resp 4 Flashcards
BRD scoring system for pre-weaned calves? post weaned? (dairy)
- what is included
- scoring system
Pre-weaned:
- eye discharge (2)
- nasal discharge (4)
- ear droop or head tilt (5)
- cough (2)
- breathing (2)
- temperature (2)
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- add scores for all clinical signs, if total score is >=5, calf may be positive for bovine respiratory disease
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Post-weaned
- sunken eyes (4)
- low body condition (5)
- cough, breathing, diurnal temp fluctuation
BRD treatment? what is our first line of defence? what is our 3 pronged approach to this disease on the feedlot?
antimicrobial therapy goals:
* Treat early
* Treat just long enough
* Use appropriate therapeutic
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Trained caretakers/pen riders:
* First line of defence
* Provide presumptive treatment
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Unresponsive animals
* Diagnostic testing important for these ones > may reveal something different eg. resistance, new disease
feedlot systems of calf BRD scoring is based on what?
what about decision trees?
- more based on behaviour vs dairy, which is clinical signs
> how alert, responsive, quick
<><> - decision tree tells penrider what to do with calf, based on eg. rectal temp, previous treatments, responsive vs unresponsive, etc.
what is the most important factor for successful treatment of ruminant respiratory disease?
Early recognition of disease
BRD treatment:
* Factors impacting first-line antimicrobial choice
- Cost
- Route of administration
- Treatment interval
- Drug label restrictions
- Need of extra-label doses
- Withholding times
- Data from susceptibility testing
- Historic drug performance
- Published treatment trials
BRD treatment
- suggested response guidelines
> response rate, fatality, chronic:die
- duration of therapy
- mass medication?
Suggested response guidelines
* 70-80% respond to first treatment
* 4-7% fatality rate
* Chronic cases to cases that die > 0.5:1.0
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Optimal duration of therapy
* At least 48 hours past clinical signs
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Mass medication?
* If # of sick animals removed is:
* 10% of population for 3 consecutive days
* 25% or > of population in 1 day
BRD treatment - when to consider a second line antimicrobial
If first line is:
* Long-acting Oxytetracycline > No response after 2-3 days
* Ceftiofur crystalline free acid > No response after 5-7 days
* Tulathromycin > No response after 7-14 days
BRD treatment - drug classes we can consider adding aside from antibiotics
- Anti-inflammatories > considered effective
- Anti-virals > none available
- Immunomodulatory therapy > some can provide positive results
Management factors associated with respiratory disease in dairy calves
- poor passive transfer
- diarrhea at a young age
- group housing, indoors (individual housing outdoors decreases disease… but consider temp)
Feedlot and stocker management factors that can contribute to respiratory disease
- Poor nutrition
- Uncontrolled parasitism
- Sale through auction markets
- Prolonged time in market channels
- Excessive dehydration from transport
- Mixing cattle from multiple sources
- Castration at arrival
- Shared water between pens
- Starting diets > greater than 75% concentrate, High in corn silage, Feeding non-protein nitrogen
risk classification for cattle respiratory disease
High risk-exposed
* Little-no preventative care
* Little-no adaptation to hay/grain diet
* Group from multiple sources
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High risk-not exposed
* Little-no preventative care
* Little-no adaptation to hay/grain diet
* Single source group
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Low risk
* Vaccinated
* Weaned
* Turned out prior to shipment
Acute Bovine Pulmonary Edema and Emphysema (“fog fever”)
- who gets this?
- clinical signs
- Cattle > 2 yo
- Dry, sparse forage → lush pasture
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Clinical signs - Within 2 weeks of pasture change
- Acute onset severe dyspnea
- Tachypnea
- Expiratory grunt
- Frothing at the mouth
- Open-mouth breathing
- Extended head and neck
- Dilated nostrils
Acute Bovine Pulmonary Edema and Emphysema
- pathophysiology?
- morbidity, mortality?
- L-tryptophan (present in lush grass) converted by ruminal micro-organisms
- To 3-Methylindole metabolized in lung > results in pneumotoxic end products
- Necrosis of type I pneumocytes and Clara cells
- Edema
- Hyaline membrane formation
- Proliferation of type II pneumocytes
- interstitial pneumonia
<><> - Morbidity rate- ~50%
- Mortality rate- ~ 30%
Acute Bovine Pulmonary Edema and Emphysema
- diagnosis, treatment
- prevention
- Dx: presumptive
- Tx: None, handling may precipitate death
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Prevention - Gradually adapt to lush pasture > Start at 2 hours/day, Transition over 10-12 days
- Delay use of lush pasture until after hard frost
- Mow and windrow pasture prior to turnout
- Turnout young stock (<15mo), other livestock first
- Use pasture before it becomes lush
- Monensin for 1 day prior to pasture and for the next 10 days
- Lasalocid for 6 days prior to pasture and for the next 10 days
> both these products decrease L-tryptophan conversion
Feedlot Acute Interstitial Pneumonia
- cause, contributing factors
- Exact cause unknown
- Likely multifactorial
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Proposed contributing factors: - Pneumotoxins
- Chronic bacterial pneumonia
- Signalment
- Chronic small airway injury
- BRSV infection
- Heat/dust exposure
- Hypersensitivity reactions
Feedlot Acute Interstitial
Pneumonia
* Clinical signs
Acute death
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Rapid onset expiratory dyspnea
* Tachypnea
* Extended headed with front legs abducted
* Open-mouth breathing
* Frothing from mouth
* Cyanosis
* Tachycardia
* Subcutaneous edema
Feedlot Acute Interstitial Pneumonia
- pathophysiology
- Dx
- Tx
- Prevention
- Pathophysiology: Unknown
- Diagnosis: Histopathology only
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Treatment - Frequently futile
- Moving cattle can precipitate death
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Prevention - Minimize abrupt dietary change
- Minimize infectious respiratory disease
4-Ipomeanol Toxicity
- what is this from? when do we see signs?
- morbidity, mortality?
- pathogenesis?
- clinical signs?
- Toxin – furanoterpenoid
- Outbreaks after feeding sweet potatoes
- Clinical signs appear 1 day after exposure
- Morbidity and mortality are high
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Pathogenesis - Toxin is absorbed and transported to lungs
- Metabolized in lung
- Damage to Clara cells, type I pneumocytes and endothelial cells
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Clinical signs - Tachypnea → dyspnea
- Expiratory grunting
- Head extension
- Flared nostrils
- Tachycardia
4-Ipomeanol Toxicity
- dx, tx, prevention
- Diagnosis: Presumptive
- Treatment: Not been investigated
- Prevention: Don’t feed moldy sweet potatoes
Perilla Ketone Toxicity
- from what plant?
- where is it found? what forms?
- pathogenesis
- signs
- dx, tx, prevention
- Ingestion of Perilla frutescens (purple mint)
<><> - Plant most common in late summer
- Green seed-stage most toxic
- Dried seed-stage less toxic, can be lethal if lots in hay
- Pre-seed stage/frosted plants low toxicity
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Pathogenesis - Very similar to 4-Ipomeanol toxicity
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Clinical signs - Often found dead
- Moderate to severe dyspnea
- Wheezing
- Frothing at mouth
- Expiratory heave or grunt
- Less severe cases pant
<><> - presumptive dx, no treatment, prevent exposure
Dictyocaulus viviparus
- type of parasite
- where it likes to live
- life cycle
- Trichostrongylid
- Present in trachea and bronchi
<><> - Eggs hatch in lungs
- Coughed up and swallowed
- Spend ~5 days on pasture in manure
- Re-ingested and migrate through intestinal wall
- Mesenteric lymph nodes → 4th stage
- Migrate via blood or lymphatic to capillaries of lung
- Enter alveoli → immature adults
D. viviparus
- clinical signs for prepatent, patent, and postpatent phases
- Unexposed cattle
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Prepatent phase (days 7-25) - Coughing
- Tachypnea
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Patent phase (days 25-55) - Intermittent-marked coughing
- Tachypnea/dyspnea
- Anorexia
- Weight loss
- Death common in untreated, heavily infected animals
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Postpatent phase (days 55-90) - Adults expelled
- Gradual resolution
- 25% of cases sudden exacerbation
D. viviparus ‘complications’
- Pulmonary edema
- Severe interstitial emphysema
- Alveolar epithelial hyperplasia
- Secondary bacterial infection
D. viviparus
- dx
- where do larva live? animal immunity?
- Tx
- prevention
Diagnosis
* Recovery of larvae from manure
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Epidemiology
* Larvae overwinter on pasture
* Immunity decreases after several
months without exposure
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Treatment
* Anthelmintics → macrocyclic lactones
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Prevention and control
* Pasture management
* Deworming program
Important Lungworms of sheep and goats
- Dictyocaulus filaria
- Protostrongylus rufescens
- Muellerius capillaris
Dictyocaulus filaria
- life cycle? pathogenesis? similar to?
- signs
- dx
- tx
- lungworm of sheep and goats
- Life cycle and pathogenesis similar to D. viviparus
- Dyspnea, tachypnea, coughing and weight loss
- Identify with Baermann technique
- Treat all animals and move pastures
Protostrongylus rufescens
- host
- signs
- dx
- tx
- lungworm of sheep and goats
- Molluscan intermediate host
- Most infection are subclinical or mild > Nasal discharge and coughing
- Identify with Baermann technique
- Treat with fenbendazole, levamisole or moxidectin
Muellerius capillaris
- prevalence
- hosts
- life cycle
- signs
- lesions
- Most common
- Goats more severe than sheep
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Life cycle - 1st stage larvae→ coughed up, swallowed, passed in feces
- Enters molluscan intermiediate host → 3rd stage larvae
- Ingested with host → mesenteric lymph nodes
- 4th stage → lungs → alveoli → adults
<><> - Many infections are subclinical
Clinical signs: - Coughing
- Dyspnea
- Unthriftiness
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Lesions - Sheep - 2-3mm grayish nodules
- Goats- interstitial pneumonia with patches
Muellerius capillaris
- dx, tx, control
- Diagnosis - Baermann technique
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Treatment: - Sheep → moxidectin
- Goats → fenbendazole, albendazole,
oxfendazole or ivermectin
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Control: - Avoid grazing on wet pastures
- Deworm before grazing season
