*
* Takes in oxygen from the environment and
delivers it to the tissues and cells of the body
* It also picks up carbon dioxide from the tissues
and cells and delivers it to the environment
*
* Nasal cavity
* Pharynx
* Larynx
* Trachea
* Bronchi
* Lungs
*
*
*
*
Short, tube-like organ between pharynx and trachea
Voice box
Commonly stretched vertically within this cartilaginous box are the vocal
cords
*
*
By contracting the lungs and forcing air past these folds of tissue, the
horse sets them into vibration and produces the sound known as:
*
*
*
*
*
Two folds of elastic tissue
Neighing
Whinnying
Nickering
Regulates the amount of air passing into or out of the lungs
Aids in preventing the inhalation of foreign objects
*
* Long tube connecting the larynx with the lungs
and is located along the lower median border
of the neck
* Composed of a series of cartilaginous rings held
together by elastic, fibrous material
*
* Branches of the trachea that connect the trachea
with each lung
* Each bronchus in turn divides into a number of
minute tubes that penetrate every part of the lung
tissue
* Branching bronchi end in groups of minute air sacs
similar to bunches of grapes
* Alveoli
* Gaseous exchange of carbon dioxide and oxygen
takes place between the circulating blood and the
air
*
*
Respiration
*
*
*
*
The act of breathing
Exchange of oxygen in the air for carbon dioxide in the blood
Interchange of these gases between the blood and the body tissues
External Respiration
*
2 movements
*
Inspiration
*
*
*
*
Brought about by a contraction of the diaphragm and an out ward rotation of the lungs
Diaphragm bulges into the airtight thoracic cavity as a dome-shaped muscle, like a piston, drawing air into the
lungs
Expiration
*
Effected by the relaxation of these muscles and a contraction of rib and abdominal muscles to force air out of the
lungs
*
Abdominal muscles are used extensively in labored breathing
Since the diaphragm plays such an important part in respiration, it follows that the distention of
the digestive tract with bulky food material interferes with normal breathing, especially when the
horse is being worked at fast gaits
*
* Contain about 1.5 Cubic Feet of air
* Normal breathing rate is 8-16 breathes per
minute
* Inhales at each respiration approximately 250
cubic inches of air
* Amount of air depends of the extent of
muscular work performed
*
*
*
Etiology
*
*
Clinical Findings
*
*
Transmission occurs when infected and uninfected horses come in either direct (nose to nose contact) or indirect (through buckets,
clothing, blankets that are contaminated) contact with nasal discharges of infected horses. The virus can travel via aerosol (in the air)
for short distances. The virus may also be transmitted by contact with aborted fetuses, placental fluids, or placentas from infected
horses. Also, following infection, horses may become latent carriers of EHV; virus may be reactivated after stress or high doses of
corticosteroids
Diagnosis and Treatment
*
*
The incubation period (period of time from exposure to development of first clinical signs) ranges from 2 to 10 days. Respiratory signs
for EHV-1 and EHV-4 include fever of 102 -107º F that lasts for 1-7 days, coughing, depression, inappetence (going off feed), and nasal
discharge. Abortion usually occurs between months 7 and 11 of gestation, about 2-12 weeks after infection. There is no evidence that
the mare's reproductive tract is damaged, and it does not affect her ability to conceive in later pregnancies. Signs of neurologic
disease for EHV-1 and EHV-4 include mild incoordination, hindlimb paralysis, recumbency (lying down and being unable to get up), loss
of bladder and tail function, and loss of sensation to the skin around the tail and hindlimb areas.
Transmission
*
*
Equine herpesviruses (EHV) are in the family Alphaherpesviridae and are enveloped double stranded DNA viruses. There are 5 alpha
herpesviruses that infect horses (EHV-1, 2, 3, 4, and 5). For the purposes of this fact sheet, we will focus on EHV-1 and EHV-4, which
are the two that result in serious clinical disease in the horse. EHV-1 and EHV-4 used to be considered subtypes of the same virus, but
are now recognized as closely related but different viruses. EHV-1 is commonly found in horse populations worldwide and was
previously referred to as the equine abortion virus. Although EHV-1 is well known for causing reproductive disease, it is also known to
cause respiratory and neurological disease. EHV-4 is also known as equine rhinopneumonitis virus and is most common among foals and
yearlings. Although EHV-4 most commonly causes respiratory disease, it can also cause abortion and neurological disease
Upon detection of clinical signs suggestive of EHV, the veterinarian may choose to take a nasopharyngeal (nose and throat) swab of the
horse, blood sample, or tissue from the aborted fetus for detection of virus in the tissues. Paired blood samples for detection of
antibody titers (levels) may also be taken. Treatment involves supportive care and treatment of the symptoms. Non-steroidal antiinflamatory drugs are commonly used to reduce fever, pain and inflammation. In uncomplicated cases, complete recovery will occur in
a few weeks. Horses with neurological disease have variable recovery rates depending on severity of the clinical signs. The prognosis
is poor if the horse is recumbent (unable to stand) for an extended period of time. The horse should be rested until fully recovered
and gradually returned to work.
Protection
*
Vaccines
*
*
Etiology
*
*
*
*
*
Equine influenza is a highly contagious viral disease that affects the upper and lower respiratory tract of the horse caused
by different strains of influenza virus. A horse contracts the virus either through contact with an infected horse or indirectly
by contaminated environments/air. Infected horses incubate the disease for 1-3 days before displaying any symptoms, which
is why outbreaks of equine influenza spread so rapidly.
The disease is endemic now, but it tends to mutate to new strains which, once developed abroad, if introduced to this
country act as epidemic infections. Foreign strains of the disease can cause local to national outbreaks. There are, however,
vaccines that are kept up-to-date for regular use to protect horses from the disease.
Symptoms
*
*
*
*
*
A rise in temperature up to 41 degrees C (106 degrees F) for 1-3 days (often undetected)
A harsh, dry cough of sudden onset that persists for 2-3 weeks or more
Clear nasal discharge progressing to thick, green-yellow discharge
Lethargy/depression
Loss of appetite
Prevention
*
*
Vaccines
Isolate new horses
Outcome
*
Equine influenza in most adult horses causes tracheobronchitis which is fairly easy to control and treat. Your horse is likely
to recover in a relatively short period of time, usually within 1-3 weeks, if the problem is diagnosed early on. In young foals,
animals that are stressed in other ways or where secondary bacterial infection of the lower respiratory tract occurs, then
there may be additional complications of pneumonia or damage to the heart muscle (myocarditis)
*
*
Etiology
*
*
Transmission
*
*
Equine viral arteritis (EVA) is a contagious disease of equids (horses, donkeys, mules) caused by equine arteritis virus (EAV) that is
present in many equine populations worldwide. The disease, referred to in the past by a variety of clinically descriptive terms, is
believed to have afflicted horses in Western Europe for centuries. Although not considered life-threatening in otherwise healthy,
older horses, EVA is of industry concern because it can result in economically significant outbreaks of abortion in pregnant mares and
very infrequently, death in young foals, as well as establishment of a long-term carrier state in stallions
Regarded as one of the more significant viral pathogens affecting the equine respiratory tract, EAV is spread most frequently
through direct contact with an acutely infected horse and exposure to infective aerosolized respiratory secretions. This is the
primary means of virus dissemination at performance events, horse sales, veterinary hospitals and also on studs, or wherever horses
are kept closely congregated with one another. While EAV is shed in various secretions and excretions by the acutely infected
individual, it is present in greatest concentration in respiratory tract secretions and in the semen of stallions
Signs
*
Where clinical signs of EVA develop, the onset of illness occurs within 3-7 days, depending primarily on route of exposure. Signs of
the disease can vary widely in range and severity and may persist for several days up to two weeks. Typical cases of EVA present
with any combination or all of the following:
*
*
*
*
*
*
*
Fever
Swelling of the dependent parts of the body (limbs, scrotum, sheath, mammary glands)
Loss of appetite and depression
Swelling above or around one or both eyes, conjunctivitis, and ocular and discharge
Stiffness of gait
Skin rash frequently localized to the head or neck but sometimes generalized.
Control
*
Vaccines
*
*
*
Etiology
*
Pleuropneumonia is defined as infection of the lungs and pleural space. In most instances, pleural infection develops secondary to bacterial
pneumonia or penetrating thoracic wounds. Spontaneous pleuritis (without accompanying pneumonia) is uncommon in horses. In the USA, ~70% of
horses with pleural effusion have Pleuropneumonia. The primary differential diagnoses for pleural effusion are neoplastic effusions, heart failure, and
hydatidosis.
*
Viral respiratory infection, long-distance transportation, general anesthesia, and strenuous exercise are common predisposing factors that impair
pulmonary defense mechanisms, allowing secondary bacterial invasion. Head restraint results in bacterial contamination and multiplication within the
lower respiratory tract within 12–24 hr and may be the single most important predisposing factor for development of pneumonia associated with longdistance transport.
Signs
*
*
*
Horses with Pleuropneumonia present with fever, depression, lethargy, and inappetence. Clinical signs specific to Pleuropneumonia include pleural
pain (pleurodynia) evident as short strides, guarding, and flinching on percussion of the chest; shallow respiration; and endotoxemia. Horses with
pleural pain have an anxious facial expression; stand with their elbows abducted; and are reluctant to move, cough, or lie down. Gait may be stiff or
stilted, and some horses grunt in response to thoracic pressure, auscultation, or percussion. Nasal discharge is a variable sign. Putrid breath or fetid
nasal discharge indicates anaerobic bacterial infection and necrotic pulmonary tissue. The respiratory pattern is characterized by rapid, shallow
respiration due to pleural pain and restricted pulmonary expansion from pleural effusion. A plaque of sternal edema is seen in horses with a large
volume of pleural effusion. Horses with toxemia have injected mucous membranes, delayed capillary refill time (>2 sec), and tachycardia.
Auscultation reveals a lack of breath sounds in the ventral lung fields and abnormal lung sounds (often crackles) in dorsal lung fields. Cardiac sounds
may be muffled or absent or may radiate over a wider area. Although uncommon, pleural friction rubs are most prominent at end-inspiration and early
expiration and are detected after thoracic drainage
Diagnosis
*
In horses with peracute pleuropneumonia, laboratory findings reflect bacterial sepsis or toxemia and include abnormalities such as leukopenia,
neutropenia, left shift, hemoconcentration, and azotemia. Horses with more stable disease have leukocytosis, mature neutrophilia,
hyperfibrinogenemia, hyperglobulinemia (chronic antigenic stimulation), hypoalbuminemia (loss in pleural space), and anemia of chronic disease.
*
Thoracic ultrasonography is ideal for investigation of pleural effusion and is indicated in horses with regions of poor to absent breath sounds, thoracic
pain, and/or dull thoracic percussion
Treatment
*
Management of horses with pleuropneumonia includes daily ultrasound examination to monitor fluid production, evaluate effective drainage, identify
isolated fluid pockets, and assess peripheral pulmonary disease
*
*
*
*
*
*
Etiology
*
*
Rhodococcus equi is the most serious cause of pneumonia in foals 1–4 mo old. It is not the most common cause of
pneumonia in this age group; however, it has significant economic consequences because of mortality, prolonged
treatment, surveillance programs for early detection, and relatively expensive prophylactic strategies. Clinical disease is
rare in horses >8 mo old. Compelling epidemiologic data indicate pulmonary infection probably originates within the first
week of life.
Inhalation of dust particles laden with virulent R equi is the major route of pneumonic infection
Signs
*
R equi infection is slowly progressive, with acute to subacute clinical manifestations. Clinical signs of disease are difficult
to detect until pulmonary infection reaches a critical mass, resulting in decompensation of the foal. Pulmonary lesions are
relatively consistent and include subacute to chronic suppurative bronchopneumonia, pulmonary abscessation, and
suppurative lymphadenitis. At the onset of clinical signs, most foals are lethargic, febrile, and tachypneic. Diarrhea is
seen in one-third of foals with R equi pneumonia and may be caused by colonic microabscessation. Cough is a variable
clinical sign; purulent nasal discharge is less common. Thoracic auscultation reveals crackles and wheezes with
asymmetric/regional distribution. Pulmonary regions with marked consolidation lack breath sounds and exhibit dull
resonance on thoracic percussion. In foals with subclinical infections, small to moderate-sized abscesses (<10 cm) may
resolve spontaneously.
Diagnosis
*
Routine laboratory evaluation of CBC and serum chemistry reveals nonspecific abnormalities consistent with infection and
inflammation. Neutrophilic leukocytosis and hyperfibrinogenemia are common, and the severity of these findings relates
to prognosis. Thoracic radiographic evaluation may reveal a pattern of perihilar alveolization, consolidation, and
abscessation. The presence of nodular lung lesions and mediastinal lymphadenopathy in foals 1–4 mo old is highly
suggestive of R equi. Bacterial culture of transtracheal wash samples is required for definitive diagnosis. Cytologic
evaluation of transtracheal wash samples reveals intracellular coccobacilli, indicating that appropriate antimicrobial
therapy should be started pending culture results
Treatment
*
Combination of erythromycin and rifampin
Prevention
*
Foals should be maintained in well-ventilated, dust-free areas, avoiding dirt paddocks and overcrowding.
*
*
Etiology
*
*
*
*
*
Acute bronchointerstitial pneumonia is a sporadic, rapidly progressive disease of foals characterized by
acute respiratory distress and high mortality
The etiology of acute bronchointerstitial pneumonia in foals is not clear. It may result from different
insults rather than a single factor, initiate a cascade of events, and result in a final common response of
severe pulmonary damage and acute respiratory distress. Warm weather (>85°F [29.4°C]) is a common
epidemiologic factor. Many foals have a history of antimicrobial therapy when clinical signs developed.
No virus is consistently isolated, and no bacterial agent has been consistently identified.
Signs
*
The age of affected foals ranges from 1 wk to 8 mo. Acute bronchointerstitial pneumonia has an acute or
peracute onset and is accompanied by high fever. The disease is rapidly progressive and may result in
sudden death due to fulminant respiratory failure. Foals are unable or reluctant to move and are usually
cyanotic. Severe respiratory distress is the most striking clinical sign. Clinicopathologic evaluation of
foals with acute respiratory distress should include arterial blood gas, CBC, serum chemistry analysis,
and thoracic radiographs. Hypoxemia, hypercapnea, and respiratory acidosis are consistent findings.
These arterial blood gas findings quantify the severity of respiratory impairment and are used to monitor
response to therapy. The hypoxemia of bronchointerstitial pneumonia is relatively resistant to
supplemental oxygen therapy. Bronchointerstitial pneumonia is similar to bacterial pneumonia in that
hyperfibrinogenemia and neutrophilic leukocytosis are seen in most foals
Diagnosis
*
Physical examination and clinicopathologic findings may appear similar to those of foals with severe R
equi pneumonia
Treatment
*
Because the cause of bronchointerstitial pneumonia is unknown, therapy is symptomatic. Treatment
includes anti-inflammatory therapy, broad-spectrum antibiotics, thermoregulatory control,
bronchodilation, supplemental oxygen, and supportive care.
*
*
*
Etiology
*
Strangles is an infectious, contagious disease of Equidae characterized by abscessation of the lymphoid tissue of the upper respiratory
tract. The causative organism, Streptococcus equi equi, is highly host-adapted and produces clinical disease only in horses, donkeys,
and mules. It is a gram-positive, capsulated β-hemolytic Lancefield group C coccus, which is an obligate parasite and a primary
pathogen.
*
S equi equi is highly contagious and produces high morbidity and low mortality in susceptible populations. Transmission occurs via
fomites and direct contact with infectious exudates. Carrier animals are important for maintenance of the bacteria between
epizootics and initiation of outbreaks on premises previously free of disease. Survival of the organism in the environment depends on
temperature and humidity; it is susceptible to desiccation, extreme heat, and exposure to sunlight and must be protected within
mucoid secretions to survive. Under ideal environmental circumstances, the organism can survive ~4 wk outside the host. Under field
conditions, most organisms do not survive 96 hr
Signs
*
*
Diagnosis
*
*
The incubation period of strangles is 3–14 days, and the first sign of infection is fever (103°–106°F [39.4°–41.1°C]). Within 24–48 hr of
the initial fever spike, the horse will exhibit signs typical of strangles, including mucoid to mucopurulent nasal discharge, depression,
and submandibular lymphadenopathy. Horses with retropharyngeal lymph node involvement have difficulty swallowing, inspiratory
respiratory noise (compression of the dorsal pharyngeal wall), and extended head and neck. Older animals with residual immunity
may develop an atypical or catarrhal form of the disease with mucoid nasal discharge, cough, and mild fever. Metastatic strangles
(“bastard strangles”) is characterized by abscessation in other lymph nodes of the body, particularly the lymph nodes in the abdomen
and, less frequently, the thorax. S equi is the most common cause of brain abscess in horses, albeit rare
Diagnosis is confirmed by bacterial culture of exudate from abscesses or nasal swab samples. CBC reveals neutrophilic leukocytosis
and hyperfibrinogenemia. Serum biochemical analysis is typically unremarkable. Complicated cases may require endoscopic
examination of the upper respiratory tract (including the guttural pouches), ultrasonographic examination of the retropharyngeal
area, or radiographic examination of the skull to identify the location and extent of retropharyngeal abscesses
Treatment
*
The environment for clinically ill horses should be warm, dry, and dust-free. Warm compresses are applied to sites of
lymphadenopathy to facilitate maturation of abscesses. Facilitated drainage of mature abscesses will speed recovery. Ruptured
abscesses should be flushed with dilute (3%–5%) povidone-iodine solution for several days until discharge ceases. NSAIDs can be
administered judiciously to reduce pain and fever and to improve appetite in horses with fulminant clinical disease. Tracheotomy may
be required in horses with retropharyngeal abscessation and pharyngeal compression.
*
* Recurrent Airway Obstruction in Horses
* Inflammatory Airway Disease in Horses
* Exercise-Induced Pulmonary Hemorrhage in Horses
* Laryngeal Hemiplegia in Horses
* Pharyngeal Lymphoid Hyperplasia in Horses
* Dorsal Displacement of the Soft Palate in Horses
* Epiglottic Entrapment in Horses
* Subepiglottic Cyst in Horses
* Fourth Branchial Arch Defect in Horses
* Diseases of the Nasal Passages in Horses
* Diseases of the Paranasal Sinuses in Horses
* Guttural Pouch Disease in Horses
*
* Pick one of the Equine Respiratory Diseases on the power point and
*
research it
Have the following
*
*
*
*
*
Etiology/Pathology/Epidemiology
Signs
Diagnosis
Treatment
Control/Prevention
*
*
You will be teaching the class about the disease
5-10 minutes long
* Poster / Paper/ Presentation
* Present in class
* 150 points
*