QUESTIONS

1. Discuss pulmonary bacterial clearance and its relevance in domestic animals (10)
2. Describe how lymphoid tissue aid in protecting the respiratory system. (10)
3. Write short notes on pathology associated with exercise-induced pulmonary
hemorrhage in horses. (10)
4. Describe the pathology associated with bloat and how it can affect the respiratory
system. (10)

ANSWERS
1. Pulmonary bacterial clearance is the removal of bacteria that has reached the exchange
portion of the respiratory system. Exchange portion comprises of bronchioles, the alveoli
ducts and alveoli. In bacterial clearance, pulmonary alveoli macrophages and anti-
microbial molecules of the alveolar lining fluid play a pivotal role in clearing of bacterial
that would have reached the alveoli. The macrophages phagocytize inhaled bacteria
without the need of an inflammatory reaction hence preventing pneumonia and other
respiratory lesions induced by bacteria to occur. Bactericidal enzymes present in
lysosomes are released into the phagosome containing the bacteria and breakdown the
bacteria. Most alveolar macrophages can be removed from the alveoli by migrating
toward the bronchiolar (transitional) region until the mucocilliary blanket is reached.
From there, pulmonary macrophages by mucocilliary flow go to the pharynx and are
swallowed thus getting rid of the bacteria. This clearance is relevant in bacteria because it
is a form of defence mechanism from bacterial invasion which can lead to pneumonia. As
a result of pneumonia, lung collapse can occur which may result in difficulty in breathing
which may lead to death.
2. The lymphoid system in the lung is primarily constituted by two types. The first is found
in the upper third (conducting system) of the airways and has many of the characteristics
of mucosal lymphoid tissue. The second is found in the lower third (exchange system)
and characterized more as being part of the systemic immune system. There is a mixture
of the two in the middle third. There is a third type of immune system, which consists of a
population of intraepithelial lymphocytes (IELs) that have distinctive phenotypes, as in
the intestine. Larger aggregates of lymphoid follicles, such as those seen in the intestine
and described as Peyer’s patches (PPs), are also found in the upper airways, especially at
bifurcations of the bronchial tree. These aggregates have been described in a large variety
of species including rodents, chickens, cats, rabbits, sheep, pigs, hamsters, guinea pigs,
and even in the human (13–16). Discrete lymphocytes are also found in mammalian and
chicken bronchial tissue and consist predominantly of immunoglobulin (Ig) A-expressing
B cells. Among the most notable are the microfold (M) cells, which are modified
epithelial cells covering the bronchial-associated lymphoid tissue (BALT), both of which
are strategically situated at the corner of the bifurcation of bronchi and bronchioles, where
inhaled particles often collide with the mucosa because of inertial forces. Inhaled particles
and soluble antigens are phagocytosed and transported by macrophages, dendritic cells,
and other professional antigen-presenting cells (APCs) into the BALT, thus providing a
 unique opportunity for B and T lymphocytes to enter into close contact with inhaled
pathogenic substances. Pulmonary lymphocytes are not quiescent in the BALT but are in
continual traffic to other organs and contribute to both cellular (cytotoxic, helper, and
suppressor T lymphocytes) and humoral immune responses. Immunoglobulin A (IgA),
produced by mucosal plasma cells, and, to a lesser extent, immunoglobulin G (IgG) and
M (IgM) play important roles in the local immunity of the conducting and transitional
systems, especially with regard to preventing attachment of pathogens to the cilia.
Chronic airway diseases, especially those caused by infectious agents such as
mycoplasmas or retroviruses, are often accompanied by severe hyperplasia of the BALT.

3. Exercise-induced pulmonary haemorrhage (EIPH) is a specific form of pulmonary

haemorrhage in race horses that occurs after exercise and clinically is characterised by
epistaxis. Only a small percentage of horses with bronchoscopic evidence of haemorrhage
have clinical epistaxis, EIPH goes undetected in many cases. The pathogenesis involves
laryngeal paralysis, alveolar hypoxia, bronchiolitis, and extremely increased pulmonary
vascular and alveolar pressures during exercise, pre-existing pulmonary injury. Necropsy
lesions in the lungs of affected horses show large areas of dark brown discolouration,
largely in the caudal lung lobes. Histopathologically, lesions are alveolar haemorrhages,
abundant alveolar macrophages containing hemosiderin (siderophages), mild alveolar
fibrosis and occlusive remodelling of pulmonary veins.

4. Bloat/ Ruminal tympany is an over distension of the rumen and reticulum by gases
produced during fermentation. Bloat can be primary or secondary. Primary tympany
(legume bloat, dietary bloat, frothy bloat) occurs after animals begin a new diet. Clinical
signs include; a distended left paralumbar fossa, a distended abdomen, increased heart
and respiratory rate. When death occurs, it is attributable to distention of the abdomen,
which compresses the diaphragm, moving it cranially (orad), with resultant decreased
pleural cavity size and respiratory embarrassment. There is also increased intraabdominal
and intrathoracic pressure, resulting in decreased venous return to the heart and ultimately
generalized congestion cranial to the thoracic inlet. Secondary tympany is caused by a
physical or functional obstruction or stenosis of the oesophagus, resulting in failure to
eructate. Breathing is difficult or laboured (dyspnea) and occurs through the mouth thus
increase in respiratory rate to 60 inhalation-exhalation cycles per minute. Bloating also
results in acquired atelectasis, specifically compressive atelectasis. It occurs as a result of
space-occupying masses in the pleural cavity which hinder proper distension of the lungs.
Death is likely caused by suffocation, when the distended rumen pushes against the
diaphragm and prevents inhalation.
References
1. Fournier M, Lebargy F, Le Roy Ladurie F, Lenormand E, Pariente R, (1989).
Intraepithelial T lymphocyte subsets in the airways of normal subjects and of patients
with chronic bronchitis. Am Rev Respir Dis;140: 737–742.
2. Goto E, et al (2000). Human bronchial intraepithelial T lymphocytes as a distinct T-cell
subset: their long-term survival in SCID-Hu chimeras. Am J Respir Cell Mol Biol;
22:405–411.
3. Zachary, J. F (2017), Pathologic Basis of Veterinary Disease, 6th edition, Elsevier
Mosby, St Louis Missouri.
 UNIVERSITY OF ZIMBABWE
FACULTY OF VETERINARY SCIENCE
PARACLINICAL DEPARTMENT

NAME : NGONGONI LLOYD ANESU

REG NUMBER : R1711634

DATE : 16 SEPTEMBER 2019

PATHOLOGY ASSIGNMENT
RESPIRATORY SYSTEM

DEADLINE : 18 SEPTEMBER 2019

LECTURER : DR VHORI