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Key To PATH 202 Practical
Key To PATH 202 Practical
Take a pus samples from lesions and place in a Petri dish and wash carefully with a little water. Yellowish sulphur
granules will become visible. Clubs can be seen if the granule crushed in a drop of 10% KOH on a slide and seen
microscopically (club colonies or rosettes)
Saw dust liver: Focal hepatitis (focal necrosis of liver)—the so-called “sawdust liver” of cattle. Necrotic areas look like
sawdust on liver cut surface
Nutmeg liver: Chronic passive congestion of liver showing pattern of nutmeg. Shrunken and congested centrilobular
areas impart the characteristic “nutmeg” appearance to the liver. This finding is most commonly associated with right-
sided congestive heart failure.
Shaggy heart (cor villosum, butter and bread pericarditis): Fibrinous pericarditis is known as shaggy heart
Heart failure cells: These are hemosiderin-containing macrophages, generated in the alveoli with left heart failure or
chronic pulmonary edema, when the high pulmonary blood pressure causes red cells to pass through the vascular
wall
Foam cells: These are the fat-laden macrophages seen in atherosclerosis. Foam cells are formed when the body
sends macrophages to the location of a fatty deposit on the blood vessel walls. The macrophage surrounds the fatty
material in an attempt to destroy it. The cell becomes filled with lipids (fats). The lipids surrounded by the
macrophage give it a "foamy" appearance.
In bronchopneumonia (lobular pneumonia), there is patchy consolidation (foci of consolidation surrounded by normal
parenchyma) around small bronchi and its usually bilateral while in lobar pneumonia there is diffuse consolidation of
entire lob and usually its unilateral.
Coagulative necrosis is the type of necrosis in which protein denaturation is more prominent than enzymatic breakdown.
There is increased eosinophilia of the cytoplasm and decreased basophilia of the nucleus; both are associated with
preservation of the general cellular architecture (the organ type is identifiable). Coagulative necrosis can occur in any
organ except brain
Liquefactive necrosis occurs in situations in which enzymatic breakdown is more prominent than protein denaturation or
in organs that lack a substantial protein- rich matrix (e.g., lipid-rich organs such as the brain). There is loss of organ
cellular architecture. In liquefactive necrosis of the brain, there are sheets of lipid-laden macrophages that replace the dead
tissue. Liquefactive necrosis is most commonly associated with organs that have a high fat and low protein content (e.g.,
the brain), or those with a high enzymatic content (e.g., the pancreas).
Difference between Hyperemia and congestion
Hyperemia: Active accumulation of blood within vessels, such as would occur in vasodilation due to acute inflammation.
Congestion: Passive accumulation of blood within vessels, such as would occur in the lungs due to left-sided heart failure,
or in the liver and extremities due to right-sided heart failure.
Hemorrhages and types
Hemorrhages: Leakage of blood from vessels.
Petechiae: Pinpoint hemorrhages (1-2 mm). Petechiae are caused by platelet dysfunction and increased vascular pressure
Purpura: Larger than petechiae and usually raised. These are commonly associated with vasculitis.
Ecchymoses: Larger than purpura (>1.0 cm) and usually caused by trauma.
Thrombosis
Pathologic coagulation of blood resulting in the formation of a solid mass (thrombus) within a chamber of the heart or
within a blood vessel. Have Lines of Zahn, which are alternating layers of red blood cells, platelets, and fibrin within the
thrombus
Factors predisposing to thrombus formation (Virchow triad)
Stasis of blood (e.g., due to congestive heart failure, obesity, immobilization). Stasis is a particularly common
predisposing condition in animals that develop venous thrombi. Hypercoagulability: Hypercoagulable states may
contribute to the development of thrombi in any location, and include hereditary conditions as well as various acquired
states. Endothelial damage: Endothelial damage plays a major role in many arterial thrombi.
Embolus
An embolus is a substance that forms within or enters the vascular system at one site and is carried through the blood
stream to another area of the body, where it lodges in a blood vessel and produces its effects (usually infarcts). If a
thrombus breaks free from where it forms and goes to another part of the body, it becomes a thromboembolus. Substances
besides thrombi, such as cardiac valvular vegetations, foreign bodies, fat, and air, can also embolize.
Infarcts
A localized area of dead (necrotic) cells within an organ. An infarct is the pathologic finding; an infarction is the process.
Hypoxia and ischemia are the two main mechanisms that result in infarction of organs. Hypoxia is lack of oxygen to an
organ, and ischemia is lack of blood flow to an organ. Ischemia is more damaging than hypoxia, since in ischemia,
decreased blood flow results in both decreased oxygen delivery and decreased delivery of nutrients to the tissue and, in
addition, there is no way to remove the toxic metabolites of cellular metabolism.
Types of infarcts: The two general types of infarcts are red and white infarcts.
Red (“hemorrhagic”) infarct: Most red infarcts occur due to obstruction of an artery supplying an organ that has a dual
blood supply or an organ that has loose parenchyma, such as the lung, which allows for leakage of blood into damaged
tissue. These look soft red area of tissue.
White (“anemic”) infarct: Organs with single blood supply and organs with solid parenchyma (e.g., heart, liver, spleen).
These look soft pale or white area of tissue.
Tetralogy of Fallot
1- Pulmonary stenosis.
2- Right ventricular hypertrophy (as a result of the pulmonary stenosis).
3- A ventricular septal defect shunts blood to the left side of the heart
4- The aorta overrides the ventricular septal defect.
Postmortem changes
Algor mortis: Cooling of the body after death, known as algor mortis.
Livor Mortis (hypostatic congestion): The purple-red discoloration of the soft tissues due to postmortem gravity-
dependent pooling of blood is livor mortis.
Rigor Mortis: Stiffening of the body after death because of a loss of Adenosine Triphosphate (ATP) from the body's
muscles
TUBERCULIN TEST FOR TUBERCULOSIS
Intradermal Test (SID): This test is very easily applicable in cattle and buffalo. The skin of middle neck is
preferred (Tail base can also be used). A 2" x 2" area is shaved. The thickness of the skin fold is measured (mm)
with a dial or ordinary caliper and 0.1 ml tuberculin or its PPD (Purified Protein Derivative) is injected intradermally
with special syringe and needle. A small pea sized elevation indicates proper placing of the antigen. The skin fold
thickness of the site is noted 72-96 hours (3-4 days) later.
Interpretation: If the thickness increases by 4 mm or more, with or without painful swelling, indicates the test
positive.
JOHNIN TEST FOR JHONE’S DISEASE (PARATUBERCULOSIS) IN BOVINES
It is applicable for the diagnosis of Johne's disease in cattle, buffaloes, sheep and goats. Single
intradermal test is used. Johnin 0.1 ml is injected in the skin of neck similar to tuberculin test. Skin fold thickness is
measured pre- and 48-72 hours post- infection. A positive test is characterized by oedematous swelling.
For the diagnosis of subclinical Johne's disease, short thermal test has been advised. One ml Johnin, diluted with 9
ml normal saline is injected intravenously. A rise in body temperature by 20 F around 5-8 hours post-inoculation
indicates the test positive.