Respiratory Flashcards
Dyspnoea at rest?
•
Cardiovascular disease
(Inadequate perfusion of the lungs)
Cardiac disease
•
congestive heart failure, acute heart failure
Peripheral circulatory failure
•
shock and dehydration
Increased blood viscosity
•haemo-
concentration including
polycythaemia
and disseminated
intravascular
coagulopathy
•
Diseases of blood
A
naemia
A
ltered haemoglobin
•
e.g.
methaemoglobinaemia
in nitrate poisoning
•Nervous system diseases
Paralysis respiratory muscles
•botulism, tick paralysis
Paralysis respiratory centre
•nicotine sulphate poisoning
Neurogenic dyspnoea
• stimulation of respiratory centre by
irritative
lesion
•General systemic states
–pain
–hyperthermia
–acidosis
•Environmental causes
–Very high temperatures, oxygen lack (high
altitude), exposure to toxic gasses
•Poisons
–Nitrate, hydrocyanic acid, urea,
organophosphate

Examination of the Resp Tract

Additional tests for respiratory
* Percutaneous transtracheal aspiration
- wide bore needle between tracheal rings
- insert long plastic catheter: withdraw needle. Leave catheter in place– passed to point approximately 10 cm beyond thoracic inlet
- infuse 20-40 ml of sterile saline and aspirate back quickly
– culture, cytological examination
* Pleural paracentesis
- ideally use a teat siphon through a skin stab wound but can use a catheter– insert below fluid line
- samples for cytology and bacterial culture
- can be of use in treatment
* Bronchoalveolar lavage (BAL)- may be done using two tubes introduced through the nares– an outer tube which is passed to the level of the trachea and an inner tube which is passed to the level of the bronchus
* Sample obtained can be used for virus isolation and bacterial culture
* Thoracic ultrasonography– pleural and pulmonary surfaces of both lung fields can be examined through the intercostal spaces between the 7th and 11th ribs
- a 3.5 MHz sector transducer is suitable for this task
Causes of pulmonary congestion and oedema
Causes:
* early pneumonia
* Inhalation smoke, fumes
* anaphylactic reaction
* hypostasis in recumbent animals
* secondary causes- CHF

Clinical signs of pulmonary congestion and oedema

Treatment for pulmonary congestion and oedema
* Adrenalin for oedema due to anaphylaxis
* Antiobiotics if early pneumonia suspected




What is pneumonia? Causes?

Classification of pneumonia

Clinical findings of pneumonia

Diagnosis of pneumonia

Treatment of Pneumonia

Aspiration pneumonia– common sequelae to what?

Acute undifferentiated bovine respiratory disease?

Agents associated with BRD

What is the most common cause of illness and death in AUS feedlot cattle?

Cause of BRD
The major pathogens of BRD are ubiquitous, and
all the major bacterial respiratory pathogens are
commensal
in clinically normal feedlot cattle.
Clinical BRD is the product of the effect of
stressors causing immuno-
suppression, thereby
allowing the colonisation of the lower respiratory
tract by opportunistic pathogens that invariably are
encountered by feedlot cattle.

Risk factors with BRD

BRD Clinical findings
* Broncho-pneumonia 10-14 days after stress
* In the early stages
- off feed depressed rapid shallow resp moist cough
* Later stages:
- febrile (40-41C)
- deep laboured resp (insp and exp)
- increased harshness of insp sounds as purulent material gathers in the airways
BRD Clinical findings


BRD Treatment
* Antiobiotics
- Usually oxytetracycline, ceftiofur, or trimethroprim/ sulphonamide combinations are used in feedlots
* NSAIDs
* Nursing- shelter and high quality feed
* Early detection of new cases and continual reassessment of the results of treatment are necessary
* Value of mass medication of feed supplies of newly arrived cattle to the feedlot
Vaccination against BRD

Pneumonic pasteurellosis
•
Combination of:
–
Viral infections of the respiratory tract
–
Effects of transportation, temporary starvation,
weaning, fluctuations in temperature, mixing, excess
handling an increase in the total numbers and
virulence of
Pasteurella
in the nasopharynx
•
Most commonly isolated
–
Mannheimia
hemolytica
–
Pasteurella
multocida




Pasteurellosis

Managing a Manheimia outbreak

Monitoring for Manheimia hemolytica

Histophilus somni disease complex?

Histophilosis respiratory form


Histophilosis Septicaemic Form

Histophilosis nervous form

Diagnosis of Histophilosis

Atypical Interstitial Pneumonia

Interstitial pneumonias include

ABPEE

ABPEE clinical findings and necropsy?

ABPEE Treatment?

Other interstitial pneumonias

Contagious Bovine Pleuropneumonia

Epi of CBPP

CBPP signs and symptoms

PM Findings in CBPP

Control of CBPP

Enzootic pneumonia of calves

Enzootic pneumonia of calves signs and symptoms
Enzootic pneumonia of calves
•
Areas of collapse with little bronchiolar reaction
•
In the later stages a dark red consolidation with
little or no fluid in the lung is detected.
•
Lesions are bilateral and
histologically
there is
an interstitial pneumonia.

Lungworm in cattle
•
Dairy calves are most vulnerable to lungworm
disease, as they are often placed on paddocks
grazed each year by successive groups of
calves
•
With high stocking rates, pasture challenge
can then reach pathogenic levels within 2 to 4
months.
•
Usually, only relatively small numbers of larvae
survive to induce low
-grade, asymptomatic
infections in a new group of susceptible calves,
which then start to re-
contaminate the pasture
and recycle the infection

Acute verminous pneumonia

Sub-acute verminous pneumonia

Lungworm diagnosis

Infectious bovine rhinotracheitis
•
May also cause an encephalitis in new
born calves
•
Infectious
pustular
vulvo
- vaginitis
(IPV),
balano-
posthitis
in adults.

Infectious bovine rhinotracheitis signs and symptoms
•
Sudden onset
•
Anorexia,
•
Fever up to 42 degrees C,
•
Severe hyperaemia of the nasal mucosa
-
greyish plaques of necrosis nasal septum
•
Serous discharge from the eyes and nose
•
Respiratory rate increased and shallow
•
Lung sounds are normal on auscultation.
•
May be short explosive cough
•
Conjunctivitis is seen in some outbreaks.



Infectious bovine rhinotracheitis calves
•
New born calves systemic form is severe
and highly fatal.
•
Signs include sudden anorexia, fever,
rhinitis, erosion of the soft palate, acute
pharyngitis.
Broncho-
pneumonia is
common.

Infectious pustular vaginitis (IPV)

•
Vaginal examination reveals plaques or
pustules of white necrotic material on the
vulva and vaginal mucosa, and a pool of
odorless
mucopurulent
material on the
vaginal floor.
•
In bulls, IPV causes a
balanoposthitis.

IBR diagnosis
Overseas, abortion is a common sequel in
pregnant cows

IBR Control

Oral and laryngeal necrobacillosis

In a calf


Oral necrobacillosis- necrotic stomatitis



•
Quite irritant -
affected animals will often rub their
noses on sticks, thistles
•
On palpating the nasal mucosa of chronically
infected
granulomatous
nodules of 1 to 4 mm in
diameter and height can be detected in both
nostrils
•
The severity of the condition in affected cattle
will often wax and wane

TB in cattle? Epi?
Caused by
Mycobacterium bovis
and is
characterised by the progressive
development of tubercles in any of the
organs in most species.
More about Epi:
* Inf by ingestion is more likely at pasture when faeces contaminate the feed and communal drinking water and feed troughts
* Drinking of infected milk by young animals is a commoin method of spread

TB spread in the body

TB clinical findings
* TB mastitis can be of major importance because of its danged to PH
* palpation of the supramammary LNs is essential in all cases of suspected tuberculous mastitis

TB clinical pathology
Basis of tuberculosis eradication
campaigns is the tuberculin test and a
knowledge of the various tests used, their
deficiencies and advantages, is essential

Single intradermal tuberculin

TB pathology

TB Diagnosis

SBE
•
caused by a chlamydia
•
characterised by inflammation of vascular
endothelium and mesenchymal tissue.

SBE Signs and symptoms
•
caused by a chlamydia
•
characterised by inflammation of vascular
endothelium and mesenchymal tissue.
•
Later, difficulty in walking stiffness with
knuckling at the fetlocks is evident at first,
followed by staggering, circling and falling
•
Opisthotonus
may be present but there is no
excitement or head pressing
.

SBE Pathology
Sporadic Bovine Encephalomyelitis
Pathology:
•
Chlamydia can be isolated from the blood in
the early clinical
•
Serological tests, including a complement
fixation test, are available
.
Pathology:
•
On post mortem a
fibrinous
peritonitis,
pleurisy and pericarditis accompanied by
congestion and
petechiation
are
characteristic.
Brisket Disease in Cattle
Epidemiology
•
the low density of the atmosphere at high
altitudes results in an environmental anoxia
•
most commonly in yearlings.
•
Brisket disease is reported commonly only
in animals maintained for some months at
altitudes above 1800 metres.
•
Continued hypoxia can cause sufficient
myocardial weakness to interfere with
cardiac compensation and thus lead to
congestive heart failure.

Poisonings which may be associated with dyspnoea
•
A number of poisons cause dyspnoea
as the prominent sign.
•
Farm chemicals including
methaldehyde
and
dinitrophenols, organophosphates
and
carbamates, urea
•
Poisonous plants including fast death
factors of algae, the weeds
Albizia
,
Helenium
, Eupatorium, Ipomea,
Taxus
spp., Laburnum
and
Erythrophloeum
spp. can all cause dyspnoea.
Nitrite/ Nitrate poisoning
Nitrate/nitrite poisoning – common
plant sources
•
Cereal crops include: immature green oats,
millet, barley, wheat, rye, Sudan grass, corn,
sorghum fodder, mangles, turnips, sugar beet
tops and rape, certain specific plants and water
from deep wells.
•
Specific plants include variegated thistle,
mintweed and a series of other plants
Nitrate/nitrite poisoning. - epidemiology
•
Cereal and root crops are likely to contain
high concentrations of nitrate when heavily
fertilised with nitrogenous fertilisers
•
When growth is rapid during hot humid
weather.
•
In cattle the maximum methaemoglobin
level usually occurs about 5 hours after
ingestion of nitrate.

Findings in nitrate/nitrite poisonings

Nitrite/nitrate poisoning- pathology
•
Post mortem
- blood is coffee brown in colour
and clots poorly.

Nitrate/ Nitrite Treatment

Hydrocyanic Acid Poisoning
Sources
•
Many plants contain
cyanogenetic
glucosides
•
Common pasture plants including
sorghum, Sudan grass and Johnson
grass.

Hydrocyanic Acid poisoning epi
Epidemiology
•
High soil concentrations of nitrogen
predispose to higher levels of hydrocyanic
acid in plants.
•
Wilted, frost bitten and young plants are
likely to more toxic

Hydrocyanic Acid poisoning
•
Animals may show signs within 10-
15
minutes of eating the toxic material and
die within a few minutes.
•
Signs observed include dyspnoea,
restlessness, moaning, recumbency and
terminal clonic convulsions with
opisthotonus.
•
Mucosae
are bright red in colour.

Hydrocyanic Acid Pathology

Hydrocyanic acid poisoning treatment
Treatment
•
Hydrocyanic acid is taken up by
thiosulphate to form
thiocyanate
which
is not toxic and is readily excreted.
•
Sodium thiosulphate should also be
given orally to fix the free hydrocyanic
acid in the rumen

Poisoning with OPs signs and symptoms
Organophosphate compounds and
carbamates
inactivate cholinesterase and
produce a syndrome of salivation, diarrhoea
and muscle stiffness indicative of
stimulation of the parasympathetic nervous
system.

Poisoning with OPs Treatment

Urea Poisoning
Urea poisoning
•
Urea is used as a feed additive for
ruminants as a source of non protein
nitrogen and as a fertiliser
•
Urea should not constitute more than
3% of the concentrate ration of
ruminants.
•
Toxic affects are due to the sudden
production of large quantities of
ammonia and signs occur within 20
to 30 minutes of feeding.
