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VMS 3010 > Approach to Upper Respiratory Tract Disease > Flashcards

Approach to Upper Respiratory Tract Disease Flashcards

1
Q

What is Equine Influenza Virus?

A
  • One of the most common infectious diseases of the URT in horses
  • Routine vaccination is helpful in preventing outbreaks
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2
Q

What is Equine HerpesVirus?

A

EHV 4:typically, upper respiratory disease in young horses
* EHV 1:respiratory disease, neurologic disease,late-term abortion, early foal death

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3
Q

What are the risk factors for Infectious diseases of the URT?

A

Horses of all ages, particularly common in young horses
* High traffic, large groupherd
* Virus transmission: air, direct nasal droplets, indirecttransmission via people, water
bucket, equipment

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4
Q

What is the clinical presentation of URT diseases?

A

Nasal discharge (often bilateral), enlarged LNs, fever, lethargy → typically,transient
* Consider LRT disease if + cough,tachypnoea
* Another ddx: oesophagealobstruction

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5
Q

How might you diagnose infectious diseases of the URT?

A

Nasal swab for respiratory PCR panel

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6
Q

How might you treat/ prevent Infectious diseases of the URT?

A

Often self-resolving
* NSAIDs: flunixin meglumine,phenylbutazone
* Supportive care: palatable foods, monitor hydrationstatus
* Vaccination

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7
Q

What biosecurity measures would you put in place to help prevent URT diseases?

A
  • Limit nose to nose contact
  • keep up with good routine hygeine practice
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8
Q

What is the aetiology of primary sinusitis?

A

either subacute or chronic, most common form of sinusitis

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9
Q

What is the aetiology of secondary sinusitis?

A

Dental/oral disease: 24%
* Sinus cyst:13%
* Others: trauma, neoplasia, mycosis, ethmoidhematoma

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10
Q

What is the pathophysiology of primary sinusitis?

A
  • URT viral infection
  • Reduced mucocilliary clearance
  • Accumulation of mucus
  • Secondary bacterial infection
  • Accumulation of purulent material ‘empyema’
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11
Q

What two ways might dental disease cause secondary sinusitis?

A

Primary dental dzs with extension into sinus
* Maxillary molars (9,10,11) roots lie within
the maxillary sinus: covered by fine layer of
alveolar bone and sinusperiosteum
* Apical tooth rootinfections of these teeth
can result insinusitis
Oromaxillary fistula

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12
Q

What is a sinus cyst?

A

Unknown aetiology
o Can occur at anyage
o Benign but expansile nature
: can distort paranasal structure

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13
Q

What is the clinical presentation of sinusitis?

A

Serous/mucoid/purulent unilateral nasal discharge
o Facial swelling/distortion (maxillary orfrontal)
o Nasal airflow obstruction: abnormal respiratorynoise
o Difficulty chewing: (usually dental disease)

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14
Q

How might you diagnose sinusitis?

A
  • Physical exam/ History
  • Oral exam
  • Imaging (radiography, endoscopy (URT sinus) CT )
    *
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15
Q

What are the three main goals of treating sinusitis?

A
  • Removal of the infective/ necrotic tissue
  • Restoration of normal drainage and mucocilliary clearance
  • Prevent Recurrence
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16
Q

How does a sinus trephination and lavage work?

A

Frontal, caudal, rostral maxillary
* Allows high volume lavage or instillation of antimicrobials

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17
Q

How does sinus flap surgery work?

A
  • Better surgical access to sinuses
  • Standing surgery
  • Extirpation, curratege to remove cysts or mass
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18
Q

What is the guttural pouch?

A

Air-filled pocket extension of Eustachian tube

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19
Q

What is the function of the guttural pouch?

A
  • Pressure equalization
  • Warming of inhaledair
  • Resonating chamber forvocalization
  • Cooling of blood to the brain during exercise
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20
Q

What is the definition of guttural pouch empyema?

A

Accumulation of exudate within the Guttural Pouch

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21
Q

What are the clinical signs of guttural pouch empyema?

A
  • Fever and related symptoms: anorexia,lethargy
  • Lymph nodes swelling
  • Unilateral/bilateral purulent discharge
22
Q

How might you treat Guttural Pouch Empyema?

A

o Supportive therapy: NSAIDs, palatablefeed
o Lavage purulent material viaendoscopy
o Removal of chondroids via endoscopy or surgery

23
Q

What bacteria causes strangles in horses?

A

Streptococcus equi equi

24
Q

What is streptococcus equi equi?

A

Gram +, β-haemolytic streptococcus, Lancefield groupC
* Highly contagious URT disease of Equidae: high morbidity (~100%) ,low
mortality (~1%)
* Endemic in many countriesincluding the UK
* Significant economic and social impact within the equine industry
* Strict codes of practice for disease control and biosecurity

25
Q

What is the pathogenesis of Streptococcus equi equi Infection?

A
  1. Inhalation/ Ingestion of S. equii
  2. Colonisation of URT epithelium tonsil tissue
  3. Rhinitis and paryngitis
  4. Spreads to local lymphatics
  5. Lymphadenopathy and abscess formation
  6. GP Emypema, Abscess Rupture
26
Q

What is the clinical presentation of mild strangles?

A

Pyrexia followed by pharyngitis and subsequent abscess formation in the submandibular and retropharyngeal lymphnodes

27
Q

What is the clinical presentation of severe strangles?

A

Swollen LNs interfering with breathing and/or swallowing → ‘strangles’

28
Q

Nmae two strangles-related conditions

A
  1. Metastatic infection- bastard strangles
  2. Immune-Mediated conditions- Purpura haemorrhagica, myositis
29
Q

What samples would you take for strangles?

A

Nasal swab: not useful
* Nasopharyngeal swab/wash: early in the dzs process with some clinical signs
* Swab from purulent discharge from an abscess: high yield
* GP wash: best dx sampling esp.in chronic carriers

30
Q

How might you diagnose strangles through bacterial culture?

A

Positive when there is live organism
* False negative if insufficient sampling

31
Q

How might you diagnose strangles through molecular diagnosis?

A

High sensitivity and specificity

32
Q

How might you diagnose strangles using serology?

A

dentify recent infection(2w)*
* Peak ~5 weeks & remain high ~6 months
* One time testis no indication of active infection
* Often miss-used as a ‘screeningtool’
* A guide for strangles relateddzs

33
Q

How would you treat Strangles with NSAIds?

A

NSAIDs: Flunixin meglumine,phenylbutazone
* Palatable food

34
Q

How would you treat strangles with antibiotics?

A
  • Penicillin gel: local infusion to theGP
  • 75% of horses develop long-term mucosal immunity as a result of infection
  • Systemic abx may interfere with the development of natural immunity
  • Systemic abx: reserve for very sick, compromisedcases
35
Q

What is bastard strangles?

A

Hematogenous or lymphatic spread ofthe organism
* Metastatic abscess: brain, abdomen, mammary, brain, eyes,etc
* A history of exposure to S. equi, recurring fever, high S. equi Ab titer
* Treatment: systemic abx

36
Q

What is immune mediated purpura haemorrhagica and myopathy?

A

Necrotizing vasculitis: edema, petechialhemorrhage
* Peripheral oedema: head, limbs,torso
* Petechiation of themucousmembranes
* A history of exposure to S. equi, suggestive CS, high S. equi Ab titer, skin biopsy
* Treatment: steroids +/- systemicabx

37
Q

What biosecurity issues are associated with strangles?

A

Highly contagious among equidfamily
* Transmission via nasal discharge material, contaminated water andequipment
o Shedding of S.equi equi usually ceases 2-3 weeks after clinical signs resolve
o Silent carriers: some horses harbourinfection in GPs
o Detection, segregation, and treatment of carrierhorse

38
Q

What should you do with a positive Strangles case?

A

Strict isolation
* Test & release: need multiple tests over weeks

39
Q

What should you do with an in-contact strangles case?

A
  • In contact with + case but no clinical signs
  • Monitoring RT &CS
  • Test if suspicious
40
Q

How would you treat a strangles carrier animal?

A

GP local abxinfusion
* Test & release
* May need multiple treatments & tests
e.g. penicillin geltreatment q 1 week x 3
then test GP wash twice over weeks apart

41
Q

What are the main differentials for epistaxis?

A

Trauma
* Ethmoidal hematoma
* Guttural pouch mycosis
* Lower airway disease: exercise-induced pulmonary haemorrhage(EIPH)

42
Q

What is the iatrogenic cause of epistaxis?

A

usually nasogastric intubation

43
Q

What is the general approach to blood loss?

A

Identify & stop the source of blood loss
Blood transfusion
* If PCV <12%
* Ongoing, moderate to severe bloodloss

44
Q

What are the clinical signs of Progressive Ethmoidal Haematoma?

A

Intermittent epistaxis: ‘mucky’blood
* Varying degrees of nasal/sinusobstruction

45
Q

How would you treat progressive ethmoidal haematoma?

A

Small lesions (<3/4 cm): intralesional formalin(10%)
* Large lesions: surgical resection via sinusflap

46
Q

What is the aetiology of guttural pouch mycosis?

A

Aspergillus fumigatus and Emericella nidulans
* Most commonly identified fungal agent +/- otherfungal spp.
* Opportunistic infection: uncertain why some horses develop clinical dzs
* Climatic factors: global warming and increasing prevalence in certain areas

47
Q

How might you diagnose Guttural Pouch Mycosis?

A

Suggestive clinical signs
* Recurrent uni/bilateralepistaxis
* Severe epistaxis
Endoscopy
* Stabilize the horse before the imagingstudy

48
Q

How might you treat Guttural Pouch Mycosis using medical management?

A

Anti-fungals: Itraconazole, enilconazole
* Topical infusion via Indwelling catheter inserted into GP +/- systemic administration
* Careful case selection:time to respond & success rates vary
* Risk of fatal haemorrhage secondary to the erosion ofthe carotid arteries

49
Q

How might you treat Guttural Pouch Mycosis using Surgical options?

A

Occlude blood supply (cranial & distal) → fungal growth stops and eventually resolve
* Balloon catheterisation
* Coil embolisation

50
Q

What is the prognosis for guttural pouch mycosis?

A

Good if treated surgically in timelyfashion
* Poor to guarded if complications (e.g. neurological dysfunction)

VMS 3010 (79 decks)

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