Livestock Respiratory Disease Flashcards
Why do ruminants develop SQ emphema, more easily that other species
1) Very few inter-alveolar pores, which normally allow for connection between alveoli and pressure equilibration.
2) Pressure can build up more easily
3) Rupture of alveoli and development of emphysematous bulla
4) Pneumomediastinum and air tract up the medaistinum to the dorsum to get SQ ephysema
Why do ruminants suffer from respiratory disease really rapidly
1) their lung is lobulated and they have a very minimal reserve capacity (unlike horses and dogs)
2) Histologically, very few inter-alveolar pores, which normally allow for connection between alveoli and pressure equilibration.
Pressure can build up more easily leading to pneumomediastinum and air tract up the medistinum to the dorsum to get SQ ephema
3) Hyper-reactive lungs - hypoxia, inflammatory, and histamine sensitive
What are ruminant lung hyper-reactive to
1) Hypoxia- pulmonary arterial constriction and subsequent pulmonary hypertension
2) Inflammatory process- macrophages and mast cells release mediators that cause disease to alveoli and interstitium
3) Histamine sensitive- significant histamine release
What occurs when there is degranulation of mast cells with anaphylaxis in ruminants
there is resulting bronchoconstriction and vasoconstriction
-resulting in pulmonary edema
How do chronic and acute respiratory disease in ruminants affect the rumen
there is decreased function of the rumen and the ability to eructate- resulting in gas bloat- distension on the rumen, pressure on diaphragm and pressure on the lungs
Why are the lungs smaller in ruminants
the rumen takes up the majority of the space
lungs are pushed cranial and smaller relative to other species
Ruminant lung anatomy
multiple lobes and within those there are lobules, which are differentiated by septal areas
Septal regions form a barrier to prevent expansion of bacterial bronchopneumonia into other areas of the lung -can have stark demarcation of disease and normal lung
What is significant about the ruminant lung anatomy and the distribution of bronchopneumonia
Septal regions form a barrier to prevent expansion of bacterial bronchopneumonia into other areas of the lung -can have stark demarcation of disease and normal lung
Maxillary sinuses in the ruminants
over the upper cheek teeth (premolars and molars)
What sinus connects to the cornual sinus in ruminants
the frontal sinus
What developmental condition of the upper respiratory tract is common in camelids
Choanal atresia
Choana
where the nasal passage opens into the nasopharynx
What are signs of upper respiratory disease in livestock
1) Nasal discharge- serous, mucopurulent
2) Sneeze
3) Cough
4) Stridor - intense musical breath sounds over upper airway, particularly the larynx, extrathroacic
5) Stertor- sonorous snoring breath sounds over the upper airway- extrathoracic
6) Decreased nasal airflow
7) Foul smelling breath
8) Facial asymmetry
9) Laryngeal swelling
10) Nasal hyperemia
11) Expanding cheeks on exhalation
11) Ocular discharge
12) Conjunctivitis
13) Respiratory distress
14) Salivation- minimally swallowing
15) Head shaking
16) Epistaxis
17) Fever
18) Quidding, dysphagia
19) Hypxemia
intense musical breath sounds over upper airway, particularly the larynx, extrathroacic
Stridor
sonorous snoring breath sounds over the upper airway- extrathoracic
Stertor
What are signs of lower respiratory disease in livestock
1) Fever
2) Cough
3) Abnormal breath sounds
4) Respiratory dyspnea- restrictive breathing pattern
5) Hemoptysis
6) SQ emphema
7) Hypoxemia
8) Bloat- inflammation of vagal nerve or enlargement of mediastinal LN putting pressure on esophagus and preventing normal eructation
Why do you see bloat of ruminants with lower respiratory disease
inflammation of vagal nerve or enlargement of mediastinal LN putting pressure on esophagus and preventing normal eructation
irritation and inflammation of mucous membrane inside the nose
rhinitis - clinical signs: sneezing, intense pruritis, nasal discharge *usually serous), stertor
What are common etiologies of rhinitis in cattle * know this
BHV-1 (IBR) *
BVDV *
PI-3 *
BRSV *
Coronavirus
MCF
What are clinical signs of cows with rhinitis
What about chronic*
sneezing, intense pruritis, nasal discharge *usually serous), stertor
chronic: lacrimation, blepharospasm, granuloma formation
What is Atopic rhinitis in cattle
allergic rhinitis
-acute, summer snuffles
-type I (IgE) allergic reaction
-older cattle
-Channel Island Breeds (Jersey, Guernsey) and Holsteins
signs: difficulty breathing, sneezing, stertor
nasal discharge (usually serous)
pruritis
chronically- develop into enzootic nasal granuloma
What cattle breeds do you see atopic rhinitis in?
Channel Island Breeds (Jersey, Guernsey) and Holsteins
What causes Atopic Rhinitis in cattle
Type I (IgE) allergic reaction
repeated exposures can lead to type IV
What causes acute summer snuffles in cattle
Atopic rhinitis- allergic rhinitis
caused by Type I (IgE) allergic reaction
What is the pathogenesis of Atopic Rhinitis in cattle
1) Antibodies (IgE) to antigen produced
2) Subsequent exposures result in type I hypersensitivity reactions
3) Repeated exposures can lead to type IV
What are the clinical signs of atopic rhinitis in cattle
difficulty breathing, sneezing, stertor
nasal discharge (usually serous)
pruritis
What occurs if atopic rhinitis develops into chronically
Enzootic Nasal Granuloma
-Chronic form
-Firm raised white granulomatous nodules
When do you see enzootic Nasal granuloma in cattle
When atopic rhinitis develops chronically
you see firm, rasied, white granulomatous nodules in the nasal passages
What are differential diagnosis for atopic rhinitis
-fungal
-foreign body
-tumor
-irritant
How do you diagnose atopic rhinitis
-Endoscopy*
-Culture (rule out)
-Biopsy
-Cytology (eosinophils)
How do you treat atopic rhinitis in cattle
-Remove allergen
-Antihistamine- often not helpful
-Corticosteroids - key treatment and useful. make sure they are not pregnant or they will abort *
What does fungal infection in the nasal passages of ruminants result in
delayed type IV hypersensitivity and nasal granuloma formation
Mycotic nasal granuloma in cows
Fungal infection leading to upper respiratory signs
-Delayed Type IV hypersensitivty forming a granuloma
Dx: endoscopy, biopsy, cytology, culute
Treatment: Surgery, Sodium Iodide, Antifungals
How do you treat Mycotic Nasal Granuloma in cattle
Surgery
Sodium iodide (IV)
Antifungals - expensive and there is a withdrawal times (contact FARAD)
What causes sinusitis in livestock
-dehorning
-tooth root infection (maxillary)
-horn injury
-respiratory disease
-nasal tumor
-actinomycosis (lumpy jaw)
-sinus cyst
-lymphosarcoma
What bacteria commonly cause sinusitis in livestock
Trueperella pyogenes
Pasteurella multocida
but any of the respiratory tract bacteria can cause it
What are the clinical signs of sinusitis in livestock
Acute: nasal discharge, fever, lethargy, anorexia, percusson
Chronic: nasal discharge, percussion, stertor, stridor, foul odor - ozena and/or halitosis, bone distortion, exopthalmos, neurological signs, unusal head carriage
If there is dehorning injury or broken horn, where does the sinusitis develop
cornual sinus that connects with the frontal sinus
How do you diagnose sinusitis in cattle
Clinical signs
Percussion
Radiograph- soft tissue density over the area of the maxillary sinus
Sinus centesis
How should you change your dehorning practices to prevent sinusitis
1) make sure you do not dehorn at later ages when the horn is communicating with the frontal sinus
2) Avoid dehorning in bad weather
3) Bandage for a prolonged time
otherwise not a lot to prevent sinusitis (esp of maxillary)
How do you treat sinusitis in cattle
Trephination- drilling a hole into the sinus and then aspirating a sample to aid in diagnosis can use for culture .Submit for aerobic and anaerobic
Aspiration
Lavage
Surgery
Antibiotics- PPG (T. pyogenes)
NSAIDs (flunixin meglumine or PO meloxicam)
Tooth extraction
Upon trephination of a cattle with sinusitis you get a sample to culture. What culture do you order
aerobic and anaerobic (although mostly aerobic)
How do you treat sinusitis in a ruminant caused by T. pyogenes
PPG - but it needs to be given twice daily and at a large volume
What is critical for the treatment of maxillary sinusitis
tooth extraction - can sometimes remove tooth orally. otherwise may need to do a maxillary surgery to remove the tooth
making a hole from the exterior into the infected sinus to allow for drainage and lavage. Use of Steinmann pin, drill
Sinusotomy (Trephination)
What bacteria is usually associated with frontal sinusitis in livestock
Trueperella pyogenes
secondary to dehorning
Tx: Penicillin
What is the most common isolate with frontal sinusitis NOT associated with dehorning
Pasteurella multocida
treat with penicillin or oxytetracycline
What should you treat pasteurella multocida caused frontal sinusitis in livestock
penicillin or oxytetracycline
oestrus ovis
nasal bots of sheep
lifecycle: spring to early fall
Signs: nasal discharge, sneezing, nose rubbing, stridor, stertor, decreased airflow (cheeks)
treatment: Ivermectin
What is the lifecycle of oestrus ovis
spring to early fall
1) Adult deposits eggs on nostrils
2) Migrate to the sinuses and go through development
3) Mature larvae migrate back down and out nostril
4) Larvae is on the ground, pupates and turn into adult fly
*Causes irration to the nasal pasages
How do you treat Oestrus ovis in sheep
Ivermectin
What is the nasal bot that occurs in llamas
Deer pharyngeal bot (Cephenemyia)
Deer pharyngeal bot (Cephenemyia)
nasal bot that occurs in llamas
What causes viral rhinitis in cattle ***
BHV-1 (IBR) *
BVDV *
PI-3 *
BRSV *
Coronavirus
MCF
What causes ovine nasal adenocarcinoma
Retrovirus
Ovine nasal adenocarcinoma
Retrovirus
Nasal signs- serous discharge, stridor/stertor, anorexia, inspiratory dyspnea, open mouth breathing, dilating/puffing out cheeks
progressive, locally invasive, not metastatic
starts unilateral but progresses to be bilateral
What is a primary sign of ovine nasal adenocarcinoma
inspiratory difficulty- some degree of open mouth breathing
livestock prefer nasal breathing but if the force mouth closed you will see them pushing their cheeks out
What is the treatment on ovine nasal adenocarcinoma
no successful treatment for it
clients may request surgery however ultimately it is locally invasive and there is no cure
Can do endoscopy and biopsy to diagnose it
rhinitis and atrophy of turbinates seen in young pigs <3weeks
Caused by Bordetella bronchiseptica and pasteurella multocida
Signs: nasal discharge, sneeze, nose rubbing +/- mild cough, nose asymmetry
Porcine Atrophic Rhinitis
What causes porcine atrophic rhinitis
Bordetella bronchiseptica and pasteurella multocida
What age of pigs does atrophic rhinitis affect
Young pigs <3weeks
Bordetella bronchiseptica and pasteurella multocida cause
rhinitis and atrophy of the turbinates of piglets < 3 weeks of age
How do you treat/prevent for porcine atrophic rhinitis
1) ID and remove carriers animals
2) Vaccination (dams immunized so there is some colostral immunity) and vaccinate piglets starting at 1-2 weeks of age.
antibiotics might not work
the location where embryologically as the nasal passage develops rostral to caudal and the pharynx develops caudal to rostral the two come together to meet
Choana
What species is choanal atresia common in
camelids - congenital condition
What are the clinical signs of camelids with choanal atresia
difficulty breathing, respiratory distress, open mouth breathing
What happens in crias with choanal atresia
crias will go to nurse and nurse vigorously and then because it is not breathing while nursing will pass out
will begin to regain consciousness
How can you diagnose choanatal atresia
1) Endoscopy
2) Radiographs with contrast- sternal. you will see pooling of contrast in the caudal aspect of the nasal passage (cannot pass through)
3) Pass a catheter
How do you treat choanal atresia
surgical options- often unsuccessful
better prognosis if just membranous choanal atresia- rather than bony
as they grow, it remains close and they need a corrective surgery
heritable so do not keep in the breeding pool
metastatic pneumonia in livestock
primary disease in other organ system (liver abscesses, jugular phlebitis, endocarditis (tricuspid valve), metritis, mastitis, foot rot
hematogenous spread to the lung
What can lead to metastatic pnenumonia in cattle
primary disease in other organ system (liver abscesses, jugular phlebitis, endocarditis (tricuspid valve), metritis, mastitis, foot rot
via hematogenous spread
What are typical causes of metastatic pneumonia in cattle
Fusobacterium necrophroum (Gram negative anaerobe)
Trueperella pyogenes (gram positive anaerobe)
T/F: metastatic pneumonia is frequently fatal with sporadic occurence
True
caudal vena caval thrombosis
septic thromboemboli originate from an abscess at the hilus of the liver
often starts in GI (rumen acidosis, rumenitis, abomasal ulcers)
showering CVC leads to septic emboli within pulmonary abscessation
Abscesses erode into bronchial wall and aneurysms can rupture into AW
Primary infection of the caudal venal caval thrombosis in ruminants is _________
often starts in GI (rumen acidosis, rumenitis, abomasal ulcers)
What is the clinical presentation of CVCT in ruminants
*Epistaxis, hemoptysis, anemia +/- dynpea
3 categories
1) Sudden death
2) Acute respiratory distress syndrome
3) Chronic bronchopneumonia
What are the 3 categories of clinical presentation of CVCT
1) Sudden death
2) Acute respiratory distress syndrome
3) Chronic bronchopneumonia
How do you control for CVCT
re-evaluate nutrition/feed management
need to prevent rumen acidosis, ruminitis, and abomasal ulcers
How do you treat CVCT in ruminants
long term penicillin, supportive care
poor prognosis
Hypersensitivity Pneumonitis in cattle
Extrinsic allergic alveolitis / Bovine Farmer’s Lung
Allergic response (Type I and IV) to dust, moldy hay, grain, plant matter
-spores: thermophilic actinomycetes (Micropolyspora faeni)
most common in dairy cows ( confined), outbreaks in winter
clinical signs: decreased milk production, appetite, weight loss, coughing, crackles on thoracic auscultation
Diagnosis: titers (exposure), identify fungi in feed
treatment: glucocorticoids, improve hay management (bailing when dry), feed hay outside, improve ventilation
How do you treat hypersensitivity pneumonitis in cattle
glucocorticoids, improve hay management (bailing when dry), feed hay outside, improve ventilation
How do you diagnosis hypersensitivity pneumonitis in cattle
Diagnosis: titers (exposure)- uncommon, identify fungi in feed
What causes hypersensitivity pneumonitis in cattle
Allergic response (Type I and IV) to dust, moldy hay, grain, plant matter
-spores: thermophilic actinomycetes (Micropolyspora faeni)
What is the major target organ in Type I hypersensitivity
the lung- shock organ
Clinical signs of anaphylaxis develop within
10-20 min
What are the clinical signs of anaphylaxis in cattle
often to vaccine, milk, drug (penicillin), insects, bee sting with signs onset of 10-20 minute
severe acute dyspnea, flaring of nostrils, extension of head and neck, open mouth breathing, urticaria (hives), pharyngeal edema
How do you treat anaphylaxis (Type I) in ruminants
1) Epinephrine (1:1000)- life saving bronchodilation (B2 agonist)
2) Corticosteroids (not in pregnant animals)- antiinflamamtion and antiedema
3) Antihistamine
4) NSAIDs- milking out/drying off (if there is a milk allergy)
Acute/Atypical Interstitial Pneumonia (AIP)
commonly non-infectious
secondary to inhalation or ingestion of toxin
usually no clinical indication of sepsis
abnormal peripheral lung sounds diffusely
*Little response to antimicrobial therapy (toxin affect)
Necropsy:
-lungs fail to collapse when thorax opened
-firm, rubbery texture with diffuse interlobular emphysema and pathcy interstitial edema
-Histo: alveolar hyaline membrane, type II pneumocyte proliferation
What are the necropsy findings of cattle with Acute/ Atypical Interstitial Pneumonia (AIP)
-lungs fail to collapse when thorax opened
-firm, rubbery texture with diffuse interlobular emphysema and pathcy interstitial edema
-Histo: alveolar hyaline membrane, type II pneumocyte proliferation
How do you treat Acute/ Atypical Interstitial Pneumonia (AIP)
Little response to antimicrobial therapy (toxin affect)
What is the etiology of Acute/ Atypical Interstitial Pneumonia (AIP)
commonly non-infectious
secondary to inhalation or ingestion of toxin
usually no clinical indication of sepsis
abnormal peripheral lung sounds diffusely
What is a severe clinical presentation of AIP in cattle
Acute Respiratory Distress Syndrome (ARDS)
sudden onset, severe dyspnea associated with gross and histological findings of AIP
Oxygenation of arterial blood to fraction of oxygen in inspired air (PaO2/FiO2) is <400
Indicates poor oxygen echange (intersitial edema)
Severe diseases fit into the AIP or ARDS category
-Acute Bovine Pulmonary edema and emphysema (fog fever)
-moldy sweet potato
-perilla mint
-feedlot AIP
-other toxic plants, gases
Acute Respiratory Distress Syndrome (ARDS) in cattle
sudden onset, severe dyspnea associated with gross and histological findings of AIP
Oxygenation of arterial blood to fraction of oxygen in inspired air (PaO2/FiO2) is <400
Indicates poor oxygen echange (intersitial edema)
Severe diseases fit into the AIP or ARDS category
-Acute Bovine Pulmonary edema and emphysema (fog fever)
-moldy sweet potato
-perilla mint
-feedlot AIP
-other toxic plants, gases
What causes Acute Bovine Pulmonary Edema and Emphysema (ABPEE)
Fog fever- lush grass that is high in L-tryptophan
Rumen converts to 3-methyllindole (3-MI)
3-MI is absorbed and circulated (pneumotoxic)- causes AIP
What are the clinical signs of Fog fever *
Develop within 2 weeks of pasture change
-tachypnea, dyspnea, frothing at mouth
*NO coughing
mortality up to 30%
What produces 4-Ipomeanol
Fusarium solani
1) Ingestion of sweet potatoes infected with Fusarium solani (sweet potatoes are used as an energy source in beed cattle diets (palatable)
2) F. solani produces 4-ipomeanol which is a pneumotoxin
3) Develops AIP/ ARDS
What is the toxicity of Moldy Sweet Potato toxicity in cattle
Fusarium solani
1) Ingestion of sweet potatoes infected with Fusarium solani (sweet potatoes are used as an energy source in beed cattle diets (palatable)
2) F. solani produces 4-ipomeanol which is a pneumotoxin
3) Develops AIP/ ARDS
What are the clinical signs of Moldy Sweet potato toxicty (4-Ipomeanol)
Occur within 1 day of exposure
-tachypnea, dyspnea, expiratory grunt, coughing*, harshlung sounds
death 2-5 days after ingestion (high mortality)
T/F: Coughing is seen with 4-Ipomeanol toxicity *
True
T/F: Coughing is seen with 3-methylindole toxicity *
False
What are the causes of pharyngeal trauma and abscess in cattle
Causes: Trauma, Iatrogenic, Sharp Feed
Bacteria:
Trueperella pyogenes *
F. necrophorum *
Actinobacillus
Pasteurella
Strep
E Coli
What are the clinical signs of pharyngeal trauma and abscess in cattle
Stertor, stridor
respiratory distress
salivation, quidding, dysphagia
Nasal discharge, oful odor
pharyngeal swelling
+/- bloat
+/- systemic signs
How do you diagnose pharyngeal trauma and abscess
-Signs
-Oral exam under sedation (Xylazine, ket-stun)
-Endoscopy
-Radiographs
-U/S
-Needle Aspiration- if abscess submit for cytology and culture
How do you treat pharyngeal trauma and abscess in cattle
1) If there is an abscess then will want to drain and lavage - if deep make sure you dont go into jugular, carotid, or vagosympathetic trunk
*Drain with needle
2) Antibiotics- PPG
3) Anti-inflammatory agents
4) +/- tracheotomy - if severe
5) +/- rumenotomy - if rumen bloat is so severe
a very common disease of calves that is a necrotic inflammatory process of the larynx
Necrotic Laryngitis/ Laryngeal Necrobacillosis/
Calf Diphtheria
What is the pathogenesis of necrotic laryngitis
Start by different factors
1) Viral upper respiratory infection- all the viruses discussed for viral rhinitis
2) Primary bacterial- F. necrophorum and T. pyogenes are associated (also M. haemolytica, Pasteurella and other respiratory)
3) Trauma/irritation from medication admin, feed, feeding too hot of mil
What are the clinical signs of necrotic laryngitis
-Excessive salivation (wet chin)
-Moist painful cough
-Fetid odor
-Inappetance (painful to swallow)
-Stertor/ Stridor
-Respiratory distress
-Swollen larynx
What are differentials for necrotic laryngitis
Trauma
IBR
Haemophuilus
Oral abscess
Pharyngeal paralysis
Tumor
How do you treat Necrotic Laryngitis *
antimicrobials (penicillin, sulfa)
anti-inflammatory drugs (IV flunixin meglumine and then switch to oral meloxicam)
supportive care
+/- tracheotomy
use a low. stress weaning
prevention: vaccination protocol and prevent trauma
What antibiotics work well fornecrotic laryngitis
Penicillin works well for necrotic laryngitis (but the downside is that it is a large volume injected and must be given twice a day)
Sulfa antimicrobials also work well for this.
Oxytetracycline works okay and NuFlor can also be used
Where are laryngeal abscesses commonly located on
arytenoid cartilage(s)
trueperella pyogenes is most commonly
What is the most common bacterial cause of laryngeal abscesses in cattle
Trueperella pyogenes
What might cause a cause a lesion that looks like laryngeal abscess in cattle
congenital lesions of arytenoids
How do you treat laryngeal abscesses in cattle
1) Long term antibiotics
2) option for surgical therapy would be to do an arytenoidectomy or other airway surgery
laryngeal papillomatosis in cattle
Warts on the larynx due to Bovine Papilloma Virus (type 4)
Feedlot
Clinical Signs- respiratory distress, stertor, cough
Diagnosis- oral exam, endoscopy
Treatment- vaccination and surgery
Diagnosis- oral exam and endoscopy
treatment: vaccination and surgery
How do you treat laryngeal papillomatosis
generally these warts will resolve on their own, but they can cause problems for temporary period.
vaccine might help increase rate of resoliton but need two doses 3 weeks apart
Do surgery to debulk the wart
Can give NSAIDS and may consider antimicrobial if there is evidence of necrosis to reduce the risk of secondary bacterial infection
What causes red nose
Infectious Bovine Rhinotracheitis (IBR)
BHV-1
Infectious Bovine Rhinotracheitis
IBR (Rednose)
caused by BHV-1
Multiple clinical syndromes (upper respiratory, lower respiratory, reproductive, and possibly neurologic)
Diagnosis- nasal/nasopharyngeal swab (PCR or VI)
Treatment: anti-inflammatory and antimicrobial for secondary bacterial infection
Prevention: vaccination
How do you diagnose IBR
do a nasal or nasopharyngeal swab and submit it for PCR or virus isolation
What are the clinical signs of tracheal collapse in cattle
-Stridor- often loudest at the thoracic inlet (level of tracheal collapse)
-Cough
-Exercise intolerance
-Respiratory distress
How do cattle get tracheal collapse
-Commonly acquired at birth due to trauma
a) dystocia results in rib fracture (1st and 2nd) at the level of the tracheal inlet. Healing callus will put pressure on the trachea resulting in extraluminal tracheal collapse/ compression - Static collapse with both inspiratory or expiratory stridor
b) Congenital tracheal collapse but this is quite rare (more common in calves)
How might dystocia result in tracheal collapse in cattle
dystocia results in rib fracture (1st and 2nd) at the level of the tracheal inlet. Healing callus will put pressure on the trachea resulting in extraluminal tracheal collapse/ compression - Static collapse with both inspiratory or expiratory stridor
Dystocia results in_________ (static or dynamic) tracheal collapse
Static tracheal collapse
dystocia results in rib fracture (1st and 2nd) at the level of the tracheal inlet. Healing callus will put pressure on the trachea resulting in extraluminal tracheal collapse/ compression - Static collapse with both inspiratory or expiratory stridor
What does static tracheal collapse mean
it is staying collapsed regardless of inspiration/ exhalation
example: rib fracture with dystocia/ traumatic birth
How do you diagnose tracheal collapse in cattle
Radiographs- dorsoventral collapse
Endoscopy
How do you treat tracheal collapse in cattle
Surgical- prostehtic extraluminally around the trachea and suture the trachea to this device and pull the trachea open- not done very commonly, varied success with this surgical treatment
Conservative Medical Therapy- NSAIDs, rest, antibiotics
What is the prognosis of tracheal collapse in cattle
good if they can breathe well enough to allow fractures to heal and the animal to grow
go more conservative medical care
Tracheal Edema Syndrome (Acute Honker Syndrome)
Acute Honker Syndrome
Southern feedlots
inflammatory condition of the upper airways that results in edema and collapse of airways. believed to be caused by either irritants or allergens in sensitized animals
results in obstructive breathing pattern with a long, slow, and deep inhalation
Clinical signs: Sudden onset of respiratory distress
Stertor, stridor
Differentials: all other causes of partial obstruction
TreatmentL antimicrobial, steroids, +/- tracheostomy
Where is acute honker syndrome typically
southern feedlots
What are the clinical signs of tracheal edema (honker) syndrome in cattle
Sudden (acute) onset of respiratory distress
Stertor, stridor
inflammatory condition of the upper airways that results in edema and collapse of airways. believed to be caused by either irritants or allergens in sensitized animals
occurs in southern feedlots
a Tracheal Edema Syndrome -
Acute Honker Syndrome
treat with antimicrobials, steroids, +/- tracheostomy
What happens when a cow with tracheal edema syndrome (acute honker syndrome) attempts to inhale
the tracheal tissue is pulled further into the lumen and the trachea collapses down
these animals have an obstructive breathing pattern with a long, slow, deep inhalation
How do you treat tracheal edema syndrome (Acute Honker) in cattle
Generally NSAIDs dont really work well
Treat with corticosteroids, often start with injectable dexamethasone and then oral prednisolone
if there is an inflammatory component to it or suspicions of bacterial infection, then use antimicrobials
What is Chronic Polupoid Tracheitis
A tracheal edema syndrome that occurs at Western Feedlots
Clinical signs are continuous dry, hacking nonproductive cough
Differentials: pneumonia
Diagnosis: history, clinical signs, endoscopy
Treatment: none
Where is chronic polypoid tracheitis
Western Feedlots
What are the two tracheal edema syndromes of cattle
1) Acute Honker Syndrome- Southern feedlots and present with sudden onset of respiratory distress, stertor, stridor Treat with Corticosteroids (dexamethasone and then pred)
2) Chronic Polypoid Tracheitis- Western Feedlots, rpesent with continuous dry hacking nonproductive cough and have no treatment
What is the treatment for Chronic Polypoid tracheitis in cattle
there is not a lot to do for these cases
How does colonization resistance occur
1) Direct microbe-microbe inhibition
2) Indirect stimulated host immunity
Host epithelium also maintains mucociliary apparatus
What is the pathogenesis of BRD
Multifactorial
1) Central dogma: immunocompromised host risk factors -> virus causes directi njury to mucociliary apparatus, tracheal epithelium, immunosuppression where the upper respiratory tract commensal overgrow leading in nasopharyngeal bacteria to invade lower airways
2) Expanded to have immunocompromised host, environment, risk factors and viral infection leads to a dysbiosis between URT and LRT
Pathobionts dominate the niche leading to pathogenic behavior expression of virulence factors: leuktoxin, endotoxin
pathobionts
commensal / mutualistic behavior colonization resistance
where there is dysbiosis of URT and LRT leading to pathogenic behavior
What are the risk factors for BRD
*Complex
-Reduce host immunity (FPI and stress)
-Genetics, sex
-Viral infection
-Group housing
-Poor airquality
-Dehydration
-Weaning
-Weather
-Transport
-Cominging
-Nutritional deficiencies
-Surgical procedures
What is the BRD epidemiology in the dairy industry
Preweaned calves (<56 days of age) endemic (up to 30% in most herds)
differentiate between aspiration vs BRD
Weaned calves (most common 2-5 months)
enzootic calf pneumonia
viral exposure, stress (mixing groups)
Replacement heifers and cows: more commonly sporadic, metastatic
What is enzootic calf pneumonia
BRD in calfs after being weaned (most common 2-5 months)
due to viral exposure, stress (mixing of groups)
What is the BRD epidemiology of beef cattle
1) Cow-calf: up to 10% pre=weaned calves (3-5 months)
nadir of IgG, short calving interval leads to herd immunity low
2) Weaned Calves (shipping fever) transport from farm of origin to stocker/feedlot. Highest morbidity during 1st 21 days after arrival
3) Finishers (Feedlot) Cows: Sporadic outbreaks, interstitial pneumonia
route out high altitidue pulmonary hypertension
When is the highest morbidity of BRD in weaned calves
during the 1st 21 days after arrival
“Shipping fever”
BRD in older animals (finishers in beef and replacement heifers/cows in dairy) is often
sporadic outbreaks
What is the epidemiology of cow-calf beef BRD
up to 10% pre-weaned calves (3-5 months)
nadir of IgG
short calving interval leading to low herd immunity
What does the pathophysiology of BRD in the lungs depend on
dominant pathobiont and/or infectious agent and passive transfer status (IgG)
innate immune system is stimulated through pattern recognition receptors (PRRs)- toll like receptors, neutrohphils, and alveolar macrophages
pro-inflammatory cascade- increases oxidative host damage
secondary invaders, opportunists- consolidation of airways, pulmonary abscess, pleuropneumonia
Mannheimia hemolytica
Gram -, Aerobic Rod
Normal nasopharyngeal inhabitant
Dysbiosis allows for niche takeover by pathogenic serovars (A1, A6) and viral co-infection increases severity
Virulence factors: leukotoxin: cytolysis of ruminant leukocytes
endotoxin/LPS: pro-inflammatory (neutrophil chemostaxis)
causes lobar pneumonia leading to necrotizing fibrinous pleuropneumonia
peracute rapidly consolidating syndrome
emerging antibiotic resistance of field strains
What are the virulence factors of Mannheimia hemolytica
Virulence factors:
1) leukotoxin: cytolysis of ruminant leukocytes
2) endotoxin/LPS: pro-inflammatory (neutrophil chemostaxis)- generates oxidative damage
What organism is commonly associated with shipping fever
Mannheimia hemolytica
What are the pathogenic serovars of Mannheimia
A1 and A6
Mannheimia hemolytica causes ______________
necrotizing lobar fibrinous pleuropneumona
Pasteurella multocida (cattle)
Gram -, aerobic coccobacilli. Normal nasopharyngeal inhabitant (A 3 most commonly pathogenic)
Opportunistic
virulence factors:
1) Endotoxin (can lead to systemic endotoxemia/bacteremia)
Pathology: purulent lobar bronchopneumonia, less likely fibrin and necrosis
often dark red cranioventral lung consildation
T/F: unless there is a co-infection Pasteurella is not as severe in cattle as Mannheimia
True
What pathology does Pasteurella cause in cattle
purulent lobar bronchopneumonia, less likely fibrin and necrosis
often dark red cranioventral lung consildation
What bug is associated with endemic disease in groups of housed calves “enzootic pneumonia”
Pasteurella multocida
Bibersteinia trehalosi (cattle)
Gram - aerobe
Normal nasopharyngeal inhabitant (pathobiont)
occasional opportunist in the lungs
Similar to Mannheimia hemolytica as it causes sporadic outbreaks in feedlots
Presentation: outbreaks with high mirtality, may lack clinical signs and lead to sudden death
Histophilus somni (cattle)
Gram -, aerobic rod or coccobaccilus
normal nasopharyngeal inhabitant that is and opportunisit in the lung and extrapulmonary sites*
Virulence Factors (dictate systemic severity)
1) LOS: induce inflammatory cascade causing apoptosis of endothelial cells (vasculitis/ thrombosis) and induce IgE, histamine (hypersensitivity leading to increased permeability of bronchial epithelium)
2) Evasion of opsonization (outer membrane protein)
**Know this: Histophilus somni is an opportunist. of the lung and ___________
extrapulmonary sites
What are the virulence factors of Histophilus somni
opportunisit in the lung and extrapulmonary sites*
Virulence Factors (dictate systemic severity)
1) LOS: induce inflammatory cascade causing apoptosis of endothelial cells (vasculitis/ thrombosis) and induce IgE, histamine (hypersensitivity leading to increased permeability of bronchial epithelium)
2) Evasion of opsonization (outer membrane protein)
What are the extrapulmonary signs of Histophilus somni **
1) sepsis
2) thrombotic meningoencephalitis
3) Otitis
4) Mastitis
5) Polyarthritis
6) Myocarditis
7) Abortion
8) Endometritis
*important pathology includes vascultis and thrombi
What pathology does Histophilus cause *
Bronchopneumonia (common in feedlots_
Extrapulmonary sites:
1) sepsis
2) thrombotic meningoencephalitis
3) Otitis
4) Mastitis
5) Polyarthritis
6) Myocarditis
7) Abortion
8) Endometritis
*important pathology includes vascultis and thrombi
What BRD bacteria has extrapulmonary sites
Histophilus somni
What is the significance of treating BRD infections with Mycoplasma bovis *
It is a facultative anaerobe with no cell wall. Will not respond to antibiotics that target cell wall
Mycoplasma bovis/ dispar (cattle)
No cell wall, facultative anerobe (wont respond to antibiotics that target the cell wall)
Primary pathogen or opportunist at pulmonary and extrapulmonary sites
Virulence factors
1) Vsp A, B, C for immune evasion
2) Adhesins associated with virulence - to adhere to synovium or inner ear to persist longer times
Pathology: fibrinosuppurative or caseonecrotic pneumonia, peribronchial lymphoid hyperplasia
-cranioventral nodules that contain abscesses of coagulation necrosis
-“cuffing pneumonia: lymphoid hyperplasia around the airways
What pathology is seen with Mycoplasma bovis
fibrinosuppurative or caseonecrotic pneumonia, peribronchial lymphoid hyperplasia
-cranioventral nodules that contain abscesses of coagulation necrosis
-cuffing pneumonia: lymphoid hyperplasia around the airways
What are the virulence factors of Mycoplasma bovis
1) Vsp A, B, C for immune evasion
2) Adhesins associated with virulence - to adhere to synovium or inner ear to persist longer times
What pathogen should be high on your differential list if you cut through the bovine lung and see a lot of abscesses/ foci of coagulation necrosis
Mycoplasma bovis
What are the clinical signs of Mycoplasma bovis
Pneumonia
Otitis (preweaned calves)
Arthritis
Tenosynovitis (weaned calves)
other signs: mastitis, conjunctivits, myocarditis, pericarditis, abortion
Important transmission route: milk and colostrum
What is an important transmission route of Mycoplasma bovis? *
Milk and colostrum
Trueperella pyogenes
gram + anaerobic coccobacillus
opportunistic pathogen
secondary or tertiary invader (co-infection is common)
Indicator of chronicity is pulmonary abscess
Virulence factor: Pyolysin: cytolytic toxin that aids in adherence
What bacteria of BRD is gram +
Trueperella pyogenes
T/F: Trueperella causes acute cases of BRD
False- it is often a secodnary or tertiary invader (co-infection is common)
What bacteria are associated with the BRD complex
1) Mannheimia hemolytica
2) Bibersteinia trehalosi
3) Pasteurella multocida
4) Trueperella pyogenes
5) Histophilus somni
6) Mycoplasma bovis
What is the pathogenesis of BHV-1 causing bronchopneumonia
1) Direct contact/ aerosol
2) Surface glycoproteins allow for host attachment and cause direct injury to epithelial cells and immunosuppresion (decrease MHC 1 expression)
3) facilitates binidng of leukotoxin (Mannheimia hemolytica)
4) Latency related transcript allows for survival of infected cells beyond message of apoptosis and latency is important for spread (recurdescence from ganglia)
BHV-1 causes direct immunosuppression by __________ which allows ____________
decrease MHC class 1 expression
facilitates binding of leukotoxin (Mannheimia hemolytica)
What bacteria is associated with viral infection of BHV-1
Mannheimia hemolytica
What is the prognosis of BHV-1 primary respiratory disease
HIgh morbidity- common in feedlots of weaned steers
low mortality unless co-infection (Mannheimia hemolytica)
What is the pathogenesis of Bovine Respiratory Syncytial Virus (BRSV)
1) Direct contact, aerosl
2) G glycoprotein induces attachment
3) Epithelial cells fuse forming multinucleated cells, syncytia
4) Suppress function of macrophages
5) Develop atypical interstitial pneumonia (emphysema, bullae)
What does BRSV cause
it causes epithelial cells to fuse (multinucleated cells, synctia)
causes an atypical interstitial pneumonia
What is the virulence associated with BRSV *
BRSV-specific IgE (mast cell degranulation and eosinophil influx) - vaccine induced disease?
Lymph node infection (tracheobronchial, mediastinal) may allow for persistance
Why might a herd with BRSV have reaction to vaccination
BRSV-specific IgE (mast cell degranulation and eosinophil influx) - vaccine induced disease?
BRSV most commonly infects
Calves <6months of age
presentation often acute and confined to respiratory tract
How do cows with BRSV typically present
Calves <6months of age
presentation often acute and confined to respiratory tract
Peracute presentation (severe dyspnea)
-Hypersensitivity (immune mediated)
-Pneumothorax (ruptured bullae)
What is the pathogenesis of Parainfluenza Virus Type 3 (PI-3) in cattle
1) direct ocntact, aerosol
2) Direct injury to ciliated epithelial cells, mucus layer, mucociliary apparatus
3) Infection of alveolar macrophages (decreased finction)
Causes immunosupression that predisposes to secondary invader
PI-3 in cattle causes
immunosupression that predisposes to secondary invader
via infecting epithelial cells, mucus layer and mucociliary apparatus
infect the alveolar macrophage and decrease function
*Disease is often mild/subclinical unless secondary bacterial infection
How does BVDV affect the respiratory tract
impairs host immunity and associated with outbreaks of BRD
coinfections with Mannheum, Mycoplasma bocis, and BRSV
What a viruses that are associated with BRD
1) BHV-1 *
2) BRSB *
3) PI-3 *
4) BVDV
5) Bovine coronavirus
6) Influenza D
7) Bovine Reovirus
8) Bovine Rhinovirus
9) Adenovirus
How do you prevent BRD
1) Colostrum management (quality and quantity) *
2) Ventilation (group housing), shelter (weather protection)
3) Nutrition (volume and quality)
4) Transport management (water access)
5) Reduce stress and reduce mixing in vulnerable age groups **
6) Herd surveillance, Treatment approach *
7) Vaccination, Herd immunity
What is important regarding the vaccination timing of cattle for BRD prevention
MLV vaccine may have lower evidence
-Stress is immunosuppressive and leads to poor vaccianre response
-Maternal inference is no no
-Preconditioning: administration of vaccine prior to weaning
-Any vacine given at arrival period leads to a suboptimal response
What are the two major risk factors in dairy and beef that contribute to BRD
1) Inadequate colostrum
2) Host immunity are major factors
What MLV vaccine has the most evidence for reducing BRD i nweaned beef cattle *
BVDB- superior to killed vaccines
What signalment and history best describes cattle at high risk for BRD?
A) 8 month Angus steer on a feedlot that arrived 6 weeks ago
B) 21 day old Holstein Heifer calf housed indoors within group pens
C) 2yo Holstein first lactation heifer that freshened 10 days ago
D) 6month old Hereford steer that was weaned 5 days ago
E) both B and D
F) Both A and D
G) All of the above
Both B and D
A) Feedlot is a risk but 6 weeks is beyond the time where BRD is typically developed (within the first 3 weeks of arriving)
B) is correct because 3 weeks is within the early pre-weaned range and also in a group pen which increases
C) Stress from first lactation but outside the common range- would have been more
D) Is correct because of weaning
A gram positve associated with BRD, commonly a secondary or tertiary invader
has pyolysin *
Trueperella pyogenes
A gram negative associated with BRD
has leukotoxin* and endotoxin
associated with viral co-infections
and causes shipping fever
Mannheimia hemolytica (A1 and A6)
A gram negative associated with BRD, has endotoxin and causes enzootic calf pneumonia
Pasterella multocida (A3)
What strain of Pasteurella is pathogenic in cattle
A3
A gram negative associated with sporadic feedlot outbreaks
Bibersteinia trehalosi
A gram negative that is associated with BRD
has LOS, IgE and causes apoptosis of endothelial cells leading to vasculitis and extrapulmonary disease
Histophilus somni
What are challenges with diagnosing BRS
-Imprecise case definitions- interpreting sequencing data requires an accurate phenotype
-thoracic auscultation may be sensitize
-Anatomic localization (URT and LRT)
-Clinical vs subclinical- does subclinical warrant treatment (judicious use of antimicrobials)
What is DART
A herd surveillance technique used in cattle for BRD
-Depression
-Appetite Loss
-Respiratroy character change
-Temperature elevation
Low sensitivity (higher risk of false negative)
High specificity
How do you detect pathogens associated with BRD
-Nasal swabs (least ideal for bacteria)
Deep nasopharyngeal swabs - are better for bacteria but still challenging to interpret because it is polymicrobial
-Transtracheal wash/ aspirate - not as practical for cattle
-Bronchoalveolar lavage fluid (non-endoscopic is typically used or endoscopic)
Deep Nasopharyngeal Swabs used for BRD
captures respiratory and associated lymphoid epithelium of nasopharynx
High risk for contamination- double guarded and cleaned nares to reduce this
Aerobic culute: often polymicrobial and challenging to determine antibioitc plan
Mycoplasma is good at getting a single positive for culture
young calves and small ruminants, placement in ventral nasal meatus is challenging
When is lower airway sampling (Transtracheal wash and BALF) contraindicated in livestock *
If the animals a dyspneic
What are potential complications of doing transtracheal wash or BALF in livestock
Subcutaneous emphysema
Wound infection
Tracheal tear
Dyspnea (inadequate fluid return)
What is important when doing sample analysis of BRD pertaining to Mycoplasma bovis
It needs to be cultured in very specific condition
PCR is more sensitive
A 3 week old pre-weaned dairy calf with a cough reduced milk consumption and a head tilit. On lung ultrasound you find lobar consolidation. The producer is concerned about BRD in their calves and would like you to definitively diagnose a pathogen to determine an optimal treatment protocol
A) Nasal swab: submit for Mycoplasma culture and mutiplex viral PCR
B) Deep nasopharyngeal swab: submit for Mycoplasma PCR
C) Bronchoalveolar lavage fluidL submit for aerobic culture and anaerobic culture
D) Deep nasopharyngeal swab: submit for aerobic culture, anaerobic culture and multiplex viral PCR
B) Deep nasopharyngeal swab: submit for Mycoplasma PCR
nasal swab is not good
multiplex viral PCR wont tell you
given dairy signalment likely mycoplasma is playing a role.
needs to be specific culture or PCR
some evidence BRD but some extrapulmonary disease evidence
What should you treat Mycoplasma bovis with **
Macrolides, florfenicol, tetracyclines labeled
-NO cell wall (beta lactams are ineffective)
What increases the clinical severity of BRD
Co-infection of viral and bacterial agents
ie. BHV-1 and Mannheimia hemolyticum
What best approximates lung bacterial overgrowth in cattle
Nasopharyngeal and lower airway sampling
What is important transmssion route of Mycoplasma bovis *
milk and colostrum
clinical signs: pneumonia, otitis (preweaned calves), arthritis, tenosynovitis
When do outbreaks of bronchopneumonia occur in small ruminants
SPring: lambs 2 weeks to 2 months of age- severe weather
Fall outbreaks- lambs, 5-7 months with the arrival at feedlots
What is the pathogenesis of bronchopneumonia in small ruminants
Stress diminishes lung’s natural defense mechanism leading to enhances in viral infections, dysbiosis of respiratory microbiome\
common stressors: FPI, transport, overcrowding, parasitism, social changes, poor nutrition, weather, diet change, dust and mold exposure
Clinical signs of small ruminants with bronchopneumonia
-Separation from herd
-lethargy
-exericse intolerance
-inappetance
-Increased respiratory rate or effort
-cough
-poor body condition
physical exam findings: acute respiratory disease- fever, tacypnea, nasal +/- ocular discharge
chronic or progressive: weight loss, cough, tachypnea
What are the most common respiratory bacterial pathogens in small ruminants
1) Mannheimia hemolytica (A2) - different strain from cattle, coinfections (bacterial, viral)
2) Pasteurella (D,F): pneumonia, sepsis, arthritis, otitis, mastitis, with coifnections (bacterial, viral)
3) Bubersteinia trehalosi - more common in sheep
4) Corynebacterium pseudotuberculosis- caseous lymphadenitis (chronic abscess)- internal/ visceral and external form
5) Mycoplasma spp
M. ovipneumonia (sheep) causes enzootic/atypical pneumonia
M mycoides and capricolum (high morbidity, low mortality, coinfections inccreases mortality, extrapulmonary disease (arthritis, mastitis, septicemia)
How do you treat sheep and goat bronchopneumonia
Antimicrobial
-Ceftiofur sodium* or others
-NSAID
-Nursing care
Contro: vaccination- sheep and goats up to 6 months of age, improves management practices, limit stress, provide high quality diet, quarantine new arrivals, isolate isck animals
What is the only FDA approved drug for treating pneumonia in goat
Ceftiofur sodium
What causes pigeon fever in horses
Corynebacterium pseudotuberculosis
chronic disease of sheep and goats (rarely in camelids)- no cure
pyogranulomatous abscesses in lymph nodes and internal organs
highly contagious
resistant in environment
zoonotic- consuming infected, unpasteurized milk, contaminated equipment, infected pus in abdrasions
Caseous lmyphadentis
(Corynebacterium pseudotuberculosis)
What are common sites for caseous lymphadenitis
Lymph nodes:
mandibular
parotid
prescapular
preforma
What species does caseous lymphadenitis infect
sheep and goats (rarely in cameids)
How do you diagnose caseous lymphadenitis
Culture
How do you control for caseous lymphadenitis in small ruminants
biosecurity is key- purchase animals from known negative herds and flocks, prevent spread on fomites like shearing equipement
testi incoming animals- know limitx of test and possibility of negative SHI test
Vaccination: may help reduce incidence in herd and # abscesses per animals
Treatment: surgical removal of infected LNs, lance and drain, cull known + animals
What are the treatments for caseous lymphadenitis
surgical removal of infected LNs, lance and drain, cull known + animals
what are causes of viral pneumonia in small ruminants
Secondary Risk factor
Parainfleunza Type 3
Adenovirus
Respiratoy Syncytila Virus
Herpes virus
Major viral pathogens: lentiviurses
-Ovine progressive pneumonia (OPP)/ Maedi-Visna
-Ovine Pulmonary adenocarcinoma/ jaagsiekte
-Caprine Arthritis Encephalitis Virus (CAEV)
What are major viral pathogens causing direct pulmonary disease in small ruminants
Lentiviruses
1) Ovine progressive pneumonia (OPP)/ Maedi-Visna
2) Ovine Pulmonary adenocarcinoma/ jaagsiekte
3) Caprine Arthritis Encephalitis Virus (CAEV)
*Lentiviruses so they have persistent infections
infects goats and sheep
progressive, debilitating disease with no treatment
horizontal and perinatal spread (colostrum and milk)
World wide distribution
High seroprevalence within the US
Caprine Arthritis Encephalitis Virus (CAEV)
Caprine Arthritis Encephalitis Virus (CAEV) causes
-Leukoencephalomyelitis (neonates)
-Arthritis (carpal joints)
-Mastitis
-Chronic pneumonia: interstitial pathogenesis (type II pneumocyte proliferation)
-Chronic encephalomyeltiis
How do you diagnose CAEV
-Screening: lung ultrasound/ CXR
-ELISA: blood and milk
-PCR: BALF/Lung, blood, synovial fluid/ tissue, brain
T/F: caseous lymphadenitis is highly contagious and zoonotic
True
Zoonotic- consuming infected, unpasteurized milk, contaminated equipment, infected pus in abrasions
External form of caseous lymphadenitis
more common in goats
external lymph nodes commonly on neck and throat
Signs: swelling associated with lymph nodes
Diagnosis: Culture
Be careful as the pus is loaded with bacteria and highly contagious
What is the visceral or internal form of caseous lymphadenitis
-More common in sheep
mediastinal and mesenteric lymph nodes, lungs, liver, kidney, CNS
Clinical signs: progressie weight loss, exercise intolerance, tachypnea, dyspnea, chronic cough
What form of caseous lymphadenitis is more common in sheep
Visceral or internal form
mediastinal and mesenteric lymph nodes, lungs, liver, kidney, CNS
Clinical signs: progressie weight loss, exercise intolerance, tachypnea, dyspnea, chronic cough
What form of caseous lymphadenitis is more common in goats
External form
external lymph nodes commonly on neck and throat
Signs: swelling associated with lymph nodes
Diagnosis: Culture
Be careful as the pus is loaded with bacteria and highly contagious
*Culture pus
How do you do diagnostics for CL
External form: Culture pus
Visceral form: Radiograph thorax for abscess + cultue/PCR TTW fluid- failure to isolate CL from TTA fluid does NOT rule out CL
Asymptomatic animals: Do a synergistic hemolysis inhibition (SHI test)
False negatives are possible, a low titer does NOT rule out disease
theoretically, lower tier = exposure vs higher titer= infection
When do you perform Syngeristic hemolysis inhibition (SHI test)
Asymptomatic animals with CL
False negatives are possible, a low titer does NOT rule out disease
theoretically, lower tier = exposure vs higher titer= infection
What are the downsides to doing Syngeristic hemolysis inhibition (SHI test) for CL
False negatives are possible, a low titer does NOT rule out disease
theoretically, lower tier = exposure vs higher titer= infection
How do you control for CAEV
1) Prevent infection in neonates
-Separate newborns from dams
-Feed only virus free colostrum and milk
2) Prevent horizontal spread- test regularly and cull positive animaals
3) Prevent introduction to the herd
-Isolate and test all newly purchased animal
-SR lentivirus or SR biosecurity panel
How is CAEV spread?
Horizontal and perinatal spread (colostrum and milk)
What causes ovine progressive pneumonia (OPP)
Maedi-Visna Virus
How is OPP spread
Horizontal and perinatal spread (colostrum and milk)
Ovine Progressive Pneumonia (OPP)
Maedi-Visna Virus
Infects sheep primarily horizontal and perinatal spread- colostrum and milk
Cross species transmission to goats is possible via infected milk and colostrum
25-30% of infected animals will exhibit clinical signs (4-5 years)
Clinical signs: interstitial pneumonia, wasting, mastitis, arthritis, neurological signs
T/F: Transmission of ovine progressive pneumonia can be spread to goats
True-
Cross species transmission to goats is possible via infected milk and colostrum
What are the clinical signs of Ovine Progressive Pneumonia
Rapid progression over 1 year
interstitial pneumonia, wasting, mastitis, arthritis, neurological signs
How do you diagnose OPP
Screening: Lung ultrasound/ CXR
ELISA: Seroconversion may take weeks to 1 year, maternal antibodies may interfere, low-cost screening on milk
PCR: Milk, BALF, lymph node
HOw do you treat/ control OPP
no treatment
-most animals die within 1 year of signs
No vaccine available
difficult to eradicate once in herd- test and cull is expensive and impractical
prevention is best- strict biosecurity: isolation and testing, dont share rams, segregate animals at shows, purchase animals from known OPP-free flocks
What causes OVine Pulmonary Adenocarcinoma
Jaagsiekte Sheep Retrovirus (JSRV) or Pulmonary Adenomatosis Virus
How is Ovine Pulmonary Adenocarcinoma Spread *
Via respiratory ecretions (ie Nasal secretion)
also shed in milk and colostrum but vertical transmission is unlikely
How do you treat ovine pulmonary adenocarcinoma
no effective diagnostic for subclinical
no vaccination
no treatment
*May cause fatal neoplasia (1-5%)
What animals are suscpetible to JSRV
young lambs
tumors develop over months to years
and cause progressive emaciation, respiratory compromise when lead is lowered (Wheelbarrow test)
pleuritis and pleural effusions in camelids can be secondary to
Overhydration
What might cause pleuritis and pleural effusion in livestock
1) Bronchopneumonia (Histophilus, Manheimia) *
2) Traumatic reticulopleuritis
3) Camelid Strep zoo. (Alpaca fever)
4) Neoplasia
5) Pulmonary hypertension *
6) Overhydration in camelids
T/F: pleuritis and pleural effusions is painful
True
What are clinical signs of pleuritis and pleural effusions in cattle
-Signs of pneumonia
-Thoracic pain: reluctance to move, abducted elbows, grunting, groaning, bruxism, decreased chest excursion, abdominal breathing
-Decreased ventral breath sounds- fluid line
-Ventral dullness on thoracic percussion
-Friction rubs
What test hsould you do to confirm a cow is painful do to pleural effusion and pleuritis
Withers test
How do you diagnose pleuritis and pleural effusions in cattle *
Ultrasound- pleural effusion +/- lung consolidation
Radiographs
Thoracocentesis with cytology +/- culture
CBC/CP: left shift with hypergammaglobulinemia
How do you diagnose JSRV
PCR on blood, nasal secretions, BALF
What do you see with JSRV
young lambs - spread with nasal secretions
tumors develop over months to years
and cause progressive emaciation, respiratory compromise when lead is lowered (Wheelbarrow test)
diagnosis: PCR ob blood, nasal secretions, BALF
How do you treat pleuritis and pleural effusions in cattle
-Appropriate antimicrobials
-Anti-inflammatory
-+/- Drainage -caution because endotoxemia
Why should you be careful draining pleural effusion in cattle
As you are draining it out, likely to leak out around needle
endotoxemia
If it is clear fluid, you can possibly just drain it
What might cause pneumothorax in cattle
1) Rupture of emphysematous bullae
-BRSV
-AIP, 3-Methyl Indole
-Lungworm
-Metastatic pneumonia
2) Rib fracture and puncture of lung - dystocia
3) Laryngeal/ pharyngeal trauma - balling gun
4) other trauma
*Usually unilateral (complete mediastinum)
Why is pneumothorax typically unilateral in ruminants
because ruminants have a complete mediastinum *
How do you diagnose pneumothorax in cattle
-Thoracic auscultation
-Thoracic percussion
-Ultrasoun (Gap between visceral and parietal pleura with no glide signs)
-Radiographs
How do you treat pneumothorax in cattle
-Thoracocentesis and suction
-Closure of opening, if applicable
-Maintenance of negative intrathoracic pressure
Pneumothorax causes *
Inspiratory effort dyspnea
Pulmonary edema in cattle is most commonly secondary to ___________ *
*Hypoproteinemia
-Protein loss from kidney or GI tract
-Cachexia, cardiac
-Fluid overload
What are clinical signs of pulmonary edema in cattle
Dyspnea with crackles
head extension
tachypnea
obtundation
abscence of fever
+.- recumbency
Causes of pulmonary edema in cattle
1) Hypoproteinemia: Protein loss from kidney or GI tract
2) Cachexia, cardiac
3) Fluid overload
4) Pneumonia
5) Toxic gases
6) Ehrlichia ruminantum
How do you treat pulmonary edema in cattle
-Reduce or stop fluids
-Diuretics (furosemide)
-Administer colloids if hypoproteinemic
-Intranasal oxygen
-Limit handing asm uch as possible
-Dexamethasone may be beneficial
What bacteria may be associated with left ventricular failure and pulmonary edema in cattle
Histophilus somni
or
Ionophore toxicity
How might cattle get diaphragmatic hernia ****
1) Congenital
2) Acquired (most common) via dystocia associated with backwards or breech presentation
or others (truma, hadware disease- reticulum)
How can dystocia lead to a diaphragmatic hernia in cattle **
Backwards or breech presentation- sternum gets pulled and tearing of the diaphragm
What is the most common cause of diaphragmatic hernia in cattle
Dystocia associated with backwards or breech presentation
How do you diagnose diaphragmatic hernias in cattle
Radiographs* +/- barium
Ultrasound
Calves with diaphragmatic hernia are often treated for
Septicemia but it is unresponsive
only treatment is surgical closure (valuable animals only)
What are the clinical signs of diaphragmatic hernia in calves
vague signs most commonly related to GI signs not repsiratory
many falsely get treated for GI diseases but diaphragmatic hernia should always be on your list for a dystocia calf
What might be occurring if it appears that a ruminant is “vomiting”
Megaesophagus - can lead to aspiration pneumonia
can be secondary to Vitamin E deficiency
What might cause megaesophagus in ruminants
Vitamin E deficiency can lead to megesophagus
thymoma (livestock)
Occur in sheep and goats
-often asymptomatic, dynpnea, nuffled lung sounds, +/- congestive heart failure, +/- rumen tympany, +/- megaesophagus
Dx: Radiographs, Ultrasounds
Cutaneous Paraneoplastic Syndrome *
Adenocarcinoma of the Thymus leading to chronic skin disease, weight loss and pruritus
How might an animal have chronic skin disease from neoplasia *
Adenocarcinoma of the thymus
Cutaneous paraneoplastic syndrome
need to take the chest film
What cancers may cause cutaenous paraneoplastic syndrome *
Adenocarcinoma of the thymus *
other differentials: adenocarcinoma, chemodectoma, thymoma
What should you recommend for an animal with extensive dermatological workups that is idiopathic*
take a radiograph
could be cutaneous paraneoplastic syndrome
What might cause thymomas in cattle
Iodine deficiencies
Where does bovine cardiac lymphoma typically occur
right atrium
What are common sites of Bovine Leukemia Virus
Heart
Uterus
Lymph node
Abomasum
are the most common sites for enzootic lymphoma in cattle
How do you diagnose Bovine Cardiac Lymphoma
ultrasound to detect pericardial effusion and possible right atrial mass
pericardiocentesis with fluid analysis -> lymphocytes
BLV serology test
What is one of the most common areas affected by bovine leukosis
the spinal cord
What might cause diaphragmatic paralysis in camelids
Suspected degeneration or trauma to the phrenic nerve
Etiologies: Vitamin E deficiency, aberrant parasite migration, trauma to cervical spinal cord or thorax, nearby abscess or tumor
How do you diagnose Diaphragmatic paralysis
Radiographs or Fluroscopy
*a must to diagnose the problem
What is the pathogenesis of caudal vena caval thrombosis (CVCT)
1) Septic thromboemboli orginate from an abscess at the hilus of the liver - primary infection often starts in GI from rumen acidosis or rumenitis)
2) Showering CVC leads to septic emboli within the pulmonary circulation
3) Abscesses erode into bronchial wall and aneurysm can rupture into AW
How do you treat CVCT in cattle
long term penicillin, supportive care
What are the most common clinical presentation of CVCT
*Epistaxis, hemoptysis, anemia +/- dyspnea/tachypnea
Hypersensitivity pneumonitis in cattle is a type ______ reaction to dust, moldy hay, grain, and plant matter associated to the spores of __________
Type I and IV
Thermophilic actinomycetes (Micropolyspora faeni)
Spores of what is associated to allergic response, causing Hypersensitivity Pneumonitis in cattle *
Thermophilic actinomycetes (Micropolyspora faeni)
Hypersensitivity Pneumonitis is most common in what kind of cow
Dairy cows (confined)
signs: decreased milk production, appetite, weight loss, coughing, crackles on thoracic auscultation
How do you diagnose hypersensitivity pneumonitis in cattle
Titers for exposure, identify fungi in feed
-Thermophilic actinomycetes (Micropolyspora faeni)
Anaphylaxis in cattle is a Type _______ hypersenitivity reaction to ________
Type I
vaccine, milk, drug (penicillin), insects, bee sting
Milk allergy in cattle
auto-allergy
Type I hypersensitivity
common in Jersey, Guernsey, Shorthorn
Risk factor: change in milking routine
Urticaria, tachypnea, tachycardia, watery diarrhea, dyspnea
What breeds of cattle have an autoallergy to milk
Jersey, Guernsey, Shorthorn
T/F: Acute/Atypical intersitital Pneumonia (AIP) in cattle is treated with antimicrobials
false- little respopnse to antimicrobials
this is commony non-infectious, secondary to inhalation or ingestion of toxin
What causes Acute/Atypical intersitital Pneumonia (AIP) in cattle
this is commonly non-infectious, secondary to inhalation or ingestion of toxin
What causes Acute/Atypical Interstitial Pneumonia (AIP) and Acute Respiratory Distress Syndrome (ARDS) in cattle characterized by severely acute interstitial edema and poor oxygenation
1) Acute Bovine Pulmonary Edema and Emphysema (fog fever)
2) Mold sweet potatio (R-ipomeanol) toxicity
3) Perilla mint toxicity
4) Feedlot AIP
Other toxic plants and gases
Cattle in ARDS have a PaO2/FiO2 of _______
<400
What is the pathogenesis of ARDS associated with lush pasture
1) Adult cattle >2 years old eat lush pasture that is high in L-tryptophan
2) Rumen converts to 3-methylindole (3-MI)
3) 3-MI is absorbed and circulated and causes AIP as it is pneumotoxic
4) Clinical signs seen within 2 weeks of pasture change: tachypnea, dyspnea, frothing at mouth, no coughing*
How do you treat/ prevent fog fever
move pasture, suportive care (NSAID/steroid)
furosemide for intersitital edema
gradual pasture introduction
feed ionophores (monensin)
Are clinical signs of 3-methylindole or 4-ipomeanol seen sooner?
4-IP: seen within 1 day of exposure while 3-MI is within 2 weeks of the pasture change
Perilla frutescens toxicity
associated with perilla mint, purple mint, wild coleus, beefsteak plant
-oils contain pneumotoxin similar to 4-IP
Common in the southeast (Aug-Oct- seed and flower stage)
Pathogenesis is similar to fog fever and moldy sweet potato toxicity
Clinical signs: sudden death, ARDS
What is Feedlot Acute/ Atypical Interstitial pneumonia
Cause is unknown but possible feed assocated pnemotoxin- BRSV?
cattle on feed more than 60 days following arrival a feedlot
-summer and fall
-more common in heifers
-high mortality
Clinical presentation
-rapid onset of dypsnea
-tachypnea
-cyanosis
-subcutaneous emphysema
*Inophores (monensin) ineffective
Feedlot Acute/ Atypical Interstitial pneumonia affects cattle that *
are on feed more than 60 days following arrival at feedlot
What causes Feedlot Acute/ Atypical Interstitial pneumonia
Cause is unknown but possible feed assocated pnemotoxin- BRSV?
T/F: Ionophores (monensin) is effective in treating/preventing Feedlot Acute/ Atypical Interstitial pneumonia
False
T/F: Inophore (monensin) is effective in treating/preventing Fog Fever
True
What are toxic gases that affect cattle
-Nitrogen dioxide in silo gas
-Zinc oxide (welding)
-Manure gas (hydrogen sulfide, ammonia, CO2, CO, methane
-Smoke inhalation
-Chlorine
Clinical signs consistent with ARDs
Treatment: move to a ventilated area, supportive care (furosemide, anti-inflammatories/ steroids)
What is the lifecycle of lungworms that cause parasitic bronchitis and pneumonia in cattle *
1) Eggs from L5 mature worms are coughed up from lungs and swallowed
2) Hatch within the GIT
3) Shed as L1 in feces
4) L1 molts 2x to become ineffective L3
5) L3 penetrates GIT and enters lymph nodes (molts to L4)
6) L4 travels to lungs in lymph/blood and incite eosinophilic exudate that blocks airways
7) L5 move to larger airways (tracheitis)
clinical signs: graudal progressive cough with possible complications of pulmonary edema, emphysema, secondary bacterial infection
What age of cows do lungworms affect
young non-immune yearlings/adults
temperate areas with high rainfall
How long does it take from ingestion of L3 lungworms intil they are in the respiratory tract
28 days
What stage of lung worms incite eosinophilic exudate that blocks airways
L4- creates inflammation
What are the clinical signs of lungworms
clinical signs: gradual progressive cough with possible complications of pulmonary edema, emphysema, secondary bacterial infection
How do you diagnose lungworms in cattle
1) Baermann on fresh feces to detect the L1 stage
-feces suspended in water
-larvae actively move into the water
-sink for collection
2) TTW or BAL- larvae or eosinophils
What stage of lungworm does Baermann detect
L1 larvae
-feces suspended in water
-larvae actively move into the water
-sink for collection
How do you treat lungworms in cattle
Anthelminthics
1) Levamisole - nicotinic acetylcholine receptor agonist
2) Benzimidazoles (-azoles)- bind tubulin and disrupt tubulin microtuble equilibrium
3) Macrocylic lactones (-mectins) : bind glutamate gated chloride channels
others: anti-inflammatories (NSAID/steroid) +/- antibiotics (secondary infection)
What is the mechanism of macrocyclic lactones like ivermectin and eprinomectin in the treatment of lungworms in cattle
bind glutamate gated chloride channels
What is the mechanism of Benzimidazoles like Fenbendazole and Albendazole in the treatment of lungworms in cattle
bind tubulin and disrupt tubulin microtubule equilibrium
What is the mechanism of Levamisole (imidazothiazole) in the treatment of lungworms in cattle
nicotinic acetylcholine receptor agonist
What causes bovine lungworm
1) Dictyocaulus viviparus
2) Ascaris suum- if exposed to high egg exposure in pigs, 10d post ingestion, causes rumen stasis interstial pneumonia via aberrant migration
Ascaris suum
a bovine lungworm if exposed to pigs (high egg exposure)
-Aberrant migration
-10days post ingestions
-Interstitial pneumonia
-Fever
-Rumen stasis
-Depression
What are different small ruminant lungworms
1) Dictyocalus filaria- 4 weeks post ingestion
2) Muellerius Capillaris- goats are more severe (interstitial) with an indirect lifecycle (snal and 6 weeks prepatent), resistant to levamisole
Muellerius capilalris is resistant to
Levamisole
Muellerius Capillaris infection are most common small ruminant lungworm and they cause severe disease in
goats- interstitial
What lifecycle does Muelleris capillaris have
indirect life cycle
snail (intermediate host)
6 weeks prepatent
You are called out to look at a pen of Angus heifers
that have had respiratory signs over the last 2 days .
The producer reports that he found 4 dead this
morning. As you get out to the dry lot pen you notice
that most of the heifers are coughing and tachypneic,
and some are dyspneic. Based on this information,
what is the most likely diagnosis and best intervention
strategy?
A. AIP/ARDS secondary to L-tryptophan ingestion; move to pasture and feed
monensin to the group
B. AIP/ARDS secondary to pneumotoxin 4-IP ingestion; investigate feed bunk
for potatoes and remove
C. AIP/ARDS secondary to aspiration of lungworm larvae; treat group of heifers
with levamisole
D. AIP/ARDS secondary to liver abscesses and pulmonary thrombi; treat group
with penicillin
B. AIP/ARDS secondary to pneumotoxin 4-IP ingestion; investigate feed bunk
for potatoes and remove
What parasite is resistant to Levamisole
Muellerius Capillaris
A second lactation Jersey cow 180 DIM was let out to
graze fresh pasture during the summer. The herd
manager decided to keep her with the dry cows and
forego milking her that afternoon. At the evening check,
the herd manager notices her standing with her head and
neck extended, tachypneic and open-mouth breathing.
Thankfully, you are already at the farm finishing up with a
dystocia (you saved the calf!)
What is the BEST next step for treating this cow?
A. You administer dexamethasone and tell the herd manager she
needs to be moved off the pasture immediately.
B. You tell the herd manager she likely has ARDS, which as a poor
prognosis, and humane euthanasia is recommended.
C. You prepare to take a deep nasopharyngeal swab that you will
submit for culture and sensitivity and treat her with flunixin
meglumine and florfenicol.
D. You administer epinephrine and flunixin meglumine and move her
to the parlor for milking immediately.
D. You administer epinephrine and flunixin meglumine and move her
to the parlor for milking immediately
Mestastic pneumonia in cattle manifest as ___________ *
epistaxis with varying degrees of respiratory distress
Rumen is primary origin of the disease
What makes you suspicious for anaphlaxis in cattle *
Respiratory distress is accompanied by pharyngeal edema and urticaria
*Give Epinephrine, glucocorticoid (if not pregnant)
