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Year 2 Equine ID > Equine Bacterial respiratory infections > Flashcards

Equine Bacterial respiratory infections Flashcards

1
Q

How would a horse with dyspnea present?

A

Dyspnea = shortness of breath

- flared nostrils, coughing, head up and down

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2
Q

List the infectious bacterial resp diseases covered in 2nd yr

A
  1. Streptococcus equi var. equi (strangles) - (mentioned in equine bacterial dermatological disease)
  2. Rhodococcus equi (rattles)
  3. Bronchopneumonia/ Pleuropneumonia = non specific lower resp disease:
    • Strep equi var zooepidemicus – main one we deal with
    • Pasteurella caballi
    • Klebsiella pneumonia
    • Bacteroides fragilis
    • Other Anaerobes
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3
Q

Streptococcus equi var. equi

- proper name and non proper

A

Contagious Equine Rhinopharyngitis (nose - pharynx - inflammation)
Strangles
INFECTIOUSSSS

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4
Q

What is strangles?

A

Contagious Equine Rhinopharyngitis
Bacteria: Streptococcus equi var. equi
- Upper respiratory tract bacterial resp disease ALTHOUGH can spread further into body causing metastatic abcesses (not just associated with the head)
Head lymph nodes favoured
- Most frequently diagnosed equine infectious disease
- causes long term latent infection in horses
- normally bacterial in glutteral pouch
- Really nasty to deal with clinically and politically

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5
Q

Morbidity/ mortality of strangles?

A

Contagious Equine Rhinopharyngitis
BActeria: Streptococcus equi var. equi

High morbidity, low mortality

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6
Q

Clinical signs of streptococcus equi var. equi

A

Strangles
Contagious Equine Rhinopharyngitis
• Swelling and constriction by the lymph nodes in the head (retropharyngeal and submandibular)
• First sign - Pyrexia before start bacterial shedding and being infective to others
• Watery nasal discharge - gets more mucusy (white and gooey) LHS
• Dull, In appetent (stops eating)
• Then lymph node abscessation (week into)
• Inflammatory changes on blood sample

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7
Q

Incubation period of streptococcus equi var. equi

What does this mean

A

Strangles
Contagious Equine Rhinopharyngitis

Variable- long = 2 days- 2 weeks
Makes it ahrder to control outbreak AND difficult to diagnose

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8
Q

Correct isolation of horses infected with Contagious Equine Rhinopharyngitis

A

streptococcus equi var. equi
Strangles
• Once start clinical signs, first being pyrexia nasal discharge and lethargy. Usually not infection to other horses until 2-3 days AFTER show these. Not shedding bacteria so can isolate at first sign of pyrexia

• Bacteria gains access to lymph nodes within first week but don’t see clinical sign of Lymph node abscesses till 1 week or so

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9
Q

How long do horses infected with Contagious Equine Rhinopharyngitis shed bacteria for?

A

streptococcus equi var. equi
Strangles
eria shedding can go on for over 2 weeks after! Some cases, reservoir of infection in guttural pouches, continue to shed infectious bacteria for loooong time. Potentially months!

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10
Q

In expreme cases of strangles what can occur?

A

Contagious Equine Rhinopharyngitis
streptococcus equi var. equi

Extreme cases: DYSPNOEA
obstruction of respiratory tract and even oesophagus = pharyngeal compression = tracheotomy required in extreme (incision in ventral neck into trachea, bypassing upper respiratory airways)

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11
Q

Strangles host - pathogen - environment interaction

A
  • Highly contagious –spread by direct contact & fomites – e..g feed buckets / hands (close contact – won’t fly for miles through the air)
  • Goes from wall/ bucket/ brush and transferred not passed through air
  • Short range drop let spread
  • Survive in environment for up to 4 weeks – affected by moisture and temperature
  • Sensitive to desiccation (drying) / sunlight / heat
  • Killed at >55oC in 30min
  • Sensitive to most disinfectants
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12
Q

What bacteria causes strangles?

Talk about this bacteria

A
  1. Streptococcus equi var. equi bacteria
  2. It is a Primary pathogen which means it isn’t found in “normal” healthy horses like Strep equi var zooepidemicus
    This means whenever found = significant
  3. Gram positive, coccoid
  4. Catalase-negative facultative anaerobe
  5. Large mucoid colonies, Beta-haemolytic
  6. Lactose fermentation negative
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13
Q

How is streptococcus equi var equi determined from other similar streptococcus equi var x

A
  1. PCR
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14
Q

Strangles how it causes disease

A

o Upper respiratory tract
o Lymph nodes of head favoured retropharyngeal and submandibular
• Lymph nodes abscesses 1 week after infection
• Lymph node abscess often burst into Guttural pouches
Causes
Guttural pouch empyema (liquid puss

Liquid puss dries to make chondroids
Bacterial shedding

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15
Q

What happens if If Gutteral pouch empyema is not treated in Strangles

A

Guttural pouch empyema = liquid puss from burst lymph node abcess
• pus thickens, dries forming:
• solid balls - chondroids which can’t leave gutteral pouch
Horse = carriers of disease, these chondroids need to be broken up and flushed out
• surgery is not easy – damage to nerves and vascular structures likely
• Chondroids don’t cause problems – can have no clinical signs and horse just continues shedding strep equi bacteria!

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16
Q

Strangles complications cause…

A
  1. Bastard Strangles
  2. Purpura Haemorrhagica
  3. Persistent Carriers
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17
Q

What is bastard strangles?

A

A Strnagles complication
Usually what happens:
• Got strangles- treated (removes and flushed chondroids, treat URT and lymph node abscesses)
• From first strangles, metastatic abscesses may form in other lymph nodes, or other tissues, other than the head
• These Disseminated abscesses difficult to treat
• most common in mysenteric lymph nodes (LHS) – difficult to heal abscesses in the abdomen, hard to access to drain due to guts and arteries and ahrd to treat with antimicrobials
- abscesses are inflamed which increases intestinal adhesions - twists and obstructions more likely = colic.

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18
Q

What is Purpura Haemorrhagica

A

A strangles complication:
• Type 3 hypersensitivity reaction – make immune response against pathogen (strangles)
2. Ab attach to pathogen.
3. Ab Ag complex circulates around body and then lodges in capillaries in small blood vessels
4. immune system attacks this, causing damage of vascular endothelium local tissue.
5. over production of immune response damages Antigen-antigen complex but also blood vessel walls – becomes leaky (leaking fluid, proteins and blood - leads to purple swellings under the skin).
• See swelling. This is PH – when capillary wall is is so damaged you get bleeding out of blood vessels into subcutaneous space purple appearance of distal limbs and muzzle predominantly.
• Vasculitis and severe illness
• See this couple weeks after worst clinical signs
• Treated with immunosuppressant’s as hypersensitivity response

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19
Q

What is going on if couple weeks after horse has been Pyrexic, Dull, In appetent (stops eating), watery nasal discharge, had lymph node abscesses, its muzzle appears purple

A

Initial clinical signs think - STRANGLES (Contagious Equine Rhinopharyngitis/
streptococcus equi var. equi)

Purple appearance of distal limbs and muzzle predominantly - due to bleeding out of blood vessels into subcutaneous space
Will also see swelling

This is Purpura Haemorrhagica

• Type 3 hypersensitivity reaction
immune response against pathogen (strangles) Ab attach to pathogen. Ab Ag complex circulates around body and then lodges in capillaries in small blood vessels and immune system attacks this, causing damage of vascular endothelium local tissue.

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20
Q

Strangles complications - persistent carriers

A

• Approx. 10% recovered horses become persistent carriers
o Mostly in glutteral pouch – not always obvious chondroids
o Can have a biofilm over the back of pharynx
o > 1 month after end of clinical signs

• Carrier status may persist for long periods
o Variable but > 5 years in some cases – very hard to deal with

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21
Q

When you deal with outbreak of strangles, what should you do on yard?

A

o Detected which horses have been infected, cure horses, after outbreak check ALL horses and look for index case (Asymptomatic case) any horses which were infected and have become persistent carriers. Should do gutteral pouch wash on every horse on yard

22
Q

Structure of streptococcus equi var equi

A

• Cell wall M-protein (target for vaccines/immunity) is antiphagocytic (stops opsonisation – why it is so pathogenic and so successful)
o Binds Fibrinogen / immunoglobulin (cant do their job)
o Mask complement binding site
o Highly variable

23
Q

How do strangles rates increase?

A

• increasing group size
• High stock density
• increased movement of horses
• increased mixing of horses
• communal feeders and drinkers
• younger horses more susceptible – immunologically naive
o apparent age-related immunity probably due to previous exposure:
o older naïve horses are still susceptible
o See strangles a lot with young horses who have been traded at market (poor biosecurity)
• E.g. older horse, no travel, low stock density – likelihood reduced but never rule out!

24
Q

How to diagnose strangles

A
  1. Culture – endoscopy and sample bacteria (although abcteria in gutteral pouch isn’t always sign of strep coc equi var equi)
  2. PCR (S equi DNA fragment) – superior test
  3. Serology (Antibodies to S equi) – increasing number over few weeks
  4. Clinical signs, history, movement, neighbour strangles status

**• A positive culture/PCR is always significant as this is a primary pathogen – doesn’t stay around as a commensal

25
Q

Talk about diagnosising strangles by serology

A
  1. Serology (Antibodies to S equi) – increasing number over few weeks
    • Only shows exposure, not infection (could have illuminated infection but still have circling antibodies)
    • Most horses seroconvert from 2 weeks
    • Remain seropositive > 6 months after infection
    • Dual ELISA – 93% sensitive / 99% specific – really good
    i. Papers in last 6 months showing this porbably isn’t as good as we once thought
    ii. Specific but not as sensitive – if high numbers of antibodies, likely but is low can’t rule out as carrier horses have been known to have low antibody numbers
26
Q

How to confirm a horse is free of strangles

A
  • Guttural Pouch Wash – only need 1 negative to be 88% sure that the horse is free of infection
  • Nasal Swabs/flush (nasopharynx) – 3 negative swabs each week for 3 weeks to inc sensitivity (= 85% sure of no infection) – lower sensitivity that GPW. +ve result know it is pos. Neg, can’t be certain
27
Q

Strangles treatment

A 
•	BIOSECURITY
•	Symptomatic treatment – feel better and maintain hydration and feed
o	Anti-inflammatory drugs
o	Antipyretic
o	Analgesic
•	Soft feeds
•	Tracheotomy
•	Antimicrobials - care
•	Removal chondroids – mash up and flush out – long process and have to do through small slit!
28
Q

What care do you have to take when administering antimicrobials when got strangles

A
  1. only use if monitoring temp
  2. only use is EARLY in course of disease
  3. DO NOT give if immature abscesses are present – the bacterial cells are protected in a fibrous abscess so giving antimicrobials or penicillin will only slow down maturation – prolong the disease won’t cure – have to wait for it to mature and drain
  4. Therefore only use if outbreak on yard, healthy horse that starts to show temp and nasal discharge because at this stage the bacteria wouldn’t have begun to form lymph node abscesses yet and to antimicrobial course is indicated.
29
Q

How do we classify outbreak of strangles on a yard

A
  • Red area: Confirmed cases – diagnostic test, or in middle of outbreak and a horse starts to show
  • Amber area: Been in contact with confirmed cases – not showing clinical signs
  • Green area: No contact with confirmed cases
30
Q

Biosecurity on yard in an outbreak

A
  • No movement on/off yard
  • Biosecurity measures – including staff (clothing etc)
  • Monitoring (daily) temps: Green/amber areas
  • Multiple owners / vets etc. to deal with
  • Have to declare all horses ‘free of disease’ before yard opens again
31
Q

Control and prevention strangles on a yard

A

• Serology all new arrivals
o Serum ELISA will detect almost all subclinical carriers
• 2 week quarantine, even if negative ELISA
• Check temperature daily
• Positive ELISA or temperature OR lots of money  Guttural pouch PCR but much more expensive than just doing Elisa
• Vaccination by submucosal injection

32
Q

Rhodococcus equi

What is it?

A

“Rattles”
Equine Bacterial Respiratory Diseases
• Suppurative Bronchopneumonia of Foals aged between 1 and 4 months of age
• Causes lesions in lung
• usually endemic to one farm/place – lives in the soil
• Adult horses do carry but tend not to show clinical signs

33
Q

Host pathogen and environment interaction of Rhodococcus equi

A

“Rattles”
• Thought that foals (in first few weeks of life) inhale rhodococcus bacteria (lives in soil)
• Evades immune system very effectively
• Acute in young foals, chronic in older foals
• Bacteria can cause Large pulmonary abscess formation - scars lungs
• Occasional diarrhoea or cholic is effects GI

34
Q

Clinical signs of Rhodococcus equi

A

“Rattles”
FOALS
• Acute – fever, anorexia, cough, nasal discharge
• Chronic – cough, dyspnoea, weight loss, exercise intolerance, loud moist crackles on auscultation
• Foals usually look miserable, dspnea, coughing. Deep suckling, warm. Probably shedding so be careful with other foals

35
Q

Long terms effects of Rattles

A

Rhodococcus equi
FOAL
o 8% Mortality, some yards extremely high morbidity.
o Reduces number of foals reaching racetrack – lung scars, stunted growth, lack of funding if infected.
o Does not affect performance of those that do race but will be harder to sell if say have had it and might be smaller

36
Q

PAthogenesis of Rhodococcus equi

A

Rattles
FOAL
similar to Mycobacterium tuberculosis (TB) in people

  1. Multiplies within alveolar macrophages – invades immune cells
  2. Destroys alveolar macrophages, mild immune response  infect more macrophages as they come to site of infection.
  3. Continual cycle of attraction and destruction leads to slow growing abscess / capsule formation
    o Slow progression
    • Destruction of alveoli in lungs
    o Mediastinal lymphadenopathy / peripheral abscessation on ultrasound
    • Destruction of Peyer’s patches in gut
    o Mesenteric lymphadenopathy / abscessation
37
Q

Incubation period of rattles

A

Rhodococcus equi -
FOAL
tion 10 d – 3 weeks – clinical signs even longer

38
Q

Complications of Rhodococcus equi

A

FOAL• Polyarthritis (immune mediated)
o Or septic arthritis
o Sterile artheritis – high protein, swollen joints and inflamed synovial membrane
• Granulomatous ulcerative enterocolitis and mesenteric lymphadenitis (M lymph nodes affected LHS)
• Corneal oedema and anterior (secondary) uveitis
o Corneal oedema, reddeninf of conjunctiva, constricted pupil, painful eye

39
Q

What is Rhodococcus equi bacteria like

A

• Gram-positive pleomorphic rod (coccoid then bacillary)
• Aerobic soil saprophyte & normal flora of GIT in adults
• Endemic farms it is everywhere in soil and faeces of adults – hard to get rid of
• There is rhodococcus equi that is pathogenic AND non!
o Pathogenic  plasmid – virulence associated protein plasmid that is only expressed under certain staings and conditions
o So diagnosis of RE doesn’t give definitive diagnosis, you need to also demonstrate plasmid

40
Q

Transmission of Rattles

A 
Rhodococcus equi  
•	Inhalation route suggested
o	Dust aerosols
o	Lung form common
o	Cranial right lung first
o	Distribution may suggests pyaemic spread to lungs
•	Oral route
o	Primary ingestion (Coprophagia)
o	Swallowing organism from airway secretions
•	Survives long time in soil
41
Q

Diagnosis Rattles

A

Rhodococcus equi
• Clinical signs – dull, nasal discharge, poor growth
• Tracheal wash and culture +/- PCR VAP plasmid definitive to identify is pathogenic
• Radiography and Ultrasonography (3 images below) – not specific for Rhodococcus equi abcesses but see cotton wool balls
• Bloods – Fibrinogen
• Normal ultrasound top, Left is conatal artefacts , Right – abscess in lung

42
Q

Treatment Rattles

A

Rhodococcus equi
• Supportive
• Low dust
• Warm
• Feed intake
• Anti-inflammatory
• Long term (weeks) antimicrobials: lipophilic so will cross cell membrane to gain access to intracellular
o These are protected antimicrobial and extremely important for human health
1. Macrolide (erythro- / clarithro- / azithro-mycin)
 V poisonous to adults – bad colitis
2. Rifampin (more recently debate over use) – particularly important for human treatment of TB
Some other side affects of these is hypothermia

43
Q

Biosecurity of rattles

A

• Reduce stock density
• R. equi is resistant to acid / alkali /disinfectants etc.
• Survives in soil 12 – 36 months
• Survives in large colon in adult horses – forms reservoir
o Foal coprophagia may be important in epidemiology (oral route)
o May be detectable in mares faeces
• Diagnosis often only at chronic stage
• Will NOT eradicate from environment
• Quarantine may work (organism is in the environment but is amplified by affected foals)
• Avoid crowding and remove foal manure from pasture as this increases dust and faecal contamination
• Reduce dust –disease most common in dry, dusty conditions
• Examine foals closely twice a week until 4 months old
• Currently no vaccine

44
Q

What is hyperimmune plasma? ROle in preventing Rhodococcus equi

A 
Rattles
Foal
Plasma with high levels of antibodies against Rhodococcus
•	2 boluses 
•	Give prior to exposure
o	24-72 hrs of age
•	If repeating give at 21 days
•	Highly efficacious on many farms
45
Q

Bronchopneumonia /Pleuropneumonia

What is it caused by?

A

Equine bacterial resp disease
• Caused by all sorts of different bacteria
• Bacterial pneumonia and secondary pleural effusion
• Aerobic, facultative anaerobes
o ß haemolytic strep. spp., - most common, in particularly Strep equi var zooepidemicus isolated from pneumonia in horses
o Pasteurellaecae, Actinobacillus spp., Enterobacteriacae, Pseudomonas.
• Anaerobes
o Bacteroides, Eubacterium, Fusobacterium
o Usually in combination with facultative anaerobes

46
Q

Clinical signs Bronchopneumonia /Pleuropneumonia

A

present with coughing, dyspnea, pyrexia

47
Q

Predisposing factors to Bronchopneumonia /Pleuropneumonia

A 
•	Long distance transport ‘shipping fever’ – crosses over from lungs into pleural cavity
o	Head elevation
o	Aspiration of dust/debris
•	Viral respiratory disease
o	Damage to respiratory epithelium
•	Aspiration Pneumonia
o	Oesophageal obstruction – mucus and food
•	Exercise
o	EIPH + aspiration of debris
•	General anaesthesia/surgery
48
Q

How Pleuropneumonia develops

A
  1. Starts as Bronchopneumonia – lower airways – some horses deosn’t develop further
  2. Acute exudative stage – proteinaceous fluid into pleural space, no bacteria. When bacteria then colonises fibrinopurulent
    • Inflammation of the lung and pleura – sterile protein rich pleural exudate
  3. Fibrinopurulent stage – forms adhesions
    • Bacteria invade and multiply in the pleural fluid
    • Fibrin deposits on pleural surfaces
    • Fibrin organises and forms tight adhensions acoss p cavity Lymphatic obstruction
  4. Organisational Stage
49
Q

Pleuropneumonia: Diagnosis

A

Signs
• Systemic illness – constant clinical signs
o Pyrexia, Depression, Increased HR, RR
• Ultrasonography
• Reduced lung sounds ventrally, dull on percussion
• Pleurodynia – inflamed pleural membrane (elbows abducted and rapid shallow breaths so as not to stretch pleural cavity)
• Soft cough
• nasal discharge
• Black anechoic area is fluid in pleural cavity – needs draining, Diaphragm the white bit – very far pushed down
Diagnosis
• Ultrasonography – extremely useful – shouldn’t be any fluid (or tiny) in plural cavity.
o Plural effusion tap sample of fluid and then do cytology and bacterial culture and sensitivity
• Thoracocentesis
• TTW and culture

50
Q

Strangles is

A

The most important bacterial respiratory condition in horse

Year 2 Equine ID (7 decks)

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