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Equine Final Year > Nasal Discharge/Sinusitis > Flashcards

Nasal Discharge/Sinusitis Flashcards

1
Q

What is the problem list?

A

–Nasal discharge bilateral – how do we get this?

–This is probably the main problem!

–Bilateral mucopurulent nasal discharge

•Not something associated with sinus disease in this case

–Lymphadenopathy

–May be bacterial, viral, fungal

–Could neoplasia

»Uncommon in horses but correct age range…

–Depressed

–Anorexia

–Pyrexia

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2
Q

What does bilateral nasal dischrage usually indicate?

A

Disease behind nasal septum

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3
Q

What diseases can cause bilateral nasal discharge? (8)(unless bilateral disease of nasal cavity (uncommon))

A

•Pharyngeal disease

–Pharyngitis

–URT viral and bacteria diseases

–Guttural pouch mycosis, tympany, empyema

»Guttural pouches close to nasal septum, can cause pus down one side or both

•Laryngeal disease

–Arytenoid chondritis

»Infection of these cartilage causes purulent discharge

•Lung disease

–Inflammatory conditions (RAO/Asthma)

–Infectious conditions (pneumonia)

–Neoplasia

–Haemorrhage

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4
Q

Where does unilateral nasal discharge originate?

A

Rostral to the caudal end of the nasal septum. Pus from one side is there as doesn’t have chance to go down both nostrils

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5
Q

What is different about the nasal septum in cows compared to horses? What is the consequence of this?

A

Shorter and quite often will tend to get more things occurring bilaterally in cows but in horses

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6
Q

What diseases can cause unilateral nasal discharge? (7)

A

–Nasal foreign body

–Nasal tumour, polyp, cyst

–Fungal rhinitis

–Nasal trauma

–Unilateral sinusitis

•May occur with mild guttural pouch disease

–GP empyema

–GP tympany

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7
Q

What is purulent nasal discharge indicative of?

A

Infection/severe inflammation

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8
Q

What might be associated with Purulent nasal discharge?

A

Foul smell

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9
Q

What can cause a Purulent nasal discharge? (7)

A

–Often due to anaerobic infection

–Or could be some kind of necrotizing tissue disease:

  • Fungal disease
  • Tumour
  • Oro-sinus fistulae and other dental diseases
  • Turbinate necrosis
  • Necrotizing pneumonia
  • Foreign bodies
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10
Q

What are the differentials for depression? (4)

A
  • Pyrexia
  • Systemic disease
  • Hypovolaemia
  • Pain
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11
Q

What are the differentials for anorexia? (6)

A
  • Pyrexia
  • Systemic disease
  • Dental disease
  • Colic
  • Pain (GI, MSK, Thoracic)
  • Hyperlipaemia
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12
Q

What are the differentials for this case? (4)

A

•Bacterial disease, due to mucopurulent discharge. Could be from:

–Guttural pouch (as it is bilateral)

–Pharynx / retropharyngeal nodes

–Lungs

  • Primary viral disease with secondary infection
  • Neoplasia / Mass
  • Foreign body
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13
Q

What examination diagnostic procedures do we have in a horse? (6)

A
  1. Body Systems evaluation
  2. Full physical examination
  3. Neurological evaluation
  4. Ophthalmic examination
  5. Aural Examination
  6. Rectal Examination
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14
Q

What labatory assessment diagnostic procedures do we have in a horse? (9)

A
  1. Haematology
  2. Fibrinogen
  3. Serum Amyloid A
  4. Serum Biochemistry
  5. PCV, TOTAL PR, LACTATE
  6. Serum triglycerides
  7. Broncho-alveolar lavage
  8. Trans-tracheal wash
  9. Serology
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15
Q

What diagnostic imaging diagnostic procedures do we have in a horse? (11)

A
  1. Endoscopy at rest
  2. Exercise endoscopy
  3. Electrocardiography
  4. Thoracic radiography
  5. Thoracic ultrasound
  6. Cardiac ultrasound
  7. Head Radiography
  8. Pharyngeal ultrasound
  9. Abdominal radiography
  10. Computed tomography
  11. Magnetic Resonance Imaging
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16
Q

When would we do a diagnostic test?

A

If it changes a treatment plan

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17
Q

What diagnostic procedures should we do? (7)

A
  • Full physical exam
  • Haematology
  • Serum amyloid
  • Serology
  • Endoscope at rest
  • Head radiographs

Note: Would need sedation

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18
Q

What does an increased fibrinogen on bloods mean?

A

Have some sort of inflammatory process going on here

–Doesn’t really go super high, if it in 7 or 8 – really need to worry!

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19
Q

What would a Leukocytosis – associated with a neutrophilia as well tell us?

A

–Starts to tell us that it probably isn’t viral disease!

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20
Q

How do we interpret PCV at bottom end of normal?

A

–Interpret this based on the animal that is presented to us! Broad range of normal, but heavier draught horses will be at lower end of the spectrum so this PCV could definitely be normal

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21
Q

What can be seen? (this picture is at the opening to the gutteral pouch)

A

–Trickle of discharge coming down

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22
Q

What can be seen? (This is within the pouch)

A

–Cannot see much due to very purulent material! Impression there is some hyperinflammatory process of guttural mucosa, so instead of a nice pink it looks more angry and red

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23
Q

What are the 2 likely organisms causing gutteral pouch empyemea?

A

•Streptococcus equi subsp equi – one we need to be most concerned about!

–‘Strangles’

»Concern about this!

•Streptococcus equi subsp zooepidemicus – can also cause this and there is also loads of other weird and wonderful things as well

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24
Q

Do we need to confirmation test for gutteral pouch emyema?

A

–Should be assumed S equi unless otherwise proved – SO YES DOES NEED TESTING FOR! As it is a disease that has high virulence and quite significance implication for other horses on the yard! The fact this horse was normal when she got it and then it got ill, was this horse ill when she bought it? Likely it was and then developed the disease on the yard – therefore one of the horses on the yard may have passed the disease to it on the yard – will affect how we manage any other horses that are there!

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25
Q

What is S. Equi usually sensitive to? (2)

A
  • Penicillin
  • Oxytetracycline (and therefore Doxycycline)
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26
Q

How do we confirm diagnosis of S. Equi? (3)

A

•Nasopharyngeal swab

–Bacterial culture

–Cotton bud on long metal swab, goes up nose, sample of bacteria, send for culture – see what grows

–Would have been gold standard 3 years ago, would have been done on 3 occasions but definitive limitations to this and it wont pick up some of the animals that are clinical carriers

–If bacteria isn’t shed into pharynx, then this will NOT pick up the disease

•Guttural pouch wash

–Bacterial culture – sterile fluid in, resample this and collect for culture

–PCR diagnosis – look at some of the DNA to see if evidence of specific sequences that are consistent with strep equi equi

•Will have a far far higher sensitivity than just random samples of bacteria at back of the throat

–Clinical signs and culture of 3x n/ph swabs 60% sensitivity, 90% if PCR

–Guttural pouch flushing’s more sensitive than nasopharynx or nasal discharge

–One of the areas bacteria like to like!

•Serology

–Sensitivity 91.5%. Specificity 90.2% of recent exposure

–Can look at specific markers for strangles bacteria

–But there are limitations for how we interpret the results

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27
Q

How do we use serology to test for S. Equi?

A

–SeM specific antibody – specific antibody to one of the antigens expressed on strangles bacteria. When is it good to use serology? What will it show:

  • recent (but not necessarily current) S equi infection,
  • determining the need for booster vaccination
  • aid in the diagnosis of purpura hemorrhagica and metastatic abscesses.

–Bastard strangles – multiple dissemination of abscesses through the body

•Does not distinguish between vaccine and infection response.

–Serum titers peak about 5 weeks and remain high for at least 6

•They will start to tail off – one of the things important to determine the quenisity of the disease based on these levels

28
Q

What is a negative serology?

A

–No SeM-specific antibodies detected.

  • No previous exposure to S equi or
  • Recent vaccine or exposure <7 days) – hasn’t had time to mount antibody response
29
Q

What is a weak postivie result in serology?

A

1:200-1:400

–SeM-specific antibodies detected at a very low level.

  • Equivocal result
  • May represent very recent or residual antibody from exposure or vaccine
  • In this situation, sensible thing would be to repeat in 7 to 14 days to confirm recent exposure.

–If response still the same – will suggest it was exposed a long time ago

–If bacterial is increased further – shows active disease and mounting an immune response

•Could be almost anything really!

30
Q

What is a moderate positive result in serology?

A

1:800 - 1:1600

–SeM-specific antibodies detected at an intermediate level.

  • 2 to 3 weeks after exposure
  • Infection occurred 6 months to 2 years previously
31
Q

What is a high positive serology result?

A

1:3200-1:6400

–SeM-specific antibodies detected at a high level. High

  • 4 to 12 weeks after infection
  • 1 – 4 weeks post vaccination

–New response to vaccine

•Vaccination is contraindicated in horses with existing high levels of antibody (>1 : 1,600)

–If using for vaccination rasons, if it has high level – doesn’t need vaccination

•Important to know clinical history of the animal

32
Q

How do we get a bacteriology sample?

A

Nasal pharyngeal swab

Direct lavage of GP

33
Q

What does this show?

A

•Gram positive cocci

–Growing in chains

–Beta haemolytic chains

•Demonstrating beta-haemolysis

–With mucoid colonies

  • Typical of S equi equi
  • Look mucus like – due to capsule of S equi equi
34
Q

How can we confirm S Equi bacteriology?

A

•Confirm by carbohydrate assay

–Does NOT ferment to sorbitol and lactose

–Need to distinguish between the different sub species of strep equi

35
Q

Where is strangles highly infectious?

A

•Highly infectious particularly weanlings and yearlings - these animals that don’t have an immune response or don’t mount one particularly effectively, so:

–Rarely affects horses >5

36
Q

Where in the body does strangles affect?

A

–Typically affects upper respiratory and lymph nodes

•Retropharyngeal LN that are key to the name of the disease. If profound lymphadenopathy, these are at the base of the guttural pouches and compress pharynx and can strangle the horse if they get larger and larger and larger – this rarely happens! It is a potential, but not seen typically!

37
Q

Strangles:

  1. Incubation period?
  2. When does it shed?
  3. Morbidity? Mortality?
A
  1. Incubation period: 3-14 days
  2. Shedding from 2d after onset of pyrexia
  3. High morbidity, low mortality
  • •20% complication rate has been reported
  • •Horses don’t die usually! But there are a number of other complications as a result of exposure
38
Q

What is the flow chart of strangles? From expsosure to the immune response

A
39
Q

Why does resolving clinical signs mean that the animal isn’t clear of disease with strangles?

A

About 10% of infected animals can then become carriers, typically keep bacteria in guttural pouch and can shed this and infect other horses, but they don’t show any signs of clinical disease themselves… Can remain carriers for a long time without anyone knowing!

40
Q

What are the major sources of strangles infection? (2)

Note: How long will it last in these situations?

A

–acutely infected horse

  • Nasal shedding occurs for 3-6 weeks after the disease, even after resolution of clinical signs – not just the pus, but other normal nasal secretions that can potentially shed bacteria!
  • Some horses for months or years (carriers)

–Fomites and contaminated environmental sources

•Bacteria can survive for a variable amount of time:

–Survives: 3 days in dirt

–7 days on a fence post

–30 days in water

41
Q

What are the non specific clincal signs of strangles? (5)

A

–Fever, depression, inappetence, sometimes get a “cough”

–Mucoid to purulent nasal discharge

42
Q

What are the specific signs of strangles? (2)

A

–Abscessation of mandibular, parotid or retropharyngeal lymph nodes

•Initially become enlarged and eventually they will burst – amount of discharge in them will cause the rupture – important moment for bacteria to be shed into the environment!

–Dyspnea and dysphagia if abscesses compress larynx or interferes with cranial nerve supply to pharynx

•Where name of disease comes from

43
Q

What is the pathogenesis of strangles?

A

•Attaches to nasopharyngeal epithelial cells = then mucosa = then lymphatics = then lymph nodes

–Multiplies extracellularly

–Resistance to phagocytosis mediated by HA capsule and antiphagocytic SeM, Mac proteins

•Difficult bacterium to shed – this is why disease signs persist for such a long time

–Abscess formation and rupture/drainage then recovery and development of immunity (hopefully!)

44
Q

What is produced and where for the immunity of strangles?

A

Mucosal IgG and IgA produced in the nasopharynx with opsonic IgG in serum

45
Q

How can the immunity against stranglescme about? (2)

A

•Natural infection - 76% do not develop the disease again for at least four years

–Can develop a good immunity to stangles!

–Animals that have the disease, don’t tend to get it again if exposed in the first 2 or 3 years after they have had it but immune respone will wane and they can get it again – isn’t a lifelong immunity!

•Vaccines (submucosal route usually) in the UK

–IM and intranasal in USA

•Different forms

–Varying amount of variability – always on and off of the market!

46
Q

How can we treat strangles in horses with early clinical signs? (1)

A

–Penicillin

•No evidence to suggest it inhibits natural immune response… but a useful way of stopping clinical signs

47
Q

How can we treat horses with strangles that have LN abscesses? (1)

A

–Poulticing and drainage of abscesses – will help resolution of clinical signs

–Antimicrobials not indicated at this stage as just going to suppress the bacteria within the LNs and may not allow natural drainage to occur

48
Q

What are the complications of strangles? (4)

A

•Anaemia (common)

–IMHA or anaemia of chronic inflammation – typically occurs commonly but can occur to the point where you have severe systemic compromise

•Guttural pouch empyema and chondroids

–Neurological abnormalities

•Dysphagia, Laryngeal hemiplegia (CN10), Horner’s syndrome

–Chondroids: initial mucoid pus, as this starts to dry out, will go into proteinaceous lumps and then will progress to mucoid, pebble looking like things lining bottom of pouch – may have live bacterium present in these! Would need to remove the chondroids as may be harbouring bacteria!

•Abscesses distant site (Bastard Strangles - rare)

–Where we get abscessation at DISTANT sites and NOT associated with URT, can occur throughout the body such as lungs and GI system and peripheral parts of muscular system etc. – anything that is causing bacteria to pass through and set up abscessation at distant sites is bastard strangles

•Purpura Heamorrhagica (rare but serious)

–Immune mediated vasculitis

49
Q

How can we diagnose and treat abdominal abscesses?

A

•diagnosis: U/S or rectal

–long term antibiotics (usually penicillin or trimethoprim sulfa/rifampin) for up to 6 weeks)

–Bastard strangles

50
Q

How can we treat gutteral pouch empyema or chondroids? (4)

A

–drainage via the pharyngeal openings

–surgical drainage

–antibiotics

–Get all material out of guttural pouch by lavage or endoscopically usually

51
Q

what causes Purpura hemorrhagica?

A

–generalized vasculitis caused by Type III hypersensitivity reaction

–1-2% of infected horses

–Thrombosis of small arteries, when we get his – get massive plaques of oedema and often mucosal/submucosa; petechial haemorrhages and can get skin and muscle necrosis

52
Q

What is seen with Purpura hemorrhagica? (5)

A
  • Skin and muscle necrosis may result
  • Ventral oedema, body swelling and petechial hemorrhages on mucus membranes
53
Q

What do we need to differentiate strangles from?

A

Streptococcus equi subsp zooepidemicus

54
Q

What is the diagnosis (3), treatment (5) and prognosis of PURPURA HAEMORRHAGICA?

A

•DIAGNOSIS

–History, clinical signs, skin biopsy

•TREATMENT

–Dexamethasone: 0.05 - 0.2 mg/kg iv

–Prednisolone: 0.5 - 1 mg/kg po

–Analgesics – NSAIDS

–IVF

–Palliative measures e.g. hydrotherapy, massage

•PROGNOSIS

–guarded

55
Q

What do we do in a strangles outbreak? (5)

A

•Isolate premises

–Isolate horses which have shown signs for at least four weeks after the signs resolve

–Prevent movement of staff and equipment between cases

–Phenolics are most effective disinfectant for equipment and areas contaminated with organic matter

–Isolate until CERTAIN there is no infection now present

•Iodophores and chlorhexidine for staff

56
Q

How can we control strangles? (3)

A
  • Quarantine and culture of incoming horses
  • Confirm resolution of disease

–3 negative nasopharyngeal swabs/GP lavages over 3 weeks tested by culture and PCR

–Or sample fluid from guttural pouch (probabl better)

•Penicillin - will prevent the disease during initial febrile period but ? Immunity amounting

57
Q

Where is the biggest threat of strangles on livery yard?

A

Biggest threat on livery yard as with high turnover of horses and young horses etc

58
Q

What is gitteral pouch tympany?

A

–Gas accumulation within GP, can potentiall affect the airway due to the swelling

–Abnormal eustachian tube ostea prevents drainage and acts as one way valve

–Non-painful swelling

–MAY AFFECT AIRWAY

59
Q

What age does Guttural Pouch Tympany affect?

A

< 1 year RARE

60
Q

How do you treat Guttural Pouch Tympany? (4)

A
  • Antibiotics
  • NSAIDs
  • Surgery – drainage into pharynx or opposite pouch (by laser to try and fenestrate the GP)
  • In dwelling catheter
61
Q

What is the affect of Nutritional secondary hyperparathyroidism on nasal disease?

A

–Occasionally causing nasal airway obstruction may be due to inability to deal with excessive dietary phosphorus

62
Q

What is the affect of foreign bodies on nasal disease? (2)

A

nasal inflammation and partial nasal obstruction

63
Q

How do Deviations of the nasal septum cause nasal disease?

A

–trauma or to space occupying sinonasal lesions.

–Occasionally so severe as to require removal of the septum.

–Might warrant removal of nasal septum if severe but unusual

64
Q

What does Abnormally large or flaccid alar folds cause? (3)

A

–airflow obstruction

–exercise intolerance

–abnormal respiratory noises during fast exercise

65
Q

How do you diagnose (2) and treat (1) Abnormally large or flaccid alar folds?

A

•Diagnosis

–Direct visual examination - excessively prominent alar folds.

–Temporarily suturing the false nostril open

•Treatment

–Resection of the alar folds is reported to offer a reasonable prognosis.

Equine Final Year (102 decks)

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