Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Clinical Sciences Exam 4 > Neonatal D+: Herd Approach > Flashcards

Neonatal D+: Herd Approach Flashcards

1
Q

what D+ agents are ENDEMIC on most livestock operations?

A
  1. ETEC
  2. crypto
  3. coronavirus
  4. rotavirus

these diseases are expected to occur at some low rate (3-5% of neonatal population)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

T/F: fecal shedding of rota and corona by dams increases as parturition approaches

A

true: creates a lower immune system and thus shedding increases from immunosuppression of pregnancy, and inexperienced immune system of younger dams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what factor greatly influences outcome of D+ cases?

A

dose of infectious agents (how many viral particles, cells etc)
neonates are biological amplifiers!! shed billions of bugs!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

IgG in colostrum must be ingested when?

A

ideally 1st 6 hours of life, but definitely the first 24 hours to be absorbed
the first cells that can engulf things are rapidly turned over

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

factors that can influence successful passive transfer

A
  • mothering instinct of dam
  • vigor of the calf and dam after delivery
  • solid bond with newborn
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is one of the first questions you should be asking about a neonate with D+

A

did it get colostral antibodies? failure of passive transfer?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

T/F: all neonates are born hypogammaglobulinemic

A

true: placenta doesn’t allow maternal antibodies to move through fetus during gestation!
immunologically naaive and rely on maternal ab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

when you correct a dystocia, when are you finished with the job?

A

when you ensure that the baby either nurses or is hand-fed! hand fed allows you to know amount that you got

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

why are calves born to 1st-time mothers more at risk of issues

A
  • first time moms not as attentive
  • first time moms have more dystocia problems
  • tired mom = weak/hypoxic neonate, delayed colostrum indigestion
    depending on fetal position and posture in dystocia, pressure can induce swelling of face, and once born the calf may not be able to suckle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

T/F: neonates born to 1st-time mothers have a higher risk of developing infectious diarrhea

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

when should you test serum or plasma of neonate after passive transfer done?

A

30-48 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

gut allows immunoglobulins to be absorbed up until ________

A

24-30 hours when gut closure takes place

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

T/F: it is not okay to feed frozen colostrum to a calf

A

false- this is fine as a lot of dams on larger operations will need to do this as the dam will be milked out right after giving birth
frozen colostrum from another dam is ok to give prompt delivery- that is what is important

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

problems with colostral intake with dairy goats and cows

A
  • not often selected for maternal instincts
  • large udders; hard for neonate to latch
  • large teats
    these animals are kept in intensive operations to produce a lot of milk and not motherly skills
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how can humans mess up passive transfer?

A
  • colotrum itself can transmit pathogens
  • colostrum and milk are excellent culture media
  • dirty environment/tools are bad!
  • letting colostrum sit at room temp is BAD

need thorough cleaning and chemical disinfection to reduce colostral infx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the target IgG levels for foals/crias?

A
  • > 800 target for foals
    1000 for crias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

why might GGT be high in a calf? should you be concerned about liver disease?

A

no- serum GGT is often secreted from mammary alveolar secretory cells during colostrum formation and GGT is readily absorbed before the gut closes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the target IgG for calves/lambs/kids?

A

want >5.5 g/dL correlates to >1000 mg/dL of IgG (using less expensive serum of total protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is SRID? what is it used for?

A

Single radial immunodiffusion: quantitatively measures serum IgG
for foals and crias measuring IgG is best means of assessing passive transfer status

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

T/F: it is okay to use serum GGT as an assessment of passive transfer success

A

no- no advantage compared to other methods and is less accurate and difficult to do in field. just expect to see an increase after neonate gets colostrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

in the absence of dehydration, what is good to use to test passive transfer in ruminants?

A

total serum solids/serum protein
>5.5g/dL = successful passive transfer
values less than 4.5 are not good
would recommend plasma transfusion and monitoring approach
these apply to the healthy hydrated neonate! dehydration will INCREASE the total protein concentration in serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

will dehydration increase or decrease total protein concentration in serum?

A

INCREASE!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

T/F: serum total protein measurement is good for assessment of passive transfer in foals and crias

A

false- you need to measure the IgG concentration specifically!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how can you increase antibodies in colostrum?

A
  1. vaccinate pregnant dams with ETEC and rota/corona killed vaccines, clostridial toxoids
    ^ effective against ETEC bc abs are in gut near time of infx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
why is vaccinating dams with ETEC important for neonatal success?
colostral ab will be at the gut mucosa during the first few days of life; and this is when ETEC can really cause infection - anti pilus abs can block pilus attachment * if infectious dose is super high, the immunity can be overwhelmed and disease may still occur
18
19
what kinds of vaccines are used for clostridium type C and D
toxoids: inactivated exotoxin to protect against exotoxins issue: large meals of substrate can provide growth media: can't just vaccinate and walk away
19
are rota/corona vaccines effective?
not really- colostral antibodies will wane in the neonate before the susceptibility period ends. also strains on farm may not = strains in vaccine!
20
are cryptosporidium vaccines effective
there are no vaccines present
21
T/F: all immunity is finite and can be overwhelmed by large infectious dose of agent
true
22
T/F: vaccination used in scours management has a great cure rate
false- vaccines can be used as a tool in scours management, but is NOT a cure-all!
23
T/F: what's on the udder gets into the baby
true!
24
what is the single most important factor in environmental management for neonates raised with their dams?
UDDER HYGIENEEEEE
25
what is the first thing in a newborn's mouth
what's pasted to the outside of the teat!
26
why is the maternity area important
- 1st extra-uterine environment encountered by the neonate - cleanliness super important since the neonate is born agammaglobulinemic
26
how can you check the cleanliness of the maternity pen?
drop to your knees a few times throughout the area; if they come up wet/manurey the same will be for udder and neonate!
26
if neonates become ill the first week of life, what should your focus be on?
1. passive transfer (colostrum) 2. maternity area hygiene
27
if neonates are getting sick in the first week of life, when were they infected?
inoculated/infected very early in life- immediately start thinking about passive transfer status and maternity area hygiene
28
if you have a neonatal D+ case, what is your hygiene protocol
- isolate IMMEDIATELY - maternity area does NOT equal sick ward - handle healthy neonates FIRST, sick ones LAST - personnel for either healthy or sick, no crossover allowed
28
what are circumstances for animals to congregate? how can this lead to issues?
- pastured animals will congregate to certain areas and amplify udder contamination during storms - open sheds and appropriate bedding reduce stress on neonates - shelter overuse can lead to hygiene problems - moist environments: concentrates fecal pathogens shed
29
how can you prevent congregation?
- rotate or increase # of bedding sites - rotate or increase # of feeding sites - clean and re-bed shelters - disperse mom-baby pairs to limit pathogen accumulation
29
how much clean pasture should each cow-calf pair have?
1000 square feet
30
scour risk is proportional to
stocking density! (# animals / area ) x time (amount of time exposed to stocking density)
31
epidemiological factors of infectious neonatal D+ (exhaustive list)
– Species involved – Timing of exposure – Magnitude of exposure – Parity of dams – Colostrum feeding / nursing – Birthing pattern (number born over a given timespan) – Climatic conditions (e.g.snow/rainfall) – Congregation activity – Facilities – Bedding/cleaning – Vaccination efficacy – Personnel (caretakers) – Out-of-herd contacts (fenceline)
32
sporadic infx D+ diseases of neonates
- wider age range (neonate to adult) - greater case fatality rate even w good treatment - less often present as endemics on a farm, more severe
33
what are examples of sporadic infectious diarrhea agents of neonates?
1. clostridiosis (clostridial enteritis, enterotoxemia) 2. salmonellosis (can be endemic, but severe signs with clinical disease) 3. BVDV: bovine viral diarrhea virus
34
clostridial enteritis
- enterotoxemia, clostridiosis - C. perfringens type C or D - feed change: excessive intake of starch or soluble protein - range animals feeding interrupted by storms - "hunker down" udder fills and hungry baby gets a big milk meal
35
T/F: clostridium perfringens exists in the GI tract and environment of most mammals
true
36
what is the pivotal event in the onset of enterotoxemia?
overeating of carbohydrate or protein - large volumes of milk or replacer - hunker down - winter storms encouraging dams to still eat and stand with hay
37
clostridium vaccines?
YES- c. perf type C and D toxoids to dams during pregnancy goal: increase colostral titers for neaonates! want abs to neutralize the potent exotoxins
38
when do neonates get immunized for enterotoxemia?
8 weeks of age with a booster! these are inactivated vaccines booster typically given 2-3 weeks after the initial immunization, then annually
39
how do you prevent C. perf?
- prevent excessive amounts of starch/sugar/soluble protein - hygiene! limit amount in food/water, clean bedding and dispersing animals
40
when do carriers of salmonella shed?
carriers shed when STRESSED, and may or may not be symptomatic when shedding
41
what stressors can trigger shedding of salmonella?
transportation, parturition, heavy lactation, severe illness
41
T/F: carriers of salmonella are typically symptomatic when shedding
false- may or may not be symptomatic when shedding
42
epidemiology of salmonellosis
- alteration of GI flora! abx, reduction in feed, surgeries - prone in equine colic cases!! - feed reduction can occur w significant illness, abx may be necessary
43
how do you prevent salmonellosis?
- don't buy it in! bring in new genetics in semen/embryos and not live animals - closed herd preferred! - QUARANTINE NEW PURCHASES! 4 week quarantine of new purchases- stress of newness can trigger shedding - ideal to also control incursion of wildlife
44
T/F: mixing of salmonella into feed is of serious concern
true! educate producers, critique feed hygiene, where they keep it should NOT haul manure or dead animals with same equipment that is used to move or haul feed salmonella and listeria love to grow in silage
45
T/F: salmonella is an opportunist
true
46
good practices to prevent salmonella?
- good comfort/shelter/parasite control - control metabolic diseases in physiologically stressed animals - control heat stress - handle sick calves LAST
47
how effective are vaccines against salmonella?
there isn't one- there are so many serotypes that can cause disease
48
immunization of salmonella?
- autogenous bacterins not great; super serotype specific and short-lived immunity - bacterins also induce humoral/antibody immunity rather than cell-mediated, and salmonella hides inside host cells where antibodies can't access them!
49
what type of immunity do bacterins induce? why is this problematic?
they induce humoral/antibody immunity rather than cell-mediated immunity - bad bc salmonella hides inside host cells/leukocytes, where antibodies cannot access them
50
when should you treat salmonellosis?
- mortality rates high - need abx susceptibility! very unpredictable susceptibility profile - doesn't consistently curtail shedding of the organism
51
prognosis of salmonella
- depends on virulence of serotype and host immune system - high virulence = acute disease crisis, severe illness with high fatality risk - less virulent = possibility of chronic D+ with weight loss - tends to be more severe/acute in animals with compromised/immature immune systems
52
what types of animals get hit hardest clinically by salmonella?
animals with immature or compromised immune systems (neonates, surgical stress etc)
53
BVDV
- bovine diarrheal virus - flavivirus, RNA virus - cattle, camelids
54
what are the sources of BVD?
- primarily animals with a persistent infection (PI) - acutely infected animal: virus encounters susceptible animal and animal sheds virus for several days
55
pathogenesis of PI infections
- became infected as fetus (mom got during pregnancy) - fetal immune system sees virus as self - PI animal sheds HUGE amounts of virus during its lifetime - source of infection for herdmates - common cause of reproduction losses/abortions
56
once born, how are PI animals a problem?
- persistent viremia: BVD present in many tissues - shed massive amounts of BVDV in all body secretions (feces, urine, saliva, tears, semen etc) - these PIs are the primary source of viral challenge to others in population!
57
what if an adult female was a PI and became pregnant?
her fetus will be infected and either be aborted or develop into PI offspring
58
what is the second source of BVDV (not PI)
- acutely infected animal - not vaccinated - or vaccinated an exposed to overwhelming dose of BVDV - or vaccinated but exposed to heterologous strain of BVD virus these animals develop fever, D+ and shed virus for several days before clearing it thru immune response
59
signs of BVDV depend on
host-viral strain interaction, so an infx can be completely subclinical
60
classic clinical case of BVDV
- high fever: 104-106 - lethargy - profuse D+ x 3-5 days - oral mucosal erosions are a big key to physical dx!!!******
61
clinpath of BVDV
- virus immunosuppressive: necrosis of lymphoid tissues - lymphopenia - secondary infections occur- what kills animals animals may die of pneumonia, septicemia and/or enteritis, but real underlying problem is the immune-crippling virus
62
why might animals with BVDV get pneumonia, septicemia and/or enteritis?
virus is immunosuppressive and causes necrosis of lymphoid tissue- the secondary infections are often what kills these animals
63
how do you diagnose BVDV?
- acutely infx animals viremic for several days - PI animals viremic for lifetime during viremic phase, lab can isolate virus from bloodstream - PI animals: can detect viral antigens or virus in blood/skin (ear notches!) - acute infx: antibody titers increase following infection by submitting acute and convalescent titers
64
how are camelids tested for BVDV?
PCR!
65
severity of signs of BVDV
- signs depend on host-viral strain interaction; can be entirely subclinical esp in camelids
66
classic clinical case of BVDV
- high fever (104-106) - lethargy - profuse D+ - virus is IMMUNOSUPPRESSIVE; lymphoid tissues attackced - LYMPHOPENIA COMMON - SECONDARY BACTERIAL INFX
67
what physical trait is commonly seen with BVDV infections?
oral mucosal lesions! very common
68
you get called to a farm to see a 3-year-old cow with profuse D+, fever of 104, and lymphopenia. upon examination of the mouth, you notice bright red lesions on the upper and lower mucosa. what is your immediate suspicion?
BVDV
69
diagnosis of BVDV summary
- isolate virus from blood, antigen or DNA in blood or skin - antibody increase: acute and convalescent titers - gross lesions and necropsy - IFA on tissues, virus, PCR on tissues
70
what organ is good for tissue collection for BVDV testing?
spleen- abundance of lymphoid tissue
71
how do you prevent BVDV?
- IDENTIFY PIS: viral detection tests, and euthanize - vaccine: MLV superior- both type 1 and 2 need to be included in a vaccine
72
T/F: you can sell BVDV infected animals as long as they aren't a PI
FALSE- PI ANIMALS SHOULD BE CULLED but can be used for meat? do not sell!
73
T/F: PI BVDV cases can be used for meat
true
74
T/F: there is no cross protection for BVDV type 1 and 2
true- vaccine needs to include both
75
what type of vaccines are used for BVDV?
MLV
76
what happens if BVDV gets into a pregnant, non-immune mom?
- fetal infection could result in babe becoming a PI!

Clinical Sciences Exam 4 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions