Diseases caused by parasitesThe parasitic diseases are classified into 2 categories:

I-Diseases cased by Protozoa.II-Diseases caused by Helminths and Arthropods.

N.B:Infestation: Parasitic invasion to the body organs without

multiplication and may be decreased.Infection: Invasion and multiplication of microorganisms in the body

tissue.Inoculation: Introduction of microorganisms or other substance in the

body tissue.

I-Diseases caused by protozoaProtozoa: They are single-celled eukaryotic animals. Classification of the Protozoa:Kingdom: Protista.Subkingdom: Protozoa.

The protozoa are divided into 2 main phyla that divided into subphylum.

PhylumSarcomastigophoraCiliophoraSubphylum1-Mastigophora

2-Sarcodina3-Apicomplixa (sporozoa)

4-Microspora

It is protozoa with cilia for locomotion e.g. Blantidium

Definitions:Mastigophora: Protozoa with one or more flagella (Giardia, Trichomonas).Sarcodina: Protozoa with pseudopodia for locomotion e.g. Entameba.Apicomplixa: Protozoa without locomotor organs and produce spores at the end life span. They are either:

A-Coccidia: It has direct life span e.g. Eimeria, Isospora.B-Hemospordia: It has indirect life span (has IMH) e.g.

Babesia, Thileria.Microspora: Protozoa have unique spores with 1–6 polar filaments e.g. Encephalitozoon.

Tissue response in protozoan infection1-Necrosis and degeneration due to production of toxic substances.

2-Tissue damage due to activation of complement system through immediate hypersensitivity type II as in African trypanosomiasis

3-Granulomatous inflammation and caseous necrosis results from cellular immunity due to intracellular invasion of some protozoa as in

case of leishmaniasis  4-Vasculitis results from formation of immune complex which deposit

under the endothelial lining in kidney and other tissue.

CoccidiosisDefinition: It is a disease caused by Eimeria or Isospora. There are 3 types:1-Enteric Coccidiosis: characterized by dysentery, dehydration and death.

2-Hepatic Coccidiosis: It is usually in rabbits less than 3 months old and characterized by enlarged abdomen and obstructive jaundice.

3-Renal Coccidiosis: in young geese and caused by Eimeria truncate or in equine, mice and guinea pigs and caused by Klossiella species.

Pathognomonic Lesions:Enteric Coccidiosis:In Schizogony Stage:

1-The intestine is hemorrhagic and eroded or ulcerated.2- Excessive epithelial necrosis.

3-Petecial hemorrhages and pin point white foci are seen the serosa, particularly with large schizonts.

4- Hemorrhagic cores in the cecum of chickens.5- Coccidia in various stages (schizogony and gametogony) are adjacent

to hemorrhagic and eroded areas.6- Villous atrophy as a result of loss of epithelial cells.

7-The schizonts are oval and with basophilic banana-shaped merozoites.In Gametogenesis:1-Regeneration and hyperplasia of the lining epithelium.2-lymphocytes and plasma cells infiltrations (predominant).3-Developmental stages of Eimeria (macro and micro gametes).

Hepatic Coccidiosis: (in rabbits less 3 months old):1-The liver is yellowish and severely enlarged. 2-Adenomatous hyperplasia in the lining epithelium of bile ducts. 2-developmental stages of E. stiedae are detected.3-lymphocytes and plasma cells infiltration are seen in the portal areas.Renal Coccidiosis: (in young geese).1-Developmental stages of Eimeria truncate in the epithelial cells of convoluted tubules without inflammation.2- Slight destruction of the renal epithelial cells.3-The protozoan maybe hyalinized and shed in the lumen of the tubules.NB: Klossiella1-Tiny gray foci on cortical surface of the kidneys.2-These foci are areas of necrosis.3- Perivascular infiltration of lymphocytes and histiocytes.4-An increase of interstitial fibroblasts.5-Numerous sporoblasts and sporocysts in the tubular epithelium.

TypesSchizogonyGametogony1-EntericIntestinal epitheliumIntestinal epithelium

2-HepaticBile duct epitheliumBile duct epithelium

3-RenalGlomerular epithelium (BC) and endotheliumTubular epithelium

4-Klossiella

NB:Sporogony: It is the sporulation of the oocysts outside the host

(formation of sporocysts).In Rabbit: The sporozoites reach the bile ducts via the portal veins or

lymphatics.In sheep and goats: The Eimeria are found in the gallbladder and

mesenteric veins.

Organ : Chicken digestive tract Disease : Coccidiosis.Macro : Inflamed small intestine due to Eimeria nicatrix (left), and inflamed ceca due to Eimeria tenella (right).

Organ : Ceca of chicken.Disease : Coccidiosis (Eimeria tenella-experimental infection).Macro : Inflamed, hemorrhagic and necrotic ceca.

Organ : Small intestine (cross-section).Stain : H&E.Disease : Coccidiosis (Eimeria nicatrix).Micro : Extensive hemorrhage and necrosis.

Organ : Small intestine of a chicken.Stain : H&E.Disease : Coccidiosis (Eimeria nicatrix).Micro : A higher magnification to show the numerous schizonts, hemorrhage and necrosis in submucosa.

Organ : Small intestine of a chicken.Stain : H&E.Disease : Coccidiosis (Eimeria nicatrix).Micro : Mature schizonts containing merozoites.

Organ : Small intestine of a chickenStain : H&E.Disease : Coccidiosis (Eimeria nicatrix).Micro : Microgammonts containing microgametes.

Organ : Kidney of goose.Stain : H&E.Disease : Coccidiosis (EImeria truncata).Micro : Gamonts in tubular eoithelial cells.

Organ : Kidney of a goose.Stain : H&E.Disease : Coccidiosis (Eimeria truncata).Micro : A higher magnification of gamonts.

Organ : Liver of a rabbit.Stain : H&E.Disease : Hepatic coccidiosis.Micro : Dilated bile-duct due to Eimeria stiedae.

Organ : Liver of a rabbit.Stain : H&E.Disease : Hepatic coccidiosis.Micro : A high magnification to show numerous macrogamonts of Eimeria stiedae in epithelium of bile-duct.

Organ : Kidney of a horse.Stain : H&E.Disease : Klosiellosis.Micro : Young budding sporont, sporont with radiating sporoblasts and mature sporocyst within tubular epithelium.

ToxoplasmosisDefinition: It is acute or chronic disease of cats (definitive host),

mammals and birds (IMH).Causes: Tissue phase of Toxoplasma gondii.

NB: The infective stage is the oocysts or tissue containing bradyzoites or tachyzoites. The tachyzoites can cross the placenta and pass with milk

and semen.Endodyogony: The tachyzoites of toxoplasma multiply by internal

budding into 2 organisms.Endopolygony: The tachyzoites of toxoplasma multiply by internal

budding into several organisms.Parasitemia: It the circulation of parasite in the blood as toxoplasma.

Pathognomonic Lesions:In Definitive Host (Cats): They are similar to coccidiosis (enteric type).

1-Necrosis of the submucosal lymphoid follicles and ulceration.2-Sexual and asexual developmental stages are seen in the lining epithelium.

3-Large granulomatous nodules in muscularis. They are consisted ofi-Tachyzoites

ii-Excessive granulation tissues.iii-Macrophages, lymphocytes and plasma cells infiltrations.

In IMH (mammals and Birds):Brain:

1-Diffuse non-suppurative meningoencephalitis. It is characterized by mononuclear cell infiltration and leukoencephalomalacia.

2-Tachyzoites (crescentic or round bodies) inside the neurons and astrocytes.3-Tissue cysts (containing more than 50 bradyzoites without inflammatory

cells.4-Small areas of necrosis and calcification.

Liver:1-Focalcoagulative necrosis.

2-Tachyzoites inside the hepatic and kupffer cells.3-Tissue cysts containing bradyzoites are seen.

Lungs:1-Small gray (tumor-like) nodules on the lungs.

2-Tachyzoites inside the type I and II pneumocytes and bronchial epithelium.

3-Focal necrosis with alveolar fetalization or pulmonary adenomatosis.4-Lymphocytes and macrophages infiltration and inside the alveoli.

Lymph nodes:1-The regional Lns are enlarged, firm and congested.

2-Focal necrosis.3-Tachyzoites inside the endothelial cells of veins.4-Hyperplasia of the lymphocytes and REC.

Myocardium:1-Tachyzoites inside the cardiac muscles. 2-Round cells infiltration.

Placenta:1-Focal necrosis and calcification.

2-Tachyzoites are seen free or inside the trophoblasts.3-Abortion with or without invasion of fetus.

4-The affected fetus show brain lesions.Eye:

1-Granulomatous chorioretinitis (choroid and retina) characterized by infiltration with macrophages and lymphocytes.

NB:Hammondiasis: Hammondia hammondi It is a non-pathogenic coccidian of cats similar to T. gondii. Its life cycle and structure are essentially as those of T. gondii with the following exceptions:

1-It has no extraintestinal cycle in cat and dogs (definitive hosts). 2-intermediate hosts (rodents) infected only by ingestion of oocysts

3-The tachyzoites proliferate in the lymphoid cells and the bradyzoites are limited in skeletal and cardiac muscles (forming tissue cysts, as in toxoplasma).

Organ : Small intestine of a cat.Stain : H&E.Disease : Txoplasmosis.Micro : Numerous asexual and sexual stages in epithelial cells with

microgamont in cell and meront in cell

Organ : Brain of mouse.Stain : PASH.Disease : Toxoplasmosis.Micro : Four cysts with PAS-positive bradyzoites.

Organ : Skeletal muscle of mouse.Stain : PASH. Disease : Hammondosis.Micro : Hammondia hammondi cyst.

Neosporiasis:Neospora caninum affects the dogs of all ages (definitive host) and

similar to toxoplasma in the IMH (cattle, sheep, goats, horses, dogs, and deer); the wall of the cyst is thicker and only found in CNS.

Pathognomonic Lesions: 1-Multifocal non suppurative necrotizing encephalomyelitis.

2-Focal gliosis, lymphoid cuffing, and hydrocephalus.3-Numerous tachyzoites found in the brain of aborted feti.

4-Tissue cysts containing bradyzoites are detected in cerebrum.5-Periportal hepatitis with focal hepatocellular necrosis.

6-Focal non-suppurative myocarditis.7-The placenta show focal necrosis, tachyzoites and neospora cysts.

Caryospora:It affects the dogs and causes pyogranulomatous dermatitis and

lymphadenitis.

Organ : Brain of aborted bovine fetus.Stain : H&E.Disease : Neosporosis.Micro : A focus of central necrosis, surrounded by inflammatory cells.

Organ : Spinal cord of a congenitally-infected bovine-calf.Stain : H&E.Disease : Neosporosis.Micro : A thick-walled tissue-cyst in a neuron.

SarcosporidiosisIt is a disease characterized by tubular cysts in the striated muscles.

Causes: Sarcocystis species or Balbiania gigantica in the tongue and esophagus of sheep.Intestinal Stage: Isospora (in final host).

Tissue Phase: Sarcocystis (in IMH).Pathognomonic Lesions:

1-Numerous intact Sarcocystis in the cardiac and skeletal muscles without inflammatory reactions.

2-These cysts are variable in sizes with clear or hyaline wall and contain strongly basophilic crescentic bradyzoites.

3-Hyaline degeneration, eosinophilic polymyositis and Zenker’s necrosis are seen in some heavily parasitized muscles.

4-The ruptured cysts stimulate granulomatous reactions.5-Focal leptomeningitis, non suppurative encephalitis, pneumonia, keratitis and

abortion are recorded in cattle, sheep and goats due to multiplication of the merozoites in the endothelial cells of blood vessels and induce vasculitis, thrombosis and necrosis of all tissue including placenta (abortion). The

placentas were thickened and edematous, and the caruncles were atrophied. 6-Enlargement of the superficial cervical lymph nodes, serous atrophy and

edema of the body fat, hydrothorax, hydropericardium and ascites are found.

Organ : Trachea of sheep. Disease : Sarcosporidiosis.Macro : Large sarcocysts.

Tissue : Muscle of bird.Disease : Sarcosporidiosis.Macro : Large sarcocysts.

Tissue : Placental lamina propria of a cow.Stain : H&E..Disease : Sarcosporidiosis.Micro : Numerous free and intracellular merozoites, and immature meronts in area of necrosis.

Organ : Heart of a calf.Stain : H&E.Disease : Sarcosporidiosis.

Micro : Immature sarcocyst, containing globular immature metrocytes.

Tissue : Bovine mesenteric artery.Stain : H&E.Disease : Sarcosporidiosis.Micro : Multinucleated first generation meront of

S. bovifelis) protruding into lumen

Organ : Tongue of a calf.Stain : H&E.Disease : Sarcosporidiosis.Micro : Numerous basophilic mature intramuscular and microscopic sarcocysts.

Tissue : Esophageal muscle.Stain : H&E.Disease : Sarcosporidiosis.Micro : Thick-walled sarcocyst of Sarcocyctis .

BesnoitosisCauses: Besnoitia besnoiti similar to Sarcocystis.

Pathognomonic Lesions:1-The skin is thick, wrinkled and hairless on legs, thighs and scrotum.

2-Large cysts containing spores in the wall of small blood vessels of skin and upper GIT.

3-Granulomatous reactions around the rupture cysts.4-These cysts may present in cardiovascular system e.g.

Antelopes: in jugular vein and veins of limbs.Impala: in S/C lymphatics and endocardium.

Enigmatic bodies: It is membrane-bounded spindle bodies with electron-dense core in the tachyzoites of Besnoitia.

Organ : Hind leg .Disease : Besnoitiosis.Macro : Numerous white raised subcutaneous cysts of Besnitia.

Organ : Skin of an ox.Stain : H&E.Disease : Besnoitiosis (globidiosis).Micro : Numerous cysts of Benoitia besnoiti in dermis.

Tissue : Jugular vein.Stain : H&E.Disease : Besnoitiosis.Micro : Numerous Besnoitia sp. cysts protruding into lumen.

Organ : Spleen.Stain : H&E.Disease : Besnoitiosis.Micro : Numerous cysts of Besnoitia sp.

CryptosporidiosisIt is a protozoal disease of most domestic and wild animals, birds, fish

and reptiles which caused by Cryptosporidium parvum. Pathognomonic Lesions:

1-Small basophilic organisms on the villi or embedded inside the enterocytes of the small intestine, colon and abomasum.

2-Atrophy and fusion of intestinal villi besides dilation of crypt. 3-The lamina propria is infiltrated with lymphocytic.

4-The parasite is stained by Giemsa or cold Ziehl-Neelsen stains.Encephalitozoonosis

(Nosematosis)It is a subclinical protozoal disease of human, rabbits, dogs and some

laboratory animals. It causes encephalitis, hepatitis and nephritis.Causes: Encephalitozoon caniculi.

Pathognomonic Lesions:1-Large areas of necrosis at cerebral cortex.

2-The parasites (Encephalitozoon) in parasitophorous vacuoles.3-Granulomatous reaction (Epithelioid cells and macrophages) around

the necrosis.

4-Perivascular lymphocytic cuffing.5-Chronic non-suppurative nephritis and focal hepatitis characterized

by granuloma and small focal scar with presence of the parasites.6-Myocarditis and vasculitis are seen.

PneumocystosisThe protozoa (Pneumocystis carinii) are found in the lungs of many

mammals, including humans and under immunosuppressant conditions.

Pathognomonic Lesions:1-The alveoli are filled with pink frothy material with the organisms.

2-The cysts are round, cup-shaped or crescentic with a thick wall.3-Each cyst contain contains 8 sporozoites.

4-Osteomyelitis in immunosuppressant human.4-The trophozoites are best visualized with Giemsa stain and the cyst-

stage with PAS stain.

Organ : Intestine.Stain : H&E.Disease : Cryptosporidiosis.Micro : Numerous developmental stages of Cryptosporidia.

Organ : Lung of horse. Stain : H7E.Disease : Pneumocystosis.Micro : Pneumocystis sp. in the lungs.

Organ : Lung of a horse.Stain : Gomori methanamine silver (GMS).Disease : Pneumocystosis.Micro : Numerous darkly-stained ovoid organisms.

Encephalitozoonosis: Brain necrosis and perivascular cuffing

Encephalitozoonosis: Brain smear to show the trophozoites

Encephalitozoonosis: Kidney with multifocal nephritis

Organ : Kidney of rabbitStain : Brown and Hopps tissue gram-stain.Disease : Encephalitozoonosis.Micro : Dark-stained immature spores.

Encephalitozoonosis: Liver with multifocal hepatitis

Organ : Liver.Stain : PAS.Disease : Encephalitozoonosis.Micro : Visible polar granule in each spore.

Organ : Muscle.Stain : Ziehl Nielsen acid-fast stain.Disease : Encephalitozoonosis.Micro : Dark-blue stained annular rings, and red-stained

(acid-fast) mature spores.

AmebiasisIt is protozoal disease of human and non-human primates and induces

severe dysentery. Causes: Entameba histolytica and Entameba bovis.

Pathognomonic Lesions:1-Flask-shape ulcers containing trophozoites in the intestinal mucosa.

2-Amebic abscesses (liquefactive necrosis without leukocytes) in the liver and brain.

3-The lamina propria and submucosa show necrotic intestinal crypts and lymphocytic infiltrations.

 NB: Amebic Meningoencephalitis (Naegleria; Acanthamoeba; Hartmannella)

1-Naegleria (N. fowleri): It induces purulent, hemorrhagic or necrotic meningoencephalitis (gray matter).

2-Acanthamoeba: It induces granulomatous encephalitis around the protozoa (microglia cells).

Preparation : Human fecal smear.Stain : Iron hematoxylin.Disease : Amoebiasis.Micro : Trophozoit of Entamoeba histolytica with small endosome and chromatin plaques at

periphery of nucleus.

Organ : Intestine of monkey.Stain : H&E.Disease : Amoebiasis.Micro : Trophozoite of Entamoeba histolytica

Organ : Heart of a dog.Stain : H&E.Disease : Amoebiasis.Micro : Trophozoite of Acanthamoeba sp.

With large dark endosome.

Organ : Brain of experimentally-infected mouse.Stain : H&E.Disease : Amoebiasis.Micro : Trophozoites of Acanthamoeba culbertsoni

with large endosome.

Organ : Brain of experimentally infected monkey.Stain : H&E.Disease : Amoebiasis.Micro : Trophozoit of Naegleria fowleri with large endosome.

GiardiasisIt is a protozoal disease affecting the small intestine and colon of

human and animals without clinical signs (may induce chronic diarrhea).

Causes: G. bovis, G. cati, G. canis, G. muris.Pathognomonic Lesions:

1-Minimal villous atrophy (stunting of the villi).2-Leukocytic infiltration in the lamina propria.

3-Presence of the parasitic trophozoites or cysts on the epithelial surface.

BalantidiasisBalantidium coli are naturally inhabitant of the digestive tract of

animals. The organisms may invade the intestinal mucosa, penetrating into the submucosa, localized particularly in lymphoid nodules.

Extraintestinal spread to mesenteric lymph nodes, liver, pleura, lungs and urogenital tract is reported. Balantidiasis as well as amebiasis is

characterized by diarrhea in calves. Enteritis, peritonitis, pneumonia and lymphadenitis are seen associated with balantidium trophozoites.

Organ : Small intestine of canary.Stain : H&E.Disease : Giardiasis.Micro : A higher power to show trophozoites of Giardia

sp.attached to intestinal villus.

Preparation : Human fecal smear.Stain : Iron –hematxylin stain.Disease : Giardiasis.Micro : Trophozoites of Giardia lamblia with two nuclei.

TrichomoniasisIt is a protozoal disease affecting cattle (bovine trichomoniasis) and

poultry (avian Trichomoniasis), and caused by the family trichomonadidae.

I-Bovine Trichomoniasis: It is venereal disease (transmitted by coitus and artificial insemination), caused by Trichomonas fetus. The

organisms live in preputial cavity of bull and vagina and uterus of cow.Pathognomonic lesions:

1-Vaginitis, endometritis (closed pyometra) and placentitis2-Early abortion (in the first half of pregnancy).

3-Pyogrnaulomatous bronchopneumonia with multinucleated giant cells in the aborted fetus.

4-In bull: Balanoposthitis, seminal vesiculitis and epididymitis.II-Avian Trichomoniasis: It is caused by Trichomonas gallinae and

affecting pigeons, turkey and chickens.Pathognomonic lesions:

1-Masses of caseated material in mouth, throat and crop.2-Necrosis and ulceration of crop.

3-Yellowish caseated nodules in the liver.

Preparation : Fecal smear of guinea pig.Stain : Protargol stain.Disease : Trichomoniasis.Micro : Trophozoites of Trichomonas with

undulating membrane and large single nucleus.

TrypanosomiasisIt is exotic disease that occurs only in tropical Africa, India, and other far-off places. This disease is most serious in humans and animals and

transmitted by arthropods, which act as biological vectors (IMH).Specific infectionCausesAffecting animals

1-DourineT. equiperdumEquines (by coitus)

2-Nagana (Tsetse-fly disease)

T. vivax, T. congolense and T. brucei

Cattle Horse, camels and dogs.

3-SurraT. evansiHorse (by horse fly).

4-Mal de CaderasT. equinumEquines

5-Chagas diseaseT. cruziHuman (by kissing bug)

Pathogenesis and Clinical Signs:The pathogenesis of trypanosomiasis is based upon the presence of the

parasites in the blood circulation, where they block capillaries, causing edema and hemolyze the erythrocytes, inducing anemia besides fever

during parasitemia, incoordination (obstruction to flow of CSF), coma and death.

Pathognomonic lesions:A-Nagana: (Tsetse-fly disease):

I-Acute form: It characterized by sudden deaths with excessive hemorrhages.

II-Chronic form:1-Emaciation and serous atrophy of fat.

2-The protozoa are detected in the blood.3-Hemosiderosis in the spleen and liver, which become enlarged.

4-Hemorrhages on pericardium and endocardium.5-Hydropericardium.

6-The lymph nodes are swollen and edematous.B-Dourine: (venereal disease, transmitted by coitus).1-Ulceration (ulcerous plaques) in the genitalia and skin.

2-Edema in the genital tract and lower abdomen.3-The protozoa are seen in the lesions (genitalia)

4-Mononuclear or granulomatous reaction.C-Surra: (transmitted by horsefly).

1-Emaciation with patches of alopecia and serous atrophy of fat.2-Edema in the lower abdomen, limbs and thorax.

3-Hemosiderosis and icterus (hemolytic type).4-Petichiae and ecchymoses on visible mucous membranes.

D-Chagas disease: (transmitted by kissing bugs).The lesions are seen in different organs and amastigotes (trypanosomes)

are found in the blood and other body fluid as well as free in tissues.1-The site of bite:

-hard, red, painful and edematous mass.-T. cruzi (leishmanial form) are present in the lesions.

2-Lymph nodes and Spleen:-Enlarged (due to hyperplasia of lymphoid tissues) and edematous.

-Intense histiocytes and giant cells proliferation contain T. cruzi.-Microabscesses may be seen.

3-Heart:-Hydropericardium and severe myocarditis (due to penetration of the protozoa

the cardiac muscle fibers) which accompanied with chronic general passive hyperemia.

4-Brain:-Non-suppurative meningoencephalitis, characterized by:

i-Edema and congestion of meninges. ii-Perivascular lymphocytic cuffing and gliosis.

5-Testes:-Interstitial lymphocytic infiltration.

-The cytoplasm of the lining epithelium contained leishmanial form.

Trypanosomiasis

Tissue : Peripheral blood-smear from infected mouseStain : Giemsa stain.Disease : Trypanosomiasis.Micro : Trypomastigotes of Trypanosoma brucei.

Organ : Heart of dog.Stain : H&E.Disease : Trypanosomiasis.Micro : Amastigotes of Trypanosoma cruzi.

Organ : Heart of a dog.Stain : H&E.Disease : Trypanosomiasis.Micro : Amastigotes of Trypanosoma cruzi, each

with a large basophilic kinetoplast.

Trypanosomiasis in brain

LeishmaniasisVisceral and cutaneous Leishmaniasis are recorded in animals and caused by

Leishmania species. The disease is transmitted by sand flies.Causes: Leishmania donovani, L. tropica and l. braziliensis.

Pathognomonic Lesions: leishmaniasis is divided into three major forms:i-Visceral Leishmaniasis: (Kala-azar, Dum dum fever):

1-Severe emaciation and anemia (pallor mucous membranes).2-The bone marrow become soft, red and heavily infiltrated with macrophages

contained the protozoa.3-All viscera (lymph nodes, spleen and liver) are enlarged and massively

infiltrated with lymphocytes and macrophages whose cytoplasm is filled with leishmaniae.

4-Ulceration of the intestine and immune complex glomerulonephritis.ii-Cutaneous Leishmaniasis:

1-Multiple nodules or ulcers of the skin that heal spontaneously by fibrous tissue proliferation.

2-The dermis is infiltrated with macrophages accompanied by lymphocytes, plasma cells and rarely eosinophils.

3-Numerous parasites are present within the macrophages.iii-Mucocutaneous Leishmaniasis: It is similar to cutaneous form but the

lesions (chronic ulcers) occur at mucocutaneous junction or oral and nasal mucosa.

MalariaCauses: Plasmodium species (P. vivax, P. falciparum, …….).

Pathogenesis and Clinical Signs:Two hosts are required:

1-Vertebrates (human or animals): in which schizogony takes place in erythrocytes and other cells.

2-Invertebrate blood-sucking insects (mosquitoes): The life cycle is started when a female mosquito penetrates the skin of vertebrate host,

introducing sporozoites into the peripheral circulation. The macro- and microgametocytes ingested by female mosquitoes are developed (in the stomach) into sporozoites which released into the hemolymph and then migrated to salivary glands of mosquito. From this site, the sporozoites are available to infect a new vertebrate host when the female mosquito

takes her blood meal.Pathognomonic Lesions:

1-The destruction of parasitized erythrocytes (hemolysis and anemia).2-Marked hepatosplenomegaly resulting from congestion, hemorrhage,

hyperplasia of REC, which contains the protozoa.3--The erythrocytes show the parasites.

4-Hemozoin (brown pigments) is seen in tissue.5-Brain hemorrhages

6-Thrombi and the blood vessels occluded with parasitized RBCs.7-Multiple infarcts in the liver and affected organs.

8-Chronic immune complex glomerulonephritis.Hepatocystis

It is plasmodial protozoa, live in the erythrocytes of monkeys, particularly in tropical countries in Africa and Asia.

Causes: Hepatocytis kochi, H. bouillezi, H. cercopitheci, H. simiae,Pathognomonic Lesions:

1-The liver show large cysts contain merozoites (called merocysts) with or without tissue reaction.

2-The most frequent reaction is granulomatous (giant cells and macrophages besides few lymphocytes).

3-The parasites (trophozoites, macro- and microgametes) are seen in the erythrocytes and hemozoin (malarial pigments) in the

tissue.

HepatozoonHepatozoon (H. canis) infect rodents, canines and others and

transmitted by arthropods. Schizonts found in the spleen and liver and the gametocytes in leukocytes of such vertebrates. Gametes

released in the invertebrate gut and undergo fertilization to form an ookinete, and then undergo sporogony to form sporozoites. In

the vertebrate host, release of sporozoites and penetrate the intestinal wall to bloodstream and then to liver and other organs.

Pathognomonic Lesions:1-Emaciation and anemia (pallor mucous membranes).

2-Splenomegaly and hepatomegaly due to extensive reticuloendothelial cell hyperplasia.

3-Focal necrosis with cellular infiltrations in the affected organs.

Preparation : Blood-smear from a starling;Stain : Giemsa stain.Disease : Plasmodiosis.Micro : Gamont of Plasmodium reluctum.

Preparation : Blood-smear from a starling;Stain : Giemsa stain.Disease : Plasmodiosis.Micro : Gamont of Plasmodium reluctum.

Organ : Lung of a penguin’Stain : H&E.Disease : Plasmodiosis.Micro : Exoerythrocytic scizont of Plasmodium sp.

Tissue : Endothelial cell of turkey-brain.Stain : H&E.Disease : Plasmodiosis.Micro : Exaerythrocytic schizont of Plasmodium durae.

Preparation : Endothelium of turkey-brainStain : H&E.Disease : Plasmodiosis.Micro : Releasing of merozoites from schizont of Plasmodium durae.

Malaria: Hemozoin in kupffer cells

Organ : Liver of a monkey.Stain : H&E.Disease : Hepatocystosis.Micro : Merocyst of Hepatocystis sp.

Organ : Liver of a monkey.Stain : H&E.Disease : Hepatocystosis.Micro : A high magnification of merocyst to show formation of merozoites.

Organ : Liver of a monkey.Stain : H&E.Disease : Hepatocystosis.Micro : A higher magnification of merozoit-formation in the wall of a merocyst.

Organ : Liver of boa constrictor.Stain : H&E.Disease : HepatozoonMicro : Developing schizont of H. sp.

Organ : Spleen of a dog.Stain : H&E.Disease : Hepatozoon.Micro : Developing schizont of H. canis.

Preparation : Blood-smear from a dog.Stain : Giemsa stain.Disease : Hepatozoon.Micro : Macrogamete or microgametocyte of H. canis in neutrophil.

Babesiosis(Piroplasmosis, Cattle tick fever, Red water fever)

Babesiosis is an infectious disease caused by intra-erythrocytic protozoan parasite, usually transmitted by ticks (IMH) and is capable of producing acute febrile and sometimes fatal infection.

Causes: B. bovis, B. bigemina, B. major and B. divergens. Pathogenesis and Clinical Signs:

The organisms live in erythrocytes and lead to intravascular hemolysis inducingIn early stage: the mucous membranes are pale (severe anemia).

In the terminal stages: the mm become yellow (severe jaundice), hemoglobinuria (red water disease and Hb nephrosis) and ascites are seen. Incoordination, mania,

convulsions, paraplegia and coma are observed due to thrombosis (DIC). Pathognomonic Lesions:

1-Emaciation of carcass with presence of ticks on the skin and serous atrophy of fat.

2-The blood is watery (anemia) with red plasma.3-Icterus is described as yellow mucous membranes.

4-The gallbladder is overdistended with dark green bile.5-The liver and spleen are enlarged (presence of hemosiderosis).6-Centrolobular hepatic necrosis (due to hypoxia from anemia).

7-The urinary bladder contains red urine (hemoglobin-urea).8-Hb nephrosis 9-Hydro-thorax - peritoneum – pericardium.10-Focal hemorrhages, thrombosis, and necrosis in the brain.

Preparation : Blood-smear.Stain : Neitz stain.Disease : Babesiosis.Micro : Intraerythrocytic Babesia sp.

Babesiosis: Hemorrhages on the brain

Babesiosis: Thrombosis in the b.v. of brain

Babesiosis: Hemorrhagic enteritis

Babesiosis: Splenomegaly

Theileriasis(Turning Disease, East Coast Fever)

Theileriasis is a hemoprotozoal infection, like Babesia, responsible for high mortality among native and imported cattle and caused by protozoan parasites of the genus

Theileria and transmitted by ticks.Causes: T. anulata (in Egypt), T. parva, T. mutans.

 Pathogenesis and Clinical Signs:Theileria, after inoculated by ticks, invaded the lymphocytes and histiocytes, first in

regional lymph nodes, then throughout all lymph nodes, spleen, liver and circulating cells. Macroschizonts (Koch’s blue bodies) and microschizonts are detected in these cells.

Released micromerozoites from the microschizonts could parasitize the erythrocytes. Fever, rough hair coat, anemia, emaciation, delirium and coma (called turning disease) are observed. Bloody diarrhea, hemoglobinuria, jaundice and corneal opacity are seen.

Pathognomonic Lesions: 1-severe emaciation of carcass.

2-All body lymph nodes are enlarged, edematous and hemorrhagic.3-The spleen is enlarged.

4-Koch’s blue bodies (macroschizonts, contain 8 or more nuclei) are seen in the lymphocytes in lymph nodes, spleen and blood.

5-Some blood vessels may be occluded with parasitized lymphocytes, producing thrombosis and infarction in the brain (turning disease).

6-Hydrothorax and Hydropericardium.

Theileriasis: Splenomegaly and lymphadenitis

Theileriasis: Hemorrhages and infarction in brain

Preparation : Blood-smear.Stain : H&E.Disease : Theileriasis.Micro : Trophozoites of Theileria in erythrocytes.

Tissue : Splenic artery .Stain : H&E.Disease : Theileriosis.Micro : Schizonts of Theileria, occluding lumen.

Organ : Lung.Stain : H&E.Disease : Theileriasis.Micro : Macrophage containing schizont of Theileria that seems to bud from endothelium of pulmonary vein.

Organ : Lung.Stain : H&E.Disease : Theileriasis.Micro : Pulmonary vessel with three developing schizonts.

Organ : Lung.Stain : H&E.Disease : Theileriosis.Micro ; Pulmonary vessel with developing and mature stages.

Organ : Kidney.Stain : H&E.Disease : Theileriasis.Micro : Capillary of a glomerular tuft with schizony.

Theileriasis: Hepatic necrosis and schizonts among hepatocytes

DiseasesSchizogony stageGametogony stage

ToxoplasmosisIntestinal epithelium of cats

Intestinal epithelium of cats Tachyzoites in tissue cells (IMH)

Bradyzoites in tissue cyst (IMH)

NeosporiasisIntestinal epithelium of dogs

Intestinal epithelium of dogs Tachyzoites in tissue (IMH)Bradyzoites in tissue cyst (IMH)

HammondiasisIntestinal epithelium of dogs

Intestinal epithelium of dogs Tachyzoites in lymphoid (rodents)

Bradyzoites in tissue cyst in cardiac and skeletal muscles (rodents)

CaryosporiasisIntestinal epithelium of rodentsIntestinal epithelium of rodents

BesnoitosisCysts contain spores in b. vs., skinTachyzoites in tissues

SarcosporidiosisIsospora in definitive host (intestine)Isospora in definitive host (intestine)

Sporozoites in endothelium (IMH)

Bradyzoites in sarcocystisCryptosporidiosisBoth are seen in intestinal epithelium of mammals and birds

TheileriasisIn lymphocytes, erythrocytes, macsIn ticks

BabesiosisIn erythrocytesIn tick

II-Diseases Caused by Helminths and ArthropodsThe parasitic helminths are classified into 3 phyla:

A-Phylum Platyhelminths (Flatworm): e.g. Trematodes (Flukes).

Cestodes (Tapeworms).B-Phylum Nemathelminths:

e.g. Nematodes (roundworms).C-Phylum Acanthocephala:

e.g. Thorny-headed worms.Pathological changes associated with helminths infection:

1-Mechanically interfere with functions:i-Obstruct blood or lymph vessels.

ii-Obstruct ducts or tracts (intestine).iii-Attach to or use functional tissue.

iv-Act as foreign bodies and displaces the normal structures.2-Invade and destruct the tissue and cells.

3-Devour blood and cause anemia.4-Devour tissues of hosts.5-Secrete toxic products.

6-Introduce bacteria or other infections.7-Induce neoplasms.

NB:The eosinophils play a major role in the body defense against helminths besides the

basophils and mast cells.

AscariasisThe ascarids, among the most common intestinal parasites of young animals, can cause digestive disturbance, enteritis and poor growth. Causes: Species of AscaridDefinitive hosts

Toxocara lumbricoides (suum)Human and swineToxocara canisDog

Toxocara catiCat, lion, leopardToxocara leonineDog, cat, lion, tiger, fox

Toxocara vitulorumCattleParascaris equorum

Ascaridia galliEquine

Chickens and turkeys

NB: Ascarid infection is rare or not present in sheep and goat.The life cycle of ascarids has 3 types of migration:

1-Tracheal migration: When the embryonated eggs containing L2 are ingested and they hatched (in the stomach and intestine) to second-stage larvae. These

larvae penetrate the intestinal wall and enter the portal vein and invade the hepatic parenchyma, where they may molt to third-stage larvae. Thereafter,

these larvae enter the general circulation to reach the lungs, bronchi, and trachea and then swallowed to intestine. In the intestine, two additional molts

occur before maturation to adult worms.

2-Intestinal migration: The second-stage larvae penetrate the intestinal wall and do not migrate further. They undergo their molts here and reenter

the lumen as fourth-stage larvae, which mature to adults.3-Somatic Migration: (Visceral Larva Migrans). It is the migration of the

ascarids larvae in paratenic hosts (abnormal hosts) without formation of adults in the intestine. When the larvae reach the general circulation, they invade all body tissues (brain, eyes, placenta, mammary gland and others) without further development. These larvae either pass with milk or across

the placenta to infect the newborn.Pathognomonic Lesions:In early stages (visceral larva migrans):1-The ascaris larvae are seen in the body tissues (liver, kidneys, lungs, heart, brain, spleen and others). 2-Several necrotic migratory tracks are represented by parasitic larvae embedded in cellular debris, extravasated erythrocytes and few leukocytes. 3-The degenerated larvae are seen inside granulomatous nodules consisting of eosinophils, giant cells, macrophages and lymphocytes. 4-Focal coagulative necrosis and hemorrhages. 5-The larvae are seen inside the portal blood vessels, bronchi and glomeruli.

In late stages (Adult):1-Numerous adult worms in the small intestine.

2-Catarrhal enteritis with eosinophils infiltrations.

3-Obstruction of the bile or pancreatic ducts with adult worms, producing obstructive jaundice.

4-Peritonitis due to penetration the wall of intestine.Ancylostomiasis

Hookworm diseaseHookworms are important parasites of mammals, and in some parts of

the world, they produce widespread disease in humans. They inhabit the small intestine and feed on blood producing anemia.

Causes: Ancylostoma species.Pathogenesis and Clinical Signs:The adult worms attach to the intestinal mucosa with hook like structures (hookworms) leading to hemorrhages and feed on blood with hypoproteinemia and anemia. There are two types of anemia: i-In acute phase is hemorrhagic (normocytic normochromic) ii-In chronic phase is iron-deficiency anemia (microcytic hypochromic).Pathognomonic Lesions:1-Hemorrhagic enteritis.2-The larvae or adult worms are seen in the intestinal lumen.3-Villus atrophy, round (blunt) and fuse together.4-Eosinophils infiltrations in the lamina propria.5-Severe dermatitis (creeping eruption, ground or water itch6-Pulmonary hemorrhages and pneumonia (due to larval migration).

Larva migrans in liver, kidney, lung, kidney brain

Adult Ascarides in intestine, make perforation, in bile duct and with milky spots on the swine liver

Ancylostomiasis (Hookworm): Hemorrhagic enteritis

NB: Creeping Eruption: It is severe dermatitis characterized by irregular

reddish patches or zigzag tunnels due to penetration the skin by Ancylostoma.Trichostrongyloidosis

I-Abomasal TrichostrongyloidosisAbomasal trichostrongyles are included Haemonchus, Ostertagia and

Trichostrongylus in the abomasum of sheep, goat and cattle.Causes: Trichostrongylus axei, Ostertagia ostertagi, Haemonchus placei (in

cattle) and H. contortus (in sheep and goats).Pathogenesis and Clinical Signs:

The lesions of Ostertagia spp. are produced by the developing larvae in the gastric glands, which lead to a rise in abomasal pH and a fall in the pepsin

concentration. The result is gastric dysfunction and diarrhea. The Trichostrongylus spp. is detected between the abomasal epithelium and

basement membrane, which induced chronic irritation with excessive mucus production. Meanwhile, the Haemonchus spp. (4th stage larvae and adults) are attached to the abomasal mucosa with their lancets (buccal teeth) and sucked

blood, leading to severe blood loss (induce anemia and hypoproteinemia).Pathognomonic Lesions:

A-Haemonchosis:1-Many blood clots or hemorrhages on the mucosa of the abomasum

(hemorrhagic abomasitis). 2-Free nematodes (Barber-pole or twisted stomach worms) on the mucosa.

3-The abomasal contents are reddish-brown. 4-Whitish nodules consist of worms, fibrous tissue and eosinophils.

5-Mucous membranes are pale (anemic). 6-Hydopericardium, hydrothorax, ascites and edema in submandibular space

(bottle jaw) are seen. 7-The body fat was edematous and gelatinous (serous atrophy of fat).

8-The liver was large, mottled and friable (due to fatty change). NB: Hypobiosis of larvae: During cold winter and hot dry seasons the larval development is arrested with the host. B-Ostertagiosis: cattle, sheep and goats.1-The abomasal mucosa is thick and granular (cobblestone appearance).2-Multiple nodules containing larvae and adult worms, giving morocco leather appearance. 3-These nodules are seen as a result of dilation of parasitized glands, which are covered by marked epithelial hyperplasia and mucinous degeneration. 4-The surrounding tissues are displaced by fibrous connective tissue. 5-Eosinophils and mononuclear cells in the lamina propria and around the nodules. 6-Focal areas of mucosal necrosis (ulceration).

C-Trichostrongylosis: Smallest type and invisible.1-Catarrhal abomasitis characterized by i-Greatly inflamed, congested mucosa with thick mucus. ii-Mucinous degeneration.iii-Hyperplasia and desquamation of lining epithelium.iv-Eosinophils infiltrations.2-Presence of the parasites which extended to the small intestine.3-Catarrhal enteritis with edematous and congested mucosa.4-Erosions and villous atrophy with increased goblet cells. 5-Loss of chief, zymogene and parietal cells leading to achlorhydria.

II-Intestinal Trichostrongyloidosis:They included Cooperiosis and Nematodiriosis that parasitize the upper small

intestine of cattle, sheep and other ruminants. Causes: Cooperia punctata, Nematodirus spathiger and N. filicollis.

Pathogenesis and Clinical Signs:Cooperia and Nematodirus species are found on the intestinal villi, inducing

villous atrophy, reduction in disaccharase and alkaline phosphatase activities in the mucosa. Thus, inappetence, weight loss and diarrhea are seen.

Pathognomonic Lesions:1-Irregular patches of mucosal atrophy with atrophic villi. 2-The intestinal glands are dilated with mucus containing the parasite. 3-Erosions of the mucosa and leukocytic infiltration of the lamina propria.

ChabertiidasisThis family Chabertiidae included the genera Oesophagostomum and Chabertia, which is similar to gastrointestinal nematode infestation.Causes: Oesophagostomum radiatum, O. venulosum and Chabertia ovina.Pathogenesis and Clinical Signs:

The larvae of these parasites developed in the wall of the ileum and the large intestine and the adults are found in the colon and cecum (sheep, goat and cattle). The heavy

infestation with these parasites induces a protein losing enteropathy and anemia. The loss of albumin into the bowel causes a diarrhea with excessive mucus contents.

Pathognomonic Lesions:A-Oesophagostomiasis (nodular-worm disease): in large intestine1-The intestinal mucosa is ulcerated and covered by mucus.2-Caseated and calcified nodules are seen in the intestinal wall (pimply gut). 3-These nodules are represented by central larvae surrounded by large numbers of eosinophils, lymphocytes, macrophages and giant cells and then encapsulated by a dense fibrous connective tissue capsule. 4-These nodules are also seen in mesentery, mesenteric lymph nodes and liver.

5-Local or generalized peritonitis.B-Chabertiasis:

1-The wall of the colon is thickened, edematous and with congested or hemorrhagic areas.

2-The intestinal nodules are absent.

Haemonchosis: Bottle jaw and worm in abomasum

Ostertagiosis in abomasum

FilariasisI-Canine Filariasis

They included 1-Dirofilaria immitis (heart worms).2-D. repens (adult in S/C)3-Dipetalonema reconditum (adult in S/C)

A-Dirofilariasis “Heart-Worm Disease”Dirofilaria immitis are found in the right ventricle of the heart and pulmonary

artery. The females are viviparous, release highly motile microfilariae which circulate in the blood. These microfilariae are taken up from the cutaneous

circulation by mosquitoes where they develop, and reinfect other host. Pathognomonic Lesions:

Adult D. immitis (in the heart):1-Presence the adult worms

i-In the right ventricle leading to general venous congestion and edema (cardiac type).

ii-In pulmonary artery producing, pulmonary embolism, thrombosis and infarctions. Hypertrophy of the right heart due to back pressure (Core

pulmonal).2-The intema of the arterial tree is uneven, rough or shaggy (due to villous

proliferation of the intema and focal proliferation of smooth muscles).3-Endarteritis with intemal infiltration of eosinophils.

4-The dead worms induce pulmonary granulomatous reactions with hemosiderosis and fibrosis.

5-Phleboscleosis of the vena cava and hepatic veins (due to fibrous C.T. Proliferation).

Microfilaria (in the blood):1-These larvae circulate in the blood with little tissue damage (congestion

and hemosiderosis).2-Dead microfilariae produce small granulomas.

3-Immune complex glomerulonephritis may be present.II-Bovine Filariasis

The adult of both sexes live in the lymphatics and connective tissues and the microflariae in the blood. They included Stephanofilaria, Onchocerca, Setaria and Parafilaria in the buffaloes and cattle.A-Stephanofilariasis:Stephanofilaria is a nematode dermatitis of buffaloes and cattle characterized by summer wound, hump or filarial sore. The microfilariae and adults are only detected in the lesions (in S/C tissue). The disease is also transmitted by various species of flies Causes: Stephanofilaria stilesi.Pathognomonic lesions:

1-The adult worms are found either in small cyst with epithelial lining in the base of hair follicles or in the dermis near the epidermis.

2-These worms are surrounded by a zone of inflammatory cells (eosinophils, neutrophils and macrophages) and a layer of fibrous connective tissue.

3-The microfilariae are found near the adults in spaces in the dermal papillae.

4-Hyperkeratosis and parakeratosis are seen in the parasitized areas.5-Severe dermatitis is detected around dead worms.

6-Chocolate blood is noticed due to formation of methemoglobin.NB: The larvae in eggs whose shells don’t stained by HE stain; but can be stained by Gram stain. B-Onchocerciasis

It is a disease of cattle, sheep and goats. The adults are seen in tunnels, nodules or cyst in the wall aorta, ligaments and connective tissues of the tendons and

fascia. They also recorded in the spleen particularly under thick capsule. Causes: Onchocerca armillata. O. bovis and O. gibsoni Pathognomonic Lesions:1-Fibrotic nodules in the wall aorta and legamentum nuchae.2-These nodules are represented by i-Centrally located adult worms and microfilariae ii-Surrounded by fibrous connective tissue iii-Chronic inflammatory cell infiltration.

3-Granulomatous reactions and local calcification are seen around degenerated larvae in the subcutaneous tissue.

4-Cracks, filled with blood, are detected in the skin of the teat. 5-These nodules are also seen in the spleen under the thick capsule.NB: In the horse, O. cervicalis is isolated from fistulous withers, poll evil, periodic ophthelmitis and remittent dermatitis.C-Bovine Setariasis (Neurofilariasis):The adults of Setaria digitata are parasitized the peritoneal cavity of cattle. The larvae are migrated randomly throughout the viscera and the microfilaria was seen in the blood. It is characterized by

i-Eosinophilia, leukopenia and anemia. ii-Splenomegaly. iii-The immature worms may seen in the brain leaving necrotic tracks. Gitter

cells and a slight to moderate infiltration of eosinophils and neutrophils surrounded these tracks. Incoordination, weakness and paralysis (lumber

paralysis) particularly in sheep, goats and horses (kumri).D-Parafilariasis

Parafilaria bovicola are seen in bovine subcutaneous nodules (firm and raised) or skin-ulcer and also isolated from hemorrhagic, gelatinous and edematous areas in the subcutis. This worm has distinct predilection sites (neck and back) as revealed

by the fixed pattern of distribution of the lesions among naturally and experimentally infected calves. Intermittent bleeding is noticed from ulcerated

skin. Microscopically, the lesions reveal eosinophilic infiltration around microfilaria and adult worms. These worms are degenerated and calcified.

III-Ovine FilariasisElaeophoriasis (Filarial Dermatosis of sheep):Elaeophora species affect sheep (filarial dermatosis), elk and deer. It is arterial

worms that found in the carotid, mesenteric and iliac arteries. The microfilariae are localized in the dermis and lead to circumscribed dermatitis

over the head, poll and face.Pathognomonic Lesions:

1-The adult worms are found in the carotid, mesenteric and iliac arteries.2-Granulomatous or necrotizing dermatitis. The lesions are accompanied by

pruritus, vesicles (bullae), ulcers and small pustules with crusts.3-Hyperkeratosis, parakeratosis and acanthosis.

4- Thrombosis of the affected arteries and infarctions (in brain and eyes).5-Eosinophils and hemorrhages around the microfilariae.

DracunculosisThis nematode is present in man and dogs. Two species of Dracunculus (guinea-worm)

Dracunculus medinensis (serpent-worm, dragon-worm or Medina-worm) is a parasite of human and D. insignis parasitizes dogs and wild carnivores.

NB: The adult females reach up to 400 cm in length and reside in the subcutis, particularly of the limbs.

Pathognomonic Lesions:1-Painful inflammatory swellings.2-Ulceration and protrusion of the worms from these swellings.

Dirofilaria immitis in heart

Dipetalonema reconditum in subcutis

Stephanofilariasis with skin lesions

Onchocerciasis in legamentum nuchae

Setariasis in diaphragm

Parafilariasis show skin injury, s/c hemorrhages, worms and meningitis

Elaeophoriasis in liver

Microfilaria in skin, liver, kidney and blood with granulomatous reaction around dead microfilaria.

Equine StrongylidosisThe family Strongylidae contains 2 types of strongyles:

A-Large StrongylesB-Small StrongylesPathogenic (in colon and cecum)Non-pathogenic (less tissue damage)

Adult live in the intestineLive in the intestineSucking bloodEating debris

There is larval migration as S. vulgarisNo larval migration

Pathognomonic Lesions:A-Strongylus vulgaris:i-With the adult worms: They are double-toothed strongyle, found in the mucosa of the cecum and colon and ingested blood.1-Enteritis with focal hemorrhages.2-The submucosa and lamina propria are infiltrated with eosinophils. ii-With the larvae They are found in the lumen and wall of anterior mesenteric artery branches

1-The wall of the affected artery is severely thickened by proliferation of fibrous tissue and showed hemorrhages, necrosis, fibrin and cellular debris accumulation

(verminous arteritis).2-Verminous aneurysm (false, thickening without dilation), thrombosis and

embolism.3-The larvae (L5) are seen in the spinal cord and brain producing verminous

encephalitis.

B-Strongylus equinus:1-The adults (triple-toothed strongyle) are found in cecum and rarely colon of equines causing catarrhal inflammation. 2-The larvae (L3) penetrate the wall of cecum or colon, causing small hemorrhages and inflammatory nodules.3-These larvae migrate into the peritoneal cavity and the liver leading to tracks of hepatic necrosis, hemorrhages and eosinophilic inflammation. 4-Larvae leave the liver (after 6-7 weeks) by way of the hepatic ligament, enter the pancreas and then the peritoneal cavity, where they molt (L5) and migrate directly to the intestinal lumen.C-Strongylus edentatus:

The adults are toothless strongyle and found in the cecum and colon of equines. The larvae penetrate the wall of the intestine and reach the liver by way of

portal veins, producing migratory tracks of necrosis, hemorrhages and eosinophilic inflammation. Larvae leave the liver also via hepatic ligament to mesentery and then to the lumen of the cecum and colon. Small hemorrhages and inflammatory nodules are seen in the large intestine. These nodules may

show central caseous necrosis besides edema, leukocytes and fibrous connective tissue.

Strongylus vulgaris in ileum with mucosal infarct and aorta.

StrognyloidosisSeveral species of Strongyloides (not to be confused with Strongylus). These

worms are similar to other intestinal nematodes.Causes: Strongyloid papillosus (cattle, sheep and goats), S. westeri (horses), S.

stercoralis (human, foxes, dogs and cat).Pathogenesis and Clinical Signs:

Strongyloides occur in the intestinal tract or as free living non-parasitic worms. The female worm is trisomic {presence of an additional “third”

chromosome of one type “xxx” or “diploid cell (2n) + 1”} and parthenogenetic (asexual reproduction without fertilization with sperms). In the intestine, the

female give three types of eggs: i-Diploid eggs (in intestine) hatch to adult females.

ii-Haploid eggs (in intestine) hatch to adult males . iii-Triploid eggs (in soil) hatch to 3rd-stage larvae. These larvae penetrate the skin of the host to enter the venous circulation, carried to the lungs and then coughed up swallowed and reach the intestine to give the adult females and males. Transmammary and prenatal infection as well as oral infection may

occur. Diarrhea and coughing are intermittently seen. Pathognomonic Lesions:

1-Allergic dermatitis and pneumonia due to migration of the larvae.

2-Catarrhal enteritis, in which the mucosa of small intestine is edematous and infiltrated with neutrophils, eosinophils, lymphocytes

and rarely epithelioid cells to form small granulomas (nodules).3-Small erosions and hemorrhages may occur in the mucosa.4-The villi become round or blunted.5-Numerous filariform larvae are present in the wall of intestine, liver, lungs and brain.

PinwormsSeveral members of the family Oxyuridae are parasitized the cecum and

colon of animals and human. These include Entrobius vermicularis (human), Oxyuris equi (equines).

Pathognomonic Lesions:1-Pruritus due to increase the activities of female worms.2-Ulcerative colitis may detect with heavy infested hosts.3-Rectal polyps are seen with Oxyuris equi in horses.

TrichuriasisTrichuris means “hair-tail” and so-called whipworm. This worm is found in the cecum and colon of cattle, sheep, goats and others.Causes: Trichuris ovis, T. discolor, T. globulosa.Pathognomonic Lesions:-Catarrhal to hemorrhagic or necrotic typhlitis and colitis according to the number of parasitized worms.

Pinworm in rectum of horse

Trichuris in colon

SpirocercosisSpirocerca lupi, esophageal worms, are usually bright red and have been found coiled in nodules in the wall of the esophagus, aorta, stomach and other organs

of the dogs with dysphagia (difficult swallowing) and vomition or sudden death.NB: The infection occurs by ingestion of paratenic host containing larvae

(beetles, frog, snake and lizard).Pathognomonic Lesions:

1-Tumor-like nodules, containing red worms are seen in the submucosa of esophagus, adventitia of aorta and serosa of stomach.2-Aneurysm of aorta, rupture and fatal hemorrhages.

3-Microscopically, these nodules are consisted of:i-Central worms and boat-like eggs are embedded in fibrous connective tissue

infiltrated with macrophages and eosinophils.ii-Mineralization and ossification are seen in these nodules.

iii-Fibroma and fibrosarcoma developed from the fibrous tissue.4-Spondylosis (degenerative changes in spin) and spondylitis (inflammation of

spin) of thoracic vertebrae are seen with the fibrosarcoma (decalcification).

Spirocerca lupi in esophagus with neoplasm

Cerebrospinal nematodiasisCertain nematodes have selective affinity for the central nervous system, and several may accidentally wander into the brain or spinal cord especially in an aberrant host. They include: i-Setaria digitata (Filaroid worms). ii-Pneumostrongylus tenuis. iii-Angiostrongylus cantonensis. iv-Halicephalobus (Micronema) deletrix.v-Migrating larvae of Strongylus vulgaris. vi-Toxocara species.vii-Horse stomach worm (Habronema megastoma).Pathognomonic Lesions:

1-Hemorrhages in the brain and spinal cord.2-Malacia (encephalomalacia or myelomalacia) and gliosis.

3-Perivascular lymphocytic cuffing.4-Some eosinophils and neutrophils infiltration adjacent the parasitic larvae

5-Eosinophilic meningoencephalitis in rats infected with A. cantonensis.6-Encephalitis and nasal granulomas in horse infected with Micronema deletrix.7-Extensive hemorrhage in the subdural space of white-tailed deer infected with

Pneumostrongylus tenuis.

Angiostrongylus lung and brain

HALICPHALOBUS DELETRIX nephritis and meningitis

Trichinosis Trichinelliasis

Trichinosis is a serious disease of human and animals (swine). Causes: Trichinella spiralis.

Pathogenesis and Clinical Signs: The females are viviparous, inhabit the small intestine and the larvae are encysted in striated muscles without specific clinical signs. Muscular pain,

nausea, vomiting, diarrhea, fever, edema of face, increased respiratory rat, and urticaria.

Invasion the larvae of cardiac muscles result in dicrotic pulse (feeble), muffled heart sound, systolic murmur or palpitation.

While, invasion the larvae of central nervous system, stupor, delirium, paralysis and coma are seen.

Leukocytosis with eosinophilia is characteristic. NB: The dicrotic pulse (feeble pulse) is measured by sphygmograph

(instrument for record movement and force of arterial pulse “sphygma = pulse”).

Pathognomonic Lesions:A-The Adults:

-The adults induce transient catarrhal enteritis.B-The Larvae:

1-The larvae are encysted in the skeletal muscle fibers (diaphragmatic, intercostals, masseteric, laryngeal, lingual and ocular).

2-The cardiac muscles rarely invaded by young larvae without encystment (active).

3-The sarcoplasm of the affected muscles is displaced by numerous large nuclei at the two poles of parasitic cysts (Nurse Cells).

4-Proliferation of sarcolemmal nuclei are seen. 5-Later on, these polar nuclei become pyknotic and the muscle fibers

become granular basophilic with loss of their striations.6-At this stage, the larvae are died and calcified.

7-Some inflammatory cells are seen around the larvae.NB: Nurse Cells: They are seen in the muscle fibers infested with the larvae of Trichinella spiralis. The sarcoplasm of these muscles is

displaced by numerous large nuclei at the 2 poles. The larvae became died and calcified when they undergo degeneration and necrosis.

Pulmonary nematodiasisLungworm Diseases

Causes:

Trichinella encysted in muscles with eosinophilic myositis

ParasitePrincipal hostsSite of adult parasite

Dictyocaulus viviparous

D. filaria

D. arnfieldi

Cattle

Sheep and goats

Horses and donkey

Bronchi, bronchioles

Bronchi, bronchioles

Bronchi, bronchioles

Metastrongylus speciesSwineBronchi, bronchioles

Protostrongylus speciesSheep and goatsBronchioles

Muellerius capillaries

Cystocaulus ocreatus

Sheep and goats

Sheep and goats

Alveoli

Alveoli

Capillaria aerophilaFoxes, dogs and catsTrachea, bronchi

Crenosoma vulpisFoxes and dogsTrachea, bronchi, bronchiole

Filaroides speciesDogsTrachea, bronchi

Aelurostrongylus abstrususCatsBronchioles, alveolar ducts

Angiostrongylus cantonensisRatsPulmonary arteries, capillaries

Pathogenesis and Clinical Signs:The migrating larvae induce little damage, until they reach the lungs, to the

intestinal mucosa, mesenteric lymph nodes and the alveolar tissue of the lungs. Adults parasitized airways produce chronic irritation, which persist for long

period. The main clinical signs were labored respiration, cough, anorexia, diarrhea and stunted growth.

Pathognomonic Lesions:A-Dictyocaulus:In Early Stage:1-Pulmonary hemorrhages and necrosis due to migration of the larva.2-Hyperplasia of type II pneumocytes, edema and interstitial thickening.3-The dead larvae are surrounded by granulomatous reaction.In Late Stage:1-Presence of adult worms in the bronchi and bronchioles.2-Catarrhal bronchitis and bronchioleitis.3-Hypertrophy of peribronchial smooth muscles with persistent cough.4-The adults may accidentally displace the alveolar tissue and become surrounded by granulomatous reactions.5-Chronic focal compensatory emphysema.NB: Filaroides, Capillaria and Crenosoma in trachea and bronchi of carnivores, produced the same lesions of Dictyocaulus.B-Protostrongylus: Similar to Dictyocaulus, where it reside in small bronchioles.

C-Muellerius capillaries (Nodular-Lungworm):1-Granulomatous nodules in the subpleura (with central caseation and calcification).2-Pulmonary hemorrhages.3-The adults, larvae and eggs are seen in the alveolar tissue.4-Numerous eosinophils, lymphocytes, macrophages and giant cells are detected around the parasites.5-Chronic focal compensatory emphysema.NB: Cystocaulus ocreatus is similar to Muellerius capillaries.D-Angiostrongylus: it is parasitized the lungs and pulmonary arteries of rat.

1-In the lungs, the eggs and larvae damage capillaries and small arterioles, leading to thrombosis and necrosis.

2-Granulomatous reaction around the parasites.3-The larvae may be seen in the brain inducing eosinophilic

meningoencephalitis.4-Some species of Angiostrongylus reside the pulmonary artery and right

ventricle of dogs and foxes as Dirofilaria immitis.NB: Angiostrongylus costaricensis is not lungworm, but a parasite of intestinal subserosal arteries and the anterior mesenteric artery of rat and characterized by eosinophilic granulomas in the wall of the intestine.

Dictyocaulus in bronchi and bronchioles

Muellerius capillaries in lung (subpleural tissue)

E-Aelurostrongylus: They reside the terminal bronchioles and alveolar ducts of cats.

1-The alveoli are impacted with eggs and larvae, which are surrounded by eosinophils, macrophages, giant cells and lymphocytes.

2-Medial hyperplasia and hypertrophy of the smooth muscle of pulmonary arteries.

F-Metastrongylus: They reside the bronchi and bronchioles of swine.1-Alveolitis and bronchitis.

2-Granulomas around dead parasites and their eggs.Dioctophymosis

The giant kidney worm Dioctophyma renale reside in the renal pelvis and is rarely seen in the peritoneal cavity (eggs pass with urine) of dogs, cats, foxes,

cattle, horses, pigs and human. Presence of the parasites in the renal pelvis lead to slight destruction of the renal parenchyma (right kidney of dogs is highly

affected). Fluid-filled sac is detected replacing the destructed renal tissue. Chronic peritoneitis is present with adhesion due to presence of worms and

eggs.Stephanuriasis

Kidney-worm diseaseThe swine kidney worms, Stephanurus dentatus, reside in the peritoneal fat and adjacent tissue. These worms form cystic cavities (tract) that communicate with

the lumen of the ureters and permit the discharge of ova with the urine.

The infection occurs either by ingestion of the larvae, which reach the liver by the way of portal vein and then penetrate the liver to peritoneal cavity or

penetrate the skin to reach the general circulation, lungs, liver and then to peritoneal cavity.

Pathognomonic Lesions:1-Subcutaneous nodules and edema due to larval penetration.

2-Liver show coagulative necrosis and extensive portal fibrosis (as migratory tacks).

3-Intense eosinophils infiltration in the affected tissue.4-The parasites are seen in the lungs, kidneys, heart and lumbar spinal cord

(paralysis).Habronemiasis

I-Gastric Habronemiasis (Stomach worms of horse):These worms include three species:

i-Habronema megastoma (Draschia megastoma).ii-H. muscaeiii-H. majus

Pathognomonic Lesions:1-Chronic catarrhal gastritis. 2-Small erosions and ulcers are seen.3-Multiple large nodules in the gastric mucosa. 4-These nodules are consisted of central parasites and necrotic debris,

surrounded by granulomatous and eosinophils.

II-Cutaneous Habronemiasis (Summer sores):It is a persistent disease of the skin of equines results from the activity of larvae of H. megastoma. The larvae are deposited on ulcerated or injured skin by flies. Pathognomonic Lesions:

1-Skin ulcers (sores) on pectoral region and between the forelegs.2-Granulomatous dermatitis (around the larvae).3-Alopacia and encrustation of the affected areas.

4-Granulomatous conjunctivitis (larvae in eyes) and pneumonia.Capillaria, Trichosomoides and Anatrichosoma

A-Capillaria hepatica: These worms are inhabited the liver of rats and mice. The adults, eggs and excreta accumulate in the liver causing necrosis and fibrosis.B-Capillaria plica (in cats) and Trichosomoides crassicauda (in rats): They inhabit the urinary bladder and occasionally ureters and renal pelvis. 1-Hemorrhages and granulomatous nodules in the urinary bladder. 2-Neoplasia (transitional cell papilloma) in the bladder.3-The adult worms and eggs are seen in lumen.C-Anatrichosoma cutaneum: This worm resides in the nasal mucosa and less frequently the skin around the nares, lips and eyes of monkeys. 1-The coiled worms and eggs are found in the submucosa or dermis, surrounded by inflammatory cells. 2-Hyperkeratosis and parakeratosis in the skin and nasal mucosa are also evident.

Stephanuriasis nephritis and ureteritis

Chronic cutaneous Habronemiasis

Capillaria in liver and urinary bladder

ThelaziasisEye worms

Thelazia species reside in the conjunctival sac and lacrymal duct of cattle, sheep, horse and humans. The flies deposit the 2nd and 3rd stage larvae in the

eyes, producing corneal opacity (with photophobia and excessive lacrimation) and blindness.

Cestodiasis (Taeniasis)Tapeworm Disease

Cestodes or tapeworms (Phylum: Platyhelminths, Class Cestoda) are common parasites of all vertebrate animals. These worms reside the intestine, interfere

with digestion and absorption, and have little apparent effect on the health except in heavy infestation induced catarrhal enteritis and eosinophils

infiltration.Causes: Taenia species, Monieza species, Stilesia hepatica (reside the bile ducts), Avitellina species and Hymenolepis species.Cysticercosis and Hydatidosis

Cysticercosis (beef or pork bladderworm disease) and hydatidosis are diseases of human and animals (IMH), caused by the presence of larva of tapeworms in

tissue.Causes:

TapewormDefinitive hostAnatomic siteType of larvaeIMH

Taenia soliumHumansSkm, heartC. cellulosaeSwine

T. saginataHumansHeart, skmC. bovisCattle

T. hydatigenaDogPeritoneumC. tenuicollisSheep, goat

T. ovisDog, fox, wolfMusclesC. ovisSheep, goat

T. pisiformisDog, fox, catLiver, peritoneumC. pisiformisRabbitsT. multiceps

T. serialisDog

Dog, Brain, sp.cord

S/CCoenurus cerebralis

Coenurus serialisSheep, goat

RabbitsT. taeniaeformisCat, dog, foxLiverC. fasciolarisRodents

Echinococcus granulosus

Dog, fox, manLiver, lung, viscera

Hydatid cystsMan, cattle,sheep, goats

E. multilocularisDog, fox, manAs E.g.Hydatid cystsMan, cattle, swine

NB: Procercoid and plerocercoid are the larval stage of Diphyllobothrium latum, which grow to form solid (not bladder-like) larvae, resembling the mature

worms in fish.Pathognomonic Lesions:I-Cysticercosis:C. tenuicollis and C. pisiformis: 1-The larvae migrate in the liver, leaving recent hemorrhagic tracks of central necrosis, fibrin exudate and erythrocytes besides numerous leukocytes.

2-Some onchospheres are surrounded by granulomatous reactions.3-Later on, these larvae mature and drop into the peritoneal cavity leaving old, yellow tracks of fibrous connective tissue infiltrated with macrophages, lymphocytes, eosinophils and siderocytes.C. fasciolaris:

1-The larvae (mature and immature) reside in the liver and are surrounded by fibrous connective tissue capsule.

2-Meanwhile, the degenerated cysts are represented by central caseation and calcification surrounded by granulomatous reactions

and eosinophils.C. bovis:

1-The larvae are found in the masseter muscles, tongue, diaphragm, heart, liver, lungs and lymph nodes.

2-These cysts are represented by small white or gray cysts (up to 1 cm. in diameter) and slightly protruded on the organ-surface.

3-The degenerated cyst is represented by focal yellowish or whitish foci of caseous necrosis and calcification.

4-The affected heart reveals Zenker’s necrosis adjacent viable and degenerated cysts.

II-Echinococcosis (Hydatidosis)The larval or intermediate stages of Echinococcus species are known as hydatid cysts, which localize in the liver, lungs and other vital organs.

There are two types of hydatid cysts:1-The granulosa hydatid cyst:

It is the larvae of E. granulosus (dog) and is unilocular cysts. This cyst consists of:

a-Germinal membrane (thick concentric and lamellated membrane without nuclei).

b-Broad capsule (contain scolices and hydatid sand).c-Daughter cysts within the parent cyst (internal).

2-The multilocularis hydatid cyst: It is the larvae of E. multilocularis (fox), and is multilocular cysts with external

daughter cysts.a-The viable cysts are surrounded by fibrous connective tissue capsule.

b-Ruptured cysts may lead to anaphylactic shock or infiltrated by eosinophils, macrophages, lymphocytes and giant cells.

c-The degenerated cysts represented by caseation and calcification, surrounding by granulomatous reactions.

d-The surrounding tissues show pressure atrophy (collapse in the lungs).

Cysticercosis and Hydatidosis

Parasitic granulomas (tapeworm)

Trematodiasis (Distomiasis)Trematodes are flat worms of family Platyhelminths (leaflike and have one or

two suckers). The term distoma is synonym to trematodes. They reside liver (bile ducts, gallbladder and parenchyma), intestine and rarely pancreatic ducts,

lungs and veins.I-Hepatic Distomiasis (Liver Flukes)

FascioliasisCauses: Fasciola gigantica is only the cause of fascioliasis in Egypt due to the presence of its IMH (Lymnae caillaudi snail); meanwhile the imported cattle showed Fasciola hepatica.Pathognomonic Lesions:A-Acute Form:

1-Recent (hemorrhagic) migratory tracks are seen in the liver. 2-These tracks are represented by cavities filled with coagulated blood, fibrin,

cellular debris, and neutrophils and eosinophils infiltration.3-Extensive hemorrhages and coagulative necrosis in liver tissue.

4-Focal peritoneitis due to initial migration of the larvae.B-Chronic Form:1-Old (yellow) migratory tracks are seen in the liver. 2-These tacks are represented by scar (fibrous connective tissue) infiltrated with macrophages, epithelioid cells, giant cells.3-Chronic cholangitis with hyperplasia of the bile duct epithelium.

4-The wall of bile ducts is thickened by extensive fibrosis, calcification and numerous leukocytes infiltration (Pipe-stem liver).

5-The adult worms are detected in the bile ducts and gallbladder.6-Adenoma and adenocarcinoma in the bile ducts and gallbladder.

NB: Pipe-stem liver: It is chronically inflamed, thickened and calcified bile ducts particularly in fascioliasis.

Fascioloides magnaIt is a large liver fluke occurs in the liver parenchyma of cattle, sheep and horses.

These flukes wander through the liver parenchyma, destroying its tissue and eliciting a reaction of the host, which encapsulates the parasites.

Dicrocoelium dendriticum (Lancet fluke)D. dendriticum is a small flukes (5-12 mm. long and 1 mm. wide), slender,

flat and lancet-shaped with pointed ends. It is parasitized the bile ducts of sheep, goats, rabbits and cattle.

The life cycle of this parasite is most unusual, where it require 2 intermediate hosts. Eggs, fully embryonated when passed in feces, are ingested by land snails (first

IMH), in which the cercariae are developed. Such cercariae are liberated from the snails during rainy periods and become massed in “slime balls”. These slime balls,

each of which contains large numbers of cercariae, are eaten by ants, Formica fusca (second IMH). In the brain of the ants, the cercariae become encysted to form

metacercaria, cause the ants to remain on herbage after normal ants return to their nest. This presumably increases the possibility that infected ants will be ingested by

grazing animals to form adult flukes in the small bile ducts.

Fascioliasis

Dicrocoelium dendriticum

NB: Hepatic Distomiasis in dogs and cats (Clonorchis sinensis) reside the bile ducts causing cholangiohepatitis characterized by biliary necrosis, hyperplasia,

and fibrosis besides leukocytes infiltration. II-Intestinal Trematodiasis or Distomiasis

ParamphistomiasisParamphistomiasis is a disease of cattle, sheep and goats. It is responsible for a high

morbidity and mortality among young animals. Causes: Paramphistomum species.

Pathogenesis and Clinical Signs:Clinical incidence is produced by the immature flukes in the duodenum, rarely ileum and

abomasum inducing acute enteritis. The mature flukes in the forestomachs cause little damage. A persistent fetid diarrhea was characteristic in early stages (with immature

flukes). Submandibular edema and pallor mucous membranes are reported with adult flukes.

Pathognomonic Lesions:1-Emaciation, subcutaneous and edema.

2-The fat in fatty depots is gelatinous. 3-The mucosa of duodenum is thickened, covered with blood stained mucus and the

serosa show patches of hemorrhages. 4-Large numbers of immature flask-colored flukes in the duodenum.

5-The paramphistomes are seen in the biliary passages and the bile ducts are cystically dilated with flukes and the wall of gallbladder is thickened and fibrosed.

6-Ulceration and necrosis in the tips of the ruminal papillae (adults).7-Lymphocytes, macrophages and eosinophils in the lamina propria.

8-Adult flukes were detected under the keratinized layer. NB: Hetrophyes, Alaria and Anophallus: They reside the intestine of dogs and cats, producing hemorrhagic duodenitis with immature flukes and

catarrhal enteritis with mature flukes.III-Other Distomiasis

SchistosomiasisThe schistosomes live in the blood vessels of the human and animals. Causes: Schistosoma mansoni, S. hematobium, S. bovis, S. jabonicum,

Pathogenesis and Clinical Signs:The principal lesions are produced by cercarial penetration of the host-skin, adult flukes in the veins, and ova (circulate in the blood as emboli)

in different tissue. Dermatitis, dysentery, and signs of cirrhosis are the common clinical signs.

Pathognomonic Lesions:1-Cercarial dermatitis with neutrophils, eosinophils and lymphocytes,

particularly around dead cercariae.2-Adult flukes are seen in the mesenteric, urinary bladder or other

veins. 3-Thrombosis, infarction and black bilharzial pigments are detected

inside the macrophages and REC.

Paramphistomiasis in rumen

4-The ova are circulated in the blood and lodged in the tissue with the formation of egg-granulomas. These granulomas are seen in the liver, intestine, spleen,

lungs, urinary bladder, nasal cavity and uterus. The granulomas are consisted of central ova, surrounded by fibrous connective tissue and granulomatous

reactions (macrophages, giant cells and lymphocytes).5-Sandy patches are elevated nodules of egg-granulomas on the intestinal serosa.

6-Hemorrhagic enteritis with small ulcers in the intestinal mucosa. 7-Numerous egg-granulomas in the liver produces cirrhosis.

ParagonimiasisParagonimus species are hermaphroditic flukes, live in the lungs of humans, dogs,

pigs and cats. The flukes are found in pairs in lung-cysts, lined with bronchial epithelium and surrounded by granulomatous reactions. Their eggs are

embedded in the lungs and cause eosinophilic granulomas. Eurytremiasis

Eurytrema pancreaticum reside in pancreatic duct of sheep, goats and cattle. Pathognomonic Lesions:

1-Mild hyperplasia and desquamation of the lining epithelium are noticed beside few numbers of the parasites.

2-Erosion of the mucosa and the parasites and their eggs are located in the lumen and on the luminal surface of the mucosa.

3-Fibrosis of the ducts with large numbers of eggs and inflammatory cells are detected in their wall.

4-The pancreatic parenchyma is displaced by fibrous connective tissue infiltrated with macrophages, lymphocytes and eosinophils.

Paragonimiasis in lungs

Eurytrema pancreaticum

Parasitic ArthropodsBiting and blood sucking insects (Pediculosis):

Many species in both of the class Insecta and Arachnid are parasite that bite or suck blood of infested animals. Biting and blood sucking insects include:

1-Horse flies 2-Stable flies 3-Tsetse flies4-Mosquitoes 5-Kissing bugs 6-Lice and fleas

i-Animals injure themselves and damage their hides by biting and scratching.ii-The hairs appear soiled by feces of the lice and the coat become rough and shaggy.

iii-The coat of the infested animals show broken hair with untidy appearance and gross excoriation of the skin with the production of raw abraded areas are seen.

iv-Dermatitis, anemia and hypersensitivity skin diseases (delayed type) are noticed.Myiasis: It is the invasion of the living tissue of animals by the larval stage of

flies. 1-Cutaneous myiasis: The larvae live in or under the skin (ox warble flies)2-Intestinal myiasis: Live in the stomach and intestine (horse bots).3-Atrial myiasis: The larvae in the oral, nasal, ocular (Oestrus ovis).4-Wound-invading myiasis: (screw-worm larvae).5-External myiasis: (blood sucking larvae).

Myiasis: Cutaneous in ram, hypoderma, Gastrophilus, Oestrus ovis

AcariasisI-External or cutaneous Acariasis

Mange, Scab or Mite infestationThe mites parasitized the skin of animals and many of them produce serous lesions. In general, each species of mites has its preferred host. Causes: Demodex, Sarcoptes, Psoroptes and Chorioptes species.Pathognomonic Lesions:A-Demodectic Mange (Follicular or Red Mange):1-Demodex folliculorum mites (cigar-shape) in the hair follicles and sebaceous glands.2-Deep folliculitis and dermatitis are detected. 3-Alopecic, scaly and eroded epidermis.4-Scab formation on eroded surface due to exudation of serum.5-Suppuration (abscesses), granulomas and lymphocytes infiltration.6-The mites may be seen in the regional lymph nodes.B-Sarcoptic Mange (Burrowing mites):

Sarcoptes scabiei mites attack cattle, sheep, dogs, swine, horses and humans. This mite burrows in the deeper parts of the stratum corneum or the superficial

layers of the prickle cell-layer of the skin, and rarely goes deeper.1-Hyperkeratosis and acanthosis due to severe itching.

2-Erosions and alopecia are seen.

3-Adults, nymphs and eggs may be detected in epidermal tunnels.4-Secondary dermatitis may be seen.

C-Psoroptic Mange (Sucking mites):Psoroptes ovis and P. cuniculi are infect sheep, cattle and rabbits, where it lives in the external meatus and produce severe lesions that may lead to middle or inner ear infection, and death. Psoroptes species do not burrow into the epidermis, but remain on the surface.D-Chorioptic mange (Scab eating mites):This type is caused by Chorioptes and localize on the legs of the horse, cattle and sheep inducing “Foot-Mange or Leg Itch”.E-Notoedric Mange: It occurs around ears, face and neck of cats and rats.F-Otodectic Mange:It occurs in ear canal of dogs and cats, producing hematoma of the pinna due to head shaking and scratching. Otitis media or interna and encephalitis (non-suppurative) are present beside the mites.G-Psorergatic Mange:This type localizes on the skin surface of sheep, causing pruritus and dermatitis.

Chronic mange: in calf, goat and with sarcoptic burrowing mites

Demodectic mange

II-Internal or Pulmonary Acariasis:PentastomiasisLinguatulasis

Visceral linguatulasis, larval or nymphal stages of Linguatula serrata, are seen in different organs especially the mesenteric lymph nodes of sheep, goats, rabbits, horse and cattle. They are the intermediate hosts of L. serrata. The adults are tongue-shaped, worm-like arthropods and recorded in the respiratory passages of dogs, foxes and human. Pathognomonic Lesions:I-With the arthropods:1-Presence of tongue-shaped, worm-like arthropods with serrated cuticle in the

respiratory passages.2-Extensive hemorrhages and granulomatous reactions around the arthropods.

3-The bronchioles are inflamed or necrotic.II-With the nymph or larvae:

1-The larvae are seen in the mesenteric lymph nodes without inflammatory reactions.

2-The degenerated larvae are represented by central caseation and calcification and surrounded by granulomatous reactions.

Pentastomiasis in the peritoneal cavity and L.n.

Pentastomiasis in the liver

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