Livestock D+: Older Animals Flashcards
1
Q
coccidia and ostertagia typically affect what age of animals?
A
juvenile: several months to a year
after they come young adults their immune system can ward these off
2
Q
winter dysentery and johne’s disease affect what age of animals?
A
older animals/adults
3
Q
T/F: grain overload/rumen acidosis can induce D+ in any age that has a functional rumen
A
true
3
Q
T/F: salmonella typically infections younger, naiive animals
A
false- can attack at any age- just like clostridium perfringens
4
Q
eimeria/isospora
A
coccidiosis
5
Q
coccidiosis epidemiology
A
- older-yearlings calves/lambs/kids/crias
- sporozoan
- host species-specific!
- fecal-oral transmission
- adults shed low #
- diseased shed billions
6
Q
T/F: horses are not susceptible to enteric disease caused by coccidia
A
true
7
Q
disease severity of coccidia is proportional to
A
of sporulated oocysts that are ingested
7
Q
what kind of D+ does coccidia cause?
A
inflammatory
8
Q
why won’t you see coccidial disease until 3 weeks of age?
A
life cycle takes approx 3 weeks; see disease around that amount of time
remain susceptible until they are yearlings!
9
Q
favorite sites for coccidia to attack
A
- distal SI (ileum)
- colon
single oocyst can develop and destroy a million enterocytes
10
Q
pathogenesis of coccidia
A
sporulated oocyst causes damage: infx amplifies, enterocytes rupture, intermediate forms of organism are released to infect new enterocytes
- rupture of enterocytes from intestinal inflammation, mucosal cell loss and cost to rebuild
- impaired digestion and absorption of nutrients
- blood and protein loss
- secondary infx
- dehydration/electrolyte loss
11
Q
where are oocysts passed?
A
feces- these are eggs
12
Q
T/F: coccidial patients shed active cysts into environments
A
FALSE: oocysts sporulate outside of host to become infective after 2-5 days; oocysts are not motile
13
Q
T/F: cecal and colonic cells are far slower to replicate
A
true: takes days to cover damaged mucosa than small intestine, which takes hours
means that more submucosa exposed for a longer time
13
Q
life cycle of infx by coccidia
A
- sporulated oocysts release sporozoites
- sporozoites invade enterocytes
- rupture and re-entry of other enterocytes occurs
14
Q
where is the primary histologic lesion of coccidosis?
A
- inflammatory ileus, typhlitis (cecal inflammation), colitis
because it takes large bowel cells longer to regenerate so more submucosa is exposed to badness for longer amounts of time
14
Q
what types of D+ are present with coccidiosis?
A
- can have maldigestion and malabsorption from damage to SI
- BUT real driver of morbidity is inflammatory response
15
Q
typhlitis
A
cecal inflammation
16
Q
how can coccidosis cause hemorrhage?
A
submucosal capillaries can be damaged by inflammation = hemorrhage into the lumen
17
Q
inflammatory ileitis, typhlitis and colitis are seen with what pathogen?
A
coccidiosis
17
Q
how can coccidiosis cause protein losing enteropathies?
A
- amount of mucosal loss triggers inflammation++
- abundant exposure of submucosa to luminal bacteria, toxins, LPS etc for long periods of time
- inflammation = increase in vascular permeability = loss of electrolytes, water, protein into gut
- exudation of protein across large area of damaged mucosa = PLE = hypoalbuminemia and hypoglobulinemia from movement of protein from plasma into the gut lumen
18
Q
when is coccidiosis triggered?
A
stress
- weaning
- handling (ie vaccination)
- bad weather
- shipping
- introduction of new animals
- confinement
- concurrent infections
18
Q
how do you diagnose coccidiosis?
A
- fecal flotation: high concentration of oocysts
- histopathology of ileum, cecum, colon
19
what determines whether coccidia are disease-causing even tho they are ubiquitous?
1. dose: amount of infx oocysts to which animals are exposed
2. host stress
3. virulence of coccidial specesi
20
why is fecal flotation not always the best for diagnosing coccidiosis?
detection of oocysts is commonplace in healthy ruminants
- severely infx animals may show few oocysts on fecal: day to day fluctuations, administration of medications, dilution by sheer volume of watery D+, infx in prepatent phase
20
what are clinical signs of coccidiosis?
- D+ red to rust color in severe cases
- +/- mucus membrane pallor from anemia
- tenesmus: straining to defecate
- rectal prolapse can result from significant proctitis
21
what is the easiest way to determine if coccidiosis is present?
sample multiple animals for fecal oocysts quantification and interpret results with clinical signs/necropsy
22
why should amprolium (corid) be diluted?
is inactive analogue of thiamin- if not diluted the animal can become thiamine deficient. dilute it for owner or do it yourself to reduce risk of polioencephalomalacia
22
what is the gold standard for coccidiosis testing?
histopathology of affected gut segments: often see hemorrhagic or catarrhal enterocolitis on histopath, and intracellular stages of the organism often seen
23
how does amprolium work? what is it used to treat?
- coccidiosis
- inactive analogue of thiamin: essential nutrient for coccidial/energy metabolism
23
what abx are used to treat coccidiosis?
SULFONAMIDES! orally, coccidiocidal
- amprolium (corid)! inative analogue of thiamin
24
what are ionophores used for?
coccidiostatic agents
24
what effects do ionophores have that are the reason why it's illegal for extra label use?
- improve feed efficiency
- increase weight gain
use only for controlling coccidiosis!!!
24
treatment protocol for coccidiosis
1. fluids and supportive care
2. NSAIDS once rehydrated - nephrotoxicosis risk
3. sulfonamide abx- amprolium/corid
4. manage owner expectations- badly damaged GIT won't heal overnight
5. blood or plasma transfusion for severe cases of high $ value
25
what are the common ionophores used for coccidiosis control?
1. monensin/rumensin: goats and cattle
2. lasalocid/bovatec: approved for sheep and cattle
26
ionophore antibiotics are highly toxic to which species?
CAMELIDS AND HORSES
27
MOA of decoquinate (deccox)
interferes with coccidia energy metabolism
28
decoquinate (Deccox)
coccidiostatic: suppresses coccidial life cycle. approved for cattle/sheep/goats and safe for extralabel use in camelids
29
how do you control coccidiosis?
1. separate feed and water from feces (elevation, concrete/gravel)
2. PEN HYGIENE: clean bedding, grade for drainage
30
coccidiosis is a disease of ____________
management
31
internal parasitism can be abbreviated to PGE: what does this stand for
parasitic gastroenteritis
32
HOT complex
- cattle
- haemonchus contortus
- ostertagia (teladorsagia)
- trichostrongylus
33
barber pole worm
haemonchus contortus (haemonchosis)
34
haemonchus pathogenesis
- coiled striping of white ovaries of female winding around blood filled intestine
- can infest all ruminants, but sheep goats and camelids more commonly develop severe clinical disease because they don't develop an effective immune response to them like cattle do
- worm suck host's blood
- anemia and hypoproteinemia result and can be lethal
- in "pure" haemonchus infections there is minimal inflammation in abomasum and no diarrhea
34
where do ostertagia/teladorsagia cause inflammation?
abomasal inflammation
in camelids, the forestomach compartment to the abomasum is the 3rd compartment, aka C3
35
ostertagia and teladorsagia cause inflammation in what part of camelid GIT?
abomasal inflammation: so C3
as a result there is inflammatory damage to the acid-secreting organ that initiates protein digestion
= inflammatory protein losses and maldigestion of protein
36
ostertagia ostertagi infect what species
cattle
37
teladorsagia circumcincta affect what species
sheep, goats
38
ostertagiasis
- ostertagia ostertagi or teladorsagia circumcinctta
- new world camelids can be affected by either or both
- 2 types of clinical disease seen in ruminants and NWCs = 2 types of ostertagiasis
- L3 larvae are the infectious ones!!!
39
what is the difference between haemonchus vs ostertagia spp?
haemonchus don't cause inflammation in abomasum and no D+
ostertagia cause abomasal inflammation (C3 in camelids)
39
type 1 ostertagiosis
- life cycle completed
- abomasal damage occurs during larval (L4) development
- larvae then molt to adults that lay eggs = detected on fecal flotation
39
what stage of ostertagia enter the abomasum?
L3: infective stage, enters parietal glands of the abomasal wall
40
what are the parietal glands of the abomasum responsible for?
HCl secretion- ostertagiasis
41
where do L3 ostertagia molt to L4?
parietal glands of abomasum
42
life cycle of ostertagia in abomasum
- L3 (infective) ingested and enter the parietal glands of abomasum wall
- inside parietal glands, L3s molt to L4s
- L4 immediately molt to adults- this is when pathologic changes occur!
- when larvae emerge from parietal glands and molt to young adults, cause inflammation and destruction of parietal glands
43
how does ostertagiosis cause D+?
- abomasitis and PLE from exudation of protein-rich serum into lumen of damaged abomasum
- protein digestion impaired from reduction in HCl secretion from damage to parietal glands
= DIARRHEA
- adults then remain in abomasum and once mature, proceed to lay eggs and thus complete life cycle
44
what are we detecting on a fecal for ostertagia?
eggs
45
type 1 ostertagiasis is characterized by
parasite promptly completing the entire life cycle
diseased animals show HEAVY FECAL EGG COUNTS as a result of adults ostertagia laying EGGS
45
typical type 1 ostertagiasis scenario
- weakened calves/lambs/kids on pasture during months of moderate weather
- pick up heavy ostertagia burden
- diseased stock show with heavy fecal egg counts
- don't undergo hypobiosis since environment is favorable for eggs/offspring to survive: so promptly molt into egg-laying adults
- once heavy burden of adult worms established, clinical disease develops
46
clinical signs of type 1 ostertagiasis
- ill thrift
- D+ bc digestion affected
- edema: protein loss
- anorexia is characteristic
can see bottle jaw!
- ABOMASITIS: PLE
- impaired protein digestion: less HCl
47
nodular abomasitis lesions are considered pathognomonic for
ostertagia infestation in cattle and telodorsagia infestation in small ruminants/camelids (C3-itis)
48
T/F: you cannot distinguish ostertagia eggs easily from other strongyle eggs
true- necropsy and documentation of "moroccan leather" nodular abomasitis is considered diagonostic gold standard for ostertagiosis
49
gold standard dx for ostertagiosis
necropsy and documentation of moroccan leather/nodular abomasitis
49
type 2 ostertagiasis
- calves ingest large # infective L3s on pasture
- adverse environment signal tells the L4s to HOLD TF UP
- go into hypobiosis (hibernation in host) and remain arrested
- northern states/CA: late fall and winter bc environment is too cold for optimal parasite survival outside of host
50
in type 2 ostertagiasis, what stage is undergoing hypobiosis?
L4 in the abomasal mucosa- some signal from environment tells L4 ostertagia that conditions aren't good, and then in spring another signal tells them that conditions now favor survival outside the host
51
pathogenesis of type 2 ostertagiasis
- simultaneous emergence of large numbers of L4s wanting to molt into young adults
- emergence = acute abomasitis and destruction of gastric glands !!!
- but not much eggs in feces yet: all are young adult worms. in type 2 disease the parasitic disease is in its PREPATENT PERIOD
52
T/F; type 1 and type 2 ostertagiasis have identical lesions in the abomasum
true
53
what is the big difference between type 1 and 2 ostertagiasis?
- clinical disease of type 2 occurs before the emergence of L4s have developed into mature egg-laying adults
- hence with type 2 disease, the fecal float is generally LOW OR ZERO in terms of egg numbers
54
in a fecal float, will you see ostertagia eggs with type 1 or type 2 eggs?
type 1: often see low or even zero eggs with type 2 bc disease occurs before L4s have developed into mature egg-laying adults
55
how do you diagnose type 2 ostertagiasis?
- D+, anorexia, hypoproteinemia
- few eggs on fecal float!!!***
- abomasal lumen pH is abnormally HIGH (pH> 5) alkaline because inflamed gastric glands cannot make normal amounts of HCl
- damaged abomasal wall leaks pepsinogen into plasma: analysis of plasma pepsinogen activity used in some labs to make dx
56
when is type 2 ostergiasis occurring?
warm climates! in southern states and tropical climates hot weather too extreme for parasites to live outside host
- ride out the hot weather by staying in as hypobiotic L4s
57
in southern, warm climates, what induces the L4 to undergo a hypobiosis?
HEAT (ostertagiasis)
58
when does emergence of type 2 ostertagiosis occur in south?
fall: weather moderates and cools off
rains more consistently
59
summary of type 2 ostertagiosis
- characterized by abomasitis created from emergence of many hypobiotic L4s when outside goes from bad to good
- disease occurs before egg production by adult occurs
- this means that there are few eggs to detect in the feces of these animals
60
abomasitis is called what in camelids
third compartment inflammation: forestomach chamber analogous to abomasum is the 3rd compartment
"C3-itis"
61
how can you treat ostertagiasis?
- benzimadazoles (fenbend, albend, oxfend)
- macrocyclic lactones (ivermectin, doramectin, etc)
cattle: ivermectin, doramectin moxidectin by injection or pour on
62
how is albendazole/fenbendazole given?
orally
63
for type 2 ostertagiasis, what is your treatment?
only modern macrocyclic lactones and benzimidazoles
64
for type 1 ostertagiasis what is your treatment?
any available antihelminthics so long as there isn't resistance
could also use pyrantel/morantel/levamisole
65
what medications would support an ostertagiasis case?
- plasma
- colloids
- appetite supplementation: B vitamins
- NSAIDS if uncomfy
