horses Flashcards
1
Q
Contagious equine metritis
A
- = acute veneral disease
- Inflammatory disease of proximal and distal reproductive tract of mare
- OIE listed
- Usually results in temporary infertility
2
Q
aetilology of CEM
A
- Gram-, non-motile, bacillus: taylorella equingenitalis, Fastidious bacteria
- Growth 3-6 days at 37oC on charcoal media,of 5-10% CO + Incubation time at least 7 days
3
Q
SOI CEM
A
Subclinical carriers = persistence of disease in population (mares and stallions)
4
Q
POE CEM
A
reproductive organ mucosae
5
Q
MOT CEM
A
natural mating, fomites + AI, vertical mare foal through birthing
6
Q
GD CEM
A
UK, now worldwide
7
Q
SIGNS CEM
A
- 10-14d after mating
- Mucopurulent vaginal discharge, early return to oestrous after shortened cycle, can be carriers for months with no signs
- Usually don’t conceive
- Stallion = asymptomatic + hold bacteria in smegma + urethral fossa
8
Q
T. asinigenitalis
A
- Donkeys are reservoirs + can be transmitted to horses
- Similar cultural + morphological characteristics to T. equingenitalis
9
Q
DIAGNOSIS CEM
A
- Bacterial isolation difficult to isolate as it’s fastidious (culture preferred)
- Swabs from endometrium (during oestrus), clitoral fossa + sinuses
- Stallions: urethral fossa, urethra, preputial cavity, shaft of penis + ejaculate if possible. Tested 3x before declared free
- Swabs in Amies (charcoal) transport medium + frozen if longer than 24h
- Culture on chocolate Eugon agar at 37oC
- Asaccharolytic but catalse, phosphate + cytochromnic oxidase +
- Serology = unreliable
- PCR = highly specific + more sensitive than culture (differentiate between the two bacteria’s)
10
Q
DIFF CEM
A
- Other metritis – s.zooepidemicus, k.pneumoniae, p.aeruginosa
11
Q
TREAT CEM
A
- Uterine infection eliminated in a few weeks
- Clean clitoral area with chlorhexidine scrub + apply nitrofurazone ointment = same for stallion
- Repeat daily for 5-7d + retest stallion after 10d
12
Q
CONTROL CEM
A
- Identify carriers + treat/eliminate from breeding program,
13
Q
public health CEM
A
NO
14
Q
equine salmonellosis
A
most common cause of infectious diarrhoea in adult horses
15
Q
salmonella aetiology
A
- Gram- Salmonella sp. (survives in environment weeks)
- 2 species: S. enterica (6 subspecies), S. bongori: Serogroup B = typimurium + agona serovars
16
Q
SOI salmonella
A
Ubiquitous, direct contact with horses shedding/ contaminated objects
17
Q
POE salmonella
A
Mouth, oral ingestion
18
Q
MOT salmonella
A
feco-oral (Healthy horses may excrete salmonella in faeces - stress)
19
Q
HS salmonella
A
all animals, young more (systemic infections) outbreaks in hospitals/studs with high density mares + foals
20
Q
pathogenesis salmonella
A
- Invade enterocytes, M cells + dendritic cells invasion to gut, LN and spleen neutrophil recruitment increase inflam mediators increase fluid secretion in intestinal lumen
- Damage of epithelial + sloughing of large areas of epithelium pseudomembrane formation
- Loss of protein into gut lumen Hypoproteinaemia
- Damage of epithelium salmonella in submucosae endotoxins release circulation septic + endotoxin shock
21
Q
signs salmonella
A
- Subclinical carrier
- Mild = 4-5d, self-limiting, depress, fever, anorexia, soft not watery faeces. Absolute neutropenia
- Severe = diarrhoea 6-24h after onset of fever. “ “ + abdo pain, profound neutropenia, faeces foul smelling, rapid dehydration sepsis + hypovolaemia
- PLE after a few days of diarrhoea bacteraemia DIC death
- Foals = haemorrhagic diarrhoea, sepsis, osteomyelitis
- Neutropenia before signs – severity related to severity of disease
22
Q
diagnosis salmoenlla
A
- isolation of bacteria = Gold standard, 3-5 daily faecal samples, blood/ tissue. 10-30g faeces. Serotype + atb testing (talk to lab)
- culture and AST
- PCR – too sensitive for high prevalence areas (dead +v. low quantities of bacteria) + no atb/serotyping
23
Q
treatment salmonella
A
- Fluids – 40-80L/d, electrolytes + acid-base correction, plasma, polymyxin B= binds circulating endotoxin
- Atb – doesn’t alter disease course or shedding but can help decrease bacteraemia. Atb diarrhoea + nephrotoxic
- NSAIDs – min effective dose, prebiotics, soft bedding, feed
24
Q
prevent salmonella
A
- Decrease stress, no overcrowding, isolate sick, clean + disinfect
25
s. abortus equi salmonella
- host restricted
- GD = endemic in Croatia + Japan due to subclinical carriers
- SOI = infected tissue + excretion, semen, subclinical carriers – causes abortion in 7-8th m
- Path = bacteraemia disseminated disease wo enteritis internalisation in macrophages through lymphatics + BV to target organs (placenta + testicle)
- Also called equine paratyphoid
- Foals = septicaemia + osteomyelitis/arthritis
- Adults = fistulous withers + orchitis
26
equine coital exanthema
- Very contagious , self-limiting, Benign venereal disease
27
Aetiology of ECE
- Equine herpesvirus 3 (EHV-3) short survival outside host (very sensitive to most disinfectants)
28
SOI of ECE
1o direct contact (venereal transmission), 2o contaminated equipment
- Reservoirs: latently infected horses – actively excreting
29
MOT OF ECE
Coitus, iatrogenic (contaminated AI equipment) and indirectly (genitonasal contact)
30
POE of ECE
- POE: Skin of external genitalia
31
GD of equine coital exanthema
worldwide
32
path of ECE
- Development of painful pustular lesions on external genitalia
- Replication of virus in stratified epithelium of dermal tissue of skin or mucocutaneous margins
- Circular red nodules vesicles erosions
33
signs of ECE
- Signs develop 4-8d after contact
- Circular red nodules 2mm on vulva, vaginal mucosa + clitoral sinus + skin
- vesicles pustules erosions that can coalesce
- oedema of perineum, stiff walking, pain
- 2nd bact w strep mucopurulent discharge
- Skin healing within 3w – maybe potential carriers
- Pregnancy rate not decreased
- Similar lesions in stallions, copulation painful, ulcers can bleed + decreased sperm viability
34
diagnosis of ECE
- Clinical findings – typical
- Confirmation: electro microscopy
- Cytology/histology = intranuclear herpes inclusion bodies
- Serology: interpret carefully due to high seroprevalence (+EHV-1 +4) isolated from genital lesions
o Paired sera + 4x increase = diagnostic
35
treatment of ECE
- treat secondary bacterial infections (topical antiseptics) and NSAIDs
36
prevention of ECE
- Sexual rest of sick animals (AI during active lesions)
- No vaccine
- Animals can return to breeding when lesion healed
37
equine infectious anaemia (swamp fever)
- Former OIE list – each country has 24 hours to report to the headquarters of world organisation
- Noncontagious (venereal) septicaemia viral disease
- Lifelong infection (like HIV) horses survive infection beginning you have symptoms and slowly decrease if they survive the 1st 3 years they won’t die
38
EIA aetiology
- Equine infectious anaemia virus (EIAV) - lentivirus, retroviridae, RNA
- Lipid membrane (sensitive to most disinfectants)
- 2 types of receptors on outer membrane (GP90, GP45 mutation in these receptors will give the clinical picture)
39
EIA GD
- GD: Worldwide distribution, Working animals, Swamp, forest areas – high humidity
40
MOT EIA
- MOT: Stomoxys calcitrans (stable fly), tabanidae (horse fly – much more capable of transmitting disease as can transfer higher volume of blood) mechanical transmission
- Iatrogenic – viable 96h on needle, aerosol (if nosebleed), in utero, venereal
41
HS EIA
- HS: All equids, horses (lifelong carriers), Donkeys usually asymptomatic (reservoir host)
42
path EIA
- Relationship between development of signs + amount of virus present
- Infection viraemia infection of macrophages increased pro-inflam cytokines (TNF alpha) increase prostaglandin E2 fever + decrease thrombocytes
- Increased TNF-alpha = decreased RBC production anaemia
- IgG + IgM bind to platelets IM destruction hepato + splenomegaly
- Acute infection controlled by immune system = signs stop until variant virus emerges that can evade immune system
- Next clinical episode is through stress (transport, pregnancy, castration, etc)
43
signs EIA
- Depends on: virulenece dose + susceptibility
- Incubation: 15-45 days or longer
- Acute/subacute phase: 1-3 days, depression, fever, thrombocytopenia, death
- Chronic: ““, increased HR + RR, anaemia, jaundice, petechiae of MM, oedema, muscle weakness
- Inapparent infection (after episode lasting 1y)
- Interval between episodes = days-weeks-months
- Anaemia – suppression of production of RBC (macrophages)
44
PM EIA
- Sago spleen: splenomegaly w prolif of white pulp (cut looks like marble) pathognomonic
- Nutmeg liver = increased w lymphohistiocytic infiltration, oedema, mucosal haemorrhage, pale kidneys, bone marrow fat replaced with red haematopoietic tissue
45
diagnosis EIA
- True diagnosis = serology – AGID/coggins test, ELISA = lots of false + so with AGID
- Western blot if conflicting results
- Serology can be – in first 10-14d PI
- RT-PCR – only for quarantine, won’t detect low loads
46
differentials EIA
- Lepto, piroplasmosis, anaplasmosis, AIGA, purpura haemorrhagic, parasites, EVA
47
treatment EIA
- no treatment or vaccine (there’s marketed vaccine in China) euthanasia/permanent isolation
48
prevent and control EIA
- Different surveillance system in places + Removal of positive animals + Vector control
- Use sterile needle syringe, and IV sets or surgical equipment
- Only administer commercially licensed blood or blood products
49
African horse sickness
- In naïve population of horse, mortality may reach 90%
- Emerging disease
50
AHS aetiology
- AHS virus, Orbivirus
- Nonenveloped, double RNA (closely related to bluetongue), 9 serotypes (VP7 + VP2 antigens)
- No cross protection between serotypes
51
AHS GD
Endemic sub-Saharan Africa
52
AHS HS
Horse: most susceptible – acute form, Mules, donkeys: mild, curable form (African horse fever), Zebras – subclinical, Dogs: fatal pulmonary forms,
53
MOT AHS
- MOT: colicoides, same one as transmitting blue tongue, Rhipicephalus spc (tick) dog = direct ingestion of infected meat + vector) (Hematophagous arthropods)
54
pathogenesis AHS
- Arthropod bite multiplication in LN viraemia replication in endothelial + mononuclear cells entry to organs multiplication 2nd viraemia damage to endothelial cells + macrophage activation cytokine release DIC/oedema death
- Organ depends on AHSV strain + tropism, lung, spleen, heart, lymphoid tissue
55
signs AHS§
- Incubation 3-15 days
- Pulmonary form – peracute, thin head. Pyrexia, dyspnoea, death due to pulmonary oedema. Incubation 3-5d, naïve animals, frothy nasal discharge, 95% fatal
- Mixed form (between pulmonary and cardiac form) – acute = most common form. Lung involvement + subcut oedema - Mortality 70-80%
- Cardiac form (subacute) – thick head – oedema of supraorbital fossa, fever, MM congestion + petechiae, incubation 1-2 weeks, fatality = 50%
- Horse sickness form just fever – mild- fever, depress, full recovery, immunised animals, donkeys + zebras
56
PM AHS
- Liquidothorax, fluid in pericardium, lung oedema, pulmonary oedema, swelling of conjunctiva
57
diagnosis AHS
- PM
- RT-PCR (blood or spleen, lungs, LN and heart) GOLD STANDARD
- Good to know serotype for control
- VI, VN, ELISA – not useful in vaccine areas
58
differentials AHS
- EVA, EIVA, Hendra virus infection, anaplasmosis, piroplasmosis, anthrax
59
treatment AHS
- Don’t treat: slaughter of confirmed cases + in-contact animals in most countries
- (in Africa there’s vaccination)
- OIE in endemic areas
o shouldn’t show signs + shouldn’t have been vaccinated against AHS in last 40 days
- No specific curative treatment
60
prevention aHS
- Movement restriction, vector control, quarantine
- Live attenuated vaccines – controversial + can’t differentiate vaccinated from infected (good but not complete protection)
- Vaccines in endemic areas annually
61
Equine influenza
- Most common highly contagious viral respiratory of horses
- Self-limiting upper respiratory infection with high morbidity (100%) but low mortality
- Outbreaks are characterised by a sudden onset and rapid spread of disease
- Worldwide – but doesn’t occur in Australia and New Zealand
- No seasonality
62
Aetiology EIV
- EI virus, Orthomyxoviridae family. RNA virus. Influenza A genus (infects people + animals, B + C = only humans) H7N7 or H3N8. Antigenic drift = Europeans + American lineages of H3N8
- Subtypes: H7N7 and H3N8 (H = haemagglutinin, N = neuraminidase) - No cross protection
63
SOI EIV
Sick/ carrier animals (incubatory + inapparent), droplets + aerosol, contaminated fomites
64
MOT EIV
inhalation of resp secretions from coughing horse, indirect + via fomites (shared water, hands) Birds natural reservoir
65
POE EIV
- POE: Mucosa of the upper respiratory tract
66
HS EIV
Equine, dogs. Naïve 1-5 years more susceptible, fatal in donkeys, zebras + debilitated horses. No carrier state but naïve + vaccinated horses can be subclinical shedders for 7-10d
- Rate of EIV infection is 100% in unvaccinated horses
67
path EIV
- Incubation = 1-5d, EIV survives hours in droplets, 2-3d on fomites + in water
- Epithelia + pneumotropic damages ciliated cells decrease mucus clearance
- Replication spreads to other cells of resp tract necrosis of epithelium exudation in to airway increase mucus but decrease mucociliary clearance
- Resp epithelium takes 21d to regenerate so susceptible to 2o bacterial infection pneumonia, chronic bronchitis
68
signs EIV
- sudden onset Fever, depress, anorexia, weak nasal discharge, dry, harsh, unproductive cough. mild = last <3d, recovery 2-3w
- severe = may convalesce up to 6m
- rare = myocarditis + COPD if return to training too soon
69
diagnosis EIV
- VI or RT-PCR from naso-pharyngeal swab
- ASAP from onset of signs
- Antigen capture ELISA. Paired serum
- can be detected before signs – take nasal swabs see if incubatory carrier – send 5-6days after signs are observed, for serology take blood samples 10-14 days later then taken 2nd sample
70
treatment EIV
- rest, no exercise, NSAIDs, maybe atb. Neuraminidase inhibitors can decrease shedding + spread of infection. Rule: For every day of high temperature, horse needs 1 week of rest
71
general protective measures EIV
- Quarantine of new horses, biosecurity, inactivated vaccine IM, MLV vaccine intranasal-induces local immunity (gives more rapid protection 5-7d)
72
public health EIV
- Zoonoses, person infected experimentally but not naturally yet
73
differential EIV
- EHV (cough more common w EIV), adenovirus
74
antigenic drift EIV
- small mutations in genes that lead to changes in HA + NA
- Drift has caused ‘European’ + ‘American’ lineages of H3N8
- H7N7 = epidemic (acutely infective horses introduced to susceptible groups)
- H3N8 = outbreaks across globe
75
Antigenic shift EIV
abrupt major changes resulting in new HA or NA new influenza subtype
76
aetiology equine viral arteritis
- Equine arteritis virus (EAV), areterivirdae, Enveloped, single stranded RNA
- Alphaarterivirus genus. North America + European lineages
- 1 serotype but antigenic variability between geographically different strains
- Survives 75d at 4oC +2-3d at 37oC, for years at -70oC, easily inactivated by detergents
77
SOI EVA
- SOI: sick + carrier (stallions), droplets/aerosol, contaminated objects/premises
78
MOT EVA
- MOT: respiratory, venereal, indirect + contact w contaminated fomites
79
HS EVA
- HS: all horses, higher incidence in warmbloods
- Persistently infected stallions can be divided into 3 groups
o Short term/ convalescent, (few weeks after recovery), Intermediate carrier state lasts 3-7 months +Long-term or chronic carrier state can last for years and even the entire life
80
POE EVA
- POE: Lung and bronchial LN/ genital tract
81
path EVA
- Resp exposure multiplies nasopharyngeal epit + tonsils + alveolar macrophages CD
- 14+ monocytes take to LN where it replicates then released to bloodstream
- Cell associated viraemia 6-8th localises in vascular endothelium of arterioles perivasculitis
- Also, in epithelium of liver, seminiferous tubules + adrenals. EAV no longer detectable after 28d
- Vascular lesions oedema + haemorrhage (max damage 10d)
- Abortion due to lethal fetal infection
- 10-70% of stallions become carriers for few weeks, few months or lifelong (no effect on semen quality)
82
signs EVA
- mostly asymptomatic, incubation 2-14d. most recover
- fever, depress, anorexia, oedema, conjunctivitis, photophobia, petechiae on MM, hives, icterus, abortion, fatal pneumonitis/pneumoenteritis in foals
- mares that abort already pregnant when exposed (3-9w PI)
- stallions = short term subfertility
- foetus = pulmonary oedema, pleural effusion, petechiae
83
PM EVA
- Oedema, congestion + haemorrhage (limbs + abdomen)
- Micro = vasculitis of smaller arterioles + venules
84
diagnosis EVA
- RT-PCR. Virus microneutralisation = gold standard
- VI – nasopharyngeal swabs, EDTA blood
- Abortion = placenta, foetal lung/liver, thymus
- Stallions = VI or RT-PCR of sperm rich ejaculate fraction (at least 2). Breed to 2 seroneg moves + check 28d later
85
differential EVA
- EHV1+4, EIA, EI, AHS, allergic urticaria
86
treatment EVA
anti-inflam, diuretics, rest, antipyretic
87
prevent EVA
- MLV + inactivated vaccines available
- Identify manage carrier stallions, screen semen for AI
- Good hygiene – prevent humans spreading
88
public health EVA
- Pathogen only of equids, no evidence to infect people
- Reportable to relevant authorities, isolation + movement restrictions (lift 3w after last confirmed case) OIE
89
equine rhinopneumonitis
- Viral rhinpneumonitis + equine abortion virus
- OIE
90
aetiology of rhinopneumonitis
- Equine herpesvirus 1 (EHV-1) and equine herpesvirus 4 (EHV-4), alphaperesvirinae, easily inactivated, survives in environment <7d
91
SOI rhino
- SOI: Sick, carrier animals (inapparent), air, contaminated objects, etc
- reservoir = latently infected horses
92
MOT rhino
- MOT: direct: nasal secretions (Aerosol), repro tract discharge, placenta/ aborted foetuses
- indirect contact by farm personnel, equipment, feed and water act as fomites
93
POE rhino
- POE: upper respiratory tract – primary infection (reactivation of latent infections)
94
HS rhino
- HS: EHV-4 = horses, weanlings, EHV-1 = horses, equids
- When infected latency occurs (reactivated by stress)
95
path rhino
- Replication in mucosa + LN of upper resp tract cell associated viraemia
- EHV-4 = resp pathogen, low tropism for endothelial cells so low viraemia no abortion/neuro
- EHV-1 = tropism for lots of cells in lymphocytes uterus + endothelium of CNS vessels
- Latency in trigeminal ganglia. Vasculitis + thromboischemia after endothelial infection EHV myeloencephalopathy (EHM)
- Abortion due to intraocular
96
signs rhino
- EHV-1 and EHV-4 cause respiratory disease, abortion and neurologic disease
- EHV-1 associated with all 3 syndromes
- EHV-4 is cause of resp disease
- Resp disease, abortion, neuro disease. Incubation 2-10d serious nasal disease, anorexia, lymphadenopathy usually no cough (unlike EI). 2o bacterial infection, fever, neutropenia, lymphopenia
- Abortion = 2-12w PI, 7-11m gestation, foetuses fresh
- EHM = EHV-1 – incoordination, recumbency, loss of bladder + tail function + skin sensation, death
97
prognosis rhino
- Decrease if 3+ d recumbent
98
PM rhino
- Ulceration of resp epithelium, multiple, tiny, plum foci in lungs
- Micro: Eosinophilic inclusion bodies in airway epithelial
- Foetuses = interlobular lung oedema, hepatic necrosis
99
diagnosis rhino
- VI = gold standard – higher sensitivity than both IF and PCR
- RT-PCR of nasopharyngeal swab or blood (false negative due to intermittent shedding)
- IgG detectable 8-10d PI, peaks at 30-40d + persists for 9+ months
- Hard to find latently infected horses
- IgM measured by CF , IgG measured by VN (virus neutralisation) and ELISA
100
treatment rhino
- Supportive, 1w rest for 1d fever, NSAIDs, valaciclovirs
101
protective measures rhino
- Inactivated combined EHV-1 + 4 vaccine at 4-6m, 4-6w later than 10-12m old q6m till 5y.
- Vaccinate through pregnancy
- Doesn’t affect latent infection
- Isolate affected, clean + dirty areas, biosecurity
102
strangles
- Very contagious bacterial infectious disease
103
aetiology of strangles
- Streptococcus equi subsp equi, Gram +, Beta-haemolytic, obligate pathogen
- Survives in environment 6-8w in damp dark places protected from light eg water bucket + stable floor. Susceptible to most disinfectant
104
SOI strangles
- SOI: sick + carriers (reconvalescent + latent), Reconvalescent carrier – shed 2- 6 w. subclinical carriers may have chondroids in G pouches – lifelong shed +Contaminated fomites
105
POE strangles
- POE: Oronasal mucosae
106
MOT strangles
- MOT: Direct + indirect contact - all routes except transplacentary. Insects – passive transmissi
107
HS strangles
- HS: all ages – most severe 1-5y. horses donkeys + mules. Morbidity 100%, mortality <10%
108
path strangles
- Inhalation or ingestion + colonise regional LN bacterial replication + neutrophil infiltration increased LN + abscessation spread in lymph + blood metastatic strangles
- SeM protein increase virulence + resistant to phagocytosis
109
signs strangles
- Incubation time 2-14 days
- Fever (shed bacteria 2-3d after + 2-3w after stops, so isolate when fever starts),
- mucopurulent nasal discharge, Swollen LN, depression, difficulty swallowing, extended neck, stridor. Abscessation of LN swallowed gut abscesses
o into G pouch cleared/ chondroid formation + carrier state
o outside signs improve (rupture 7-14d after signs start)
110
complications strangesl
- Bastard strangles – abscesses in abdomen/thorax/brain/lungs. Inadequate atb may predispose. Often fatal
- Purpura haemorrhagica –2-4 w after contact with strep antigen
o Immune mediated vasculitis. Hives, oedema, colic, arrhythmia, haemorrhage,death
- Myositis, sinus infection, keratitis, meningitis
111
diagnostic strnagles
- Culture - S. equi subsp equi = gold standard
- Sampling: nasopharyngeal swab/ wash (good for sick not carriers) g pouch wash (increased sensitivity good for carriers) + PCR of g pouch wash
112
treatmetn strangles
- Atb- penicillin, 22,000 IU/kg IM q12h or IV q6h
- Yes, if severely ill + before LN swelling
- No if LN increased already – decreased maturation of abscesses, predisposes to bastard
- Supportive – warm compresses to increase abscess maturation, fluids, NSAIDs, drain + flush abscesses, feeding
113
control strangles
- Isolate sick + in contact, take temp 2x1d – isolate if fever, quarantine new arrivals
- Biosecurity, disinfection, PPE, avoid same grazing for 4w
114
prevent strangles
- Post expose immunity long after disease if no atb given + Only vaccinate healthy horses
- Inactivated vaccine (IM) – prevents disease in 50% cases if outbreak. Common local reaction
- MLV (intranasal) – duration of immunity 3m decrease vaccine reaction
- 2-3 vaccines 3 w apart + then 1q 6-12m check risks of individual horse before vaccination
- Don’t vaccinate in outbreak esp if horses have been in contact with ill
- Horses can shed for 4-6w post recovery. Screen for shedding 3w after no signs (PCR of G wash)
115
strep equi subsp zooepidemicus
- Can cause disease similar to strangles
- B-haemolytic
- Pathogen or commensal
- Not species specific – disease in animals + humans
- Resp or repro infection – depending on strain virulence
116
rhodococcus equi foal pneumonia aetiology
- Rhodococcus equi, g+, facultative intracellular, pleomorphic bacteria, ubiquitous in soil on horse farms, virulent strains (VapA gene) + avirulent survival in soil pH dependent 7.5-8
117
SOI rhodococcus
- SOI: soil + manure
118
MOT rhodo
- MOT: Inhalation of contaminated dust (aerosol) + ingestion of contaminated mucus
119
risk rhodo
- Risk: dry, warm, windy weather, dusty soil with no grass –contribute to development of aerosol
120
HS rhodo
- HS: 1-5m old foals. Disease rare if >8m. pulmonary infection in first 1-2w of life
121
path rhodo
- Inhaled + taken up by alveolar macrophages macrophages destroyed by intracellular replication
- Migration of inflam + protective cells necrosis of cells + damage to surrounding tissue granuloma formation
122
signs rhodo
- Signs 3-24 weeks of life,
- Subacute-chronic suppurative bronchopneumonia
- Pulmonary abscesses + suppurative lymphadenitis. Stress increases signs
- Lethargy, fever, cough, increased RR
- Crackles + wheezes on auscultation
- Weight loss/failure to grow
123
non-pulmonary signs rhodo
- Consequence of pulmonary or independent intestinal/mesenteric abscesses – fever, depress, colic, diarrhoea, anorexia (50% w pulmonary)
- Polysynovitis – non-septic inflam from bacteraemia, hock/stifle effusion. No lameness
- Septic physitis/osteomyelitis – 1 joint affected, lame, spinal cord compression/fracture
- Panophthalmitis, guttural pouch emphysema, sinusitis, pericarditis, hepatic/renal abs
124
diagnosis rhodoc
- AM diagnosis - presence of bacteria in tracheobronchial aspirate (TBA) = gold standard
- PCR/culture from tracheal wash/nose isn’t confirmatory due to ubiquitous nature
- US – can miss deeper lesions. X-ray
- Cytology – intracellular bacteria. Neutrocytosis, hyperfibrinogenemia
125
treatment rhodoc
- Macrolides difficult as resistant + intracellular for 2-12w. stop if no US/X-ray signs + foal better
- Clean environment fluid, oxygen, NSAIDs, nutrition
- Abscesses <11cm maybe no treatment
126
prognosis rhodoc
- 60-90% survive if good treatment
127
prevent rhodo
- ¬decrease aerosol formation + density of foals, compost manure for 7d, serial monitoring?
- Administration of hyperimmune plasma (HIP) in 1st few days of life, maybe decrease incidence + severity
- No vaccine is effective enough yet to be commercially available
128
public health rhodo
- Emerging pathogen. Can cause disease in immunocompromised people. Rarely in immunocomptent. Endemic on farms
129
west nile
- Emerging arthropod-born pathogen, causes disease in human and horse + birds
- OIE listed
130
aetiology west nile
- West Nile virus (has at least 6 lineages, 1-2 in Europe), Flaviviridae, genus: flavivirus
- Enveloped, spherical, single-stranded RNA
131
SOI WN
- SOI: Birds and mosquitos (transovarial transmission - overwintering)
132
POE WN
- POE: skin
133
MOT WN
- MOT: Mosquitoes (culex)
134
HS WN
- HS: avian– natural reservoir and amplifier for the virus, Horse and humans (dead end host)
135
path WN
- Infection starts in keratinocytes + immune cells in epidermis (langerhaans + dendritic cells)
- Infected dendritic/keratinocyte LN viraemia disseminated to organs (spleen, liver, kidney, CNS)
136
mechanism for euro-invasion WNV
- 1.direct infection of vascular endothelium and entry into CNS
- 2. viral passage through vascular endothelium due to BBB damage by vasoactive cytokines
- 3. “trojan horse” - infected monocytes are trafficked into CNS
- 4. retrograde axonal transport into CNS after infection of peripheral neurons
- in brain, WNV replicate in: neurones, astrocytes + microglial cells necrosis/apoptosis of neuronal cells neuro-invasive disease
137
signs WN
- incubation: 5-15 days, 80% asymptomatic
- 20% = flu-like – fever, anorexia, depression
- <1% = encephalomyelitis, anxiety, fever, muscle weakness, tremors, ataxia, paresis/paralysis, inability to swallow, sensitive to light + noise
- 20-40% lethal, 80-90% fully recover in 1-6m
- 20% = residual complications – weight loss, cran nerve decrease
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PM WN
- petechiae in rhombencephalon and spinal cord
- micro = mild-severe polioencephalomyelitis of brain stem + ventral horns of thoracolumbar spine
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diagnosis WN
- blood test w increase IgG antibodies to WNV (7d PI), PCR/VI of blood, CSF and brain
- IgG can be from last year, IgM is from acute present infection + IgM = confirmation of WNV
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differential WN
- Herpes
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treatment WN
- complete recovery after 1-6 months 80-90%
- symptomatic treatment, anti-inflam electrolytes, decrease stress
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protective measures WN
- insect control – remove standing water, clean troughs, indoors when mosquitoes highest
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immunoprophylaxis WN
- inactivated whole WN virus vaccine – 2 x every year
- non-replicating live canary pox recombinant vector vaccine
- 2 primers at 1m interval + booster annually
- NOT vaccinating in Croatia
- inactivate flavivirus chimera vaccine
- mosquito human yes
- horse human no (but care at necropsy)
