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Module 20: Global Vet Med > Equine Diseases of the Northern Hemisphere > Flashcards

Equine Diseases of the Northern Hemisphere Flashcards

1
Q

what is the most important viral respiratory disease of equids

A

equine influenza A

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2
Q

how is equine influenza A transmitted

A

Direct/indirect contact, aerosols

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3
Q

is there a carrier state for equine influenza A

A

no carrier state

requires circulation

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4
Q

what is the incubation period of equine influenza A

A

1-5d

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5
Q

what type of virus is equine influenza A

A

RNA

H3N8 strain circulating

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6
Q

what is responsible for attachment of virus to host cells in equine influenza A

A

hemagglutinin

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7
Q

what breaks down mucus bonds in the resp mucous in equine influenza A

A

neuraminidase

allows access of virus to underlying epithelial cells

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8
Q

what is the role of hemagglutinin (HA) and neuraminidase (NA) in equine influenza A virus

A

they both undergo antigenic drift which alters the antigenicity

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9
Q

what are the subdividisions of eqiune influenza A

A

clade 1 and 2

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10
Q

what are the signs of equine influenza A

A

Typically URT signs, extreme pyrexia

  • 39-40ºC

Lymphadenopathy

Nasal discharge

  • Serous

Acute signs decrease after 7 days, with harsh cough for 3-4 weeks

Can result in secondary bacterial pneumonia

Swollen legs/vasculitis/myositis/myocarditis may occur

Life threatening dysrhythmias

  • Should be evaluated for myocardial polypeptides, muscle enzyme before return to training
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11
Q

how is equine influenza A diagnosed

A

History, clinical signs, high morbidity rate

Viral isolation

  • Useful for strain surveillance — vaccine implications

Paired serology

Rapid antigen detection tests (ELISA)

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12
Q

what is the morbidity and mortality rate of influenza A

A

High morbidity

High mortality rate in foals and elderly

Reduced morbidity with improved immune status (ex. prior infection/vaccine)

Age is predictor of disease risk

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13
Q

how long does immunity last post infection in equine influenza A

A

1 year

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14
Q

what are the risk factors of equine influenza A

A

Prolonged journey is risk factor for horses developing equine influenza in UK (ex. importation from Europe)

New horses should be quarantined for 4 weeks after arrival

AHT maintains map of confined cases, and strain types

Lapse of vaccination

Prior vaccination does not prevent but reduces severity

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15
Q

what are the vaccination requirements of equine influenza A

A

Essential to know strain of circulating virus

Maintain up-to-date vaccine reservoir

OIE supplies information on circulating strains

Vaccines for international market should contain both clade 1 and clade 2 viruses of the Florida sub lineage

ProteqFlu has both clade 1 and clade 2 strains

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16
Q

what are the compulory vaccine for equine influenza A

A

FEI:

  • 1st vaccine at 4 months
  • 2nd after 21-92 days
  • 3rd after 150-215 days
  • Thereafter 6 monthly booster required

BHA:

  • As above, compulsory annual booster given on or prior to anniversary

Individual horse societies/events vary in rules

ProteqFlu vaccine

  • Canary pox vector
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17
Q

how is equine influenza A treated

A

Symptomatic

Particularly severe in naive individuals

Prolonged rest, NSAIDs, fluid therapy if severe

  • Post-viral syndrome and viral myocarditis relatively common
  • Sufficient nursing and rest duration vital in recover
  • May take 6 weeks for complete recovery to occur

Antibiotics may be required

  • Secondary bacterial infections common
  • May progress to interstitial pneumonia
  • Disease of high morbidity, particularly if vaccination has lapsed
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18
Q

what are the diseases that equine herpesvirus causes

A

EHV1:

  • Respiratory disease, abortion, neurological signs

EHV2:

  • Respiratory disease, keratitis, conjunctivitis

EHV3:

  • Coital exanthema

EHV4:

  • Respiratory disease, (abortion)

EHV5: Respiratory disease

  • Nodular pulmonary fibrosis?
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19
Q

what are the signs of equine herpesvirus respiratory tract infection

A

pyrexia (39-40C)

lymphadenopathy

URT signs but short duration

serous nasal discharge

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20
Q

what is the importance of EHV infections

A

common

performance limiting

contagious

spread from young to broodmares and neurotropic strains

abortion, neurological disease less common but high mortality

latent infections and recrudescence

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21
Q

why is important to know about the latency and recrudescence of EHV infections

A

disease prevetion

detection

disease transmission

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22
Q

how is EHV1 and 4 transmitted

A

Infection via inhalation or recrudescence of latent infection

Virus circulates in young horse population

Pregnant mares and visiting youngstock should be kept separate

Direct (nose to nose contact) or indirect (contaminated buckets, clothing, blankets contact with nasal discharges of infected horses)

Virus can travel via aerosol for short distances

Virus may also be transmitted by contact with aborted fetuses, placental fluids, or placentas form infected horses

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23
Q

what is the incubation period of EHV1 and 4

A

2-10 days

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24
Q

how long does shedding last of EHV1 and 4

A

up to 14d from onset of pyrexia

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25
how is EHV1 and 4 controlled
3 week quarantine period of incoming horses Separation of horses into suitable age groups Consider vaccination to reduce circulating virus but does not prevent infection
26
how is EHV resp infection diagnosed
qPCR on fresh tracheal was specimen or nasopharyngeal swab Serology not useful as virus is ubiquitous May be useful to test several individuals
27
what is the disease progression of EHV resp infections
Self limiting in 3-7 days May be secondary infections or vasculitis Major risk due to abortion or neurological signs in susceptible individuals Young animals should be quarantined for sufficient period to reduce likelihood of viral shedding
28
how are EHV resp infections treated
Symptomatic treatment only required NSAIDs Soft feed Stable rest Occasionally require treatment of vasculitis and limb edema, uveitis Will remain carriers of infection and therefore concurrent disease or corticosteroids could induce recrudescence in future
29
what does rhodococcus equi infection affect
foals of 2-3 months most susceptible waning colostral immunity
30
how is rhodococcus equi transmitted
Inhalation of contaminated dust * Intestinal lesions due to contaminated sputum * Parasites may introduce R. equi into tissues * Hematogenous spread rare Increase by crowding, poor ventilation, dust
31
how does rhodococcus equi become endemic on stud farms
Will have high burden in the soil and will spread to successive foal crops May be a significant annual problem A proportion of foals will harbour infection, develop pulmonary abscesses and then have natural regression of these abscesses Others develop clinical signs and require treatment to prevent/reduce mortality
32
what is the pathogenesis of rhodoccocus equi infection
Survives intracellularly in macrophages (difficult for antibiotics to reach) * Causes degeneration and necrosis of cells then further bacterial release Polisaccaride capsule resists phagocytosis VapA virulence factor Exoenzyme virulence factors — phospholipase
33
what is the mortality and morbidity of rhodococcus equi
morbidity 10-15% mortality \>50%
34
what is the incubation period of rhodococcus equi
variable incubation period clinical signs only apparent after few weeks most presenting at 2-4 months old
35
what are the clinical signs of rhodococcus equi infection
**initial pyrexia** **Bronchopneumonia** * Polypnea, coughing, wheezing * Abdominal effort, cyanosis * May be nasal discharge, lacrimation **Ulcerative colitis +/- mesenteric LN abscess** * Weight loss, poor thrift, poor haircoat * Low grade colic, lethargy and inappetance **Rarer clinical signs** * Polysynovitis, joint sepsis, or osteomyelitis * Specific organ disruption ex. hepatic encephalopathy * Uveitis and hypopyon
36
how is rhodococcus equi diagnosed
**May be cultured from transtracheal aspirate (TTA) or blood** * Negative culture does not rule out infection as intracellular organism **Neutrophilia and high fibrinogen levels** **Metabolic acidosis if struggling with oxygenation** **Positive serology indicates exposure only** **Usually clinical diagnosis made on evaluation of diagnostic imaging together with clinical pathology** * Cavitating abscesses may be present * Compression of trachea may cause stertor
37
how is rhodococcus equi treated
**Combination of erythromycin & rifampin most common** * Need a lipophilic antimicrobial to penetrate the immune cells * Erythromycin may cause diarrhea, hyperthermia and tachypnea **Long term course of 4-9 weeks required**
38
what is used to guide duration of therapy of rhodococcus equi infection
Ultrasonographic appearance and resolution of acute phase response used to guide duration of therapy in addition to clinical response Consensus guidelines according to lesion classification (U/S)
39
what antibiotics may have greater efficacy in rhodococcus equi
Drug resistant R. equi huge problem in endemic areas (ex. Kentucky) **Newer macrolides have greater efficacy:** Azithromycin Clarithromycin Tulathromycin
40
what is the prognosis for racing of rhodococcus equi infections
Good for continued athletic function if recover
41
what is the intestinal presentation of rhodococcus equi infection
Settle in the abdomen in the lymph nodes Failure to grow adequately Diarrhea May or may not be concurrent involvement of thorax Difficult to treat, large abdominal abscesses and can adhere omentum and parts of bowel and major organs
42
how are rhodococcus equi infections treated
Old stud farms Heavy population Hot, dry, dust Infected foals isolated **Early recognition:** * Observe foal lagging behind * Measure WCC and fibrinogen * Ultrasound screening repeated during first month of life * Hyperimmune plasma at 48 hours and 3-4 weeks thought previously to decrease incidence but individual variation in susceptibility and strain pathogenicity
43
what is the causative agent of equine protozoal myeloencephalitis (EPM)
sarcocystis neurona also incriminated -- neopsora hughesi
44
where is equine protozoal myeloencephalitis (EPM) reported
USA canada france? seroprevalence \>\>\> disease
45
what are the risk factors for equine protozoal myeloencephalitis (EPM) infection
age (\<1.5yo and \>13) season presence of definitive hosts watering/feeding management adverse health events
46
what is the definitive host of equine protozoal myeloencephalitis (EPM)
opossum fecal excretion of infective sporocysts onto pasture
47
what are the intermediate hosts of equine protozoal myeloencephalitis (EPM)
raccoon armadillo skunk develop sarcosysts in muscle
48
what are the incidental hosts in equine protozoal myeloencephalitis (EPM) life cycle
horses
49
what does equine protozoal myeloencephalitis (EPM) cause in horses
multifocal distribution of lesions expulsion of parasite --\> asymptomatic CNS lesions --\> EPM
50
what are the clinical signs of equine protozoal myeloencephalitis (EPM)
**Highly variable** **Often insidious** **Most have spinal cord lesions** * Ataxia & paresis often asymmetrical **5-10% have muscle atrophy** \<5% have brain/brainstem lesions often persistent, but may wax and wane * Inflammatory response to the cyst in the nervous tissue Multifocal disease possible **EPM = differential for many chronic neurological disorders in endemic areas (herpes virus)**
51
how is EPM diagnosed
Problematic due to widespread seroconversion Relies on compatible signs and interpretation of relevant but non-definitive Signalment, history, clinical signs Exclusion of Ddx Immunoblots (westner blot) — serum/CSF antibody ratio * High sensitivity, low specificity Response to treatment
52
how is EPM treated
**Anti-protozoals** * Ponazuril (toltrazuril sulfone) * Anti-coccidial, crosses BBB * Prolonged course of medication required * Sulphonamine-pyrimethamine **Ancillary therapy** * NSAIDs * Corticosteroids/DMSO? * Vitamin E * Protect the myelin sheath * Immuno-modulators
53
what is the % of horses that imrpove and relapse after EPM infection
60-70% improve Relapse rate —\> 10-20%
54
how is EPM prevented
difficult aim to limit exposure of forage and pasture to definitive host
55
what is the causative agent of potomac horse fever
Neorickettsia risticii
56
how is potomac horse fever treated
Fluid therapy * Colitis Tetracyclines (doxycycline, OTC) * 7 day course Tetracyclines may correct pyrexia within 48 hours
57
how is potomac horse fever prevented
Vaccination highly successful in reducing incidence Avoidance of risk factors Stabling to avoid ingestion of infected trematodes at risk times of year
58
what type of bacteria causes equine monocytic ehrlichiosis (aka potomac horse fever)
neorickettsia risticii intracellular gram negative coccus
59
where is equine monocytic ehrlichiosis (aka potomac horse fever) distributed
USA, canada, europe
60
what is the vector of equine monocytic ehrlichiosis (aka potomac horse fever)
Virgulate (rod shaped) trematode of freshwater snails Methods of transmission is unknown Possible ingestion of immature stages in aquatic insects
61
what is the pathogenesis of potomac horse fever
Infects monocytes * Obligate intracellular organism Predilection for colon tissue, macrophages, crypt cells, mast cells * Loss of microvilli * Reduced electrolyte transport * Watery diarrhea * Dose dependent effect
62
what is the prediliction site for potomac horse fever
colon tissue, macrophages, crypt cells, mast cells
63
what are the clinical signs of potomac horse fever
**Typhlocolitis** * Biphasic fever (up to 41ºC) * Edema * Anorexia * Diarrhea * Endotoxemia * Laminitis **Sub-clinical disease** **Abortion** * Usually at 7 months * Maladjusted foals
64
how is potomac horse fever diagnosed
history, signs serology (IFAT or ELISA) fecal PCR
65
what are ddx for diarrhea in young foals
Clostridium difficile Rotavirus infection Strongyloides westeri — high burdens (epg \>2000) leads to diarrhea Strongylus vulgaris — cause verminous arteritis and colic signs Cryptosporidia — more likely to occur in more intensive stud farms Giardia Parascaris equorum becomes significant in foals \>3 months Antibiotic induced diarrhea also common as in adults
66
what are the viral causes of diarrhea in foals
rotavirus
67
what are the epidemiological features of rotavirus
highly contagious short incubation period rapid spread
68
what are the signs of rotavirus in foals
depressed and anorexic
69
what age does rotavirus affect
2 days to 6 months
70
how is rotavirus diagnosed
fecal antigen testing and electromicroscopy
71
what are ddx for rotaviral infection in foals
adenovirus coronavirus parvovirus bacterial causes of diarrhea
72
what is the morbidity of rotavirus in foals
high effective barrier nursing disinfection required vaccination in subsequent years
73
how is foal diarrhea treated
**Fluid therapy most important** * IV or oral * Electrolytes, glucose * Hyperimmune plasma for Rotavirus infection **Intestinal protectants** * Bismuth subsalicyclate * Activated charcoal * Bio-sponge **Anti-ulcer therapy** **Antibiotics if pyrexic with secondary infection** **Probiotics**
74
how is foal diarrhea prevented
Vaccination of mare at 8, 9, and 10 months of pregnancy to increase production of antibodies in colostrum to protect foals
75
what causes proliferative enteropathy of foals
lawsonia intracellularis
76
what age of horse does lawsonia intracellularis affect
weanlings
77
what type of bacteria is lawsonia intracellularis
obligate intracellular gram negative organism
78
where does lawsonia intracellularis invade
GI cyrpt cells loss of villi and malabsorption
79
at what time are horses affected by lawsonia intracellularis
around time of loss of colostral antibody protection 4-7 months
80
what are the clinical signs of lawsonia intracellularis
Fever Lethargy Peripheral edema \* Diarrhea Until final stages of condition Colic Weight loss Profound hypoproteinemia * Albumin falling to 10 g/l (ref 30-33 g/l) in some cases * Foal may collapse due to hypotension * Better prognosis with earlier diagnosis and treatment
81
how is l intracellularis diagnosed
Clinical signs and signalment Extreme hypoalbuminemia Fecal PCR * Intermittent shedding * Pool fecal samples or submit sequential samples for analysis Serology * Seroconversion in high proportion of adults, but seropositivity in foal with clinical signs is suggestive of active infection US appearance of small intestine * Cartwheel appearance * Narrowed lumen
82
how is l intracellularis treated
**Oxytetracycline** * 4-6 weeks required * Doxycycline also effective **Colloidal oncotic support** * Hetastarch or plasma **Full recovery can be made with early diagnosis and sufficient duration of treatment**
83
how is l intracellularis preveted
difficult ## Footnote Wildlife reservoir Vaccination of mares Licensed equine vaccine

Module 20: Global Vet Med (21 decks)

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