RT Infections Flashcards
How does the body non-immunologically defend itself from respiratory infections?
Increase in Inertial Impaction
- Holding head in vertical position
- Anatomy of nasal conchae creates turbulent airflow
Resident (Normal) Flora
- Colonization resistance in URT (no space for pathogenic bacteria to adhere to target cell)
Sneezing and Coughing
Mucociliary Clearance Mechanism
How does the body immunologically defend itself from respiratory infections?
Pulmonary Alveolar MØ
- predominant inflammatory cell in the normal LOWER airway // MAJOR defense mech. of alveoli
Mucosal Immunnity
- APCs, phagocytosis, lymphoid tissue in bronchi with humoral IRs
What are predisposing (risk) factors that allow for animals to contract respiratory infections?
Transportation
- prolonged transport
- decreased effectiveness of mucociliary clearance due to postural changes
Age and Co-Mingling
- young (imunologically naive) and intesive housing (cattery)
Viral Infections
- bacterial infection often follows viral due to way the virus infects/damages the pulmonary alveolar macrophages (PAMS) and mucociliary clearance
Housing
- stables, barns, sheds
Intense Exercise and Exercise-Induced Pulmonary Hemorrage in HORSES!
- impairs function of PAMs and decreases peripheral lymphocyte fuction, increases cortisol serum for up to 24h
General Anesthesia and/or Aspiration
- anesthesia can decrease pulmonary defenses
- aspiration due to positioning
How do microorganisms enter the respiratory tract?
Ventilation
- most common route
Perfusion / Hematogenous
- all venous return from systemic circ. passes through the lungs!
- pulmoary capillaries frequently exposed to blood-borne pathogens (e.g., Histophilus somni)
Where is Streptococcus equi ss equi (Strangles) located in carrier animals? What does this bacteria manifest as in infected animals?
Location in carrier animals = the guttural pouch
is a major, global, contagious equine disease in the carrier state
Manifests as cervical lymphadenitis
Clinical manifestations of Strangles
Cervical lymphadenitis (submandibular, retropharyngeal, LNs) and pharyngitis –> fever, nasal d/c, anorexia
High morbidity, low mortality
What is equine “purpura hemorrhagica” following a Strangles infection?
A type III hypersensitivity reaction (due to deposition of antigen/antibody complexes in the vasculature)
What disease in YOUNG PIGS (3-7 weeks old) causes destruction of nasal turbinates and conchal bones of the snout?
main clinical sign: epistaxis
Atropic Rhinitis:
What are the 3 most common infectious disease of teh tracheobronchial compartment?
laryngitis, tracheitis and bronchitis
What is the morphology of Mycobacterium and how did they stain?
Gram+ rods, Acid-fast; strict aerobes
Factors that predispose cattle to Mycobacterium bovis and routes of infection.
- crowded, dirty environment; genetics
- aerosol, contaminated feed
What lesions does M. bovis produce?
Granulomas with areas of central necrosis, surrounded by mø and giant epithelia cells
What is the major source of M. bovis for infection of grazing cattle in countries where the disease is largely eradicated (like the U.S.) and therefore complete eradication very difficult?
Wildlife reservoirs (deer, buffalo in the U.S.)
How are mycobacteria infections diagnosed/controlled (for tuberculosis)?
Tuberculin tests and Comparative Cervical Tuberculin test (CCT) to determine a reactor or suspect cow
- inject purified protein derivative of M. bovis into cervical region or caudal (tail) fold in cattle -> monitor for hard swelling >5mm @ 72h and if positive, due CCT to compare with PPD of M. avium -> if >4mm, reactor only
How do bacteria cause pneumonia?
Gets to the pulmonary capillaries in HIGH numbers via increased aerosol concentration
risk factors: shipping fever, intense exercise causing aspiration of oro-pharyngeal organisms, changes in anatomical structures like tie-back in horses
How can the prognosis of pneumonia in horses be determined?
By determining which stage of the infection the horse has
Evidence of bacteria and inflammation in cytology sample for diagnosing RT infection:
- tracheal wash: increased % of polymorphonuclear neutrophils (PMN)
- pleural fluid: increased # of PMNs and/or increased protein
