Different lesions are identified at slaughter houses and are included in this report

1. Report on pathological lesions identified at Lilongwe abattoir,Malawi
DATE:3rd
JULY,2017.
AUTHOR: SHAREEF NGUNGUNI
AIM
To diagnose the lesions presented at the abbatoir
INTRODUCTION
Slaughter houses provide an excellent opportunity for detecting diseases of both economic and
public health importance. Frequent encounters of bovine pathological lesions in the lungs, heart,
intestine, kidney and liver have been constant features in the annual reports of various
government stations in Malawi. According to Cabana (2001) numerous abattoir surveys of
bovine pathological conditions have been conducted to investigate macroscopic and microscopic
abnormalities. The slaughterhouse and its regulations, represents a key control point of livestock
production chain. Any observation and information obtained at slaughterhouse can contribute to
the understanding of slaughtered animals’ diseases. The pathological examination represents a
useful tool to make a diagnosis within the slaughter line.
Meat inspection ensure that only apparently health, physiological normal animals are slaughtered
for human consumption and that abnormal animals are separated and dealt with accordingly.
These objectives are achieved by ante mortem and postmortem inspection procedures (Peacok,
1996). Postmortem inspection provides necessary information for the scientific evaluation of
pathological lesions. According to (Rastogi, 2007) it also requires observation of all parts of the
carcass, dressing procedures, equipment, and facilities to prevent contamination of edible parts.
Routine postmortem examination of carcass is carried out as soon as possible after the
completion of dressing in order to detect any abnormalities so that products only conditionally fit
for human consumption are not passed as food.It is often observed that improperly performed
postmortem examination is characterized by voluminous information that has little importance to
the diagnosis of a particular case in question but absence of information vital to the formulation
of a diagnosis thus confusing the understanding of a disease process. A systematic approach in
performing postmortem examinations is required so that appropriate and adequate information is
gathered during the examination.
Specimens taken from suspected contagious / zoonotic cases should be adequately labeled to
warn others about the potential of spreading the infection or pose danger to the biological system
or to those handling the specimen. During the practical the lungs, part of rumen, liver, aortawas
presented with pathological lesions. The lesions were examined grossly; diagnosis and
microscopic examination is based on reference.

2. LUNGS
Lungs are vulnerable to many infectious agents and pathological conditions in lungs of
slaughtered cattle were studied. Grossly, the lungs were pale with small dark-red
spots/hemorrhages. The hemorrhages were pin pointed and paint brushed. According to (Kumar
et al,2005) pin pointed hemorrhages are also known as petechiaehemorrhages; they are of about
1-2mm and occurs in skin, mucous membranes or serosal surfaces; they are typically associated
with locally increased intravascular pressure, low platelets counts, defective platelets function
and defects in clotting factors. The painted brushed ones are Echymoses hemorrhages and they
are larger hemorrhages that are about>1 to2cm (Barret et al, 2010) and occur in subcutaneous
tissues.
The lungs were also inflated, appearedballoonshaped and that expansion makes is to lose
elasticity (McGavinet al, 2001), a puffy or spongy texture was observed after pressing its
parenchyma with fingers. This suspects the pulmonary emphysema. According to Stockhalm
and Scott et al, (2008) pulmonary emphysema is abnormal enlargement of air spaces distal to the
terminal bronchioles with destruction of the alveolar septa with little or no fibrosis. It is caused
by air pollutants, inhalation of chemicals, fumes, dust etc. These pollutants change the structure
and functions of the lungs by causing irritation and inflammation of the narrow airways. This
leads to release of enzymes in the lungs that destroy lung tissues and increased size in the air sac
eventually leading to emphysema. The destroyed lung tissues form bullae (holes) and lose
elasticity. According to (Kumar et al, 2005) under microscope, pulmonary emphysema is
characterized by distension of many alveoli with wide openings due to rupture of alveolar walls,
the alveolar wall is thin and atrophic. Emphysema can be classified based on the part of the
respiratory acinus(lobule) which is damaged. According to Kumar et al (2005) the classification
includes;
[1] centralacinar emphysema which involves primarily the bronchioles and commonly occurs
in the upper lobes
[2] paracinar emphysema involve entire respiratory acinus from bronchioles to alveoli, occurs
more commonly in the lower lobes, especially basal segments and anterior margins of the lungs
[3]paraseptal emphysema occurs primarily adjacent to the pleura and connective tissue septa
especially in the upper lobes. Extensive involvement of the lung is rare.
[4] paracicatrial emphysema is an irregular emphysema associated with scarring. There is no
relationship to the acinus.
Other types of pulmonary emphysema include [5] Interstitial emphysema commonly found in
connective tissue of the peribronchovascular sheaths, interlobular septa and visceral pleural.
Interstitial emphysema is created when air burst or ruptures through tissue from the alveoli and
bronchioles into the perivascular tissue of the lung.

3. [6]Bullousemphysema.This refers to any form of emphysema that produces large subpleural
bullae(spaces >1cm in diameter in the distended state and occasionally occur in the apex.
Rupture of the bullae leads to pneumothorax.
[7]Compesatory emphysema. This is type of emphysema in which there is dilatation of the
alveoli but not destruction of the septal wall in response to loss of lung substance elsewhere.
[8] senile emphysema which refers to over distended, sometimes voluminous lungs found in the
aged animals. When aging the lungs alters their internal geometry by having larger aveolar ducts
and small alveoli but this occur without loss of elastic tissue or destruction of lung tissue.
All in all, only interstitial pulmonary emphysema was identified on the lung with pathological
changes as explained above.
LIVER
Grossly the liver occupied nodules, its architecture showed to be destructive, and broad scars on
the parenchyma and due to the scars, a firm and hard texture was identified. This is a
characteristic of hepatic cirrhosis. According to (Peacock, 1996) liver cirrhosis is characterized
by replacement of multiple adjacent lobules by fibrous tissues leading to scars, parenchymal
nodules created by regeneration of encircled hepatocytes,the nodules varies from (<3mm in
diameter called micro nodules)to large (several centimeters, called macro nodules), disruption of
the architecture of the entire organ of liver. Microscopically there is deposition of liver lobules
with type 1and type 3 collagen creating broad septal tracts, loss of sinusoidal endothelial cells
due to continued deposition of collagen in space of disse. The amount of fibrous tissue exceeds
that of normal liver and no longer arranged acini or lobules.
So from observed gross lesion, the liver was undergoing cirrhosis. The nodules occur due to
disorganized hepatocytes that regenerate in a nodular way (Peacock, 1996). This condition is
caused by viral hepatitis, biliary diseases, primary hemochromatosis, protein deficiency, and
ingestion of toxin from plants (Kumar et al, 2005). For example, exposure to aflatoxins is
probably also an important factor in tropical areas like Malawi, likely because of the suboptimal
storage of certain food items such as peanuts. Ongoing hepatocyte injury from aflatoxins
increase liver cell turnover, leading to the formation of regenerative nodules (Kumar et al,2005).
According to cabana (2001), the formation of regenerative nodules is an attempt by the liver to
replace the damaged hepatocytes and compensate for lost liver function. Within regenerative
nodules, some hepatocytes can undergo further genomic changes and hence progress to liver cell
dysplasia/disorganized. With these changes, the nodules increase in size and cellularity, giving
rise to the formation of dysplastic nodules.
The parenchyma of the liver also was observed with small multiple fleshly masses of palegray-
white soft tissue; each mass sharply demarcated and appeared as centrally

4. opened/perforated.This suspects the presence of angioma in the liver. According to (Rastogi,
2007) Hepatic angioma is a benign tumour of the liver composed of hepatic endothelial cells.
They usually appear at or near the surface of the liver. They are solitary and rarely exceeding a
few centimeters in diameter. Hepatic angioma is mostly idiopathic but can be associated with
exposure of cattle togrowth promoters such asarsenicals and polyvinyl chloride used in plastics.
They begin as small, sharply demarcated, asymptomatic, and often become large with areas of
hemorrhages. Microscopically, there is no definite blood vessels and they are marked atypical,
endothelial cells appear spindle shaped, necrosis of endothelial cells and hepatocytes.
Although microscopic examination wasn’t done, and based on reference the lesion was hepatic
angioma.
AORTA
Grossly, the aorta was dilated, thickened, with elevated atheromatous plaque on the intima
surface and the worms within a nodule were usually observed. From these gross findings, the
aorta was harboring onchoncerca species. This is due to grossly this species are associated with
formation of nodules , dilation and plaque formation in the aorta (Kumar et al 2005).
Histological examination reveals parasitic granuloma present in the aorta characterized by the
infiltration of eosinophils, numerous sections of the parasites in the wall of aorta, parasites
embedded or encysted in the inner most layer of aorta , chronic granulomatous reactions
characterized by accumulation of macrophages, lymphocytes, plasma cells, giant cells,
calcification and fibrosis around degenerate and dead parasites, presence of neutral fat in
parasites and surrounding cells (cabana, 2001). As per said, the results suggest the occurrence of
onchocercosis in the examined aorta. According to Soulsby(1968)Onchocercosis is a parasitic
disease caused by the different species of nematodes belonging to the genus Ochocerca affecting
both humans and animals.Ochocercaarmillta, O. gutturosa and O. gibsoni affect mainly cattle,
and also buffaloes. Progressive O. cervicalis is found in the ligamentum nuchae and possibly
other sites in Equidae. In cattle, O. gutturosa locates in the ligamentum nuchae, O.lienalis in the
gastrosplenic ligament and O.armillata is found in the aorta.
From that reference the examined pathological aorta was affected with O.armillata.
RUMEN
Forestomaches are lined by stratified squamous epithelium, but each has a characteristic surface
structure. Reticulum looks reticulated, rumen has so many papillae for optimal absorption and
omasum also known as “the book” it has many thin folds that resemble pages of a book
(Stockhalm and Scott et al,2008). The part of the rumen which was examined showed multi-focal
superficial sites of mucosal destruction, the destroyed part looked whitish and this is a
characteristics of rumen ulcers. According to (Rastogi, 2007)rumen ulcers are characterized by
destruction of superficial portion of the mucosa, natural local buffering surface cells is lost, and
the proliferative compartment of the gland, which is near the surface, is obliterated, preventing a
local epithelial reparative process hence rumen epithelia atrophies. And when the rumen mucosa

5. is atrophied, there is poor digestion and fermentation, so ingesta can’t be broken down, they just
move on through, carrying water with them causing diarrhea. Microscopically necrosis of the
muscularis mucosae is observed. If the necrosis continues, the ulcer may extend through the
muscularis and serosa and results in perforationof the rumen wall. Rumen ulceration is mostly
caused by ruminal acidosis due ingestion of diets high in grain (carbohydrates). Increased
fermentation of carbohydrates lowers the rumen PH (<5) due to accumulation of volatile fatty
acids in the rumen. The volatile fatty acid damages the rumen mucosa resulting in ulcers and
erosions. These erosions and ulcers may be secondarily infected with fungi resulting in mycotic
rumenitis. Ulcers often provide a breach for Fusobacterium necrophorumor Corynebacterium
spp. to gain entry to the blood supply and cause hepatic abscesses and hepatic necrosis. These
hepatic lesions are common in feedlot cattle fed high concentrate diets.
The lining of the rumen also was also attached with pear-shaped, pink-red short flukes and many
of the ruminal papillae have become darker. Pear-shapedrumen flukes are paramphistomes
(Soulsby, 1968) so the rumen was manifested with paramphistomiasis. According to Soulsby
(1968) grossly adult rumen flukes are small, Cornical shaped, maggot-like flukes about 5 to 13
mm long and 2 to 5 mm wide, and they are light red or pinkish in colour. Microscopically their
egg resembles that of Fasciola hepatica being large and operculated, but it is clear rather than
yellow.In large numbers/severe cases rumen flukes can cause: ruminal or intestinal ulceration,
severe diarrhea, weakness and death.
INTESTINE
The intestine showed grayish-whitish nodules on the surface. Small and larger nodules were
visible, some showed to be gritty and others soft. The intestine was thickened with some areas of
reddening and edematous. This is a characteristic of nodular worms since these worms are
associated with formation of parasitic nodules in the intestinal mucosa and serosa (Peacock,
1996). Nodular worms includes oesophagostomumradiatum which is found in
cattle,oesophagostomumcolumbianum in sheep and oesophagostomumdentatum in swine causing
nodules or pimply gut or knot gut in intestines (Soulsby, 1968).The presented intestine was
manifested with oesophagostomiasis which is a parasitic infection of ruminants and swine
(Soulsby 1968).According to microscopically granulomatous reaction characterized by
infiltration of inflammatory cells such us eosoniphils ,plasma, giant cells is observed and the
mucosa is encysted with the larvae of nodular worms. The helminth that was causing
oesophagostomiasis in the presented intestine was the larvae of O.radiatum since it is found in
the intestines of cattle (Soulsby, 1968). The intestines affected with nodular worms are
condemned and also its carcass.

6. Conclusion
All in all, it was easy to identify the organs presented at the abattoir and their pathological
lesions grossly. However, histopathological examination was not conducted to those lesions to
see microscopic changes. Still more the aim of diagnosis was achieved based on gross
examination of the lesions.
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