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Fluids, Respiratory, Muscles > Equine Respiratory Disease > Flashcards

Equine Respiratory Disease Flashcards

1
Q

What is one of the most common medication conditions encountered by equine vets in the USA

A

Infectious Respiratory Disease

26.4% of horses tested positive for one or more pathogen

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2
Q

What are the clinical signs of equine viral airway disease

A

Fever, lethargy, anorexia, serous nasal discharge, lymphadenopathy

treat as if they are suffering from any of the viral causes

+/- multiple horses affected (more likely to be viral than bacterial)

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3
Q

How do you treat equine viral airway disease

A

Supportive care
-Rest
-NSAIDS
+/- antibiotics
+/- antivirals

treat as if they are suffering from any of the viral causes because they are indistinguishable

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4
Q

If you multiple horses affected with airway disease, what does this tell you about the etiology

A

It is less likely that it is caused by a bacteria

*Think that you are dealing with an equine viral airway disease

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5
Q

Why do you need to test for etiology in horses with viral airway disease

A

Influence outbreak control measures
1) biosecurity measures (mode of transmission)
2) length of quarantine period
3) Vaccination protocols
4) EHV-1 is reportable

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6
Q

how do you test for etiology in horses with viral airway disease

A

Antigen or genome (Virus culture, PCR, immunodetection, ELISA assays)

Antibody- serology

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7
Q

What do you need when diagnosing etiology in horses with viral airway disease using serological assays

A

typically requires demonstration of seroconversion

*possible exception: EHV-1 serology

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8
Q

What is the downside of serology testing for etiology in horses with viral airway disease*

A

it is retrospective. you need to wait 14 days to see if titer levels (seroconversion) is high enough

not good for outbreak and quaratines

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9
Q

What serology assay in horses with viral airway disease does not require demonstration of seroconversion *

A

EHV-1 CF serology

great test but no commercial labs in US have this

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10
Q

When you have a barn of horses with a possible respiratory outbreak, which animal should you sample

A

Sample sick horses (varying stage) +/- healthy contacts

collect all potential samples (serum, whole blood, swabs)
immunologoically naive animal

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11
Q

Which horses have longer duration of shedding and higher titers of viral airway disease

A

naive animals

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12
Q

is the length of shedding shorter in a horse that is partially immune or naive

A

partially immune animal

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13
Q

What kind of herpesvirus family do horses get (EHV-1,3,4)

A

alphaherpesviridae

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14
Q

What causes equine coital exanthema

A

EHV-3
*genital lesions

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15
Q

If a horse has genital lesions, what herpes virus caused this

A

EHV-3 (Coital exanthema

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16
Q

Which Equine Herpesvirus causes CNS disease

A

EHV-1

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17
Q

Which Equine herpesvirus causes abortion

A

EHV-1 and EHV-4

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18
Q

Which Equine herpesvirus causes respiratory disease in young horses

A

EHV-1 and EHV-4

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19
Q

Which equine herpesvirus causes ocular disease

A

EHV-1 and EHV-4

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20
Q

What equine herpesvirus is in the family gammaherpesviridae

A

EHV-2
EHV-5
AHV-2
AHV-4
AHV-5

*longer periods of active replication, more opportunities for spread

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21
Q

How do equine gammaherpesviridae typically differ from alphaherpesvirdiae

A

Gamma has longer periods of active replication, more opportunities for spread, typically more host adapted

*gamma clinical significance is unknown

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22
Q

What equine herpesviruses are in the alphaherpesvirdiae family

A

EHV-1
EHV-3
EHV-4

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23
Q

What is Equine Multinodular Pulmonary Fibrosis (EMPF) associated with

A

EHV-5 (gammaherpesvirdiae)

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24
Q

EHV-5 is a ___________ that is associated with _________

A

gammaherpesviridae that causes Equine Multinodular pulmonary fibrosis (EMPF)

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25
Q

What is Equine Multinodular Pulmonary Fibrosis (EMPF)

A

EHV-5 *gammaherpesviridae
potentiall impacts healing of the pulmonary fibrosis

present with coughing, weight loss, +/- fever, exercise intolerance, respiratory distress

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26
Q

Horses with EMPF present with ______________

A

coughing, weight loss, +/- fever, exercise intolerance, respiratory distress

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27
Q

What other species can EHV-1 affect

A

Ruminants and Camelids (neuroglocial disease, ocular disease- blindness, retinitis, chorioretinitis, optic neuritis)

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28
Q

What does EHV-1 infection cause in camelids

A

1) Neurological Disease
2) Ocular Disease: blindness, retinitis, chorioretinitis, optic neuritis

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29
Q

Camelids with neurological or ocular disease (blindness, retinitis, choriorentinits, optic neuritis) might have

A

EHV-1

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30
Q

When do abortions due to EHV-1 (or 4)

A

occur 9-120 days post infection (majority 10-20dpi) or often during late gestation (after 7 months)

fetuses typically fresh, especially with EHV-1

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31
Q

What lesions do the aborted fetuses from EHV-1 typically have

A

they look typically fresh and normal

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32
Q

How might neonatal foals fro EHV-1

A

in utero infection or immediately after birth

born sick or become sick within 1-2 days
rapidly progressive viral pneumonitis
may survive 1-2 weeks

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33
Q

How might a neonatal foal get EHV-1

A

born sick (in utero infection) or immediately after birth (within 1-2 days)

rapidly progressive viral pneumonitis

may survive 1 to 2 weeks

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34
Q

Equine Herpesvirus Myeloencephalopaty (EHM)

A

causes by EHV-1
severity of clinical signs can vary widely
slight hindlimb incoordination to paralysis or urinary incontinence
recovery depends of severity and extent of damage

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35
Q

Do horses with EHV-1 typically have more central NS or spinal NS signs

A

typically spinal NS signs are more common but cranial nerves can be affected

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36
Q

If a horse has neurological signs but no fever, can you rule out EHV-1

A

No it is not a ruleout

they may not have a fever

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37
Q

T/F: EHV does not cause respiratory signs in adult horses

A

True

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38
Q

T/F: EHV does not cause respiratory signs

A

False- it does in young horses

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39
Q

T/F: Respiratory signs of EHV are typically present before abortion

A

False

*monitoring for respiratory disease does not provide any warning

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40
Q

T/F: it is important to monitor for respiratory disease to detect EHV in horses

A

False

*monitoring for respiratory disease does not provide any warning

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41
Q

Is elimination of equine herpes virus possible?

A

NO- equine herpes viruses are ubiquitous (lacency)

elimination from horse populations is impossible

do not rule out if the horse hasnt had any contact with other horses because it could be latent

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42
Q

When is EHV reactivated?

A

during periods of stress
then virus is shed in the nasal sections for the infection of susceptible contacts
those horses then shed the virus in nasal secretions and there is establishment of latency

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43
Q

What might cause stress and subsequent reactivation from latency of EHV

A

observed in field after
-transport
-handling
-rehousing
-weaning
-high periods of steroids (10X)

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44
Q

How do you detect EHV latency carriers

A

Antibody (serology)
but vaccines make it difficult

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45
Q

Reactivation from latency of EHV due to stress is associated with

A

typically asymptomatic “silent” shedding

potential for disease appearance in closed horse populations

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46
Q

How do horses that have Reactivation from latency of EHV due to stress present

A

typically asymptomatic “silent” shedding

potential for disease appearance in closed horse populations

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47
Q

Does EHV-1 or 4 have a longer viremic period

A

EHV-1*

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48
Q

What is the pathogenesis of EHV-1 *

A

1) Inhalation of virus
2) Infection and replication in the respiratory epithelium
3) Shed into nasal secretion or go into epithelium and then infect leukocytes and spread to lymph nodes
4) Replication within the lymph nodes
5) Leukocytes leave LNs and create cell-associated viremia
6) Distribution throughout the body - cells go from leukocytes to endothelial cells leading to vasculitis, thrombosis and tissue destruction
7) Fetus and nervous system issues via endothelial damage

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49
Q

What is EHV-1 cell associated viremia

A

the horse will have a viremia but the virus isnt free, it is within the leukocytes

1) test buffy coat, virus will not be detected within the plasma/serum
2) Harder to eliminate via antibodies- vaccines arent as efficacious

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50
Q

What do you need to be careful about when sampling blood for EHV-1 infection

A

the virus lives within the leukocytes so it will be detectible in the buffy coat, not the serum/plasma

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51
Q

Why is the vaccine for EHV-1 not that efficacious

A

because the virus lives in leukocytes (cell associated viremia) and its not as susceptible to the antibody response

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52
Q

How does EHV-1 cause myeloencephalopathy *

A

it doesnt necessarily harm the neurons but it causes vasculitis and thrombosis via endothelial damage

*vascular injury after endothelial cell infection
-vasculitis, thrombosis, ischemia of neuropil

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53
Q

How does EHV-1 cause abortion

A

it causes vasculitis and thrombosis via endothelial damage

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54
Q

How long can EHV-1 cell associated viremia persist

A

can persist for up to 21 days even if they stopped shedding the virus
can lead to
-abortion
myeloencephalopathy

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55
Q

What is needed for EHV-1 to cause abortion and myeloencephalopathy

A

cell associated viremia causing damage to the endothelial cells

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56
Q

vascular injury after endothelial cell infection leading to vasculitis, thrombosis, and ischemia of neuropil

A

Myeloencephalopathy from EHV-1 infection

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57
Q

What is the difference between
-Non- neuropathogenic
and
-Neurpathogenic EHV-1

A

Non: AA substitition absent in 95% of non-neurologic isolates

Neuropathogenic: single AA substitution in the polymerase gene: 83% neurologic isolates

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58
Q

What would you see in neuropathogenic EHV-1

A

single AA substitution in the polymerase gene in 83% of neurologic isolates

*this produces higher levels of cell associated viremia and higher chance of neuro disease

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59
Q

Why might infection with neuropathic EHV-1 strain not result in nervous system disease

A

1) Age (EHM typically not in younger horses, more middle ages )
2) Infectious dose
3) immunity
4) Breed (ponies less likely to get EHM)

*Neurological attack rate varies between outbreaks

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60
Q

T/F: ponies are less likely to get EHM from EHV-1

A

true

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61
Q

How might you sample for the diagnosis of EHV-1

A

1) Nasal swab sample (PCR, virus isolation, etc)

2) Whole blood sample (PCR, virus isolation)

3) Tissue sample- fetal tissues (PCR, virus isolation, etc)

4) Serum sample for Serology (VN or CF) but this is retrospective and it doesnt tell you if it is herpes or not, need to demonstrate seroconversion and lab will report to state vet

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62
Q

How might EHV-1 be further spread after a lot of abortions

A

contact of fetal membranes and fluids to other horses

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63
Q

Is EHV-1 reportable to state vet

A

yes

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64
Q

How do you control EHV-1/4

A

1) Husbandry- isolation for 28 days after last new infection

2) Vaccination- Inactivated or Modified live, no vaccine protects against neurological disease

3) Antiviral drugs

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65
Q

What should you keep in mind when doing serology with serum for EHV-1 diagnosis

A

this is retrospective and it doesnt tell you if it is herpes or not, need to demonstrate seroconversion and lab will report to state vet

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66
Q

How long should you isolate horses wit EHV-1/4

A

isolate for up to 28 days after last new infection

spread primarily through contact (limited aerosol spread) so need to be careful

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67
Q

Vaccination for EHV-1 /4

A

Inactivated EHV-1: elicit VN antibody response, reduce virus shedding, reduction in the incidence of abortions, protect from respiratory disease

Modified live virus vaccines: cytotoxic T cell response is better?

*No vaccine protects against neurological disease

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68
Q

What should you keep in mind about the EHV-1 vaccine *

A

they reduce shedding, elicit antibody response, lowe abortion incidence, and protect from respiratory disease

but DO NOT PROTECT AGAINST NEUROLOGICAL DISEASE

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69
Q

What dictates the quarantine and biosecurity protocols with EHV-1

A

the state veterinarian
*EHV-1 is a reportable disease in Colorado

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70
Q

Vaccination against EHV-1 may protect from _________ and __________ but does not ____________

A

it may protect from infection and reduce shedding but does NOT protect from neurological disease

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71
Q

What family of virus is equine influenza virus in

A

orthomyxoviridae
(A)

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72
Q

What are the two strains of equine influenza virus

A

H3N8 (eqine 2) *
H7N7 (equine-1)

genetic evolition resulted in H3N8 two distinct lineages: European and American

3 American Sublineages: South American, Kentucky, and Florida (clade 1 and clade 2 are the predominate)

*antigenic drift forms multiple different lineages

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73
Q

What is needed to make an effective Vaccination against Equine Influenza virus

A

If it offers protection from the Florida sub-lineage clades 1 and 2 because those are the predominate types

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74
Q

What are the clinical signs of Equine Infuenza virus

A

it is the same as other equine respiratory virus
-fever
-lethargy
-anorexia
-serous nasal discharge
-lymphadenopathy
-cough (especially apparent)
+/- multiple horses affected

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75
Q

Most of the clinical signs of equine viral respiratory disease are the same but what is significant about equine influenza virus

A

these horses cough a ton!!!

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76
Q

What is the pathogenesis of Equine Influenza virus

A

1) Inhalation of infectious virus
2) Infection and replication in the respiratory epithelium (cells die)
3) Following release from cell virus spreads quickly throughout the respiratory tract
4) Complications: bacterial pneumonia, myocarditis because of loss of cilia function -> reduced airway clearance

*efficient replication of virus in airways
(efficiently spread through direct contact, fomites, respiratory droplets, aerosols)

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77
Q

How is equine influenza virus spread

A

*efficient replication of virus in airways
(efficiently spread through direct contact, fomites, respiratory droplets, aerosols)

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78
Q

What is the sequalae of equine influenza virus

A

Bacterial pneumonia, myocarditis, etc

-influenza infected airway tissue, airway cells are damaged = loss of cilia function
reduced airway clearance can result in bacterial bronchopneumonia

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79
Q

Why do you typically get bronchopenumonia after equine influenza virus infection

A

-influenza infected airway tissue, airway cells are damaged = loss of cilia function
reduced airway clearance can result in bacterial bronchopneumonia

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80
Q

How do you diagnose Equine Influenza virus?

A

1) Nasal swab sample (PCR, virus isolation)
2) Serum sample (serology)

*No viremia so you cant use whole blood sample, only detect for serology via antibody

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81
Q

Why cant you use antigen test for Equine Influenza virus

A

*No viremia so you cant use whole blood sample, only detect for serology via antibody

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82
Q

How do you control for Equine Influenza

A

1) Husbandry - isolation for 21 days after last new infection (very efficient spread by droplets- up to 50 yards)

2) Vaccination is effective: Inactivated, LV, recombinant

3) Antiviral drugs

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83
Q

What are the different vaccinates for Equine Influenza

A

*Effective

1) Inactivated: quantity, quality, virus strain, adjuvants, protect against homologous virus

2) MLV: intranasal (preferred), single dose, protects up to 12 months, IgA

3) Recombinant: canary pox vector, protected against challenge with recent isolates

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84
Q

What family of virus is equine viral arteritis virus in

A

Arteriviridae

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85
Q

What is significant about equine viral arteritis virus when it comes to doing AI

A

at subfreezing temperature (cryopreserved semen) the virus can stay viable for years

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86
Q

A lot of the equine viral respiratory disease have the same clinical signs (fever, lethargy, anorexia, serous nasal discharge, lymphadenopathy, cough),
But what is significant about equine viral arteritis virus

A

Lot of variation between strains but you also see vasculitis
-Nasal discharge
-Ocular discharge
-Pink eye
-Photophobia
-Skin rash around head and neck
-Ventral edema, lower limbs, scrotum, mammary glands
-Abortions

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87
Q

When might equine viral arteritis virus cause abortion

A

Exposure of mare > 3months pregnant to EAV may lead to abortion

Abortion occurs 1-3 weeks after viral exposure

Abortions rates may range from 10-70%

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88
Q

How are foals with equine viral arteritis virus typically infected

A

in utero

may die within 2-4 days after birth due to severe progressive interstitial pneumonia or enteritis

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89
Q

neonatal foal equine viral arteritis virus

A

often infected in utero

may die within 2-4 days after birth due to severe progressive interstitial pneumonia or enteritis

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90
Q

How might equine viral arteritis virus be transferred

A

1) Semen from stallion (carrier state)
2) Nasal secretion from an acutely infected horse

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91
Q

What is up with the carrier stallion with equine viral arteritis virus

A

Possible short term infertility due to increased temperature and scrotal edema

-Subsequent fertility not impaired
-virus may localize in accessory sex glands (30-50% carrier rate)

Carrier state is a testosterone dependent condition

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92
Q

Is is needed for the carrier state condition of equine viral arteritis virus

A

testosterone

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93
Q

How do you diagnose equine viral arteritis virus

A

1) Nasal swab sample (PCR, virus isolation)

2) Whole blood sample (PCR, virus isolation)

3) Tissue sample of fetus (PCR, virus isolation)

4) Semen (PCR, virus isolation)

5) Serum sample (serology)

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94
Q

What should you do regarding vaccination against equine viral arteritis virus *

A

Consult with animal health officials to ensure that use of vaccine is in compliance with the state/s control program for EVA

Keep in mind that it is not possible to differentiate vaccine titers antibodies from natural infection and some countries prohibit importation of seropositive horses
*collect serum sample for EVA serology testing prior to vaccination

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95
Q

What should you do prior to vaccination against EVA *

A

Collect serum sample for EVA serology testing prior to vaccination
*Not possible to differentiate vaccine titers antibodies from natural infection
Some countries prohibit important of seropositive horses

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96
Q

T/F: you can differentiate vaccine titer antibodies against EVA from natural infection

A

False

Collect serum sample for EVA serology testing prior to vaccination
*Not possible to differentiate vaccine titers antibodies from natural infection
Some countries prohibit important of seropositive horses

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97
Q

What should you do when you diagnose EVA

A

report it to the state vet because they will dictate quarantine +/- biosecurity protocols

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98
Q

What should you do if your client wants to you vaccinate their stallion against EVA

A

talk to the state vet on the best protocol
will likely need serology prior to vaccination because you cant differentiate vaccine from natural infection

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99
Q

What are the two broad ways of controlling contagious disease

A

1) Minimize exposure
2) Optimize disease resistance

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100
Q

Why are vaccines only a supplement to controlling contagious disease

A

very few (if any) vaccines protect all animals from disease
vaccines may lessen severity of clinical signs, but do not prevent shedding of contagion
dfiferent levels of efficacy between different vaccines
Vaccines failuresL Inadequate response, timing (maternal antibodies), and vaccine/pathogen mathc

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101
Q

What are risk factors for bacterial pneumonia in horses?

A

-Foals
-Race training
-Racing
-Transportation
-Air quality (ammonia paralyze the cilia)

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102
Q

What are the differences in horses with pneumonia vs pleuropneumonia *

A

Pneumonia: cough, fever, lethargy +/- anorexia, mucopurulent nasal discharge, Increased RR +/- effort

Pleuropneumonia: often no/mild cough, fever, severe lethargy, anorexia, mucopurulent nasal discharge, increase RR and respiratory effort, edema forelimbs and chest

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103
Q

What are the clinical signs of pneumonia in horses

A

cough,
fever,
lethargy +/- anorexia mucopurulent nasal discharge
Increased RR +/- effort

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104
Q

What are the clinical signs of pleuropneumonia in horses

A

often no/mild cough, fever,
severe lethargy, anorexia, mucopurulent nasal discharge,
increase RR and respiratory effort, edema forelimbs and chest

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105
Q

What is the pathogenesis of pneumonia in horses

A

1) Airways exposed to >10,000 L of air/day (dust, chemicals, microorganisms)
2) >10um dont get past upper resp, 3-10um get removed via mucociliary, 1-5um are able to get to lower airway to cause disease
3) Overwhelming of defense mechanisms (anesthesia, drugs, viral infection, toxic gases, congestion, edema, secretion

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106
Q

What are the airway defense mechanisms

A

Upper airway: coughing, sneezing, swallowing

Trachea: Mucociliary clearance

Lower airway: phagocytic cells, cellular immunity, humoral immunity

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107
Q

What might result in loss of cough, leading to impaired defense mechanism against respiratory pathogens *

A

-Anesthesia
-Neuromuscular
-Drugs
-Pain

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108
Q

What might result in loss of epithelium (mucociliary clearance) leading to impaired defense against pathogens *

A

-Viral infection
-Toxic gases (eg. ammonia)

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109
Q

What might result of lowering of lower airway defense mechanisms (phagocytic cells, cellular immunity, and humoral immunity) leading to impaired defense against pathogens *

A

Loss of clearance:
1) congestion
2) edema
3) secretion

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110
Q

What are common bacterial etiologies of pneumonia in horses

A

Gram +:
-Strep. zooepidemicus*
-Strep pneumoniae
-Rhodococcus equi (foals)
-Strep. equi (rare)

Gram -:
-Pasteurella spp.
-E. coli
-Enterobacter spp.
-Klebsiella spp.

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111
Q

Commonly, pleuropneumonia occurs as

A

an extension of pneumonia into the thoracic cavity

exceptions: penetrative trauma

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112
Q

What is the pathogenesis of equine pleuropneumonia

A

1) Exudative stage: increased permeability and leakage of sterile fluid into the cavity
2) Fibropurulent stage: bacterial invasion, WBC transmigration, and fibrin deposition.
3) Organization stage: Fibroblast growth, Inelastic membrane forms= pleural peel

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113
Q

Pleural peel

A

inelastic membrane as a result of pleuropneumonia that is permanent and impairs lung function

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114
Q

What are common etiologies of pleuropneumonia in horses

A

Gram -: Pasteurella spp., E coli, Enterobacter, Klebsiella

Gram +: S. zooepidemicus

Anaerobes: Clostridium spp and Bacteroides spp.

Good drugs: broad spectrum like Metronidazole or (Penicillin and Aminoglycoside)

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115
Q

What is a good drug for pleuropneumonia in horses *

A

broad spectrum like Metronidazole or (Penicillin and Aminoglycoside combo)

Bacteroides are often resistant to penicillin so a combo of these three are used

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116
Q

What kind of things do you hear on thoracic auscultation of a horse with pneumonia or pleuropneumonia

A

Rebreathing exam: lung sounds, tracheal sounds, cough, tolerance, recovery

Secretion sounds, crackles and wheezes, lung sounds, no or only bronchial sounds, cardiac sounds over wider area

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117
Q

What do you see on bloodwork of a horse with pneumonia or pleuropneumonia *

A

-Inflammatory leukogram
-Neutrophilia (or neutropenia if early on)
-Hypergamma-globulinemia (Increased plasma protein)
-Increased fibrinogen

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118
Q

What do you see on radiograph of a horse with pneumonia

A

alveolar pattern (classical)
air-bronchogram

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119
Q

What do you see on radiograph of a horse with pleuropneumonia

A

often unrewarding (effusion is present)

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120
Q

What do you see on ultrasound of a horse with pneumonia

A

Comet-tails- take with a grain of salt, might be because horse is older but then to be more cranioventral
Consolidation
Abscessation

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121
Q

What do you see on ultrasound of a horse with pleuropneumonia

A

Consolidation- increased intrathoracic pressure (Exudative sage
Fibrin deposits and abscesses that form

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122
Q

How do you obtain a sample for culture in horses with pneumonia

A

Transtracheal* wash or transendoscopic wash to get the bugs in the trachea

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123
Q

What is the best method to get a sample for pneumonia

A

transtracheal wash

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124
Q

gets cells and secretions from the distal smaller airways. If done blind, the disease process must be diffuse. Superior for small airway cytology

A

Broncho-alveolar lavage

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125
Q

procedure for non-homogenous sample of cells and debris from anywhere in the distal airways. Superior for focal disease and culture

A

tracheal wash

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126
Q

What method if best for small airway cytology in horses

A

Bronchoalveolar lavage

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127
Q

What method if best for focal disease and culture of horses with pneumonia

A

tracheal wash

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128
Q

How should you perform a tracheal aspirate/ wash in horses

A

1) Ideally, prior to ABC administration or stop ABC for 24-72 hours
2) Cytology +/- gram stain, fluid analysis (color, turbidity, small, cell count, protein, cytology, culture)
3) Aerobic and anaerobic culture

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129
Q

What should you do if you see a horse with fluid in thoracic cavity

A

thoracocentesis 6th or 7th ICs, U/S guided if possible

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130
Q

How should you do antimicrobial therapy for horses with pneumonia and pleuropneumonia *

A

Ideally: culture and sensitivity
Broad spectrum: gram +/- and anaerobes
long term administration
antimicrobial treatment of anaerobes usually empiric

Metronidazole
(Penicillin and Aminoglycodes

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131
Q

What are the different inflammatory, non-infectious airway conditions in horses

A

1) Mild to Moderate Equine Asthma: Inflammatory airway disease (generally younger horses)

2) Severe Equine Asthma: Recurrent airway obstruction (ROA/ Heaves): older horse >7 years of age

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132
Q

Inflammatory airway disease is _________and generally occurs in

A

mild to moderate equine asthma
generally in younger horses

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133
Q

Recurrent airway obstriction is ________- and generally occurs in

A

severe equine asthma “Heaves”
older horses >7 years

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134
Q

What is the clinical presentation of horses with asthma

A

Mild equine asthma: exercise intolerance, prolonged recovery, occasional cough, +/- nasal discharge

Moderate asthma: exercise intolerance, prolonged recovery, occasional cough, +/- nasal discharge

Severe asthma: expiratory dyspnea, heave line, coughing , respiratory compromise at rest

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135
Q

What is the clinical presentation of severe equine asthma

A

expiratory dyspnea leading to heave line (hypertrophy of expiratory muscles), coughing , respiratory compromise at rest

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136
Q

What type of hypersensitivity is associated with heaves

A

Type I (IgE mediated) hypersensitivity to inhaled antigens

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137
Q

What causes heaves (RAO)

A

Type I (IgE mediated) hypersensitivity to inhaled antigens

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138
Q

What is the pathophysiology of heaves

A

1) Type I (IgE mediated) hypersensitivity to inhaled antigens
2) Airway obstruction caused by
a) Mucous production (hypersecretion by goblet cells)
b) Neutrophil accumulation
c) Bronchoconstriction via inflammatory mediators and autonomic NS

*Hyperresponsive to nonspecific stimuli (cold air, road dust)

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139
Q

What causes the airway obstruction in heaves

A

a) Mucous production (hypersecretion by goblet cells)
b) Neutrophil accumulation
c) Bronchoconstriction via inflammatory mediators and autonomic NS

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140
Q

Horses with heaves are hyperresponsive to

A

nonspecific stimuli (cold air, road dust)

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141
Q

You do a bronchial lavage of a horse with heaves. What will you see on cytology?

A

Horses with RAO will have 50-70% neutrophils (Normal is <5%)

Positively correlated to hypoxia, pulmonary function (high resistance, poor lung compliance), and airway hyperreactivity

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142
Q

Why do you see more neutrophils with RAO horses

A

Horses with RAO will have 50-70% neutrophils (Normal is <5-10%) on BAL cytology
correlated to disease severity

Positively correlated to hypoxia, pulmonary function (high resistance, poor lung compliance), and airway hyperreactivity

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143
Q

What is the pathophysiology of inflaamatory airway disease in horses (mild form)

A

unclear etiology but
dust exposure?- positive correlation to stabling
viral infection
bacterial infection
parasitic
most likely multiple etiologies

Three forms
Eosinophilic (5-40%) form
Mixed (Neutrophilia, Lymphocytosis, Monocytosis)
Mast cell (>2% mast cells)

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144
Q

What is the point of doing hematology and biochemistry in horses with respiratory disease

A

used to rule out pneumonia (neutrophilia, hyperfibrinogenemia, etc.)

if normal, think of asthma

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145
Q

T/F: radiology is important in diagnosis equine asthma

A

False- often unrewarding but you can use it to rule out pneumonia

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146
Q

T/F: endoscopy is important in diagnosis of equine asthma

A

false- fluid accumulation and airway mucous is a common sign but not specific to asthma

bronchoscopy might be more helpful to see hyperactivity bronchi though but still not very useful

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147
Q

Is tracheal wash or BAL more helpful for equine asthma diagnosis

A

BAL is the best- cells and secretions from the distal smaller airways. If done blind disease process must be diffuse. Superior for small airway cytology

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148
Q

Why do you use BAL for equine asthma diagnosis

A

BAL is the best- cells and secretions from the distal smaller airways. If done blind disease process must be diffuse. Superior for small airway cytology

*It is diffuse condition and doesnt necessarily matter where you sample, it can be blind

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149
Q

Cytological evaluation of RAO

A

look for neutrophilic inflammation
-tracheal aspirate RAO: opportunisitic MO
-Culture indiciated if BAL sample shows degenerative cells of intracellular bacteria

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150
Q

How do you treat horses with RAO and IAD

A

Environment: monst important, minimize exposure to mold, dust, endotoxin
Most important sources is hay and bedding*
Maintained at pasture, pelleted feed supplement
Control dust exposure (stall cleaning, feeding, and eating)

Medical Treatment:
Corticosteroid
Bronchodilator (ie albuterol
*Choice depends of severity of signs, cytological results, financial means, owner compliance

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151
Q

What is the most important sources of mold, dust, and endotoxin that you want to control in horses with RAO and IAD

A

Hay (Round bale hay has the most dust) and bedding

*Maintain at pasture and pelleted feed supplement

*Control dust exposure (stall cleaning, feeding, eating, indoor arenas, road dust)

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152
Q

Albuterol is a

A

bronchodilator

can be used to open the airways in equine asthma

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153
Q

Most management is environmental but what do you use for medical therapy in horses with asthma

A

Corticosteroids
a) *Systemic administration- more powerful than inhaled but greater risk of systemic complications (laminitis, infection)
b) Aerosolized delivery- short acting, not prolonged benefit

Bronchodilators
a) Systemic administration- greater risk of adverse effect (excitation, tachycardia, sweating)
b) *Aerosolized delivery- more powerful than systemic but expensive

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154
Q

What is a metered dose inhalant (MDI) system

A

rapid administration aerosolized drug therapy
consistent dose delivery
minimal risk of pulmonary contamination with environmental microorganisms
no maintenance is required
no electricity required
widely available

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155
Q

Clenbuterol is a

A

Beta 2 agonist for long term therapy of equine asthma
used in combination with corticosteroids
monotherapy results in downregulation or desensitization of b2 receptors (treatment failure)

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156
Q

What does monotherapy of clenbuterol or albuterol result in?

A

monotherapy results in downregulation or desensitization of b2 receptors (treatment failure)

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157
Q

Albuterol is a

A

Beta 2 agonist for long term therapy of equine asthma
used in combination with corticosteroids
monotherapy results in downregulation or desensitization of b2 receptors (treatment failure)

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158
Q

Competition horses being treated for asthma have to

A

zerol tolerance
horses have to come off steroids and bronchodilators

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159
Q

Medical treatment for equine asthma typically involves corticosteroids +/- bronchodilators. What else is there but are ineffective

A

Mast cell stabilizer- Sodium cromoglycate
Antihistamines
NSAIDS
Singulair: expensive

160
Q

How should you manage pregnant mares with asthma

A

Corticosteroids (Ideally aerosolized), some risk with systemic

Clenbuterol- take off close to term, reduces uterine contractility

*Hypoxia is detrimental to the foal

161
Q

Why should you take a pregnant mare off of clenbuterol close to term

A

it reduces uterine contractility

162
Q

What are the risk factors for the development of bacterial pneumonia

A

Risk factors for the development of bacterial pneumonia in adult horses include respiratory viral infection (e.g. equine influenza, equine herpes virus-1/4), transportation, race training, racing, general anesthesia, neuromuscular disorders (e.g. botulism), exposure to certain noxious gases (e.g. ammonia), and a recent history of esophageal obstruction (e.g. choke). In foals, predisposing factors include overcrowding, heavy parasite burden, poor nutritional status, heat stress, congenital immunodeficiencies, and concurrent disease.

163
Q

A 7 year-old Warmblood mare is presented with a history of increased respiratory rate, coughing, and weight loss. Thoracic ultrasound and x-ray findings are shown below.

T/F: A bronchoalveolar lavage (BAL) is the diagnostic modality of choice to evaluate the type and degree of pathology present in this mare.

A

False- As this horse presents with evidence of localized disease (i.e. the thoracic x-ray and ultrasound findings are indicative of pulmonary abscessation), the diagnostic modality of choice for this horse is a tracheal aspirate. The tracheal aspirate allows collection of cells that originate from anywhere in the lower respiratory tract and accumulate in the distal trachea before being cleared from the airways by mucociliary clearance. In contrast, the BAL samples cells and secretions from small airways in a discrete area of the lungs (i.e. where the BAL tube gets lodged). Therefore, BAL is most useful in the diagnosis of homogeneously distributed small airway disease such as equine asthma.

164
Q

What are the clinical signs of Equine Arteritis Virus

A

Fever, serous nasal discharge, and a cough are clinical signs commonly seen with any equine respiratory virus. Because EAV infection results in inflammatory changes in small blood vessels (particularly the arterioles), clinical signs associated with equine viral arteritis also include conjunctivitis (“pink-eye”), limb edema, supraorbital or periorbital edema, and urticaria (as well as abortion).

165
Q

You examine a horse showing respiratory distress and a rapid and shallow respiratory pattern. Auscultation identifies increased intensity of bronchial breath sounds heard over the trachea. There is increased intensity of bronchovesicular breath sounds in the dorsal lung fields on the left and right. Breath sounds are absent in the ventral lung fields on the left and right sides in the standing animal. What would be the best clinical interpretation of the most likely respiratory pathology?

A

Pleural Effusion. The increased intensity of breath sounds over the trachea and dorsal lung fields suggest any combination of hyperventilation, airway inflammation, or pulmonary consolidation. However, the absence of, or quieter breath sounds ventrally in the standing animal is highly suggestive of fluid in the pleural cavity. Pneumothorax can also result in decreased intensity of thoracic breath sounds but this would be throughout the ventral and dorsal fields in the standing animal, not just in the ventral lung fields.

166
Q

What are the different types of nasal discharge

A

1) Serous (often normal)
2) Mucoid / Catarrhal
3) Seromucoid discharge
4) Purulent
5) Hemorrhagic/ Sanginous (Epistaxis)
6) Ingesta

167
Q

Seromucoid discharge in horse

A

due to inflammation of the nasal cavity
increased glandular secretions
can be due to acute viral disease or dust/ environmental irritants

168
Q

What might cause ingesta nasal discharge in the horse

A

1) dysphagic
a) mechanical- cleft palate, swelling (strangles), extraluminal compression
b) Functional- nerve damage (CN IX)

2) proximal GI obstruction (choke)- emergency, distress, retching, stretched out neck, copious nasal and oral secretions

3) oro-maxillary fistula (sinusitis)

169
Q

Purulent nasal discharge in horses

A

more severe inflammation
bacterial invasion

increased neutrophils in airway secretions create color of milky, white, yellow, or green

170
Q

What does malodorous nasal discharge in a horse tell you

A

necrotic with anaerobic bacterial component

171
Q

Where might be the source of sanginous nasal discharge in the horse

A

Really anywhere (especially the guttural pouch)

172
Q

Why is it really important to scope the soft palate in foals

A

milk from nursing can be there. If large volumes, could be due to a cleft palate

173
Q

How might there be nasal discharge of ingesta in a horse due to dysphagia

A

a) mechanical- cleft palate, swelling (strangles), extraluminal compression
b) Functional- nerve damage (CN IX)

174
Q

What are the causes of (muco)purulent nasal discharge in a horse

A

*Bacterial infection
a) Upper airway- Sinus or Guttural puch
b) Lower airway- inflammatory airway disease (asthma) or bronchopneumonia
c) Secondary to trauam, epistaxis, cysts, or neoplasia

(also fungal or parasitic)

175
Q

What are the clinical signs associated with upper respiratory tract disorders in horses

A

nasal discharge
epistaxis
swelling or pain in the throatlatch region
swelling or pain over the sinuses,
facial swelling
mandibular lymphadenopathy
abnormal respiratory sound
epiphora
poor performance
occassionally dyspnea and/or dysphagia

176
Q

What should you do if you suspect an issue with the upper respiratory tract in the horse *

A
  • Do upper airway endoscopy to find the source of the discharge

(can also do other imaging- oral exam, skull radiographs, and head CT or ancillary tests- nasopharyngeal lavage, biopsy, CBC, titers)

177
Q

Infection of what teeth in the horse can cause sinusitis

A

The last three of four cheek teeth

108-109/ 208-209: Rostral maxillary sinus

110-111/ 210-211: Caudal maxillary sinus

*Common cause of sinusitis in the horse

178
Q

Primary vs Secondary sinusitis in the horse

A

Primary: no detectable predisposition to bacterial infection other than possible respiratory infection

Secondary: dental sinusitis, oro-maxillary fistula formation, progessive ethmoid hematoma, sinus cysts, trauamtic sinusitis, sinus neoplasia, mycotic sinusitis

179
Q

What might cause secondary sinusitis in the horse

A

1) dental sinusitis **
2) oro-maxillary fistula formation
3) progessive ethmoid hematoma
4) sinus cysts,
5) traumatic sinusitis, 6) sinus neoplasia
7) mycotic sinusitis

180
Q

What clinical sign is indicative of sinus cysts or neoplasia in the horse

A

firm facial swellings or facial distortion and nasal airflow obstruction

181
Q

primary sinusitis in the horse

A

typically purulent discharge
normal oral exam

variable free fluid in sinus possible filling of ventral conchal sinus

182
Q

What is seen in sinusitis secondary to dental disease in horses *

A

purulent and malodorous nasal discharge *
see various dental disease on oral exam

see loss of lamina dura, sclerosis and lysis, free fluid and soft tissue opacity centered over affected tooth on radiography

183
Q

What do you see with trauma to the upper respiratory tract

A

hemorrhagic nasal disacharge
depression fx. soft tissue swelling, tissue gas crepitus *

184
Q

Malordorous exuate is usually associated with what in horses

A

anaerobic bacterial infections. frequently due to dental associated secondary sinusitis

can also be primary though

185
Q

Hemorrhagic nasal discharges are most commonly seen in horses with

A

traumatic sinusitis and progressive ethmoidal hematoma
10% of sinus neoplasias

186
Q

How does epiphora occur in horses

A

sinusitis that compresses the nasolacrimal duct as it courses via the dorsolateral aspect of the maxillary sinuses and is present in 20% of cases

187
Q

Are sinusitis cases in horses bilateral or unilateral

A

Unilateral but can be bilateral in a small percentage of cases

188
Q

What are the primary signs of sinusitis in horses *

A

1) unilateral mucopurulent or purulent nasal discharge
2) Ipsilateral submandibular lymphadenopathy (infectious)

Less common: epistaxis, facial swelling, epiphora, nasal airflow obstruction, abnormal resting respiratory noises, head shaking

189
Q

What would you see on radiograph of a horse with sinusitis

A

fluid lines in the sinus

*helpful but CT is better

190
Q

T/F: CT is very helpful in the diagnosis of sinusitis in horses

A

True

191
Q

What is the use of CT in diagnosing sinusitis in horse

A

helpful for diagnosing sinus and nasal passage idsorders in the horse. Major advantage of CT compared to radiogrpahs is lack of superimposition
CT can be used to plan a surgical approach but cannot determine if a lesion is benign or malignant

192
Q

What is the prpose of Scintigraphy in diagnosis of URT disease in horses

A

can be used to detect the presence of apical infection, with affected teeth having a marked, local increased radionucleotide uptake at the apex of the affected tooth

193
Q

Sinoscopy use for diagnosing Upper respiratory disease in horses

A

minimally invasive technique that enables the visualization of inspissated pus in some primary sinusitis cases, explaining their chronicity and non-response to sinus lavage

can also ID intra-sinus progressive ethmoidal hematoma and mycotic lesions and the detection of food in the sinus

194
Q

What might be needed to perform sinoscopy

A

Trephination - surgical procedure in which a hole is created in the skull by the removal of circular piece of bone

195
Q

What is Trephination

A

a procedure done with standing sedation, local anesthesia, steinmann pin, sample collection and drainage in the horse

196
Q

How is sinusitis treated in horses?

A

1) Antimicrobials
2) Lavage through existing openings
3) Tooth extraction
4) Surgery (standing or general)
-sinoscopic lavage
-create sinonasal fistula
-breakdown maxillary septum
-breakdown ventral conchal bulla
-maxillary flap
-nasofrontal flap

197
Q

What are common treatments for horses with primary sinusitis

A

rest and/or antibiotic therapy
sinus lavage in less severe cases and sinusotomy in the remainder

typically all horses receive sinus lavage following sinusotomy. maxillary or nasofrontal sinusotomy is performed under general anesthesia or under standing sedation

198
Q

What is the prognosis of sinusitis in horses

A

Excellent long term response to treatment
91% fully cured
7% partially cured
following a median of 1 treatment

Sinus neoplasia- only 22%cured

199
Q

What structures are found within the equine guttural pouch

A

1) Cranial Nerves: IX, X, XI, XII
(cranial nerves V, VII, VIII run in close proximity to pouches and can be affected by guttural pouch disease)
2) Cranial cervical ganglion
3) cervical sympathetic trunk
4) internal carotid
5) external carotid
6) stylohoid bone

200
Q

How do you tell what guttoral pouch you are in when scoping.

A

The lateral compartment is the smaller compartment
tells the direction

201
Q

What cranial nerves are affected when there is disease in the guttoral pouch

A

CN IX, X, XI, and XII

202
Q

guttural pouch empyema

A

accumulation of exudate (pus) in the guttural pouch
secondary to respiratory tract infection

failure of empytinh mechanism

associated with Strangles- lymph node abscessation into guttural pouch

may accompany guttural pouch tympany (air filled guttural pouch)

203
Q

How can strangles lead to guttural pouch empyema *

A

lymph node abscessation into guttural pouch

204
Q

What is the number one cause of guttural pouch empyema **

A

Strangles- Steptococcus equi ssp. equi or ssp. zooepidemicus

lymph node abscessation into guttural pouch

even if it does not culture positive for strangles

205
Q

What are the clinical signs of Guttural pouch empyema

A

1) Unilateral or bilateral nasal discharge
2) Thick purulent
3) Continuous/ intermittent
4) External enlargement not always noticeable

complications: airway obstruction, chondroid formation

Diagnosis: Endoscopy and Radiographs

206
Q

What are the complications of Guttural pouch empyema

A

1) Airway obstruction
2) Chondroid formation - severe and carry strangles - need to do something about it

207
Q

What are the two questions you ask when you see a horse with epistaxis

A

1) Does it occur during exercise or at rest
2) Is it unilateral or bilateral

208
Q

What might exercise-induced epistaxis tell you in a horse

A

Exercise induced pulmonary hemorrhage (EIPH) - seen occasionally with pleuropneumonia, pulmonary abscess, and others

209
Q

What might cause epistaxis in a horse when it is a rest/spontaneous

A

1) progressive ethmoidal hematomas
2) trauma
3) guttural pouch mysosis
4) Coagulopathies
5) Neoplasia
6) Fungal infections

210
Q

What is EIPH? *

A

Exercise Induced Pulmonary Hemorrhage in horses that occurs after hard exercise

Mechanism: unknown but possibly stress failure of pulmonary capillaries or role in inflammatory airway disease

clinical signs: epistaxis 1-10%
typically bilateral (can be unilateral)
cough
poor performance

diagnosis: Tracheal endoscopy 60-90 min after exercise
BAL: RBCs and hemosiderophages > 150 days after last episode
some radiographic changes

Treatment: Rest, NSAIDs, furosemide

211
Q

How do you diagnose EIPH in horses

A

1) Tracheal endoscopy 60-90 min after exercise - see hemorrhage
2) BAL: RBCs and hemosiderophages > 150 days after last episode (remain there)
3) some radiographic changes in dorsocaudal lung lobe (10%)

212
Q

How do you treat EIPH in horses? *

A

Rest
NSAIDs
Furosemide (illegal to race in)
Nasal Strips

213
Q

What does the epistaxis being unilateral or bilateral tell you in the horse

A

Unilateral: Nasal passage, paranasal sinuses, guttural pouch

Bilateral: Guttural pouch, pharynx, larynx, lower respiratory tract

214
Q

What are differentials for epistaxis from lower respiratory tract in a horse

A

EIPH*
Pulmonary Edema
Necrotizing Pleuopneumonia
Hemothorax

215
Q

What are differentials for epistaxis from upper respiratory tract in a horse

A

1) progressive ethmoid hematoma*
2) Guttural Pouch Mycosis *
3) Rupture of Longus Capitis *
4) Mucosal Erosion/ Rupture Small vessels

216
Q

What are causes of epistaxis in the horse

A

Upper Airway:
1) progressive ethmoid hematoma*
2) Guttural Pouch Mycosis *
3) Rupture of Longus Capitis *
4) Mucosal Erosion/ Rupture Small vessels

Lower Airway:
1) EIPH*
2) Pulmonary Edema
3) Necrotizing Pleuopneumonia
4) Hemothorax

others: trauma, foreign body, coagulopathy, fungal, neoplasia

217
Q

How might a horse rupture the longus capitis

A

horses flip over backwards and damage their basisphenoid bone
causing epistaxis of uper respiratory tract

218
Q

What is your diagnostic choice for determining where epistaxis is coming from

A

Upper Airway Endoscopy

219
Q

What is a progressive ethmoid hematoma (PEH) in horse?

A

slowly expanding yet benign lesion of ethmoid region and paranasal sinuses of horses
unknown etiology but resumed lesion is hemorrhage in submucosa of the respiratory eputhelium, causing the mucosa to stretch, thicken, and form a capsule around the slowly expanding hematoma

220
Q

What are the clinical signs of progressive ethmoid hematoma

A

-Unilateral discharge
-Bloody or mucopurulent
-partial airway obstruction
-facial swelling
-exopthalmos (protrusion of eyes)
-head shaking
-malodorous breath

221
Q

How do you diagnose Progressive Ethmoid Hematoma in horses

A

1) endoscopic examination of the nasal passages and ethmoid turbinate area is the most common diagnositc technique used to evaluate the upper airway in horses with epistaxis or respiratory stertor
PEH may be deep red to purple or have a yellow, green or bronze color

(2) Biopsy for definitive diagnosis

222
Q

How do you treat progressive ethmoid hematoma in horses

A

*Determined by size and location of mehatoma

1) Formalin injection- multiple injections of smaller lesions
2) Laser or cryosurgery- large lesions
3) Surgical removal- paranasal sinus surgery, hemorrhage, cross match for blood transfusion

223
Q

What is the likely etiology of guttural pouch mycosis

A

Aspergillus; Emericella

224
Q

Guttoral pouch mycosis *

A

commonly caused by aspergillus
plaques develop on mucosal walls of the guttoral pouch
usually dorsal - associated with carotid artery
Erosion through the wall creating an emergency

*Middle aged to older horses

225
Q

Why can guttural pouch mycosis develop into an emegency

A

Aspergillus can erode the carotid artery leading to severe epistaxis

226
Q

Clinical signs of guttural pouch mycosis

A

1) None
2) Nasal discharge- yellow, epistaxis (unilateral or bilateral), can be fatal
3) Cranial Nerve deficits- dysphagia and facial nerve paralysis, pharyngeal paralysis, laryngeal hemiplegia, horner’s syndrome

227
Q

Why is there commonly dysphagia with guttural pouch mycosis

A

dmaage to the glossopharyngeal nerve and pharyngeal branch of the vagus nerve

228
Q

T/F: its rare to have neoplasia in the guttural pouch

A

true- but could cause epistaxis

229
Q

How do you diagnose guttural pouch mycosis

A

endoscopy, cytology/culure

230
Q

How do you treat guttural pouch myocosis in the horse

A

1) Surgery-
a) arterial embolization (balloon or coil) to stop bleeing
b) common carotid artery ligation
c) Salpingopharyngeal fistulation- connecting guttural pouches, changes the environment there
*Need to stop the bleeding

2) Blood transfusion
3) Antifungal application

231
Q

What is the gold standard method for treating guttural pouch mycosis induced epistaxis

A

Transarterial coil embolization techniques

232
Q

What is the prognosis of guttural pouch mycosis

A

Untreated- 50% mortality
Embolization- 80-90%
Common carotid artery ligation- 80%
Salpingopharyngeal fistulation: novel report is promising

complication: prognosis depends on function, pharyngeal function, dysphagia, corneal ulceration, horner syndrome, blindness

resolution following surgery is 2-4 months

233
Q

How might rupture of head flexor muscles of horses lead to epistaxis

A

1) longus capitus and rectus capitis ventralis
2) Avulsion and rupture from basisphenoid or occipital bones when horses rear or fall over backwards
3) Epistaxis +/- neurologic signs
Diagnose via endoscopy

Conservative management

234
Q

Rupture of what muscles in horse can lead to epistaxis

A

longus capitus and rectus capitis ventralis
-strap muscles

235
Q

What are the clinical signs of Strangles in a horse

A

1) Pyrexia
2) Pharyngitis ]- dysphagia and abnormal head positions
3) Abscess formation in lymph nodes (Submandibular and Retropharyngeal)
4) Nasal Discharge if the lymph nodes ruptured into guttural pouch)
5) Pyrexia: 3-24 days after exposure
6) Cough
7) Lymphadenopathy
8) Upper Respiratory Tract Obstruction

*Severity of disease is correlated with the dose and frequency of infectious challenge- varies with immune status

236
Q

Strangles forms abscesses in what lymph nodes of horses

A

Submandibular and Retropharyngeal

237
Q

Does Strangles cause Upper or Lower respiratory tract obstruction

A

Upper

238
Q

What is the pathogenesis of Strangles? *

A

1) Portal of entry: mouth and nose
2) S. equi attaches to cells within the crypts of the lingual palantine tonsiles and to the epithelium of the pharyngeal and tubal tonsils
3) Few hours later, organism is within epithelial cells and subepithelial tonsilar follicles
4) Translocation to mandibular and retropharyngeal lymph nodes
5) 3-5 days later there is complement derived cheomtactic factors that attract large numbers of neutrophils: Abscessation
6) Final disposal of bacteria is dependent on lysis of abscess capsule and evacuation of its contents

239
Q

When does nasal shedding of S. equi typically occur *

A

usually begins 2-3 days after onset of fever and persists for 2-3 weeks in most animals

240
Q

How long does S. equi shedding typically persist for

A

2-3 weeks in most animals

241
Q

What is the portal of entry of Strangles

A

Mouth and nose - horse contact but commonly fomites

242
Q

When does abscessation after S. equi infection typically form *

A

3-5 days after exposure

once you have abscessation- treatment with antibiotics is not ideal
can use antibiotics prior to these 3-5 days

243
Q

S. equi causes lymph nodes to rupture where? *

A

1) Through the skin to the outside
2) Into the respiratory tract- nasopharynx and guttural pouch *

244
Q

10% of horses experience failure of guttural pouch drainage mechanism resulting in empyema, why is this significant

A

can persist subclinically for months to years

detection is best achieved via endoscopy

245
Q

What would you see on endoscopy of guttural pouch disease due to S. equi

A

1) empyema
2) chondroids

246
Q

T/F: cranial nerve deficits is commonly seen with S. equi infection of guttural pouch

A

False- unlikely despite there being a lot of inflammation

247
Q

How do you diagnose strangles guttural pouch disease

A

do a lavage and submit for culture for S. equi in horses thatn no longer have clinical signs to see if it persist
*not sterile and not interested in contaminates

248
Q

What is the microbe of choice for horses with Strangles

A

Penicillin (monotherapy)

249
Q

What is catarrhal or atypical Strangles

A

mild form of Strangles seen in animals with limited susceptibility
-older horses with residual immunity
-foals with waning maternal antibody protection
-vaccinated animals

*These animals shed virulent S. equi

250
Q

Why might a horse have the catarrhal or atypical Strangles? *

A

1) Older horses with residual immunity
2) foals with waning maternal antibody protection
3) Vaccinated animals

*These naimals shed virulent S. equi

251
Q

Do horses with catarrhal or atypical Strangles shed S. equi

A

Yes

252
Q

After S. equi infection, is there immunity?

A

75% (not treated with antibiotics) have long term immunity

20-25% are susceptible within several months- failure to produce/maintain antibodies

*Good for young horses to get strangles and develop natural immunity

253
Q

T/F: it is good for young horses to get strangles and let it run its natural course so they can develop long term immunity

A

true

254
Q

Why is transmission of S. equi of outwardly healthy animals of great importance

A

1) Horses that are incubating the disease and go on to develop signs of Strangles- Nasal secreton are source onf infection

2) Outwardly healthy convalescent horses that continue to habor the organism after full clinical recovery. Consider all recovered horses potentially infectious for at least 6 weeks after their purulent discharges have dried up

3) Long term subclinical S. equi carriers- outwardly healthy horses that carry and at least periodically shed S. equi for prolonged periods after apparent full and uncomplicated recovery

255
Q

How long should you consider horses that recovered from S. equi infections to be infectious *

A

Consider all recovered horses potentially infectious for at least 6 weeks after their purulent discharges have dried up

256
Q

What blood work changes will you see in a horse with Strangles

A

Leukocytosis
Neutrophilia
Hyperfibrinogenemia
Hyperglobulinemia

257
Q

How do you sample for Strangles diagnosis

A

*Guttural pouch lavage if in there
also:
-Nasopharyngeal wash (most sensitive)
-Nasopharyngeal swab
-Rostral nasal swab
-Aspirate of abscess

258
Q

What is the most sensitive method to sample a horse with Strangles

A

Nasopharyngeal wash- more mucosal surface and best way to rule out the animal isnt infectious anymore

or guttural pouch lavage if abscessation into guttural pouch

259
Q

After optioning a sample for S. equi. What should you do for further diagnosis

A

1) Culture- Beta-hemolytic streptococci but can be unsuccessful for incubation, early clinical phases, when bacterial count is low during convalescence

2) PCR: SeM- gene for antiphagocytic M protein of S. equi
qPCR- seel superantigen- encoding gene
3x more sensitive than culture

260
Q

What are you culturing for when doing a culture for Strangles

A

Beta-hemolytic Streptococci

261
Q

What protein does PCR detect in strangles

A

SeM: gene for antiphagocytic M protein of S. equi

can do qPCR for seel superantigen encoding gene
3x more sensitive than culture

262
Q

What should you do for detection of S. equi in subclinically infected carrier animals

A

PCR testing of an endoscopically guided GP lavage

263
Q

What suggests Strangles infection, despite lavage is negative for S. equi

A

visual detection of inflammation of the guttural pouch respiratory epithelium and the presence of empyeme, chondroids, or enlarge retropharyngeal lymph nodes on the floor of the guttural pouch

264
Q

SeM antibody titer

A

detection of recent infection evidenced by a 4 fold or greater increase in titer of antibody in paired sera taken 10 days apart

to support a diagnosis of existing S. equi associated purpura hemorrhagica (titer >12,800)

To support diagnosis of metastatic abscessation (titer >12,800)

to identify animals with existing high levels of antibody that might predispose to purpura hemorrhagica, especially useful if within 1 year of disease or exposure

265
Q

What SeM antibody titer consititutes a Strnagles infection *

A

4 fold or greater increase in titer of antibody in paired sera taken 10 days apart

266
Q

What SeM antibody titer value tells you the patient has S. equi associated purpura hemorrhagica or metastatic abscessation

A

Titer > 12,800

267
Q

You should not vaccinate if the SeM antibody is titer is

A

> 3,200

268
Q

What SeM antibody titer value might support diagnosis of existing S. equi associated purpura hemorrhagica

A

> 12,800

269
Q

What SeM antibody titer value might support diagnosis of existing S. equi metastatic abscessation

A

> 12,800

270
Q

To vaccinate against Strangles, horses should have titers that are ________ *

A

< 3,200

271
Q

Why should you not do any procedures in horses on the same day that received Strangles vaccination

A

horses might develop abscesses or complication related to abscessation

272
Q

When does Shedding of S. equi typically occur

A

begins about 2 days after the onset of pyrexia
*possible to isolate new cases before they can transmit infection

273
Q

Nasal shedding of S. equi typically persists for ________ in most animals but horses may be infectious for at least ______ after their purulent discharges have dried up

A

2-3 weeks; at least 6 weeks

274
Q

What might result in persistent shedding of S. equi for years

A

persistent guttural pouch infection

275
Q

How do you quarantine and screen animals for S. equi

A

Limit exposure
Implement biosecurity measures
quarantine- 3weeks for new arrivals
screen for sublcinical carriers: GP endoscopy and Culture and PCR testing

276
Q

What biosecurity measures should you make for S. equi

A

Quarantine and screening of new arrivals
appropriate disinfection and cleaining
pasutrues should allow a few weeks of rest (exposure to direct sunlight and dry periods are beneficial to denaturing bacteria)

education of caretakers- dedicating personnel and equipment, waste feed and manure from infectious animals should be composted in an isolated areas

277
Q

How do you treat Strangles

A

Majority require no treatment
Supportive: rest, comfortable stall, soft, moist, palatiable food

acute febrile cases in stalls benefit from fan assisted ventilation

empyema/chondroids- use lavage

in many cases, antibiotics is unnecessary .

cases where necessary:
-acute infection w high fever
-profound lymphadenopathy and respiratory distress
-metastatic abscessation
-purpura hemorrhagica
-guttural pouch infections

278
Q

T/F: you should always treat Strangles with antibiotics

A

False- in many cases antibiotics are unnecessary

concerns:
1) delay in maturation of abscesses or recurrence when antibiotics are discontinued
2) Diminish the development of protective immunity - a suboptimal immune response could leave horses susceptible to reinfection

279
Q

What are your concerns with using antibiotics to treat Strangles

A

1) delay in maturation of abscesses or recurrence when antibiotics are discontinued
2) Diminish the development of protective immunity - a suboptimal immune response could leave horses susceptible to reinfection

280
Q

Antibiotics are typically not indicated for treatment of Strangles. When are they indicated *

A

1) Acute infection with high fever and malaise before abscess formation
2) Profound lymphadenopathy and respiratory distress
3) Metastatic abscessation
4) Purpura hemorrhagica treated with corticosteroids
5) Guttural pouch infections treated locally and systemically to eliminate carrier state

Penicillin

281
Q

T/F: Antibiotics should be used as a preventative in animals that my have been exposed to Strangles *

A

False- they should NOT unless you are in the day 1-3 period (before abscessation and imbedding in tissue)

overuse of antibiotics promotes resistance, provides a false sense of security, and convalescent immune responses may not be induced

282
Q

How do you treat empyema/ chondroids in horses with Strangles

A

1) Lavage- transendoscopic, uterine pipette, and guttural pouch catheter

2) Transendoscopic grasping instruments

3) Surgical
a) transcutaneous- modified Whitehouse approach
b) Salpingopharyngeal fistulation (transendoscopic/laser)

283
Q

What is the metastatic spread of S. equi called

A

Bastard Strangles
via hematogenous, lymphatic, close association

common: lung, mesentery, liver, spleen, kidneys, and brain

284
Q

What are common sites of metastatic spread of S. equi

A

via hematogenous, lymphatic, close association

common: lung, mesentery, liver, spleen, kidneys, and brain

285
Q

How do you diagnose Bastard Strangles?

A

1) History of exposure to S. equi
2) Intermittent low fever
3) Very high SeM specific antibody titers (>12,800)
4) Labratory findings consistent with chronic infection: anemia, hyperfibrinogenemia, leukocytosis, neutrophilia, and hyperglobulinemia

286
Q

What are the immune mediated consequence disease of S. equi infection

A

1) Purpura hemorrhagica

2) Myositis
a) muscle infarctions, b) rhabdomyolysis with acute myonecrosis
c) rhabdomyolysis with progressive atrophy

3) Myocarditis triggered by streptococcal antigen

*Need steroids

287
Q

Aseptic necrotizing vasculitis caused by the deposition of immune complexes in blood vessel walls
see edema and petechial/ ecchymotic hemorrhages

A

Purpura hemorrhagica

288
Q

How do you treat purpura hemorrhagica in horses

A

Dexamethasone

289
Q

severe manifestation of purpura hemorrhagica where prognosis is guarded even with aggressive therapy
rhabomyolysis- elevation in CK and AST with stiff and recmenet

A

Muscle infarctions

Rhabdomyolysis with acute myonecrosis

Rhabdomyolysis with progressive atrophy

treat with corticosteroids +/- antibiotics if severe concurrent infection

290
Q

Strangles typically affects horses that are _________ of age while Rhodococcus affects _________

A

> 1 year of age;

weanling foals (3weeks to 6 months)

291
Q

What is the leaning cause of bronchopneumonia in foals with a high morbidity and mortality

A

Rhodococcus equi

292
Q

What does Rhodococcus have that allows growth in mamcrophage

A

VapA

293
Q

What are the bug basics of Rhodococcus equi

A

Gram +
Coccoid/pleomorphic
Facultative intracellular
Aerobic
partial acid fast

294
Q

What are the virulent strains of R. equi characterized by?

A

their ability to survive and replicate within the macrophages - associated by their presence of a large virulence plasmid- VapA

295
Q

What is the prevalence on endemic farms of R. equi? What is the mortality?

A

Prevalence: 13-25%- highly variable between farms and years- unrecognized, sporadic, endemic

Mortality 0-30%

296
Q

What is the source of R. equi

A

1) Passive carriage in adults leads to shedding of the organism in manure
2) Under suitable conditions (warm temp, low soil moisture, low neutral pH) it multiplies further
3) Acquisition from contaimated soil
4) Inhalation of aerosilized bacteria within the first few days or weeks of life (increased by dry and dusty areas

297
Q

At what environmental conditions does R. equi replicate in

A

-Warm temp
-Neutral pH
-Low soil moisture

298
Q

What acts as a source of virulent R. equi

A

Mares

-foals shed higher concentrations and more virulent of R. equi in manure when compared to adults

299
Q

What route is R. equi introduced to the foal

A

Inhalation of dust particles contain virulent R. equi

300
Q

What are risk factors of R. equi

A

-Foal density
-Large farms
-Transient mares
-Host factors

301
Q

At how old are foals typically exposed to R. equi

A

Exposure: Birth to several days old

Susceptible to infection: within the first 3 weeks

Occurrence of disease: 120 days to 180 (first few months)

302
Q

What is the timeline of foals with R. equi

A

Exposure: Birth to several days old

Susceptible to infection: within the first 3 weeks

Occurrence of disease: 120 days to 180 (first few months)

303
Q

What are the clinical spectrums of R. equi

A

Variable depending on severity
early signs may be subtle
subclinical disease
advanced signs are easier to recognize
Clinical signs: 3 weeks to 6months, often <4 months

*Primarily respiratory but also Nypoyon Nephritis and Polysynovitis Septic Arthritis

304
Q

What are the clinical signs of foals with R. equi *

A

Pulmonary disease: pyogranulomatous bronchopneumonia with abscessation, abnormaly lung sounds, tachypnea, suppurative lymphadentis

Abdominal: with or without concurrent respiratory disease
Colic and Diarrhea
Enterocolitis, typhilitis, abdominal abscesses, peritonitis

Bone and Joint: Arthritis, Osteomyelitis, vertebral osteomyelitis, painful/ lame, neurological deficits

Non-septic polysynovitis (25-33% of foals)- immune mediated and most commonly at the tibiotarsal and stifle joints, variable degree of joint effision, minimal lameness

Others: Ulcerative lymphangitis. SQ abscesses, Hypopyon, Uveitis, Nephritis, Renal abscesses, Hepatitis, Cholangitis

305
Q

50% of foals with bronchopneumonia caused by R. equi have

A

GI lesions

Colic and Diarrhea
Enterocolitis, typhilitis, abdominal abscesses, peritonitis

306
Q

Where do foals typically get non-septic polysynovitis from R. equi?

A

tibiotarsal and stifle joints

*minimal lameness

*Respond well to NSAID treatment

307
Q

T/F: Foals with non-septic polysynovitis from R. equi are experience significant lamness

A

False- there is minimal lameness

308
Q

R equi in foals causes respiratory, abdominal, bone/joint disease, and non-septic polysynovitis. What other body systems might be affected

A

1) Ulcerative lymphangitis
2) SQ abscesses
3) Hypopyon
4) Uveitis
5) Nephritis
6) Renal abscesses
7) Hepatitis
8) Cholangitis

309
Q

Why is it important to differentiate R. equi from other causes of pneumonia

A

there is different antibmicrobial

310
Q

How do you diagnose R. equi

A

Blood work: neutrophilia and hyperfibrinogenemia

Serology- reflex exposure, cannot identify disease by the time standard methods

Ultrasound: tell you R. Equi pneumonia with peripheral lesions

Thoracic radiography: alveolar pattern with regional consolidation. Often discrete nodular and/or cavitary lesions compatible with pulmonary abscessation

Culture: Treacheal wash via endoscopt (gold standard)

PCR: VapA rapid identification of R. equi strains. highly sensitive and can identify infection in negative cultures

311
Q

How do you sample for R. equi

A

A tracheal wash for bacterial culture

312
Q

What is the gold standard for diagnosing R. equi

A

Bacterial culture

obtain a sample via transtracheal wash or via endoscopy

313
Q

How might there be false negatives for R. equi

A

1) animals are cultured after having been admin antimicrobials
2) Mixed bacterial
3) since and intracellular organism is more difficult to isolate

*PCR is more sensitive

314
Q

What does PCR for R. equi detect

A

vapA gene

315
Q

Why might you need to use clinical signs in addition to culture to diagnose r. equi

A

if animals are subclinically infected or on endemic farms, they might have dust with the pathogen on it and might not outright manifest the disease

316
Q

How do you treat R. equi infections *

A

Combination of Macrolide and Rifampin

Macrolides (Erythromycin, Azithromycin, Clarithromycin, and Gamithromycin)

or Getamicin (IV or nebulized), oxygen, IV fluids, NSAIDS, nutrition

317
Q

What are the adverse affects of Macrolide +Rifampin treatment for R. eqio

A

Diarrhea (mare)
Hyperthermia
Respiratory distress
Red Urine

318
Q

What do you need to be careful about when treating a foal for R. equi with Macrolide + Rifampin *

A

can cause a fatal colitis in adult horses. He careful when they are sharing a stall together

319
Q

Why do you combine a macrolide (erythromycin, Clarithromycin, azithromycin, or gamitromycin) with rifampin to treat foals with R. equi?

A

Because rifampin allows for penetration of the drug into abscesses

320
Q

What should you warn the clients about when treating R. equi with rifampin

A

the foal might have red urine

321
Q

What is the prognosis of R. equi

A

Survival rate: 60-90%

Possible prognostic indicators- radiographic scores, US findings, heart rate, fibrinogen concentrations

Prognosis is poor for foals with joint sepsis/osteomyelitis (84% mortality)

322
Q

How do you control for R. equi

A

Limit exposure dose related to outcome
enviroment
1) Decrease foal density
2) Removal of manure (how it is spread)
3) Reduce dust in the area

323
Q

How do you perform screening of foals for R. equi

A

Screen starting at 3 weeks of age
-Temperature
-WBC: >13000 on endemic farms
-U/S
-Fibrinogen
-SAA
-R equi anitbodies

324
Q

What is the vaccine for R. equi?

A

there is no vaccination

you can administer hyperimmune plasma containing high anti-vapA antibodies titers

Typically 1L admin IV within the first 24 hours of life and the another one 21-25 days later

325
Q

There is no vaccination for R. equi available. What should you do instead

A

there is no vaccination

you can administer hyperimmune plasma containing high anti-vapA antibodies titers

Typically 1L admin IV within the first 24 hours of life and the another one 21-25 days later

326
Q

How do you screen foals for foals for R. equi

A

routine practice at many endemic farms

Lesion score: sum of the largest diameter of all pulmonary lesions >1cm

88% of foals with a lesion score of 1-10cm recover without treatment.
treatment of these foals leads to antimicrobial resistance

Treatment of foals with median score of 1..5 cm associated with mortality of 0.6%

327
Q

What lesion score of R. equi foals recover without antimicrobials

A

88% of foals with a lesion score of 1-10cm recover without treatment.

328
Q

What is the lesion score in foals with R. equi

A

Lesion socre: sum of the largest diameter of all pulmonary lesions >1cm

88% of foals with a lesion score of 1-10cm recover without treatment.
treatment of these foals leads to antimicrobial resistance

Treatment of foals with median score of 1..5 cm associated with mortality of 0.6%

329
Q

What do you examine on endoscopy of the arytenoids

A

the corniculate process

330
Q

Disease process that decrease the sie of the rima glottidis results in

A

Increases to airway resistance leading to dynamic airway collapse and noise

331
Q

What is result of decreased rima glottidis size in horses *

A

1) Increased negative inspiratory pressure
2) Hypoxemia, Hypercarbia
3) Metabolic acidosis
4) Musculoskeletal fatigue

332
Q

What are the different grades of laryngeal hemoplegia in horses in standing unsedated

A

1: All arytenoud cartilage movements are syndromous and symmetrical and full cartilage abduction can be achieved and maintained

2: Arytenoid cartilage movements are asynchronous and/or larynx is asymmetric at times but full arytenoid cartilage abduction can be achieved and maintained

3: Arytenoid cartilage movements are asynchronous and/or asymmetric. Full arytenoid cartilage abduction cannot be achieved and maintained

4: Complete immobility of the arytenoid cartilage and vocal fold

333
Q

Name the grade of laryngeal hemoplegia in standing unsedated horse:

All arytenoud cartilage movements are syndromous and symmetrical and full cartilage abduction can be achieved and maintained

A

Grade 1

334
Q

Name the grade of laryngeal hemoplegia in standing unsedated horse:

Arytenoid cartilage movements are asynchronous and/or larynx is asymmetric at times but full arytenoid cartilage abduction can be achieved and maintained

A

Grade 2

335
Q

Name the grade of laryngeal hemoplegia in standing unsedated horse:

Arytenoid cartilage movements are asynchronous and/or asymmetric. Full arytenoid cartilage abduction cannot be achieved and maintained

A

Grade 3

336
Q

Name the grade of laryngeal hemoplegia in standing unsedated horse:

Complete immobility of the arytenoid cartilage and vocal fold

A

Grade 4

337
Q

What are the grades of laryngeal hemoplegia in the horse during exercise

A

Grade A: Full abduction of arytenoid during inspiration

Grade B: Partial abduction of affected arytenoid cartilage (between resting position and full abduction)

Grade C: Abduction less than resting position, including collapse into the contralateral half of the rima glottidis during inspiration

338
Q

Name the the grade of laryngeal hemoplegia in the horse during exercise:

Full abduction of arytenoid during inspiration

A

Grade A

339
Q

Name the the grade of laryngeal hemoplegia in the horse during exercise:
Partial abduction of affected arytenoid cartilage (between resting position and full abduction)

A

Grade B

340
Q

Name the the grade of laryngeal hemoplegia in the horse during exercise:

Abduction less than resting position, including collapse into the contralateral half of the rima glottidis during inspiration

A

Grade C

341
Q

paralysis/ paresis of arytenoid abductor muscle

usually left sided due to left recurrent laryngeal neuropathy (axonal degeneration) affecting the crico-arytenoideus dorsalis muscle function

A

Laryngeal hemiplegia

342
Q

What is damaged in laryngeal hemiplegia

A

usually left sided due to left recurrent laryngeal neuropathy (axonal degeneration) affecting the crico-arytenoideus dorsalis muscle function

343
Q

How do you diagnosis laryngeal hemiplegia in horses

A

Endoscopy
Ultrasound

344
Q

How do you treat laryngeal hemiplegia in horses

A

*1) Prosthetic laryngoplasty (tie-back): suture to mimic function of CAD muscle (permanent)

*2)Ventriculocordectomy= sacculectomy (bilateral) + vocal cordectomy (uni-/bilateral) can be more dysphagic

3) Neuromuscular pedicle graft

4) Arytenoidectomy (partial)

345
Q

What are differential for right laryngeal hemiplegia in horses

A

1) Chondritis
2) Neuropathy - peri-vascular injection is most common
3) Laryngeal dysplasia (4-BAD)
4) EPM

*rules out

346
Q

bilateral laryngeal paralysis in horses

A

uncommon
risk of acute death due to asphyxiation
causes:
-arytenoid chondritis
-organophosphate, lead toxicity
-CNS disease- EPM
-Hepatic dysfunction/ encephalopathy
-Secondary to general anesthesia- head unsupported

Treatment:
-Steroid, NSAIDs, Vitamin E
-Tracheostomy: permanent if underlying cause not resolved
-Unilateral laryngoplasty- usually not necommended- airway contamination can be severe

347
Q

What causes bilateral laryngeal paralysis in horses

A

-arytenoid chondritis
-organophosphate, lead toxicity
-CNS disease- EPM
-Hepatic dysfunction/ encephalopathy
-Secondary to general anesthesia- head unsupported

348
Q

What is Arytenoid chondritis in horses

A

inflammatory condition of arytenoid cartilage
caused by respiratory trauma
fixed obstruction= inspiratory and expiratory noise

clinical signs: coughing, dysphagia, nasal discharge, respiratory noise, exercise intolerance

Diangosis: endoscopy to see distortion of corniculate process- mildly thickened, cartilage exposure with granulomas/ ulcers
kssing lesion on opposite aryenoid
or ultrasound

MEdical: Rest, NSAIDs, antimicrobials, pharyngeal spray
severe cases could require tracheostomy

Surgical treatment: Arytenoidectomy (partial) to remove part of the affected arytenoid

349
Q

Arytenoid chondritis is caused by

A

inflammatory condition of arytenoid cartilage cause by respiratory trauma

350
Q

What do you see on endoscopy of a horse with arytenoid chondritis

A

endoscopy to see distortion of corniculate process- mildly thickened, cartilage exposure with granulomas/ ulcers
kssing lesion on opposite aryenoid

351
Q

How do you treat arytenoid chondritis in horses

A

MEdical: Rest, NSAIDs, antimicrobials, pharyngeal spray
severe cases could require tracheostomy

Surgical treatment: Arytenoidectomy (partial) to remove part of the affected arytenoid

352
Q

What causes epiglottis in horses

A

mucosal and/or cartilage inflammation- edema, reddening, thickening, cartilage may be exposed at tip

epiglottis may or may not be trapped

353
Q

How do you treat epiglottis in horses

A

Stop exercise
Anti-inflammatories, antibiotics, corticosteroids

354
Q

What is the most common condition of the epiglottis in horses

A

epiglottic entrapment
apex entrapped by aryepiglottic folds

can be intermittent or persistent
predisposes to DDSP

Clinical signs: abnormal respiratory noise, exercise intolerance, dysphagia, coughing, nasal discharge

diagnosis endoscopy

355
Q

What is epiglottis entrapment in horses

A

epiglottic entrapment
apex entrapped by aryepiglottic folds

can be intermittent or persistent
predisposes to DDSP

Clinical signs: abnormal respiratory noise, exercise intolerance, dysphagia, coughing, nasal discharge

diagnosis endoscopy

treatment: surgery

356
Q

How do you treat epiglottic entrapment in horses

A

Surgery (standing endoscopy)
1) Transnasal axial division with guarded hook blade
2) transendoscopic axial division with diode laser
3) or resection via laryngotomy (TIVA)
4) Transoral axial division with hook blade

357
Q

What is dorsal displacement of the soft palate in horses

A

intermittent or persistent
common cause of respiratory noise and poor performance- estimated in 10-20% of race horses

etiology:
Primary Disease:
1) dysfunction of pharyngeal nerves/ associated muscles (thyrohyoideus m. dysfunction- palatal instability) or
2) hypoplastic epiglottis

Secondary Disease:
a) Disruption to palatal-epiglottic seal- caudal palatal or subepiglottic ulcer, subepiglottic cyst
b) Increased caudal position of the larynx- pharyngitis/ lymphoid hyperplasia and lower airway disease

358
Q

soft palate dislodge from subepiglottic position and obstricts rima glottidis at exercise

A

Dorsal displacement of the soft palate

359
Q

What are the clinical signs of dorsal displacement of the soft palate in horses

A

Respiratory noise- expiratory
Exercise intolerance

Decreased performance (open mouth breathing)

Increased swallowing prior to displacement

Soft palate billows up over rima glottidis leading to increased tracheal expiratory pressure and impedance. The decreased minute ventilation leads to hypoxia and hypercarbia

360
Q

What are the effects of dorsal displacement of the soft palate

A

1) increased tracheal expiratory pressure and impedance.
2) The decreased minute ventilation leads to hypoxia and hypercarbia

361
Q

How do you diagnose dorsal displacement of the soft palate

A

Historical information

Resting endoscopy- persistant DDSP, evaluate palatal border, under epiglottis

Dynamic endoscopy

Radiographs

362
Q

How do you treat dorsal displacement of the soft palate in hroses

A

Treat primary etiology- ulcer or pharyngitis or lower airway disease

tongue tie has questionable scuess

Cornell collar- prevent caudal retraction of the larynx

laryngeal tie forward: goal is to elevate and advance the larynx rostral to mimic the thyrohyoideus muscle
-suture pulls ventral thyroid cartilage towards the basiphyoid to advance larynx rostral and dorsal

363
Q

What is the laryngeal tie forward

A

goal is to elevate and advance the larynx rostral to mimic the thyrohyoideus muscle
-suture pulls ventral thyroid cartilage towards the basiphyoid to advance larynx rostral and dorsal

typically combined with sternothyroideus myotenectomy

364
Q

What is pharyngeal lymphoid hyperplasia/ pharyngitis in horses

A

Caused by local immune response to inhaled antigens

Young race horses <3yo racehorses

Exercise intolerance and respiratory noise

Diagnosis with endoscopy and investigate lower airway disease

treat with ant-inflammatories and pharyngeal spray

365
Q

What needs to be done for obstructions (upper respiratory disorders) in horses *

A

perform an emergency trachetomy- often before a definitive diagnosis is made

366
Q

What are the clinical signs of obstructions (Upper respiratory) in horses

A

-slow, exaggerated respiration
-Stridor (high pitch whistle= larynx/trachea)
-Stertor (low pitch girgle= nanso/oropharynx)
-Facial swelling/edema (snake bite envenomatin)
-Pharyngeal/ laryngeal swelling- laryngospasm (post-anesthetic anaphylaxis, HYPP), Strangles, Chondritis, SCC

367
Q

How might a horse that got a snake bite envenomation have upper respiratory obstruction

A

from facial swelling or edema

368
Q

What might pink foam coming from the nostrils in a horse mean

A

Pulmonary edema secondary to profound negative inspiratory pressure
-Treat with Lasix +/- antibiotics

369
Q

Emergency (Temporary) Tracheostomy

A

secure airway before diagnostics if in distress
Promixal 1/3 to 1/2 of neck

Vertical incision through skin, paired sternothyrohyoideus to incise between cartilage rings

Temporary tracheostomy tube options: J-tube, self retaining, nasotracheal tibe, jug handle, foal tubes

Requires daily cleaning to remove concentrations
heals by second intention in 3 weeks

+/- Furosemide for pulmonary edema

370
Q

What is the difference between intra-thoracic obstructive versus restrictive disorders in horses

A

Intra-Thoracic Obstructive: High airway resistance -> expiratory or mixed inspiratory/ expiratroy distress (Increased abdominal effort) - Equine asthma or heaves

Inthra-Thoracic Restrictuve Disorders: Low compliance -> respiratory distress without noise (nostril flare, increased respiratory rate/effort)
caused by pneumonia, pleuritis or pneuothorac

371
Q

What are some causes of Intra-thoracic obstructive disorders in horses

A

Equine Asthma or Heaves

High airway resistance -> expiratory or mixed inspiratory/ expiratory distress
(Increased abdominal effort)

372
Q

What are some causes of intra-thoracic restrictive disorders in horses

A

1) Pneumonia, pleuritis- will head absence ofl ung sounds ventrally (pleural effusion)

2) Pneumothorax- auscultation: absence of lung sounds dorsally

Low compliance leads to respiratory distress without noise

373
Q

In horses, Intra-thoracic ________ disorders such as asthma or heaves leads to ________________ sounds while, Intra- thoracic _________ disorders such as pneumonia leads to ________ sounds.

A

Obstructive

Expiratory/inspiratory distress

Restrictive leads to no noise

374
Q

How can you differentiate between intrathoraic repsiratory disorders in horses

A

Do an ultrasound

375
Q

How do you treat intra-thoracic respiratory disorders in horses

A

Aim at the primary problem

Asthma crisis
a) give beta-2 agonist like albuterol
b) clenbuterol (ventipulmin oral) uptake is slow
c) N- butylscopolammonium bromide (buscopan) is a potent bronchodilator but effect dissipates within an hour
d) Dexamethasone is not a rescue drug but will decrease inflammation
e) Atropine is effective but can cause ileus and tachycardia

Epi for anaphylactic shock

Do pleurocentesis for pneumothorac

Give oxygen (15-30L/min)(

376
Q

Is Albuterol or clebuterol uptake slower

A

clenbuterol uptake is slower because it is oral (ventipulmin)

377
Q

N- butylscopolammonium bromide (buscopan) is a potent bronchodilator but ___________

A

effect dissipates within an hour

378
Q

Injury to the left recurrent laryngeal nerve leads to affects the ________ muscle function

A

Crico-arytenoideus dorsalis

379
Q

suture procedure to mimic the function of the crico-arytenoideus muscle in cases of laryngeal hemiplegia

A

Prosthetic laryngoplasty (tie back)

380
Q

Severe cases of arytenoid chondritis may require

A

tracheostomy

mild/early cases can be treated medically with rest, NSAIDs, antimicrobials, pharyngeal spray

Some may require arytenoidectomy (partial) to remove the affected arytenoid

380
Q

T/F: In horses, bacterial pneumonia is always caused by a single pathogenic bacterium, such as Rhodococcus equi or Streptococcus equi subspecies equi.

A

False

Correct. In adult horses bacterial pneumonia is most commonly caused by Streptococcus equi subspecies zooepidemicus. In addition, gram-negative microbes such as Pasteurella spp., E. coli, Enterobacter spp., Klebsiella spp., and Pseudomonas spp. often complicate streptococcal pneumonias. While anaerobic bacteria are not usually primary isolates in pneumonias, they are isolated from horses with pleuropneumonia (e.g. Bacteroides spp. and Clostridium spp.)

381
Q

What respiratory noise do you hear with dorsal displacement of the soft palate *

A

Expiratory

382
Q

A 15-year old Paint mare is presented with a history of fever (103.5 F), colic, tachycardia, tachypnea, increased respiratory effort, and bilateral mucopurulent nasal discharge. On thoracic ultrasound examination, pulmonary atelectasis, pleural roughening, and a large amount of pleural effusion with free bright gas echos is seen. A teat cannula is inserted in the 6th intercostal space to drain the pleural effusion and to collect a sample for cytology, culture and sensitivity testing.

The aerobic culture reveals the following:

Heavy growth of Streptococcus equi subspecies zooepidemicus
Moderate growth of Klebsiella pneumoniae
Moderate growth of E. coli
The anaerobic culture shows the following:

Moderate growth of Bacteroides fragilis
Based on these culture results, which of the following antimicrobial therapies would likely provide appropriate antimicrobial coverage?

A

Potassium penicillin, gentamicin, metronidazole

While the antimicrobial susceptibility pattern may indicate differently (e.g. Klebsiella spp. resistant to aminoglycosides), the choice of an antibiotic with broad gram positive coverage (K penicillin), gram negative coverage (gentamicin), and anaerobic coverage (metronidazole) is indicated. While antimicrobial sensitivity testing is often not available for anaerobic bacteria, familiarity with antimicrobial susceptibility patterns is helpful in formulating the treatment regimen when an anaerobe is suspected. While Penicillin is typically an effective drug to combat anaerobic infections, Bacteroides fragilis is an anaerobe that is routinely resistant to penicillin. Metronidazole has activity against a variety of obligate anaerobes including B. fragilis.

383
Q

The following statement is true or false?

Thoracic radiographs are often of limited value in the diagnosis of equine pleuropneumonia.

A

True

As radiographic evaluation of the equine thorax is limited to right and left lateral projections, pleural disease is superimposed on the lung and pleural fluid accumulation causes an increase in total opacity of the thorax (particularly ventrally). Changes in the dorsal aspects of the lung that may still visible can be difficult to interpret as lung volume is compressed and interstitial patterns are enhanced.

384
Q

T/F: airway allergies is a risk factor for horses developing bacterial pneumonia

A

False- Risk factors for the development of bacterial pneumonia in adult horses include respiratory viral infection (e.g. equine influenza, equine herpes virus-1/4), transportation, race training, racing, general anesthesia, neuromuscular disorders (e.g. botulism), exposure to certain noxious gases (e.g. ammonia), and a recent history of esophageal obstruction (e.g. choke). In foals, predisposing factors include overcrowding, heavy parasite burden, poor nutritional status, heat stress, congenital immunodeficiencies, and concurrent disease

385
Q

A 16-year old Quarter Horse gelding is presented with a history of fever (103.9 F), anorexia, bilateral purulent nasal discharge, and a soft, infrequent cough. On examination, additional findings include tachypnea, increased respiratory effort on in- and expiration, a soft grunt heard during expiration, and the finding depicted in the image below.

Based on the horse’s presentation, what is the most likely diagnosis?

A

Bacterial pleuropneumonia

In horses, clinical signs of pleuropneumonia include fever, anorexia, cough, respiratory distress, stiff gait, weight loss, colic, pectoral/sternal edema and limb edema affecting primarily the front limbs.

386
Q

Which of the following clinical signs can only be encountered in horses with moderate to severe equine asthma (heaves), but not in horses with mild to moderate equine asthma?

A

Dyspnea and heave line

Although a cough, bilateral serous to mucoid nasal discharge, and impaired performance (i.e. exercise intolerance and prolonged respiratory recovery after exercise) can be seen in horses with the mild to moderate form of equine asthma, dyspnea is not a feature of mild to moderate disease and is only seen in horses severe heaves.

387
Q

Which of the following are benefits of using inhaled fluticasone compared to oral dexamethasone for the treatment of a horse with severe equine asthma.

A

1) Less adverse affects - While inhaled corticosteroids such as fluticasone, beclomethasone, and budesonide are less powerful than systemic steroids, they carry a lesser risk of systemic complications (e.g. suppression of endogenous cortisol, increased risk of infection, laminitis).

2) No need to wean off - As fluticasone is minimally absorbed from the equine lung, it does not result in substantial suppression of endogenous cortisol production. Therefore, there is no need for weaning.

388
Q

T/F: The following statement is true or false?

Airway obstruction in horses with moderate to severe equine asthma (heaves) is due to the following mechanisms:

Bronchoconstriction
Excessive mucous production
Inflammatory cell accumulation within the lumen of the small airways

A

True

In horses with heaves, airway obstruction results from three distinct mechanisms: excessive mucous production, inflammatory cell accumulation within the small airways and bronchoconstriction.

389
Q

What is the test of choice of a horse that presents with evidence of localized disease (i.e. the thoracic x-ray and ultrasound findings are indicative of pulmonary abscessation),

A

Tracheal aspirate
The tracheal aspirate allows collection of cells that originate from anywhere in the lower respiratory tract and accumulate in the distal trachea before being cleared from the airways by mucociliary clearance. In contrast, the BAL samples cells and secretions from small airways in a discrete area of the lungs (i.e. where the BAL tube gets lodged). Therefore, BAL is most useful in the diagnosis of homogeneously distributed small airway disease such as equine asthma.

390
Q

The following statement is TRUE or FALSE?

Inactivated equine herpes virus (EHV)-1 vaccines are highly efficacious in protecting horses from developing equine herpesvirus myeloencephalopathy (EHM).

A

False

While circulating and mucosal antibodies each play a role in protection from EHV-1 infection and reduction of virus shedding, the most important component to protect from viremia and its sequelae is the cytotoxic CTL response. Unfortunately, inactivated vaccines are weak inducers of cell-mediated immunity and currently, none of the commercially available vaccines has shown to be able to protect horses from EHM.

391
Q

Which of the following test result(s) is/are highly suggestive of an active (acute) EHV-1 infection?

A

1) Positive EHV-1 whole blood PCR:
Following virus replication in the respiratory epithelium, cell-to-cell spread of virus first results in the presence of virus in the regional lymph nodes. This is followed by a lymphocyte-associated viremia. Demonstration of viral DNA in whole blood (or buffy coat) is confirmatory of active EHV-1 infection.

2) Complement fixation (CF) titer of 1:2048

3) Positive EHV-1 immunofluorescence in aborted fetal tissue
Direct immunofluorescence is a rapid, specific and moderately sensitive test that can be used to detect virus antigens in nasal secretions or tissue samples. Following EHV-1 induced abortion, fetal membranes and tissues typically contain high viral loads and thus, are useful samples to collect to diagnose abortions caused by EHV-1.

392
Q

T/F: Because EAV infection results in inflammatory changes in small blood vessels (particularly the arterioles), clinical signs associated with equine viral arteritis also include conjunctivitis (“pink-eye”), limb edema, supraorbital or periorbital edema, and urticaria (as well as abortion).

A

True

393
Q

The carrier stallion is of central importance to the maintenance and spread of equine arteritis virus (EAV) in the horse population.

Which of the following would allow demonstration of lack of EAV persistence (i.e. non-carrier status) in a EAV seropositive stallion?

A

Lack of seroconversion in a seronegative mare following test breeding

A stallion with a serum titer of >1:4 without documented history of vaccination must be considered a putative EAV-carrier (as 30-50% of stallions become carriers following infection). As virus contaminated semen (fresh, fresh-cooled, or frozen) poses a significant risk of introducing EAV into a susceptible population, such a stallion must be tested for the presence of virus prior to breeding to a seronegative mare. The carrier state can be confirmed either by virus isolation or detection of viral nucleic acid by RT-PCR in a sample of semen containing the sperm-rich fraction of the ejaculate. A slower, more expensive but very reliable alternative is to test breed a suspect stallion to two seronegative mares which are monitored for clinical signs and seroconversion.

394
Q

Which of the following statements regarding equine viral arteritis (EVA) vaccination is CORRECT?

A

The vaccine can be used to prevent the establishment of a carrier status in stallions
One of the indications for vaccination against EVA is to protect stallions against infection and subsequent development of the carrier state. Remember that prior to initial vaccination, all stallions shall undergo serologic testing and be confirmed negative for antibodies to EAV. Testing should be performed shortly prior to, or preferably at, the time of vaccination. Negative certification is of importance should a vaccinated stallion be considered for export at a later date. All first-time vaccinated stallions should be isolated for 3 weeks following vaccination before being used for breeding.

395
Q

Within a 48-hour period, a group of 25 yearling horses at a sale barn develop high fevers (up to 105 F), serous to mucopurulent nasal discharge, lethargy, and inappetence. While examining several of the most severely affected horses, you notice submandibular lymphadenopathy and very frequent, hacking coughing.

Which of the following sample - diagnostic test combination would allow you to confirm your suspect diagnosis?

A

Nasal swab sample, RT-PCR test

Based on the history (rapid spread of a febrile illness) and clinical presentation (fever, lethargy, anorexia, nasal discharge, lymphadenopathy, and severe coughing) the most likely diagnosis is equine influenza. To detect the genome of an RNA virus, a Reverse Transcriptase (RT)-PCR test is required. As influenza replicates efficiently in the upper respiratory tract and respiratory tract secretions typically contain high viral titers (especially early in infection), a nasal swab sample submitted for equine influenza virus RT-PCR testing is likely to provide an etiological diagnosis.

396
Q
A

Fluids, Respiratory, Muscles (7 decks)

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