Pigments

Forms:
• Endogenous pigments
– haemoglobinogenous pigments
• haemoglobin
Pathologic pigmentation – szulfmethaemoglobin, haemiglobin, carbon-
monoxid-haemoglobin, formaldehyde pigment,
haematin
• haemosiderin
• haematoidin and bilirubin
• porphyrin

– anhaemoglobinogenous (autochtonous) pigments

• Exogenous pigments

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 Topics
• 31. Pathologic pigmentation caused by
hemoglobin and haemosiderin
• 32. Pathologic pigmentation caused by
hematoidin, and bilirubin
• 33. Pathologic pigmentation caused by
porphyrins
• 34. Pathologic pigmentation caused by melanin,
lipofuscin, and ceroid
• 35. Exogenous pigments
• 36. Concretions (lithiasis) and pseudoconcretions

31. Pigmentation caused by haemoglobin

and haemosiderin Hemoglobin forms:
• Haemoglobin • Sulfhaemoglobin (H2S): greenish  fades
– Haemolysis haemoglobinaemia
– Haemoglobin cylinders in renal tubuli
• Methaemoglobin (Fe++, - Fe+++): dark brown
(benzidine +) • Carboxi-haemoglobin (CO-intoxication)
• Causes of haemolysis: – cherry pink discoloration, clearly visible in brain
– Autointoxication
– Chemicals (arsenic, cupper, phenol,
trichlorethane)
– Drugs
(sulphonamides, atebrin, phenacetin)
– Physical effects
(radiation, thermal injuries)
– Bacteria, viruses, parasites (Babesia)
– plant poisons

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• Hemosiderin
– Brown, amorphous, granular, iron-containing
pigment
– Develops in RES cells (macrophages)
– Siderin: injection of iron-dextran preparates
– Histology:
• Prussian blue (Perl’s reaction)
• Turnbull’s technique
– Local haemorrhages: siderophor cells
– Pseudomelanosis: hemosiderin + H2S
(putrefaction)

 Hemosiderin
– Pseudomelanosis: hemosiderin + H2S (putrefaction)

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 32. Pigmentation caused by hematoidin
and bilirubin

• Hematoidin
– Brownish pigment
– Old haemorrhages
– Iron free derivate of haem!
– Needle-shaped or rhomboid crystals
• Bilirubin (biliverdin: oxydized): bile pigment
– RHS (MPS) cells (indirect bilirubin)
– Liver cells (direct bilirubin – conjugated to
glucuronic acid)

Simultaneous presence of haematoidin and haemosiderin

in subcutaneous tissue

Jaundice - icterus
• Bilirubin in tissues: solute and
precipitated to proteins
• Staining the tissues yellow
(conjunctiva, sclera, intima of blood
vessels…)
• Bird liver: green (biliverdin)

• Staining:
– Forsgren method (reddish-blue)

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 Jaundice - icterus
• Posthepatic
• (stagnation or resorption)
– Obstruction to the outflow of bile
(bilirubin I)
– In the blood and urine: bilirubin II
• Prehepatic (hyperfunctional or
hemolytic)
– Intensive haemolysis
– (bilirubin I in blood)
– Icterus neonatorum
• Hepatic (toxic or retention)
– (bilirubin I and bilirubin II)
– In the urine: bilirubin II, urobilinogen
– Cell necrosis

Cholelithiasis ( posthepatic icterus)

Intrahepatic accumulation of bilirubin

HE; 200x

33. Pathologic pigmentation

caused by porphyrins

HE; 600x

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 Porphyria Porphyria
• Hereditary
• Porphyrin
– Haem synthesis • Toxicoses (Pb, As, anilin etc.)
– Protoporphyrin + Fe + globulin = Hb • Spongy bones are coloured
– Porphyrin synthesis: liver + bone marrow • Dental cement brown
– Affinity to bone • Dentin pink, reddish-brown
– Photosensitization
• Enamel: white
– Brownish-violet, fluorescence under UV light
• Cartilage, ligaments, tendons:
– Uro- and coproporphyrin = excreted with urine and faeces
uncoloured
– Hereditary porphyria
– Toxicoses: lead, arsenic, CCl4, benzene, anilin
• coproporphyrin

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 40. HGCE - Pyometra complex

Pigments
Forms:
• Endogenous pigments
– haemoglobinogenous pigments
34. Pathologic pigmentation caused by • haemoglobin
melanin, lipofuscin and ceroid – szulfmethaemoglobin, haemiglobin, carbon-
monoxid-haemoglobin, formaldehyde pigment,
haematin
• haemosiderin
Autochton pigments • haematoidin and bilirubin
• porphyrin

– anhaemoglobinogenous (autochtonous) pigments

• Exogenous pigments

34. Pigmentation caused by melanin,

Anhaemoglobinogen pigments lipofuscin and ceroid
Autochtonous (non hemoglobinogen
pigments)

• melanin Melanin
• Insoluble in water, acids, fat solvents
• lipofuscin • Solubile in K-OH, Na-OH
• H2O2 – bleach
• ceroid • Ectodermal origin cells produce it
• Tyrosinase enzyme initiates
• ceroid-like pigment melanin synthesis
• Melanocyte-stimulating hormone (MSH)
stimulates, but also ACTH has
influence on the pigmentation
• Brownish-blackish pigment – no iron

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 Melanocyte
Melanin
• Produced by: melanocytes
• Stored by: melanophags
tirozin
Tirozinase (oxidation)
melanin
Hypophysis (MSH, ACTH)
Under physiological conditions
• skin
– epidermis, corium
• during pregnancy
– nipples, face, middle line if the belly (chloasma gravidarum)
• eye
– retina, iris, chorioid
• ganglion cells
– nucleus niger
• leptomenings
• mucous membrane of the oral cavity
• mammary gland in special swine breeds (Berkshire)
• Serous membrane of reptils and some birds
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 Three variations of abnormal pigmentation

• Hyperpigmentatio
– Radiation, arsenic treatment
– Naevi (naevus pigmentosus)
– Focal melanosis
– Melanoma
– Acanthosis nigricans
– Addison’s disease
• Hypopigmentatio
– Leukoderma (surgical
treatment)
– Vitiligo (pigmentfree area)

• Albinismus

Melanosis maculosa

Melanoma benignum
(melanocytoma)

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Acanthosis nigricans

• Disease of unknown origin

• Hyperpigmentation of the
axillae, ventral thorax,
inguinal and circum-anal
region
• Uneven proliferation of the
epithelial cells in stratum
spinosum
• Skin thickened, surface
uneven
• Velvety touch

Hypopigmentation
• Age
• Vitiligo (hamartia)
• Leukoderma (focal absence after injury)
• Trophoneurotic problems
– dourine in horses
• Trypanosoma equiperdum infection
– depigmented areas
• pale areas after maceration

• Albinism
– pathological absence of melanin
– congenital in rodents

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 • Lipofuscin
Golden-brown pigment
protein + lipids, no iron
Formed in lysosomes
Ageing cells
Autooxidation of unsaturated lipids
all three germ layer cells may contain
insoluble in water, acid, alkali
Liver, kidney tubuli, adrenal gland,
chorioid plexus, muscle cells
EM: dense, amorphous autophagosomes
+ granules and lipids

Lipofuscin containing histiocytes Lipofuscin in heart muscle

cells

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• Brown bowel syndrome
– Dogs
– Diarrheal diseases
– Steatorrhea • Ceroid
– Pancreatic acinar deficiency – Lipogenous pigment
– Malabsorption – Partially oxidized and polymerized unsaturated
– Intestine: brown fatty acid bound to proteins
• Smooth muscle cells
– Produced in macrophages and hepatocytes
– Ziehl-Neelsen positive
• Neuronal ceroid lipofuscinosis
– English setter, cattle, sheep, cat
– Intracellular accumulation • Yellow fat disease
– Progressive loss of cells in the – Alcohol soluble - icterus
brain and the cerebral function
– Ether soluble - yellow fat disease

Ceroid-like pigment
yellow
Appearance
• lipocytes
• macrophages
• MPS-cells

• The fat tissue is yellow

– yellow fat disease
– cause: high amount if unsaturated fatty
acid in the feed

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 Ochronosis (alkaptonuria)

• inherited disturbance of the protein

metabolism (tyrosine, phenilalanine)
amino acids (aromatic)

homogentisic-acid
oxidation colored substance

• Cartilage, tendons, ligaments become greenish

• The bones do not get discolorated

Pigments 35. Exogenous pigments

Forms: • Anthracosis
• Endogenous pigments – Phagocytic activity against fine coal
– haemoglobinogenous pigments
• Pneumoconiosis
• haemoglobin
– Siderosis (Fe), Chalicosis (CaCO3),
– szulfmethaemoglobin, haemiglobin, carbon-
monoxid-haemoglobin, formaldehyde – Silicosis, asbestosis, tabacosis…
pigment, haematin
• haemosiderin • Tattooing
• haematoidin and bilirubin • Pseudoicterus
• porphyrin – karotinoids
• Medicines
– anhaemoglobinogenous (autochtonous) pigments – Trypanblue
– Silver preparations (argyria)…
• Exogenous pigments

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 Exogen pigments
• Either colored or non-colored
• Enter the body
– Aerogenously
• pneumoconiosis
– Per os (enterogen)
• Food, plants (common madder - alizarin)
– Skin wound (tattooing)
– Parenteral way
• In the lungs
– Alveolar macrophages + histiocytes
– Gets to the regional lymph node

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 Exogen pigments
Powders, chemicals, drugs, feed particles
• soot, dust = anthracosis
• quartz = silicosis
• iron = siderosis
• lime, whiting = chalicosis
• asbestos = asbestosis
• tobacco = tabacosis
• silver products = argyrosis
• karotin = karotinosis (pseudoicterus)

• Any substance in the lung - pneumoconiosis

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 Exogen pigments 36. Concretions and pseudoconcretions
Drug, feed
• blackberry = skin, tendons Lithiasis, calculus formation
• pannage = fascia, mesenteric lymphnodes • Solid substances
– From secretions of certain organs
• alizarin = osteogenesis
– Lined by mucous membranes
– madder (Rubia tinctorum)
– fine red dyeplant
• Reason for the precipitation
– used to colour fabric and timber – Increased concentration of crystalloids
• picric acid = yellow – Decreased protective colloid content
• Lithogenous material + binding material →
• tripaflavin = yellow Microlith
• trypan blue = tendons • calculus, sediment

Predisposing factors Composition of different

Lithogenous material in increased amount
• Metabolic disorders
• Nutritional factors
Inflammation of hollow organs
• Changes in the pH
• Enzymatic destruction of the colloids
• Desquamation of the epithelial cells
Stasis of excretions
concretions
• Calcium-carbonate
– Food is contaminated with limestones
• Phosphate calculi
– Feeding with forage, bran
• Oxalate stones
– High amount of fodder beet
• Cystine or xanthine stones
– Due to metabolic disorders in urinary tract

Structure

• Microlith – crystallization centre

– Foreign body, fibrin, necrotic cells
• Lithogenous material
– Salts of organic or inorganic acids
– Cholestrol, bilirubin, cystine, xanthine
• Binding material
– Protein or mucous like

• Concentric layering

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 Localization
• Mainly in the urinary tract
– Pelvis of the kidney, urinary bladder
• besides that
– ducts of the salivary glands
– ducts of the pancreas
– gallbladder, biliary ducts
– intestines
– oral cavity (dental plaque, tartar)

• Liths in the large intestine of the horses

– Composition: magnesium-ammonium-phosphate
– high amount of forage, bran = magnesium(II)-phosphate
– during putrefaction of proteins ammonium is produced

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„Facetted stones” Concentric layering

„Enveloped stone”

Uroliths from the renal

pelvis of a horse

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 Enterolith, horse, large intestine Sand deposition, horse
Stone in the urinary
bladder of a dog

Sialolith from the parotid gland Sialolith in human

of a horse submadibular gland

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 Concrements
• Size of the stones
– differ
• What happens with the stones?
– small concretions exit from the lumen
– in some cases dissolve
– in other cases break into smaller pieces
– stay in the organ constantly
• Harmful effects
– Stenosis or complete obstruction of the lumen
– Mechanical trauma (rough surface)
– Heavy stones cause pressure, atrophy, necrosis
Obstipation (coprolith)
Inspissation of the intestinal content
Zootrichobezoars
Pseudoconcretions
• Inspissation of content
• Impaction of foreign materials
• Types:
– Simple solidification of the excretions
• Fossae of the tonsils, prepuce, guttural pouch, bronchi, oviduct
• Secondary calcification
– Knotted animal hair (zootrichobezoars)
• Effect of the movements of the stomach (Ru, sus, ca, oryct)
• Bones, fur, fish-scale – in predators
– Knotted plant elements (phytotrichobezoars)
• Straw, barley chaff (horse, birds)
– Conglobates
• Undigested non-food fragments and foreign bodies
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 Zootrichobezoar in stomach, swine Zootrichobezoar in stomach, swine

Phytotrichobezoars
Phytotrichobezoar in large intestine

barley chaff bezoar, pig

Conglobates

Conglobate in the gizzard of day-old poultry

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 Pseudoconcretions formed from eggs Pseudoconcretion from eggs

• Multifactorial disease
– The egg gets stuck in the oviduct
– new eggs are also formed
– abnormal decomposition of the eggs start
– fibrin accumulates between the eggs
– results in inflammation
– the wall of the oviduct gets reconstructed…..

Consequences

• Local irritation
• Pressure
– resulting in atrophy, necrosis, ulceration
• Narrowing, impacting the lumen of the organ
– painful spasm
– ileus
• Causing disorders of the passage
– obstruction, gas accumulation (tympany)

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