Health and diseases exam 2 content Flashcards
(170 cards)
1
Q
what is peritonitis?
A
inflammation/ infection of the peritoneal cavity
2
Q
what is the peritoneum?
A
the membranous lining of the abdominal cavity closely assoc. w/ abdominal wall. looks like Saran Wrap and holds the sterile fluid (no bacteria)
3
Q
What is localized peritonitis?
A
When the body tries to wall off infection by forming a connective tissue wall around It
4
Q
what is generalized peritonitis?
A
life threatening infection spreads throughout peritoneal cavity.
5
Q
what is the etiology/pathogenesis of peritonitis?
A
- rupture of intestine/stomach/uterus/bladder
- puncture by foreign body
- Necrosis of abdominal structure of organ (intussusception/ liver lobe torsion
- contamination during Sx (iatrogenic)
- infectious disease (FIP)
6
Q
what is the definition of iatrogenic?
A
self created (ex: can be from surgery that is not sterile)
7
Q
what is septicemia?
A
blood poisoning
8
Q
what is necrosis?
A
tissue death
9
Q
what are the clinical signs of peritonitis?
A
- abdominal pain (severe), don’t want to move, guard abdominal area by being hunched over
- fever
- anorexia, vomiting, ABD distention
- Toxemia ,septicemia , shock
- colic in horses
cattle (decreased rumination, decreased milk production)
Generalized peritonitis: Very sick animal= death if not treated
localized peritonitis: painful, febrile, ill, recovers with appropriate treatment
10
Q
Dx for peritonitis
A
-hugely increased WBC count (leukocytosis)
- X-rays show glass appearance to abdominal contents, poor organ definition
- peritoneal tap done in standing position put needle in then suck out fluid with syringe if easy to get fluid and there is alot of it, its most likely peritonitis.
- may need to do exploratory surgery ( abdominal surgery) to determine the cause of the peritonitis
11
Q
What is the treatment of peritonitis?
A
- immediate antibiotics/ fluid Tx to combat shock and fight infection
- surgery is often needed to localize and repair cause (if ruptured organ, foreign body, etc)
12
Q
intestines: intussusception what is it and who is it most common in?
A
most common noninfectious intestinal problem in young animals less then 1 year old
13
Q
What is the etiology of intussusception
A
unknown, gut (intestinal) irritability may predispose (internal parasites, Gl dz (Parvo, corona in dog, etc)
14
Q
What is the pathogenesis of intussusception
A
Pathogenesis - gut becomes hyper irritable,
telescopes inside itself causing partial, then full
obstruction
Get intestinal dilatation proximal to obstruction
Subsequent vascular obstruction can lead to necrosis
-> tissue death and toxic shock
15
Q
what are the clinical signs of intussusception?
A
Usually previous Hx of diarrhea, diarrhea
stops ( only have small amount of jelly-like stool)
anorexia
repeated vomiting
dehydration => shock => death over a 1-2 week course of
illness
16
Q
what is the diagnosis of intussusception?
A
C.S., abdominal radiographs, age, palpation of
abdomen (can sometimes feel the intussusception)
17
Q
What is the treatment of intussception?
A
Surgery - support w/ iv fluids, antibiotics
intestinal resection & anastomosis
treat any predisposing cause (parasites, infection, etc)
18
Q
What is the prevention of intussusception?
A
good deworming / vax programs & minimize
digestive upsets
19
Q
What is neonatal scours of calves
A
diarrhea
20
Q
what animal is neonatal scours common in
A
1-10 day old calves. If treated, calf can dehydrate and die
21
Q
What is the etiology of neonatal scours?
A
Etiology - May be primary
enteropathic (toxin producing)
E.coli bacteria, or may also be
concurrent (or primary) viral
(corona/rota viral)
infections
Lack of maternal protective
antibodies predisposes calf to
scours (no colostrum, or dam
(colostrum donor) not exposed to
pathogen)
22
Q
what is the pathogenesis of neonatal scours?
A
- Newborn calf (lamb, kid) exposed to pathogenic
E.coli or rotavirus or coronavirus from environment (manure,
feco-oral transmission)
Pathogen colonizes gut lining (enterocytes) and causes output of
fluids and salts (electrolytes) beyond capacity to resorb (gut
epithelial cells are damaged)=> uncontrolled watery diarrhea=>
severe dehydration, decreased urine output, weakness, death
from dehydration (excess blood potassium stops heart)
Gut epithelial lining takes 3-5 days to heal (new cells replace
damaged cells)
Occasionally can lead to septicemia (blood
poisoning: bacteria/viruses penetrate damaged GI epithelial
cells and get into blood stream (very serious); pathogen can
then infect joints, eye (hypopyon), many tissues
23
Q
what are the clinical signs of neonatal scours?
A
1-10 day old calf, watery diarrhea, dehydration
24
Q
what is the diagnosis of neonatal scours?
A
Can test for pathogens if needed, rarely
done
25
What is the treatment of neonatal scours?
Goal: to keep calf alive and hydrated until new functional GI
cells replace the old damaged cells
Early on - give oral electrolytes (replace fluid/salt loss ) for 24-48
hrs (stops scours) then gradually change back to milk or milk
replacer. If very bad can give iv fluids + antibiotics
26
what is the prevention of neonatal scours
Colostrum, 2 liters in first 2 hours of life.
Clean calving environment.
If severe problem can give rota/corona pre-made antibodies at birth;
can also vaccinate colostrum donor with rota/corona virus and E.coli
vaccine 1 month prior to calving to increase antibody levels in
colostrum.
27
What are the signs of dehydration?
tacky gums, pull up sling and let go if it stay up for a while dehydrated, sunken eyes really deep into head
28
What does colic mean?
Abdominal pain
29
what type of colic makes up most of equine colic?
gastrointestinal
30
where is 80% of equine colic?
large intestine
31
where is 20% of equine colic?
small intestine and stomach
32
Is stomach and small intestine colic or large intestine colic more severe?
small intestine and stomach
33
Why is colic common in horses?
Because of there anatomy
diameter of the gastrointestinal tract ranges from large to small
"hairpin turns" really small diameter
makes obstruction more likely
34
What are the predisposing causes of simple obstruction?
- Equine GI anatomical features
- decreased water intake
- low fiber diet ( horses need fiber since there energy comes from cellulose)
- Increased chunkiness of food (poor teeth so insufficient chewing, poor quality roughage)
- intestinal parasites (roundworms)
- foreign body (sand from putting hay on sand< enteroliths (roll and layer)
35
What are the potential causes of strangulating obstruction?
- twist in intestine, cutting off circulation
- entrapment of intestine in other abdominal structure
- external strangulation of intestine such as with pendunculated lipoma ( fatty tumor benign)
36
What are the clinical signs of equine colic?
- kicking at abdomen
- looking at abdomen
- stretching (relives some of the pressure)
- rolling
- anorexia (food is backed up so don't want to eat)
- not making much manure
- increased heart rate due to stress
- increased respiratory rate due to stress
- fever if strangulation
37
What is the diagnosis of equine colic
- clinical signs
- evaluate severity and likelihood of strangulation or rupture
- pain level (usually given IV inflammation medicine to see if gets rid of pain)
- mucous membrane color, CRT (capillary refill time push of gums release see how long it take to turn back pink should be 1-2 seconds not longer
- rectal palpitation (feel for things that shouldn't be in large intestine
- response to pain medication (if don't respond well more severe)
- peritoneal tap if indicated (look for rupture
38
What is medical treatment for simple obstruction? (equine colic)
- laxatives (eg mineral oil via stomach tube
- stool softener
- pain control drugs (ex: bute)
- iv fluids if needed (to provide more fluid)
- hand walk to enhance GI movement (for hours makes gut move--> NEED TO DO IT)
39
Surgical treatment for strangulating obstruction/rupture
abdominal exploratory to detect and correct problem if possible
40
What does dog sitting in horses indicate?
- gastric stomach colic
- need to get vet to make sure not stomach rupture
41
What is the prevention for equine colic?
- good quality, consistent feed
- reasonable amounts of grain, multiple small meals, regular time schedule
- high quality hay in reasonable amounts (roughage/fiber
- always have water available
42
When is most water consumed in horses?
80% of water consumed is consumed within 2 hours of eating
43
What type of disease is Lyme diseases an example of?
multi-systemic disease which means it effects multiple body systems
44
What is the causative agent of Lyme disease (spelling counts)
Borrelia Burgdorferi (gram negative spirochetal bacterium)
45
Why is Borrelia burgdorferi difficult to culture?
- requires enriched liquid BSK media
- microaerophilic conditions (does not like too much air)
- take a long time (sometimes up to a month
46
What is Borrelia burgdorferi sensitive to?
- dehydration
- heat
- does not survive freely in the environment
47
What is the vector for Lyme disease?
Ixodes specie of ticks
48
How long is the lifecycle for a tick?
2 years, 3 stages
49
can BB be tranovarial transmitted?
no if a mother tick is infected with BB and lays eggs the eggs will not be infected.
50
What are the common reservoir hosts of borellia burgdorferi?
While footed mice (keeps the infection going)
White tail deer (place for adult female ticks to mate)
51
How long do ticks need to feed before transmitting BB to the host?
12+ hours
52
Larva stage (what season, how tall can it crawl, what hosts)
- summer
- can crawl one inch on vegetation
- takes blood meal from either bird or rodent then mults to nymph
53
Nymph stage ( what season, how tall can it crawl, what host)
- spring
- can climb vegetation 6 inches
- take blood meal if infected as larva they transmit Lyme disease to host
- have the chance to be get BB from blood meal
- mult into adult
- people, foxes, maybe deer
54
Adult stage (what season, how tall can it crawl, what host)
- Fall
- can climb about a foot up vegetation
- stays till male inseminates
- if don't get meal in the fall will quest for meal in the spring
- eggs laid in the spring
- sometimes people, but mainly deer and animals like foxes
55
Do males ticks suck blood?
No
56
What ticks are the most common in southern New England
Ixodes scapulars (deer tick) --> may spread Lyme disease
Dermacentor Variabilis (dog tick --> unlikely to spread Lyme disease
57
How to tell if a tick is a Deer tick (common vector of Lyme disease)
- all brown
- long mouth parts
- smaller in size then dog ticks
- blood filled adult ticks may be fairly large
58
How to tell if a tick is a Dog tick (not likely to transmit Lyme disease)
- brown body with white stripes near the mouth parts (female)
- brown body with white stripes on back (male)
- larger than deer ticks
59
What is the pathogenesis for Lyme disease?
Uninfected tick bites (usually reservoir, such as
infected mouse) host, ingests blood containing Bb
Borrelia burgdorferi (Bb) present within the
infected tick multiply and modify their surface
proteins, then migrate to the tick’s salivary glands
Infected tick bites the next host, and Bb secreted
by tick into skin; local infection follows
Takes 12-24 hours of feeding before Bb is
transmitted
60
Who can get a skin rash from tick infected with BB?
- humans
- cattle
- rabbits
61
Who cannot get a skin rash from tick infected with BB?
- Dogs
-Cats
- Horses
62
Where may BB persist?
- joints, central nervous system (can cross blood brain barrier, connective tissue)
63
What are the clinical signs of Lyme disease? (human)
Early skin rash (~70% of people)
* Early flu like symptoms (fever, aching joints, headache,
fatigue) (first month after infection)
* Neurological involvement (peripheral neuropathies;
cognitive dysfunction) (1-6 months after infection)
* Later symptoms include arthritis (joint inflammation) and
arthralgia (joint pain) (months to years after infection)
* Diagnosis can be difficult- non-specific symptoms and
suboptimal dx tests
* Treatment is most successful in early stages of disease
64
clinical disease of Lyme disease dogs
Acute onset of systemic febrile disease with
whole body weakness, malaise, depression
(dishrag)
– Less severe waxing and waning lameness,
often in carpus or hock, with or without obvious
swelling; usually also has low grade fever (102.5
F); can look like injury, but no radiographic
changes
– Some breeds (retrievers, etc) may rarely develop
renal disease, renal failure
– Only ~ 5% of infected dogs develop clinical
disease
65
Clinical disease of Lyme disease horses?
Clinical signs in approximately 9% of infected horses,
others subclinical infection
* Primary clinical complaint: shifting large joint lameness (eg
not usually in the hoof)
* Behavior change (crabby, unwilling to work) common
clinical sign; Sensitivity to touch, saddle, other stimuli
* Need to rule out other causes of lameness (differential
diagnosis)
* Negative serology (Bb antibody testing) can help rule out
Lyme disease in horses; positive serology supports a
clinical diagnosis
66
What is the diagnosis for Lyme disease?
* Symptoms (clinical signs)
* History of tick exposure (geographical likelihood)
* Differential diagnosis (rule out other diseases
with similar symptoms/clinical signs)
* Laboratory testing (to support or minimize
likelihood of Lyme disease dx)
* Response to treatment (clinical and laboratory)
67
Laboratory testing for Lyme disease
Serological (antibody) Tests (Elisa, IFA, Western Blot)
– Antibody titers (levels) are often not detectable until 3-4 weeks
after infection (tick bite)
* Antigen (Borrelia burgdorferi bacteria) Tests (Specialized culture
to grow Bb in the lab), PCR (polymerase chain reaction) to detect
DNA of B.burgdorferi))
– Limitations (difficult to culture, Bb not present in blood for long
so PCR of blood of limited value)
* Magnitude of serological response (eg how high the antibody titer
is) does not correlate with degree of illness
* Domestic animals often have subclinical infection (eg infected with
Bb but do not show clinical disease)
68
Treatment for Lyme disease
* Treatment (certain antibiotics) is most effective if given early
(first month) in course of disease
* Doxycycline family antibiotic TX most common, 3-4 weeks most
common (other regimens possible)
* Chronic / recurrent Bb infection: other antibiotics may be used:
treatment length may be extended
* Jarrish Herxheimer reaction can occur (<5%) and may
precipitate temporary worsening of CS for a few days after start
of treatment –careful of laminitis in horses, check feet ( do not take off of antibiotics give antinflammatories)
* Humans: some individuals experience post-Lyme syndrome:
immune mediated inflammation after resolution of infection
69
What is the prevention for Lyme disease?
**Daily tick check; prompt removal**
* Wash tick removal site with antiseptic; apply bandaid and
antibiotic or antiseptic ointment
* Test ticks for Bb if desired (place in ziplock, submit to
CVMDL for tick borne disease testing)
* Minimize tick habitat: mow yards, pastures, rake debris
around stone walls, rodent control (ticks need moisture and
reservoir hosts)
* Don’t feed deer
* Use tick repellents when in tick-rich environments
- knowledge of the vector and its lifecycle
- tick repellents humans (feet) animals (permethrin)
- for people permethrin can only be used on clothing not skin
70
What is the etiology of rabies?
Rhabdovirus that causes fatal encephalitis. all mammals are susceptible. Birds reptiles and amphibians are not susceptible
71
what are the most common species to transmit rabies in North America?
Fox, Bat, Skunk, and racoon
72
what is the species most likely to transmit rabies globally?
dog
73
what is the most risky species to infect you with rabies and why?
bat due to being able to bite you while your sleeping you wouldn't feel it or see it so most likely would not known you have been exposed
74
What is the cycle for rabies ( important memorize it)
- animal with clinical signs of rabies (shedding virus in saliva) bites another animal, An animal bit is not infectious until the animal has rabies encephalitis
- Virus incubates at bite wound for weeks to months, and then travels via peripheral nerves to the spinal cord then to the brain
- rabies virus in the brain causes encephalitis, clinical signs, and death in 10-14 days. the virus infects cranial nerves to the salivary glands and is shed in saliva
75
When does rabies enter the saliva?
the virus only enters the saliva during the last stage of rabies infection, when the animal has virus infection in the brain (rabies encephalitis) and is showing clinical disease
76
What is the incubation period for rabies?
the incubation period (time between rabies infected bite wound and development of clinical signs is variable, from 1-6 months. It is shorter if the wound is closer to the head (brain) as less time is needed for the virus to travel up peripheral nerves
longer incubation period for wounds near the toes
77
What are the clinical signs of rabies?
- encephalitis
- fever, behavior change (aggression or lethargy)
- may act blind
- wild animals may act friendly
- drooling due to pharyngeal nerve paralysis (can't swallow)
- anorexia and often can't drink
- will often bite many rohr animals, spreading infection
- death within 7-14 days o the onset of clinical signs
78
What is the diagnosis for rabies?
no antemortem (before death) diagnosis
- post mortem diagnosis: brain smear is fixed and stated wit anti-virus fluorescent antibody (approximately 2 hours)
- should do post mortem test if animal you think has rabies is dead
- histologically negri bodies (inclusion bodies) can be seen in neurons infected with rabies virus. This requires brain tissue formalin fixation (takes 24-48 hours) then examination by. pathologist (a total of 2-3 days for results)
79
What is the treatment for rabies?
-there is no treatment one the disease enters the CNS
- post exposure prophylaxis available for humans not animals ( you are able to have prevention after being exposed due to the incubation period being so Long)
- For prophylaxis
* A LARGE DOSE OF PREMADE ANTI-RABIES ANTIBODIES (GLOBULIN)(given by bite)
* A SERIES OF RABIES VACCINATIONS (USUALLY
5) TO STIMULATE THE PERSON TO PRODUCE
THEIR OWN ANTI-RABIES ANTIBODIES
* POST EXPOSURE PROPHYLAXIS WORKS BECAUSE THERE IS SUFFICIENT TIME FOR THE PERSON TO MAKE ANTIBODIES WHILE THE
VIRUS IS INCUBATING AT THE WOUND SITE (EG BEFORE IT REACHES THE CNS). THIS TREATMENT IS VERY EFFECTIVE, BUT EXPENSIVE.
80
What is the prevention for rabies?
- pre exposure vaccination required by law on all dogs and cats 3 months of Age and older in CT
- pre exposure vaccination is also available for at risk people ( ex: veterinarians, animal control officers, farmers, traveling to places with bad control, spulnkers ...)
It is important to keep record of rabies vaccination just incase your animal bites someone also need to keep them current
81
What animals are licensed rabies vaccines available for?
- dogs
- cats
- horses
-cattle
- sheep
- ferrets
but only required for dogs and cats in CT
82
what animals can get the rabies vaccine off license?
- goats
- swine
- etc
83
how often do dogs and cats need to get rabies prevention vaccine?
first vaccine given at 3 months which is good for one year then the boosters after that are good for 3 years
84
how often do horses, cattle, and sheep get rabies prevention vaccine?
they get boosters annually
85
What does CT law say if an animal who was not vaccinated for rabies bites someone?
* CT LAW SAYS: IF A DOMESTIC ANIMAL BITES SOMEONE, THEY ARE QUARANTINED AT THE
HOME FOR 2 WEEKS; THE ANIMAL CONTROL OFFICER WILL CHECK THE ANIMAL TO MAKE
SURE IT IS ALIVE AT THE END OF 2 WEEKS. IF THE ANIMAL IS STILL ALIVE, IT COULD NOT HAVE
BEEN SHEDDING RABIES VIRUS IN THE SALIVA AT THE TIME OF THE BITE, AND NO FURTHER
ACTION IS REQUIRED.
* IF THE ANIMAL DIES FOR ANY REASON DURING THE QUARANTINE PERIOD, ITS BRAIN MUST BE
TESTED FOR RABIES. (IF THIS WAS POSITIVE, THE PERSON BITTEN WOULD UNDERGO POST
EXPOSURE PROPHYLAXIS).
86
What should you do if an animal suspected to have rabies bites a domestic animal that is vaccinated for rabies?
THE ANIMAL IS WASHED WITH DISINFECTANT SOAP
(USE GLOVES), THE WOUND AREA IS CLEANED BY THE VETERINARIAN (USE GLOVES), AND THE
ANIMAL RECEIVES A RABIES VACCINE BOOSTER.
87
What does CT law say if an unvaccinated animal is bitten by an animal suspected of having rabies?
* IF AN UNVACCINATED (OR NOT CURRENTLY RABIES VACCINATED) ANIMAL IS
BITTEN BY A RABIES SUSPECT ANIMAL (EG ABNORMALLY ACTING RACCOON
BITES YOUR UNVACCINATED DOG OR CAT), THAT ANIMAL (THE BITTEN DOG OR
CAT) IS REQUIRED BY LAW TO BE STRICTLY QUARANTINED (AT AN APPROVED
FACILITY, AT THE OWNER’S EXPENSE) FOR 6 MONTHS (THE LONGEST
INCUBATION PERIOD) OR EUTHANIZED.
* IF THE ANIMAL THAT BIT THE DOMESTIC ANIMAL CAN BE TESTED FOR RABIES
(EG THE RACCOON IS KILLED IN ITS FIGHT WITH YOUR DOG, YOU CAREFULLY
PUT IT IN A BAG (DO NOT TOUCH) AND BRING TO THE LAB (CVMDL IN PVS OR
CT STATE VIROLOGY LAB) FOR RABIES TESTING), A POSITIVE FA TEST WOULD
NECESSITATE THE 6 MONTH QUARANTINE OR EUTHANASIA RULE. IF THE FA
TEST WAS NEGATIVE, THE DOMESTIC ANIMAL WOULD NOT NEED TO BE
QUARANTINED /EUTHANIZED.
* TAKE HOME MESSAGE: KEEP RABIES VACCINATIONS CURRENT, EVEN IF ANIMAL
STAYS INDOORS; KEEP RECORDS OF RABIES VACCINATION.
88
What is the Etiological agent of brucellosis?
Brucella SPP bacteria
89
what are the characteristics of Brucella SPP bacteria
- intracellular bacteria
- can survive in cool, moist environments for months
- direct sunlight kills them in a few hours
- zoonotic disease
- world-wide distribution
90
What are the routes of transmission for Brucellosis?
-oral, milk, direct exposure via skin/ mucous membranes, transplacental, venereal
- most commonly transmitted through contact with infected aborted fetus
91
What is the most common way brucellosis is transmitted to humans in the United States?
raw milk
92
what is a select agent? Is brucella SPP bacteria a select agent?
a select agent is a infectious agent that has potential to be a bioterrorist
yes
93
B. abortus
cattle
94
B. melitensis
goats, sheep, camels
95
B.Suis
pigs
96
B. canis
dogs
97
B. Ovis
sheep and goats
98
What is the incubations period for brucellosis?
2 weeks from infection until clinical disease but many be months
99
What is the typical pathogenesis? Brucellious
TYPICALLY, COW INGESTS ORGANISM, BECOMES BACTEREMIC (BACTERIA IN BLOOD) -
BACTERIA SETTLE IN REGIONAL LYMPH NODES (SUPRAMAMMARY LN IN PARTICULAR), OFTEN
STAYS DORMANT UNTIL THIRD TRIMESTER OF PREGNANCY WHEN ERYTHRATOL FROM
PLACENTA INCREASES AND CAUSES INCREASED GROWTH OF ORGANISM
THEN ORGANISM MOVES FROM LYMPH NODES TO UTERUS - PLACENTA – FETUS, CAUSING
ABORTION
Also moves to mammary gland and is shed in milk
100
What is the diagnosis for Brucellosis?
blood angulation test (AB test) or ELSIA (also milk agglutination test for dairy cows)
used to screen diary cows if positive milk test from milk tank need to test each cow individually slaughter the infected ones
101
What is the treatment for Brucellosis in cows?
slaughter
102
What is the treatment for brucellosis in small animals and humans?
tetracycline family antibiotics usually doxycycline
103
What is clinical disease in Brucellosis?
-clinical signs involve reproductive system
- abortion occurs with variable incubation period usually in late gestation
- stillborn or weak offspring, retained placenta
- males have orchitis (testicular inflammation) and infertility
- even without clinical disease infected animals can be a source of infection for other animals
- shed in reproductive fluid and milk in females and semen and accessory fluids in males
104
What is the diagnosis for brucellosis?
- Blood agglutination tests or ELISA
- mandatory screening of milk, blood
- testing for blood antibodies to brucellosis in livestock going to slaughter if positive found traceback to herd is done all are tested infected ones are slaughtered
- serology is the most common diagnostic test culture is less common now
105
what is the treatment for Brucellosis?
O TREATMENT ALLOWED IN CATTLE (TEST AND SLAUGHTER PROGRAM)
* DOGS: NEUTER ANIMAL; CAN TREAT WITH TETRACYCLINES
* OTHER SPECIES: VARIES WITH USE/VALUE OF THE ANIMAL: UNLIKELY TO
BE USEFUL AS BREEDING ANIMAL AFTER THIS INFECTION
* VACCINE NO LONGER USED IN CALVES IN BRUCELLA-FREE STATES; NOT
AVAILABLE FOR OTHER SPECIES
* HUMAN: TETRACYCLINES (DRINK PASTEURIZED MILK ONLY!)
106
What are the zoonotic aspects of brucellosis?
* UNDULANT FEVER
* ESPECIALLY NASTY DISEASE WITH B.MELITENSIS
* SYMPTOMS IN HUMANS:
* WAXING AND WANING FEVER, ACHY JOINTS, MALAISE, RARELY CAN CAUSE
ABORTION
* TREATMENT WITH DOXYCYCLINE
* PREVENTION: DO NOT CONSUME RAW DAIRY PRODUCTS; AVOID CONTACT
WITH ABORTED FETUSES; USE PPE (PERSONAL PROTECTIVE EQUIPMENT)
107
what is the definition of Enzootic?
prevailing in animals at a low level
108
Brucellosis in Yellowstone (how much seropositive?, bison management plan, disease transmission)
-up to 50% seropositive
Bison management plan
- maintain a wild free- ranging bison population
- minimize risk of transmission to domestic cattle
disease transmission
- contaminated birthing fluids, soil
109
What are the clinical signs of brucellosis in wildlife?
Elk
- abortion
- no retained placenta, infertility
Moose
- debilitation, death
predators act as vectors
- coyotes, crows, vultures, and bears (eat dead fetuses then spread it)
110
What is colibacillosis?
Any localized of systemic infection caused by entirely or partly by Escherichia coil
111
What is the occurrence of colibacillosis
All type and age groups of poultry, other birds and many kinds of mammals
Most reported outbreaks in poultry have been in chickens, turkeys, and ducks
Outbreaks due to low standard sanitation, poor environmental conditions
Immunosuppressive diseases
Most frequent in youngnger birds
Common throughout the world
112
What is the etiology of colibacillosis
E.coli
3 stereotypes are frequently identified in disease outbreaks
1:k1, 2:k2, and 78:k80(B)
113
What are a couple diseases that colibacillosis can cause?
peritonitis, airsac disease, synovitis, and avian cellulitis (muscle infection)
114
What are the clinical signs for colibacillosis?
airsaculitis, enteritis, synovitis, and pericarditis
115
what is coccidiosis
infection of the gastrointestinal tract by protozoal parasite
116
What is the pathogenesis of coccidiosis?
ingestion of the infective agent oocyst which releases sporozoites that invade the intestinal epithelium destroying the intestinal mucosa
117
What is the Etiologic agent of coccidiosis?
Eimeria spp and Isospora spp (more common)
118
What are the clinical signs of coccidiosis?
- reduced food and water consumption
- lethargy
- rumpled, puffed up feathers
- bloody, runny droppings to diarrhea
- high mortality events
119
what type of disease is coccidiosis
protozoal disease
120
what is coccidiosis characterized by
diarrhea and enteritis
121
What does coccidiosis primarily effect
gastrointestinal tract beside geese which affects renal (kidneys)
122
What is the diagnosis of coccidiosis
- clinical signs
- fecal analysis under microscope
- necropsy in high mortality events
123
what is the prevention for coccidiosis
- limited exposure to oocysts in litter to develop immunity
- anticoccidials in the feed (amprolium or monensin)
124
What is the treatment for coccidiosis
anticoccidial drugs such as ionophores in feed and water
housing on wire which separates birds from droppings
vaccination ( low doses of live oocysts)
125
what is the pathogenesis of mareks disease
highly infectious viral infection which targets feather follicles and immune cells resulting in both severe immunosuppression and lymphoma formation
126
what is the etiology of mareks disease
Gallid Herpesvirus-2
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What are the clinical signs for mareks disease
- lymphoid neoplasms in the skin and internal organ
- changes to the color and shape of iris. eye is grey.
- neural form: transiet paralysis and ataxia to flaccid paralysis (range paralysis)
- sudden death
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What is the diagnosis for mareks disease?
- history of clinical signs
- postmortem examination
- virus isolation, PCR
- immunohistochemsitry
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What is the prevention for mareks disease?
- known infected premises should be depopulated and should be cleaned and disinfected
- left vacant for a few weeks
- all in all out brooding system
- vaccinate day old chicks at hatchery
- in ovo vaccination
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What is new castle disease?
fatal virus disease affecting the respiratory, nervous, and digestive system
worldwide and can affect all species of birds including those who are vaccinated
spreads through contact or body fluids from infected birds
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What is the etiology of new castle disease?
paramyxovirus
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what are the clinical signs of Newcastle disease?
- sudden death and increased death loss in flock
- sneezing, gasping for air, nasal discharge, coughing
- greenish watery diarrhea
- decreased activity, tremors, drooping wings, twisting of head and neck, circling, complete stiffness
- swelling around the eyes and neck
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what is the diagnosis of new castle disease?
- history of clinical signs
- definitive diagnosis
- RT-PCR (sampling intestine or trachea)
- ELSIA
- serology
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What is the prevention for new castle
- vaccinate + biosecurity
- permit only essential workers and vehicles on premises
- clean and disinfect all vehicles
- provide clean clothing and disinfection to employees
- all in all out flock management
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What is the etiology of avian influenza?
- orthomyxoviridae
- RNA viruses, medium sized, pleomorphic
- 3 types A,B, and C
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What type of influenzas can humans get
A,B, and C
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What species get Type A influenza?
humans, swine, horses, mink, seals, and whales
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What is avian influenza?
* Disease of birds caused by influenza Type A viruses
* This virus has been isolated from >100 species of birds, worldwide
* Wild birds, in particular waterfowl like duck are considered a reservoir
host
* These birds develop mild or no signs of disease (asymptomatic carriers)
* Influenza A viruses are categorized as low pathogenic (LPAI) or high
pathogenic (HPAI)
* Based off the molecular characteristics of the virus and its ability to cause
mortality in experimental settings
* Based on two groups of viral proteins: hemagglutinin (H proteins) and
neuraminidase (N protein)
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How is avian influenza transmitted
* Infected birds shed virus in saliva, nasal discharge, feces
* HPAI can spread rapidly from farm to farm
* Migratory birds, particularly waterfowl, can transmit virus to
poultry
* The virus remains viable in the environment for long periods,
especially at low ambient temperatures and it can survive freezing
* LPAI can mutate into a high-pathogenicity strain
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What are the clinical signs of avian influenza?
* LPAI: no signs to mild signs of lethargy, ruffled feathers, drop in egg
production
* HPAI: High mortality, sudden death
* swelling of head, comb, eyelids
* Lethargy and inappetence
* Nasal discharge, coughing, sneezing
* Diarrhea
* Decreased egg production or abnormal, soft-shelled or misshapen eggs
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what is osteoporosis ( etiology, and pathogenesis)
* Also called Cage Layer Fatigue
* Etiology/Cause: Inadequate dietary
calcium, phosphorus, vitamin D at
and around the time of egg
production
* Pathogenesis: Slow, ongoing loss of
calcium stored in the skeleton
which occurs during the laying
period in addition to lack of
mechanical stress on the bones in
hens housed in cages.
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What are the clinical signs, diagnosis, and treatment/ prevention of nutritional disease
* Clinical Signs: Leg weakness, vertebral fractures, posterior paralysis, sudden
death
* Diagnosis: History, clinical signs, and response to treatment
* Treatment/Prevention: Supplement calcium (oyster shell)
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What is everything about hemorrhagic liver syndrome
* Hemorrhagic Liver Syndrome
* Also called fatty liver hemorrhagic
syndrome
* Most common in birds with an
increased energy intake and limited
exercise. Common in egg-laying hens
* Pathogenesis: Estrogen levels
increase during egg production
resulting in lipid (fat) accumulation in
the liver
* Clinical Signs: Often the only sign is sudden
death
* Diagnosis: Postmortem examination
* Treatment/Prevention:
* Monitor body weight and daily feed intake
* Allowing access to areas for exercise
* Substituting fat sources of energy with
carbohydrates
* Selenium supplementation
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What is the etiology of tetanus?
clostridium tetani: bacteria that produces toxin toxic to CNS
looks like chicken wing under microscope
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What is the pathophysiology of tetanus
Most common route of infection is through wound contamination with soil (containing C. tetani spores), including umbilical stump.
C.tetani inoculated into deep wound (frequently puncture wound), with subsequent wound closure, providing an anaerobic environment.
In the anaerobic environment the bacteria multiply, produce toxin
Toxin enters the peripheral nerves and travels via nerves to the CNS (generally spinal cord) where it inhibits action of inhibitory neurons. By abolishing inhibitory modulation of motor neurons in the spinal cord, motor neurons have uncontrolled transmission of stimulatory motor impulses throughout voluntary nervous system. Excessive muscle contraction results.
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Tetanospasmin (tetanus toxin)
INTERFERS WITH RELEASE OF INHIBITORY NEURO-TRANSMITTERS & CAUSE SPASMODIC,TONIC CONTRACTIONS OF VOLUNTARY MUSCLES
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What is the mechanism of the toxin that causes tetanus
TETANUS TOXIN ENTERS PERIPHERAL NERVES & TRAVELS TO SPINAL CORD BY RETROAXONAL TRANSPORT. THERE TOXIN BLOCKS INHIBITORY NERVE NETWORK* & RESULT IN UNCONTROLLED STIMULATORY MOTOR IMPULSES & EXCESSIVE MUSCLE CONTRACTION
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What would case of no history of wound be due to (tetanus)
Case with no history of previous wound may be due to:
Wound too small to notice.
Wound and disease onset too far apart to associate the two.
Other species (non-human/horse): less severe clinical disease
Humans: lockjaw
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What are the clinical signs In horses for tetanus
Incubation period three days to one month and occasionally up to four months.
Inability to retract third eyelid (flashing third eyelid) (pathognomonic) and reluctance to feed off the ground.
Stiffness of muscles begins and spreads to the head making eating difficult.
The tail becomes stiff and extended and "saw horse" attitude develops.
The horse goes down, lapses into a coma and finally death occurs.
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what is the definition of pathognomonic
a clinical sign that is unique to a specific disease
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What is the treatment for tetanus in a horse
Antisera - doubtful value once toxin is in CNS
Clean wound if possible (get air in wound) (reduces bacterial growth).
Tranquilizers and muscle relaxants
Antibiotics especially penicillin may help early in disease.
(Can Tx in dog (less susceptible)
Quiet, darkened stall.
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What is the prophylaxis for tetanus
Tetanus toxoid: initially two shots four to six weeks apart with one annual booster. Vaccinated animals that suffer puncture or deep wounds should be given additional toxoid.
Mares - antibodies given to foals thru colostrum and passive immunity is superior to that gained by tetanus antitoxin at birth. Therefore, give dam toxoid during last month of pregnancy. Actively immunize foals at four to six months.
Tetanus Antitoxin following injury to non-vaccinated horse.
Tetanus Antitoxin and toxoid can be administered at same time to unvaccinated animal at risk, which is better than using Tetanus Antitoxin alone. Different sites. Don't forget second toxoid in one month. (lambs at castration/tail docking)
Humans: tetanus toxoid given in combination with other vaccines; booster q. ~10 years, or after potential exposure event
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What is the difference between tetanus toxoid and tetanus antitoxin
antitoxin is premade antibodies usually given to foals that didn't get colostrum
toxoid is a vaccine that allow them to build there own antibodies to toxin
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What is the etiology of tuberculosis
infectious dISEASE of all vertebrate species caused by mycobacterium spp BACTERIA
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What are the 3 main types of tuberculosis
M.tuberculosis
M.Bovis
M.Avium
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M.Tuberculosis
Humans
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M.Bovis
cattle
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M.Avium
Birds
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can all 3 main types of tuberculosis spread amoung all species
yes
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What is the pathogenesis of tuberculosis
primary focus of bacteria in lungs in mammals (digestive tract in Birds) - lymphatic drainage brings mycobacteria to regional lymph nodes and spreads to other places.
If bacteria get into the blood stream , they can seed many organs.
Mycobacteria can form walled off areas of infection - called NODULES - that can stay inactive for years, or can open and serve as a source of bacteria that spread throughout the body.
Nodules in lungs can look like tumors on XR.
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What is the transmission of tuberculosis?
TB typically spreads by coughing up organism followed by aerosol transmission, or via infected Sputum contamination of water or food
(man-spittoon-dog-child)
in cattle, Cough, swallow infectious sputum , bacteria in digestive tract excreted with manure, and can contaminate pasture or feedstuffs. contaminated food then ingested by another animal.
Organisms are also shed in milk of infected animals.
Organisms resistant to chemical treatments and drying and can live up to 3 years in the environment.
They are killed by pasteurization
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What are the clinical signs of Tuberculosis in animals?
- chronic cough
- progressive wasting in spite of good care (get really skinny bad coat)
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What is the diagnosis for Tuberculosis in animals?
- clinical signs
- TB test (dairy cattle routine)(every 3 years screening test is performed in dairy cattle)
- intradermal inoculation with tuberculin (cell wall preparation) recheck in 72 hours, look for swelling, inflammation which would indicate previous exposure to mycobacteria
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What is the diagnosis for tuberculosis in humans?
PPD screening test
- if positive PPD test follow up with chest X-ray
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What is latent tuberculosis?
- no symptoms
- does not feel Sick
- can't spread TB to others
- Positive skin test
- normal xray
- needs treatment for late TB infection to prevent TB disease
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What are the clinical signs for a person with tuberculosis?
- bad cough 3 weeks or longer
- pain in chest
- coughing. up blood or sputum
- weakness or fatigue
- weight loss
- no appetite
- chills
- fever
- sweating at night
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What are the characteristics for a person with TB disease?
- usually feels sick
-may spread TB bacteria to others
- may have a abnormal chest x0ray, or positive septum smear or culture
- needs treatment to treat TB disease
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What is the treatment for tuberculosis?
- In cattle test and slaughter
- humans and pets a drug isonicotinic acid (25% reoccurrence after treatment)
- other drugs available for humans- problem with multi drug resistant TB
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What is the prevention for tuberculosis?
- pasteurized milk
- federal test and slaughter cattle program
- no spitting
TB testing PPD screening test
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