Pigmentation - Pathology

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Exogenous Pigmentation

  • Enter body from environment

Carbon (Anthracosis)

  • This occurs where carbon particles are inhaled over a long period of time.
  • Carbon particles are phagocytosed by alveolar Macrophages.
    • Are carried to a peribronchiolar location and the local bronchial lymph nodes.
  • It is common in animals that live in cities.
    • There is air pollution due to smoke.
    • Mostly seen in dogs.
  • Can occur in the mesenteric lymph nodes of pigs that feed on ash heaps.
  • Carbon is insoluble and results in minimal irritation.

Gross Appearance

  • Black or grey speckles in lungs.

Histological Appearance

  • Black extra- or intra-cellular granules .
    • Resistant to solvents and bleaching agents.
    • Can cause slight fibrosis in alveolar walls.


  • A serious pigmentation.
  • Results from repeated inhalation of irritating mineral dust, e.g.
    • Coal
    • Silica
    • Asbestos
  • Leads to pulmonary fibrosis.
    • Varying shades of grey.
  • Asbestos may also cause pulmonary, pleural and peritoneal tumours.
  • Seen more in man than animals.
    • Occupational hazards.


  • Also known as lipochrome.
  • Carotenoids are fat-soluble greenish-yellow pigments that bind to lipids in body.
    • Derived from carotenes and xanthophyll in plants.
    • Can be seen grossly in a number of normal places
      • Adrenal cortex.
      • Testes.
      • Corpus luteum.
      • Liver.
      • Yolks of eggs.
      • Fat of horses and Channel Island cattle.
  • May be confused with a jaundiced liver or subcutis.
    • Adding minced tissue to a mixture of ether and water can distinguish the two.
      • Carotenoids are fat-soluble and dissolve in the ether fraction.
      • Bile pigments dissolve in the water fraction.


  • E.g.
    • Iron injections in piglets.
    • Coloured antiseptics.
    • Tattooing.

Endogenous Pigmentation

  • Pigments are formed inside the body.


  • Normally gives visible colour to the skin, hair, and iris.
  • Melanin synthesis is controlled by melanocyte stimulating hormone (MSH).
    • MSH is produced in the pituitary.
    • Melanin is derived from tyrosine (an amino acid) utilising a copper-containing enzyme, tyrosinase.
  • Melanosis occurs when excessive quantities of pigment are deposited in internal organs.
    • The lungs and aorta, pleura, brain and meninges, and liver are often affected.

Gross Appearance

  • Black/brown pigmentation is seen, either as spots or as larger areas.
    • Larger areas can give the lungs or liver a chequer-board pattern.
  • No change in structure occurs.

Histological Appearance

  • Round granules of brown/black are seen in the cytoplasm of cells.
    • Can be bleached out by chlorine or KMNO4.
    • Stain black with silver stain Masson Fontana.


  • There is no significance of melanosis when it occurs in the internal organs.
  • There is also no significance in hyperpigmentation of the skin.
  • Melanosis may be associated with chronic irritation.
    • For example, in wound healing.
  • Hyperpigmentation may be significant in excess cortisol states such as Cushing’s Disease.
    • There may be tumours of melanocytes.
  • Albinos have no pigment in their hair or skin, and have pink irises.
    • Lack sufficient tyrosinase enzyme in their melanocytes.
    • Albino rabbits, rats and mice are seen.

Blood Pigments

  • Blood pigments causing pigmentation may be
    • Normal derivatives of haemoglobin, which have accumulated in excess.
      • Haemosiderin.
      • Bilirubin.
    • Pathological
      • Methaemoglobin (chocolate brown) in nitrate poisoning.
      • Carboxyhaemoglobin (bright cherry red) in carbon monoxide poisoning.
      • Parasitic acid haematin.


  • Results from excessive phagocytosis or haemolysis of red blood cells.
    • Haemoglobin is freed into the plasma which becomes red.
  • If there is sufficient haemolysis, the haemoglobin overspills into the urine.
    • Haemoglobinuria.
      • Both the kidneys and the urine appear dark red.
  • Can be caused by a variety of agents including:
    • Bacteria
    • Protozoa
    • Chemicals
      • E.g. excessive copper in the liver of sheep.
    • Immune mediated conditions
      • E.g. autoimmune mediated haemolytic anaemia.
  • Haemoglobin is not usually seen in the tissues.


  • Haemosiderin is a golden brown/yellow pigment.
    • Derived from splitting haemoglobin into an iron-porphyrin compound and globulin.
  • Excessive quantities of haemosiderin arise from increased red cell breakdown by:
    • Phagocytosis
    • Haemolysis
  • Large amounts of haemosiderin diffusely spread throughout the spleen usually indicates a haemolytic disorder.
  • Local production of haemosiderin is responsible for the appearance of bruising in injury.
    • Other haemoglobin breakdown products are also formed.
  • Haemosiderin also accumulates in chronic congestion of the vascular system due to heart failure.
    • Seen in highly vascular tissues such as the lung, liver and spleen.
Gross Appearance
  • Grossly, very little can be seen unless there has been substantial breakdown of haemoglobin.
    • In this case the organ may appear brownish.
  • Also seen as bruising.
  • Usually not appreciable in the lung in heart failure.
  • In repetitive exercise induced pulmonary haemorrhage of horses, the affected area of the dorsal lung may be brownish in colour.
  • The equine liver often contains stores of haemosiderin giving them a brownish colour.
Histological Appearance
  • Accumulates in the cytoplasm of macrophages.
  • Chronic congestion in the lung can be seen due to heart failure.
    • Some of the red blood cells escape out of the alveolar capillaries and are engulfed by alveolar macrophages.
      • Called "heart failure" cells.
  • Prussian blue stains specifically for haemosiderin.
    • Granules stain blue.


  • There are 2 types of haematin.
    • Acid haematin
    • Parasitic haematin.
Acid Haematin
  • A pigment artefact.
  • Acid in unbuffered formalin binds with haemoglobin to form a brownish-black granular pigment.
  • Only seen microscopically.
  • Can be formed in areas of ante-mortem ulceration of the stomach.
    • There is increased acidity due to hydrochloric acid.
  • Acid haematin is iron negative.
  • Must remove acid haematin prior to staining sections to allow haemosiderin to be distinguished.
    • A useful clue in the untreated section is the presence of the pigment in the red blood cells of vessels.
Parasitic Haematin
  • Certain parasites in other parts of the world (e.g. Schistosoma sp.) take up blood.
    • Break haemoglobin to haematin.
    • Regurgitate the pigment back into circulation.
  • Fasciola hepatica in this country causes chronic damage to the bile ducts of the bovine liver.
    • Produces acid haematin, which lines the bile ducts.
    • The fluke and its spines damage the duct lining and feed on blood liberated from the blood vessels.
      • This is regurgitated by the fluke and passes down the bile duct to the intestine together with the proteins liberated.
        • This parasitic haematin is in an un-resorbable form, and so the flukes lead to hypoproteinaemia and anaemia.



  • Haematoidin is bile pigment laid down in areas of focal haemorrhage where red blood cells are lysed.
    • I.e. it is unconjugated bilirubin in tissues.
  • Has a clear yellow colour.
  • Can sometimes be granular.
    • Could be confused with haemosiderin.
      • Unlike haemosiderin, haematoid does not contain iron.
        • Does not stain with Prussian Blue.


  • Porphyrin is a component of haeme.
  • Porphyria is a rare heritable condition in cattle, pigs and cats, where there is imperfect synthesis of porphyrin.
    • Due to defective enzymes.
    • Leads to a degree of anaemia in affected animals.
  • Porphyria is best-documented in cattle.
    • Porphyrins (brownish in colour) accumulate in bone, teeth and other internal tissues.
    • Excess porphyrins also circulate in the blood stream and are excreted in the urine.
    • Urine has a reddish colour.
  • Porphyrin is a fluorescent pigment.
    • Urine will also fluoresce under ultra-violet light.
Histological Appearance
  • Porphyrin is a fluorescent pigment.
    • Is related to chlorophyll.
  • UV light acts on porphyrins as they circulate in the blood under the white skin.
  • The inflammation caused may look like sunburn, but is actually a necrotising dermatitis.
    • Affected areas slough off.
    • Large areas of the dermis are exposed to infection.
    • Death due to toxaemia can ensue if it is severe.
  • Removing animals from sunlight causes the lesions to regress.

  • The most common and important form of photosensitisation in animals is due to liver damage coupled with a diet containing a lot of chlorophyll.
    • I. e. animals on green pasture.
  • A wide variety of plants and fungi have been implicated in causing acute toxic damage to the liver.
    • Including grasses, clovers and Brassica sp.
    • This liver damage may cause the imperfect breakdown of chlorophyll and raised phyloerythrin levels.
      • Causes photosensitisation.
  • The common form in sheep is facial eczema.
    • The face and head are swollen, raw and bleeding.

  • A third form of photosensitisation occurs in the absence of liver damage and is due to certain plants containing excessive fluorescent pigments, e.g.
    • Buckwheat (Fagopyrum esculentum)
    • St. John’s wort (Hypericum perforatum)


  • A yellow-brown granular pigment composed of lipid, phospholipid and protein polymers.
    • Thought to be derived from the lipid peroxidation of cellular membranes.
  • Lipofuscin is the ageing pigment.
    • Can be seen in senile animals in
      • Muscle
      • Myocardium
      • Neurones (particularly those of horses)
      • Normal liver of middle-aged cats.
  • Xanthosis is when lipofuscin is a prominent feature in the tissues of Ayrshire cattle.
    • Lipofuscin is found in the heart, diaphragm, masseter muscles, kidney and adrenal cortex.
  • Pathologically, lipofuscin is associated with Vitamin E/ Selenium deficiency.
    • There is excessive lipid peroxidation of cellular membranes by free O2 radicals.

Gross Appearance

  • Xanthosis - gives a brown colour to the organ.
  • Senility
    • May impart a brownish colour to the heart.
      • Sometimes called ‘brown atrophy’.
    • In other areas, lipofuscin is only visualised microscopically.

Histological Appearance

  • Granular
  • Brown- yellow in colour.
  • Lies in the cytoplasm...
    • ...At either end of the nucleus in the heart.
    • ...Scattered throughout in the liver and neurones


  • Is a variant of lipfuscin.
  • Stains acid fast.
  • Occurs in:
    • Hepatocytes
      • E.g. in choline deficiency in cirrhosis
    • Macrophages
    • A variety of tissues including fat, cardiac muscle, splenic trabeculae and intestine in Vitamin E deficiency.
      • Sometimes being so prominent as to be grossly visible.

Also see Liver Pigmentation.