,
averaging about 7 days.
9
10. Pathogenesis
Wound
Exotoxins
Spore germinate –anaerobic condition
Disseminate via blood and lymphatics
Toxin reaches CNS along nerves
Producing clinical signs
Ascending
tetanus
Descending
tetanus
Tetanospasmin & Tetanolysin
10
12. CLINICAL SIGNS
Human beings
Painless spasm of the
muscles of the jaw
Difficulty in opening the
mouth “lock Jaw”,
Contraction of the muscles
on the forehead and mouth
The board like rigidity of the
abdominal wall are
characteristic
12
13. CLINICAL SIGNS
RUMINANTS
Bloat
Constipation & retention of urine
Lateral recumbency with extreme extension
of limbs, tail and all muscles
Rigidity of legs and opisthotonous
SHEEP and GOAT
Fall to the ground and opisthotonus
13
17. CLINICAL SIGNS
DOGS AND CATS
Long incubation period
Localized tetanus
Stiffness and rigidity in limb ,stiffness
may progress to opposing limb and
may advances anteriorly.
Generalized tetanus is also there but
rare
17
18. DIAGNOSIS
Clinical signs and history
of recent trauma
Detecting tetanus toxin in
serum
If wound is apparent –
gram stained smears and
by anaerobic culture
18
22. Animals
Cattle and sheep
Horses
Birds and poultry
Mink and ferrets
Uncommon in dogs and pigs
Fairly resistant
No natural cases documented in cats
22
24. Neurotoxins
Seven different types: A to G
Different types affect different species
All cause flaccid paralysis
Only a few nano grams can cause illness
Binds neuromuscular junctions
Toxin: Destroyed by boiling
Spores: Higher temperatures to be inactivated
24
25. Neurotoxins
Neurotoxin A B C D E F G
Human X X X X
Horses X X
Cattle X X X
Sheep X
Dogs X X
Avian X X
Mink & Ferret X X X
4/28/2016
26. HISTORY
1793, Justinius Kerner
“Botulus” = Latin for sausage
1895, Emile von Ermengem
Isolated organism during
Belgium outbreak
U.S. outbreaks led to improved
industry processing
Justinus Kerner (1786–1862)
26
28. Human Disease
Three forms
Food borne
Wound
Infant
All forms fatal and a medical emergency
Incubation period: 12-36 hours
28
29. Infant Botulism
Most common form in U.S.
Spore ingestion
Germinate then toxin released and colonize large intestine
Infants < 1 year old
94% < 6 months old
Spores from varied sources
Honey, food, dust, corn syrup
29
30. Food borne Botulism
Preformed toxin ingested from contaminated food
Most common from home-canned foods
Asparagus, green beans, beets, corn, baked potatoes,
garlic, peppers, tomatoes; type A
Improperly fermented fish (Alaska); type E
30
31. Wound Botulism
Organism enters wound
Develops under anaerobic conditions
From ground-in dirt or gravel
It does not penetrate intact skin
Associated with addicts of black-tar heroin
31
32. Adult Clinical Signs
Nausea, vomiting, diarrhea
Double vision
Difficulty speaking or swallowing
Descending weakness or paralysis
Shoulders to arms to thighs to calves
Symmetrical flaccid paralysis
Respiratory muscle paralysis
32
34. Cattle and Sheep
Ingestion of toxin
Incubation
24 hours to 7 days
Sources
Spoiled stored silage or grain
Silage using poultry litter or products
Phosphorus deficiency in cattle
Carcasses: Baled or chopped into hay
34
35. Ruminants: Clinical Signs
Progressive ascending ataxia(Symmetric muscular paralysis)
Recumbent & Head turned into flanks
Cranial nerve dysfunction(dysphagia, drooling, tongue paresis,
and facial muscle paresis)
Eye effects include decreased pupillary light reflex, ptosis and
mydriasis
Rumen stasis; bloat
Atonic bladder - loss of urination
35
36. Affected animal lie in strenal recumency with the head
on the ground or turned to the flank
36
37. Horses
Horses, especially foals, are highly sensitive to botulism toxin
Type B & C toxins
Incubation period
24 hours to 7 days
Sources
Contaminated feed
Wound infections
37
39. Foals
“Shaker Foal” syndrome
Most 2 weeks to 8 months old
On a high nutrition plane
Spores in contaminated feed
Usually type B
39
40. Birds and Poultry
“Limber neck”
Types C and E
Good sentinel species
Sources:
Decomposed vegetation or
invertebrates
Ingest toxin or invertebrates
with toxin
Contaminated feed or water
of chickens
40
41. Birds and Poultry:
Clinical Signs
Occurs 12-48 hours after ingestion
Droopy head
Drowsy
Wing and leg paralysis
Unable to hold their head up
Unable to use their wings or legs
Eyelid paralysis
41
42. Mink and Ferrets
Type C
Occasionally A and E
Sources
Chopped raw meat or fish
Improper storage of meat by-products
Vaccine available for type C
42
43. Dogs
Progressive symmetric ascending weakness
Rear limbs to forelimbs
Cranial nerve deficits
Respiratory paralysis
Lose ability to urinate and defecate
43
44. Dogs
Rare
Type C; few cases type D
Source
Ingestion of carrion
Wetland areas with avian botulism epizootics
Incubation period
Few hours to 6 days
44
45. Cattle and Sheep: Diagnosis
History
Bloodwork and CSF tap: Normal
ELISA test available for type C & D
Definitive diagnosis
Demonstration of toxin in serum, gut contents or organs(mouse bioassay)
Electromyography (EMG)
45
46. Differential diagnosis
Hypocalcemia
Hypomagnesemia
Carbohydrate overload
Toxicosis, including from mycotoxin, lead, nitrate, organophosphate, atropine or
atropine-like alkaloid
Tick paralysis
Paralytic rabies
46
47. Ruminants: Prevention
Good husbandry practices
Rodent and vermin control
Prompt disposal of carcasses
Avoid spoiled feedstuff or poor quality silage
Vaccination in endemic areas
47
48. Product name BoNT type Animal species Dosage
Ultravac
botulinum
(Pfizer Animal
Health)
C ,D Cattle, sheep 2.5 ml cattle
1 ml sheep
1st dose; 2nd
dose after 4-6
weeks Annual
booster
Long range
(Pfizer Animal
Health)
C ,D Cattle 2.5 ml 1st dose from 6
weeks Annual
booster
Singvac 1-year
botulinum
(Virbac Animal
Health)
C ,D cattle 2 ml 1 dose Booster
after 36 months
Botulism Vaccine
(Onderstepoort
Biological
Products)
C,D Cattle Horses
Mules Sheep
Goats
1.0ml sheep
and goats 2.0ml
cattle, horses,
and mules
1st dose; 2nd
dose after 4-7
weeks Annual
booster
48
50. Acnitis
Consumption
Great white plaque
Great white scourge
Pearl disease
Pott’s disease
Pthisis
Rajayakshman
Swollen gland
Caption of the men of death
Going into a decline
52. Mycobacterium bovis:
tuberculosis in cattle
Mycobacterium avium complex (MAC)
Mycobacterium avium &
Mycobacterium intracellulare
causes generalised TB in cattle
zoonotic disease called mycobacteriosis
53. EPIDEMIOLOGY
1882- Robert Koch
isolated M.tuberculosis
1898- differentiated M.bovis
and M.tuberculosis
Many countries have eradicated bovine TB
Prevalent in many African, Asian and middle
East countries.
Robert Koch
54. TB- second most leading cause of death by single infectious agent
128 out of 155 countries reported the presence of M. bovis
infection and/or clinical disease in their cattle population between
2005 and 2008 (Michel et al, 2010)
55. 2013, world:
9 million (1.1 m with HIV)- affected
1.5 million (360000 with HIV)- death
2013, India:
22,00,000 – new cases of TB reported
38,000- death WHO, 2013
58. HOST
M.tuberculosis reservoirs in man
M.bovis mainly cattle, domestic and wild
animals and man.
M.avium causing generalized TB
59. TRANSMISSION
Tubercle bacilli transmit from person to
person, person to animal
man can infect animals with both strains
self limiting in animals
Ingestion- unpasteurized and contaminated
meat
60. Animal-to-animal
Inhalation of droplets
Ingestion of milk
Bite of infected hard tick
Infected pastures
Animal-to-man
Direct exposure
Ingestion of infected
material
70. DISEASE IN ANIMAL
CATTLE:
Lymphadenitis
Progressive hardening
and swelling of udder
Watery, flakes in milk
Emaciation
Diarrhea with capricious appetite
Fluctuating temperature
72. DIAGNOSIS
1. Microscopic detection of organism
2. Delayed type hypersensitivity assay
a. single intradermal tuberculin test
b. stormont test
Acid fast bacilli
detected in the
impression smear
from omentum
73. c. short thermal test
d. subcutaneous tuberculin test
e. opthalmic test
3. Animal inoculation
4. Isolation and identification of pathogen
Suspected
material
Guinea
pig
Tubercular
lesions
Lowenstein jensen medium
74. 1. Microscopic detection of organisms
2. Montoux test
Fluorescent auramine
staining showing
Mycobacterium sp in
sputum sample
75. 3. Radiography
4. Gas chromatography
5. Radiometric determination of bacterial
growth
6. PCR
7. ELISA
8. Isolation of pathogens
76. PREVENTION AND CONTROL
Test and slaughter – best
Test and segregation
Slaughter surveillance
Cleaning and disinfection
5% phenol, iodine solutions, moist
heat(121˚C, 15min), glutaraldehyde and
formaldehyde
Herd density
Vaccination
77. Condemnation of milk from infected animal
Treatment of infected meat
Abattoir control
Milk pasteurization
Health education
78. LYME DISEASE
The spirochete bacteria Borrelia burdorferi
A zoonotic disease
A disease affecting the many organ systems
Lyme borreliosis, is an infectious disease caused by bacteria of the Borrelia type
In North Americai Borrelia burgdorferi sensu stricto,
Europe and Asia, the bacteria Borrelia afzelii and Borrelia garinii are also causes of
the disease.
79. SYMPTOMS
Erythematous lesions
Fever
Headache,
Joint pains,
Severe headaches with neck stiffness,
Heart palpitations,
If untreated, symptoms may include loss of the ability to move one or both sides
of the face,
82. TRANSMISSION
Lyme disease is transmitted to humans by the
bite of infected ticks of the Ixodes genus.
The tick must be attached for 36 to 48 hours
before the bacteria can spread
Deer tick
83. Lyme disease is classified as a zoonosis, as it is transmitted to humans from
a natural reservoir among rodents by ticks that feed on both sets of hosts.
Hard-bodied ticks of the genus Ixodes are the main vectors of Lyme disease (also
the vector for Babesia).
Most infections are caused by ticks in the nymphal stage, as they are very small and
may feed for long periods of time undetected
Larval ticks are very rarely infected.
Although deer are the preferred hosts of deer ticks, and the size of the tick
population parallels that of the deer population, ticks cannot acquire Lyme disease
spirochetes from deer.
84. ZOONOTIC IMPORTANCE
Lyme disease is the most common disease spread by ticks in the Northern
Hemisphere
It is estimated to affect 300,000 people a year in the United States and 65,000
people a year in Europe(Shapiro, ED (1 May 2014). "Clinical practice. Lyme
disease.". The New England Journal of Medicine 370 (18): 1724–
31.doi:10.1056/NEJMcp1314325. PMID 24785207.)
85. NERVOUS SYSTEM IMPLICATION
B. burgdorferi may induce astrocytes to undergo astrogliosis which may
contribute to neurodysfunction.
The spirochetes may also induce host cells to secrete Quinolinic acid, which
stimulates the NMDA receptor on nerve cells, which may account for
the fatigue and malaise observed with Lyme encephalopathy
In addition, diffuse white matter pathology during Lyme encephalopathy may
disrupt grey matter connections, and could account for deficits in attention,
memory, visuospatial ability, complex cognition, and emotional status.
87. LEPTOSPIROSIS
Leptospirosis field Fever, Rat catcher's yellows, Pretibial fever
t is also known as Weil's disease
L interrogans most pathogenic
Leptospira is a flexible, spiral-shaped, Gram-negative spirochete with internal
flagella. Leptospira interrogans has many serovars based on cell surface antigens.
Infection caused by corkscrew-shaped bacteria called Leptospira.
Signs and symptoms can range from none to mild such as headaches, muscle
pains, and fevers; to severe with bleeding from the lungs or meningitis.
88. Up to 13 different genetic types of Leptospira may cause disease in humans.
It is transmitted by both wild and domestic animals.
The most common animals that spread the disease are rodents.
It is often transmitted by animal urine or by water or soil containing animal urine
coming into contact with breaks in the skin, eyes, mouth, or nose.
In the developing world the disease most commonly occurs in farmers and poor
people who live in cities. In the developed world it most commonly occurs in
those involved in outdoor activities
89.
90. Pathogenesis
Leptospira
Damage to small
blood vessels
Vasculitis
Direct cytotoxic injury
Immunological injury
Massive migration of fluid from
Intravascular to interstitial compartment
Renal dysfunction, vascular
Injury to internal organs
91. SIGNS AND SYMPTOMS
Leptospirosis is a biphasic disease that begins suddenly with fever accompanied by chills,
intense headache, severe myalgia (muscle ache), abdominal pain, conjunctival suffusion (red
eye), and occasionally a skin rash.
The symptoms appear after an incubation period of 7–12 days. The first phase (acute or
septicemic phase) ends after 3–7 days of illness.
The disappearance of symptoms coincides with the appearance of antibodies
against Leptospira and the disappearance of the bacteria from the bloodstream. The patient
is asymptomatic for 3–4 days until the second phase begins with another episode of fever.
The hallmark of the second phase is meningitis (inflammation of the membranes covering
the brain).
95. PREVENTION
Effective rat control
Avoidance of urine contaminated water sources
Pre-exposure prophylaxis may be beneficial for individuals traveling to high-risk
areas for a short stay.
96. Epidemiology
Leptospirosis is a worldwide zoonosis affecting many wild and domestic animals.
Humans acquire the infection by contact with the urine of infected animals.
Human-to-human transmission is extremely rare.
It is estimated that seven to ten million people are infected by leptospirosis
annually.
One million cases of severe leptospirosis occur annually, with 58,900 deaths.
Annual rates of infection vary from 0.02 per 100,000 in temperate climates to 10
to 100 per 100,000 in tropical climates.
This leads to a lower number of registered cases than likely exists.
97.
98. LISTERIOSIS
Listeria primarily causes infections of the central nervous
system (meningitis, meningoencephalitis,brain abscess, cerebritis)
and bacteremia in those who are immunocompromised.
Synonyms
Silage Disease
Circling disease
Listerellosis
mononucleosis
99. Special features of organism
Can withstand refrigeration temperatures
Can withstand batch method of pasteurisation
Can withstand high salt concentration
Can grow over a wide pH range 4.5-9
Extensive survivability
100. CAUSE
Listeria monocytogenes is ubiquitous in the environment and most pathogenic organism.
The main route of acquisition of Listeria is through the ingestion of contaminated food
products. Listeria has been isolated from raw meat, dairy products, vegetables, fruit
and seafood. Soft cheeses, unpasteurized milk are potential dangers.
Rarely listeriosis may present as cutaneous listeriosis. This infection occurs after direct
exposure to L. monocytogenes by intact skin and is largely confined to veterinarians who
are handling diseased animals, most often after a Listerial abortion.
101. Route of transmission
Direct indirect contact through conjunctiva & Intact mucous membrane
Ingestion of Milk and meat
]Through water and soil
Perinatal infection –Through trans placental and trans mammary route
Organism excreted through semen
Through inhalation –very rare
102. Treatment
Bacteremia should be treated for 2 weeks,
Meningitis for 3 weeks,
Brain abscess for at least 6 weeks.
Ampicillin generally is considered antibiotic of choice; gentamicin is added
frequently for its synergistic effects.
103. Prevention
The main means of prevention is through the promotion of safe handling, cooking
and consumption of food. This includes washing raw vegetables and cooking raw
food thoroughly
Another aspect of prevention is advising high-risk groups such as pregnant
women and immunocompromised patients to avoid unpasteurized milk and foods
such as soft cheese
104. REFERENCES:
ZOONOSES AND COMMUNICABLE DISEASES
COMMON TO MAN AND ANIMALS-Third edition
ZOONOTIC DISEASES OF PUBLIC HEALTH IMPORTANCE-NATIONAL
INSTITUTE OF COMMUNICABLE DISEASES (DIRECTORATE GENERAL OF
HEALTH SERVICES)
www.WHO.in
www.cdc.in
www.oie.org