Introduction

Infectious diseases

Infectious agents are the most common causes of the diseases worldwide. Infectious diseases occur due to invasion of the animals by viruses, bacteria, parasites or fungi, which lead to dysfunction or tissue damage.

Virulence is the capacity of an organism to achieve infection. The infective agents must gain access to the body, avoid host defense, accommodate itself to growth and parasitizes the living tissue.

Host defense against infection is the mechanism by which the bodies prevent infections. Skin, aerodynamic filters of the upper air way and mucociliary blanket of the airway are anatomical barriers beside mucus membrane of gastrointestinal tract and microflora.  Moreover, gastric acid and bile salts chemically destroy the microorganisms.

Diseases caused by viruses

Viruses produce disease by cells damage results from intracellular replication of viruses. Viruses are one of the smallest of all life forms. Viruses are obligate intracellular parasite that contain only one type of nucleic acid, not contain cell organelles and not divide by binary fission. Moreover, viruses don’t have ribosomes to synthesis protein, so it use cellular organelles to synthesis its protein and shutting off cellular protein synthesis.

Mechanisms of virus induced disease

1. Bind to the cell surface

Virus should be capable to attach itself to the surface of target cells. The viruses have specific surface viral protein (legends) that binds with specific cellular protein on the surface of host cells. The viral tropism is depending on the presence or absence of surface particular protein.

2. Entering the cells and replication

After entering the cell, the virus kill host cells and cause tissue damage through several ways

1. Viruses inhibit host cell DNA or RNA and protein synthesis.

2. Damage cell membrane or promote cell fusion

3. Replication of viruses inside cells results in host cell lysis

4. Killing the infected the host cells by immune system which recognize the viral protein on the cell surface.

Diseases caused by poxviridae

Poxvirus are brick. shaped virus which have a complex internal structure including double stranded DNA genome (130. 260 kb) and associated enzyme. The poxviruses have affinity to epidermis. Most poxviruses produce epidermal proliferative lesions that form vesicles, and then pustules.  The Poxviridae and Iridoviridae are the only DNA virus that form intracytoplasmic inclusion bodies.  A mature virions may be released by budding (enveloped) or after cell lysis (unenveloped).

The member of poxviridae induce infectious diseases that infects most domestic, wild, laboratory animals, man and birds and characterized by the production of skin lesions.

Pathogenesis

Infection is usually transmitted mechanically through invasion of broken skin or insect biting and in most cases remains localized. The pox lesions develop due to proliferation of epidermal cells and ischemic necrosis results from proliferation and necrosis of endothelium.

After a latent period a small focal non. elevated area of erythema (macule) appears.

The virus continues replication at the site of inoculation causing epidermal hyperplasia and subepidermal edema leading to elevated localized area (papule) (Fig. 1).

The epidermal cells progressively enlarged and suffered hydropic degeneration. Moreover, some cells lysis and serous fluid accumulate in tiny cystic space called vesicles. The secondary bacterial infection lead to accumulation of neutrophils and fibrin forming pustules and crusts (Fig.s2&3). Finally, the lesion heals leaving a scar. 

Fig. 1: Pigeon infected with pox showing nodules on beak (papules).

Pigeon infected with pox showing pustules.

Fig. 2: Pigeon infected with pox showing pustules. 

Fig. 3: Pigeon infected with pox showing crust.

Systemic disease is rare, except for those viruses cause major plagues as sheep pox and small human pox.

Host defense

Intact skin considers the first line of defense against poxvirus. Interferon, non. specific inflammation and pyrexia play a role in limiting infection during the early stage. Immunity is mainly cellular.

Cowpox

It is a mild and self. limiting infectious skin disease of cattle characterized by the formation of pox lesions (macules, papules, vesicles, pustules and crusts) in the udder and teats.

Cause

It causes by orthopoxvirus closely related to, but distinguishable, from variola and vaccina.

Route of transmission

The infection occurs during milking from cow to cow

Milker's nodules are occurs in milkier contact with infected cows and characterized by nodules in hands.

Macroscopic appearance

The pox lesion (macules, vesicles, pustules and crusts) are seen on teat and udder (Fig. 4). The vesicles are round on the udder and ovals to elongated on teats and are surrounded with an inflamed rim. The contents of the vesicles are at first clear but become turbid later on.  The vesicles show a depressed center. Later on, The pustules are formed and contain a thick purulent discharge. Pustules then dry forming a crust and finally healing occurs leaving a scar.

Fig. 4: Cattle mammary gland showing pox nodules.

Microscopic appearance     

Congested blood vessels and lymphocytic aggregation are the first changes observed in the dermal papillae underlying the affected epidermis.

Hyperplasia and swelling of the epidermal epithelium are seen. Moreover, eosinophilic intracytoplasmic inclusion bodies (Guarnieri bodies) composed of many minute spherical granules (Borrel bodies) which are the elementary particles of the virus. As necrosis occurs in the affected epithelium, a clear vesicle forms and soon is filled with neutrophils.

Buffalopox

It is a contagious disease of water buffaloes characterized by pox lesions on teat and udder (Fig. 5).

Fig. 5: Buffalo showing pox nodules, ulceration and crusts on the teat.

Sheep Pox

It is a serious infectious disease of sheep caused by Capripoxvirus and characterized by the cutaneous form (particularly in area devoid of wall) and generalized or visceral form causing high morbidity and mortality.

Signs

Incubation period usually ranged from 4. 7 days. Fever, which followed by development of pox lesions especially in area devoid from wool, is seen. Moralities in systemic form reach 50% and may reach 100% particularly in lambs.

 Lesions

The pox lesions on skin of the head, nostrils, and lips begin as erythema then papules, vesicles, and end as pustules, scab and scar (Figs 6 & 7 ).

Fig. 6: Sheep pox skin form, nodules on lips and muzzle.

Fig. 7: Sheep showing numerous pox nodules in cutaneous form of pox.

In generalized form typical nodules may be formed in the mouth, pharynx, and abomasum (Fig. 8).   Moreover, the trachea and lungs may show grayish nodules (about 3 cm in diameter) which may be caseated or not (Fig. 9). The pleura may shows serofibrinous inflammation, which may cause death in some cases.

Moreover, whitish nodules may be seen in liver, kidneys and heart (Fig. 10&11). Microscopically, the epidermal shows localized acanthosis and vesiculation starting from the middle layer of the epithelial cells, which isolated by serous fluid. Intracytoplasmic inclusion bodies are seen in infected keratinocytes (Fig. 12&13).

The edematous dermis and subcutis contain many sheep pox cells (Cellules claveleuses), which contain intracytoplasmic inclusion bodies. The sheep pox cells are concentrated around blood vessels and between collagen bundles.

Severe necrotizing dermis and vasculitis results in ischemic necrosis and intense infiltration by neutrophils.

Lesions in the respiratory and digestive tracts in cases of generalization occur in the same manner as in the skin. The sheep pox cells may notice in heart, liver, kidneys, adrenal and others.

Fig. 8: Sheep buccal cavity showing pox nodules in lips, hard palate and dental pad.

Fig. 9: Lungs of sheep infected with generalize form showing grayish nodules

Fig. 10: Sheep pox, kidney showing enlargment due to presence of sheep pox nodules.

Fig. 11: Liver of sheep infected with pox showing grayish white pox nodules.

Fig. 12: Microscopic picture of skin sheep pox showing vesiculation and necrosis of stratum spinosum besides presence of eosinophilic intracytoplasmic inclusion bodies. H&E

Fig. 13: Microscopic picture of skin sheep pox showing  presence of eosinophilic intracytoplasmic inclusion bodies. H&E

6. Fowl pox

It is slow spreading disease characterized by nodular proliferative skin lesionon the non feathered part of the skincutaneous form)  (Fig. 14) or fibrinonecrotic and proliferative lesions in the mucous membrane of the upper respiratory tract,esophagus and mouth (diphtheretic form).

The disease cause by Avipoxviruses (Canarypox, Pigeonpox and Turkeypox)

Fig. 14: Pigeon showing pox nodules on unfeathered part

Fig. 15: Pigeon pox showing intracytoplasmic inclusion bodies (Bollinger) in hyperplastic epithelium of stratum spinosum. H&E

Fig. 15, 16: Pigeon shin section showing hyperplastic epithelium containing Bollinger body besides bacterial colonies on the stratum corneum. H&E

Fig. 17: Pigeon shin section showing hyperplastic epithelium containing Bollinger body besides necrotic of superficial layer. H&E

Fig. 18: Pigeon shin section showing hyperplastic epithelium containing Bollinger body besides caseous necrosis. H&E

Fig. 19: Skin of pigeon showing vasculitis. H&E

Fig. 20: Trachea of bird infected with pox diphtheritic form showing hyperplastic eroded epithelium containing Bollinger bodies. H&E

Lumpy Skin Disease

It is a highly infectious skin disease of cattle and less common in buffalo characterized by generalized cutaneous nodules. 

Cause

The disease is caused by poxvirus (Neethling virus), which is closely related to sheep. pox and goatpox.

Route of Transmission

The disease is thought to be transmitted mechanically by biting insects such as flies and mosquitoes.

Susceptible hosts

Lumpy skin disease is primary a disease of cattle and less common in buffaloes.

Signs

The disease usually occurs is hot season. The incubation period is about two to five weeks.

Persistent fever, anorexia, reduce milk production, emaciation besides generalized suddenly skin nodules is observed.  The skin nodules are most numerous on the neck, brisket, back, thighs, legs, perineum, udder, scrotum, and around the muzzle and eyes.  Morbidity is high but mortality is generally low, but may be approach 10%.

Lesions

Skin shows generalized round firm nodules of 0.5 to 5 cm in diameter. The nodules usually undergo necrosis and separated from the surrounding skin forming a cone of necrotic tissue (Figs. 21, 22, 23, 24 & 25). Moreover, other organs as lungs, pharynx, trachea, bronchi, rumen, abomasum and kidneys show similar to these in the skin. The superficial lymph nodes are enlarged., muscles, , lung.

Microscopically, The dermis shows edema, perivascular infiltration by lymphocytes, macrophages and neutrophils.

Acanthosis, parakeratosis and hyperkeratosis are seen in the epidermis. Moreover, eosinophilic intracytoplasmic inclusion bodies are seen in keratinocytes, macrophages and fibroblasts (Fig. 26). Later on the hyperplastic cells undergo vesiculation and necrosis, which requires three to 5 weeks to heal.

The lungs show coagulative necrosis, surrounded by mononuclear cells mainly lymphocytes and plasma cells and finally followed by fibrous tissue. Other organs show necrosis infiltrate by round cells.

Fig. 21: Cattle showing numerous nodules due to lumpy skin disease.

Fig. 22: Cattle showing lumpy nodule in nostril.

Fig. 23: cattle showing lumpy nodule in teat.

Fig. 24: Cattle showing nodules usually undergo necrosis and separated from the surrounding skin forming a cone of necrotic tissue

Fig. 25:  Cattle showing nodules usually undergo necrosis and separated from the surrounding skin forming a cone of necrotic tissue leaving ulcer.

Fig. 26: Microscopic picture of cattle skin infected with lumpy skin disease showing hyperplastic epithelium containing intracytoplasmic inclusion bodies. H&E

Fig. 27 Microscopic picture of cattle skin infected with lumpy skin disease showing hyperplastic epithelium containing intracytoplasmic inclusion bodies. H&E

Diseases caused by Herpesviridae

Herpes viruses is composed from a core containing double strand DNA genome, enclosed by capsid surrounded by amorphous protein coat called tegument and finally by glycoproteins bearing lipid bilayer envelope.

Herpes viruses are divided into three groups: Alpha, Beta and Gammaherpesvivinae. Alphaherpes viruses are cytocidal (necrotizing) viruses. The Betaherpes viruses are cytomegalo viruses, which lead to extremely large cell with intranuclear inclusion body. The Gamaherpes viruses are lymphotropic viruses for either B or T lymphocytes.

Disease caused by Alphaherpesviruses

 Infectious Bovine Rhinotracheitis

Infectious Pustular vulvovaginitis, coital exanthema, vesicular venereal disease and vesicular vaginitis.

It is an acute infectious disease of cattle caused by herpes virus type 1 and characterized by respiratory, neonatal, abortion and genital forms.

Cause

The disease is caused by herpes virus type 1 (BHV. 1). 

Susceptible host

The disease occurs mainly in cattle. Sheep and goats are less susceptible to rhinotracheitis but may be affected with vulvovaginitis.

Route of infection

IBR is transmitted by direct contact with the infected animals. The infection occurs through inhalation of infected droplets, through conjunctiva or through coitus and artificial insemination.

Pathogenesis

In case of infection through inhalation the viruses have affinity to the epithelial lining of the respiratory system mainly upper respiratory. The virus initially multiplies in the upper respiratory tract resulting in rhinitis, bronchitis and pneumonia.   In young animals The leukocytes carry the virus from the initial focus of infection to various organs and lymph nodes. The viruses reach conjunctiva through direct contact or secondary to viremia.

In case of the infection occurs through coitus, the viruses enter the mucosa of genital tracts leading to vulvovaginitis and balanoposthitis.

1. Respiratory form

It is infectious disease especially among young cattle with 100% morbidity and up to 10% mortality. The incubation period of the disease is 10. 20 days. Conjunctivitis often accompany the respiratory form or occurs independently.

Signs

An acute febrile illness (temperature up to 42 C), anorexia, nasal discharge besides severe hyperemia of the nasal mucosa  (red nose), are seen (Fig. 28).

The most characteristic signs are sever respiratory dyspnea in the form of explosive cough due to obstructive bronchitis, and bronchopneumonia. Diarrhea and conjunctivitis may be seen (Fig. 29).

Lesions

The muzzle is hyperemic and red (red nose). Early there is mild rhinitis but in more advanced cases, the inflammation becomes more severe and extends into the pharynx, and the exudate becomes fibrinous and adheres to the mucosa (Fig. 30). Later, the mucosa covered with mucopurulent exudate. The wall or respiratory tract becomes edematous.

Petechial hemorrhages are commonly found in the frontal sinus, larynx and trachea.

The lung, especially the ventral tips of the apical and cardiac lobes, is congested and firmer than normal .

Microscopically, degenerative changes and necrosis of upper respiratory tract epithelium, which infiltrated with neutrophils, are seen. The ulcerated mucosa is covered with fibrin threads.  Eosinophilic intranuclear inclusion bodies are seen in remaining cells covering the upper respiratory tract (Cowdry  A type inclusion bodies) (Fig. 31).

The submucosa shows congestion of blood vessels and infiltration of leukocytes mainly neutrophils, lymphocytes, and variable number of plasma cells and histocytes.

The lungs show necrosis and desquamation of the epithelial lining of bronchi and bronchioles, which fills the air passages.

Bronchopneumonia results from secondary bacterial infection may be seen particularly in fatal cases.

2. Neonatal form

It is occurs in very young calves. It is generalized and fatal without respiratory signs.

Lesions

The neonatal form characterize by wide spread of necrotic foci in respiratory epithelium, mucosa of oral cavity, esophagus, forestomach, liver, kidneys, spleen and lymph nodes.

Microscopically focal areas of coagulative necrosis, which infiltrated with round cells besides intranuclear eosinophilic inclusion bodies are seen (Fig. 32).

3. Genital form

The genital and respiratory form are rarely found in the same herd at the same time.

The female shows red vulvular mucosa with dark foci which later form vesicles and pustules (Fig. 33&34). The pustules coalesce with each other and form a yellowish membrane, which is soon detached leaving ulcer.

Male show vesicles, pustules, and erosions on the penis and prepuce (Figs. 35 & 36).

4. Abortion form

It is characterize by abortion of about 60% of pregnant cow at any time of pregnancy particularly between 4.5 to 6.5 months.

The aborted fetus is autolyze because it dies 24 to 36 hours before abortion. The aborted fetus shows diffuse hemorrhages and coagulative necrosis in liver, spleen, kidneys and lymph nodes. Edema especially in the subcutis, interlobular septa of the lung and fetal membranes are seen. Accumulation of blood tinged fluid in the abdominal and thoracic cavities Moreover, intranuclear inclusion bodies are seen in the previous organs. The cow is completely normal.

Fig. 28: Cattle infected with IBR showing severe congestion of muzzle and nasal mucosa (red nose)

Fig. 29: Cattle infected with IBR showing breathing through the mouth due to bronchitis and bronchopneumonia beside salivation in a bovine affected with IBR.

Fig. 30:Cattle infected with IBR showing  I Acute inflammation of the larynx and trachea.

Fig. 31: Cattle infected with IBR showing eosinophilic intranuclear inclusion bodies in the remaining epithelial lining of the upper respiratory besides accumulation of inflammatory cells.  H&E

Fig. 32: Kidney of cattle infected with IBR showing coagulative necrosis of the lining epithelium of renal tubules besides intranuclear inclusion bodies and leukocytic infiltration. H&E

Fig. 33: Cattle infected with IBR showing congested red vulva

Fig. 34:Cattle infected with IBR showing pustules and and yellowish membrane covered the vulva and vagina.

Fig. 35: Penis of cattle infected with IBR showing pustules, and erosions.

Fig. 36: Prepuce of bull infected with IBR showing infiltration of the lamina propria with round cells. H&E

Disease caused by gamaherpesviruses

Bovine malignant catarrh

Malignant Catarrhal Fever

It is an acute infectious disease of cattle and buffaloes, which characterized by high fever, emaciation, catarrhal and mucopurulent inflammation of eye and nostrils, erosion in oral mucosa, enlargement of lymph nodes, corneal opacity and nervous manifestation.

Cause

The disease is caused by gammaherpesvirus

Route of infection and susceptible hosts

The disease is not transmitted by direct contact with infected animals. Infection may occur through insect bits. Congenital infection may occur. Cattle and buffaloes are susceptible to natural infection.

Signs and gross lesions

Fever and catarrhal conjunctivitis and rhinitis with stream mucopurulent discharge from nostril and conjunctiva. Later on the discharge dries and adheres. 

Rapid emaciation, corneal opacity beside dries and eroded skin of the muzzle is seen (Figs. 37, 38 & 39). Congestion of the oral mucosa may be with sharply irregular erosion is seen with the start of fever (Fig. 40).

Diarrhea may be noticed beside nervous manifestation in the final stage. The esophagus, omasum, rumen, abomasum and intestine are congested edematous and eroded (Fig. 41).

Brain shows cooked appearance with broth odor. Generalize enlargement of the lymph nodes are constant signs. The cut section is granular and pink. Moreover, in mild form thickening and peeling of neck, axillae and perineum skin are seen.

Enlargement of liver and kidneys with grayish white foci are seen.

Microscopic appearance

The blood vessels in almost all organs show a pathognomonic lesion in the form lymphocytic arteritis, which characterize by necrosis of media, endothelial swelling of the intema and infiltration with lymphocytes (Fig. 42).

The lymph nodes show hyperplasia of the reticuloendothelial cells, edema and dilated lymphatics. Destruction and loss of the mature small lymphocytes and much of their debris is ingested by macrophage.

The liver and kidneys show foci of lymphocytic aggregations.

Alimentary and upper respiratory epithelium show erosions and necrosis. Infiltration of inflammatory leukocytic cells in the submucosal connective tissue is noticed.

Brain shows meningioencephalitis characterized by edema of the meninges and leukocytic infiltration of all types of inflammatory cells in the meningeal spaces. Moreover, perivascular edema and lymphocytic cuffing infiltration in Virchow. Robin space are seen. Necrotic vasculitis and neuronal degeneration are recorded.

Corneal epithelium undergoes degeneration and vesiculation beside edema of the lamina propria.

Iridocyclitis beside fibrinous exudate in the anterior and posterior chambers are observed.

Fig. 37: Cattle infected with malignant catarrhal fever showing  corneal opacity.

Fig. 38: Cattle infected with malignant catarrhal fever showing  corneal opacity.

Fig. 39: Cattle infected with malignant catarrhal fever showing  red muzzle besides presence of dried crusts.

Fig. 40: Cattle infected with malignant catarrhal fever showing congestion of the tongue with sharply irregular erosion

Fig. 41: Malignant catarrhal fever showing congestion and hemorrhages in distal colon. “Tiger striping”.

Fig. 42: Cattle infected with malignant catarrhal fever showing lymphocytic arteritis, which characterize by necrosis of media, endothelial swelling of the intema and infiltration with lymphocytes. H&E

Diseases caused by Adenoviridae

Adenoviruses are highly species specific, double. stranded DNA viruses, which replicate in the nucleus forming basophilic intranuclear inclusion bodies (masses of virions). The majorities are not producing serious diseases except canine hepatitis. Adenoviruses commonly infect the respiratory and enteric tract.

Infectious canine hepatitis

Hepatitis contagiosa canis

It is one of the few mammalian adenoviral diseases characterize by pharyngitis, tonsilitis, diarrhea, enlarged necrotic and congested liver with basophilic intranuclear inclusion body. The majority of infections are a symptomatic, and infection that results in disease usually is not fetal.

Cause

The disease is caused by canine adenovirus.

Pathogenesis

The virus is disseminating through urine excretion and infection usually occurs through naso-oral infection. The virus has a tropism to vascular endothelium and hepatocytes. The viruses firstly replicate at the pharynx leading to pharyngitis and tonsillitis. The virus gets entry to blood and localize in different tissue, which replicate in the endothelial cells of blood vessels inducing their damage leads to disseminated intravascular coagulation and hemorrhagic diathesis. The viruses particularly replicate in the hepatocytes inducing its necrosis. Later on platelets and coagulation cascade inhibit leading to bleeding. 

Signs

It is mostly occurs in young dogs. The course usually short and the signs appear shortly before death.

The diseased dogs show anorexia, thirst, vomiting and diarrhea. Hemorrhage and abdominal pain expressed by moaning sound are observed.

Nervous manifestations are uncommon, and when observed, take the form of clonic spasms of the extremities and paralysis of hindquarters. The mucous membranes are usually anemic and sometime icteric.

Congestion of the conjunctiva with copious lacrimation and diffuse cloudiness of the cornea (blue eye) are seen.

Lesions

Wide spread hemorrhages particularly in stomach and serosal surface are seen.

Congestion and enlargement of the liver and kidneys, besides edematous wall of gallbladder are observed. The spleen and lymph nodes are edematous and congested and may be hemorrhagic.

Microscopically, The liver shows periportal necrosis besides basophilic intranuclear inclusion bodies in degenerating hepatocytes adjacent to necrosis (Figs. 43, 44 & 45). Moreover, the inclusion bodies are seen in reticuloendothelial cells and endothelium of the spleen and lymph nodes.

Hemorrhage and edema are seen particularly in lymph nodes, tonsils, stomach, mesentery and under serosal surfaces.

Brain shows symmetrical hemorrhages with intranuclear inclusion bodies in endothelial lining. Moreover, encephalomalacia and gliosis are seen.

The cornea is edematous and infiltrated with neutrophils, lymphocytes and macrophages. Inclusion bodies may be seen in ciliary body and iris.

Fig. 43: Microscopic picture showing widespread periportal hepatic necrosis caused by Infectious Canine Hepatitis .H&E

Fig. 44: Liver of dog infected with infectious canine hepatitis showing hepatic coagulative necrosis, hemorrhage and congestion besides intranuclear inclusion bodies. H&E

Fig. 45: Liver of dog infected with infectious canine hepatitis showing hepatic coagulative necrosis and congestion besides intranuclear inclusion bodies. H&E

Diseases caused by Picornaviridae

Picornaviruses are divided into enteroviruses, rhinoviruses and cardioviruses and aphthviruses. They are single stranded RNA viruses.

Diseases caused by Aphrhoviruses

Foot and Mouth Disease (Aphthus Fever)

Foot and mouth disease (FMD) is an acute widespread infectious epitheliotropic viral disease of all cloven-hoofed animals and characterized by the formation of vesicles and erosions in the mouth and on the feet in adult animals and high morality in young age

Cause

It is the only disease caused by the viruses of Aphthovirus group. It is the first animal viral to be recognized in the history. There are 7 main serotypes O, A, C, SAT 1, SAT 2, SAT 3 and Asia 1

In Egypt, The serotype O type is the only one present in Egypt. Although the signs and lesions produced by different serotypes are similar, infection with one virus serotype does not immunize against others.

Susceptible hosts

The disease mainly occurs in cloven-hoofed animals, the most important in which are cattle, buffalo, sheep, swine and goats.

Camels appear to be less susceptible. Moreover, humans can take the natural infection with formation of vesicles in hands, feet and oral mucosa.

Route of infection and pathogenesis

The infected animals excrete the virus in the saliva, nasal discharges, urine, feces, milk and semen. Recovered cattle can carry the virus up to 2 years, but recovered sheep can carry the virus up to 6 years.

The virus can be carried not only by the infected animals but also mechanically by humans and others animals, shoes, migratory birds, and animals byproducts.

The infection is spread directly through air born route and ingestion. Following infection, the virus replicates in the pharynx or respiratory tract, then reaches the lymphatics in the mucous membranes of the oropharyngeal region to the blood with subsequent to viremia and less localization particularly in the epithelium of the mouth and feet, and to a extent, the teats.

Signs

The signs usually related to lesions. After incubation period of 2-6 days, fever anorexia, salivation (Fig. 46) and painful eating with smacking of the lips and the tongue is noticed. Vesicles appear on the tongue, dental pad, and buccal mucosa. Moreover, the vesicles can be seen on lightly haired skin such as udder, vulva and conjunctiva.

Lameness occurs due to development of vesicles in the feet, particularly the cleft, heel and coronet (Fig. 47)

In young animals such as calves and lambs mortality rate is very high due to myocarditis and gastroenteritis (Fig. 48). Mortality rate in adults is about 2%, but in calves it is up to 20%

Gross lesions

The distribution of vesicles and erosion in buccal cavity is characteristic. The vesicles are seen on oral mucosa, dental bad, over the lips , palate and dorsum of the tongue (Figs 49 & 50).

Also, vesicles and erosion and erosions near the coronary band and adjacent to interdigital clefts are common. Moreover, vesicles and erosion are seen in lightly haired skin as teats and vulva. Rumen, reticulum, omasum show vesicles also. 

Abomasum may shows focal hemorrhages and diffuse edema of the mucosa. The small and large intestine show focal hemorrhages, congestion, or diffuse edema of the mucosa.

In young calves and lambs, lesions in the myocardium are most common in the fatal disease. These consist of small, grayish foci of irregular size in the wall and septum of left ventricle. The necrosis may give the myocardium a somewhat stripped appearance (tiger heart).

Microscopic appearance

The lesions of the epithelium of tongue, dental pad, buccal mucosa are started in stratum spinosum. The intercellular bridges of the epithelial cells retract and then disappear, and the cells become loosened from one another. The cells undergo hydropic degeneration and liquefactive necrosis.  These changes are associated with infiltration of edematous fluid leading to the formation of small vesicle (aphthae).  The vesicles coalesce to form larger ones  (bullae) which compressed the surrounding epithelium with intact basal cell layer

The rupture of the vesicles lead to formation of erosions. The dermis is heavily congested and infiltrated by inflammatory cells. Vesicles in the feet and erosions are formed in the same manner as that in the oral mucosa.

 Heart shows hyaline degeneration and coagulative necrosis of the cardiac muscle fibers besides intense infiltration of inflammatory cells, mainly lymphocytes, between the cardiac muscle fibers (Fig. 51).

Fig. 46: Cattle infected with foot and mouth disease showing excessive salivation resulted from oral lesions

Fig. 47: Sheep infected with foot and mouth disease showing lameness occurs due to development of vesicles in the feet, particularly the cleft, heel and coronet.

Fig. 48: Cattle infected with foot and mouth disease showing rupture gum vesicles.

Fig. 49: Cattle infected with foot and mouth disease showing rupture tongue vesicles.

Fig. 50: Died calf infected with foot and mouth disease due to myocarditis

Fig. 51: Microscopic picture of myocardium of died calf infected with foot and mouth disease showing necrotic myocarditis infiltrated with lymphocytes. H&E

Diseases caused by Reoviridae

Reovirus replicate in the cytoplasm and many of them produce eosinophilic cytoplasmic inclusion bodies. It contains 6 genera. The genus orbivirus contain the most important pathogens for animals, such as bluetongue, and African horse sickness. The rotaviruses cause many enteric affection in animals.

1. Bluetongue (Soremuzzle)

It is an infectious insect born disease of sheep and occasionally other ruminants caused by orbivirus and characterized by edematous and cyanotic tongue, stomatitis, rhinitis and lameness.

Cause

The disease is caused by double stranded RNA orbivirus, which multiplies in arthropods as well as in vertebrates. There are 24 serotypes.

Susceptible hosts

Bluetongue is mainly a disease of sheep. Cattle and goat are less susceptible. In cattle the infection usually not apparent. The cattle can carry the viruses and viremia occurs from time to time adequate for insect transmission.

Route of infection and pathogenesis

The virus is transmitted through insects biting of genus Culicoides. The virus gets entry to the host through insect biting. After the entry of the virus, it multiplies in the hematopoietic cells, and then reach to blood resulting in viremia. The virus has affinity to replicate in the endothelial cells of blood vessels, resulting in endothelial swelling and necrosis. The damaged endothelial cells lead to widespread hemorrhages, infarctions and edema. The tongue is edematous and cyanotic due to hemorrhage in lingual papillae and among the muscle bundles, which become necrotic.

Signs

In sheep after incubation period (4 to 7 days), the diseased animal shows high fever associated with reddening of the buccal and nasal mucosa and excessive salivation (Fig. 52).

Watery nasal discharge, which later become mucus and dry to form crusts (Fig. 53). Edematous swelling are seen involving lips, muzzle, tongue and intermandibular. The tongue shows severe edema and cyanosis that they have given the disease its name.

As the fever subside, the cornets become worm and tender. The pink perioplic band turns red, so the animal become stiff and lame (Fig. 54)

The disease may be terminate with sever emaciation. Moreover, abortions occur in pregnant animals after slight febrile reaction and slight reddening of the buccal mucosa.

In cattle, the disease is not always a symptomatic and occasionally severe signs are seen (Fig. 55)

Macroscopic appearance

The muzzle, tongue, cheeks and lips are hyperemic, edematous cyanotic with erosions and even ulceration of the mucosa (Fig. 56). Hard palate, dental pad, esophagus, reticulum and rumen show erosion, congestion and hemorrhages (Fig. 57).

The subcutaneous tissue of head, neck and intermandibular space are edematous. The wall of the hoof shows red streaks (Fig. 58). The skeletal muscles particularly above the scapula show petechiae and pale areas

The spleen is congested and enlarged besides moderate inflamed and edematous lymph nodes. The heart show sub endocardial hemorrhages in the left ventricle

Microscopic appearance

Fig. 52: Sheep infected with blue tongue showing reddening of the buccal and nasal mucosa

Fig. 53: Sheep infected with blue tongue showing lameness

Fig. 54: Sheep infected with blue tongue showing dried crusts around the nostrils.

Fig. 55: Cattle infected with blue tongue showing  excessive salivation.

Fig. 56: Sheep infected with blue tongue showing   Intense congestion cyanosis and swelling of lips and gums and tongue.

Fig. 57: Sheep infected with blue tongue showing congestion and hemorrhages in esophagus

Fig. 58: Blue tongue. Lesion on the coronary band of a sheep.

African Horsesickness

It is a highly fatal infectious disease of Equidae caused by an orbivirus that is transmitted by several species of Culicoides and characterizes by hydrothorax and pulmonary edema or hydropericardium and cardiac degeneration with ascites.

Cause

The disease is caused by an orbivirus closely related to bluetongue virus. There are several serotypes, which is not entirely cross protective.

Susceptible hosts

Horses, mules donkeys, goats, dogs and ferrets are susceptible to natural infection. The disease in mules is less severe than in horse, but more severe than in donkeys.

Dogs and foxes are found to be susceptible to infection by ingestion of infected meat.

Route of infection and pathogenesis

The disease is transmitted through biting of blood sucking insects as Culicoides. The pathogenesis has not been completely understood. The endothelial damage is not obvious as in case of bluetongue.

Signs

The clinical signs take on of four forms

1. The mild form is often seen in partially immunized animals specially donkeys. The diseased animals are febrile for more than 1. 2 days, anorexia, dyspnea and conjunctivitis. Recovery is occurred rapidly.

2. Acute pulmonary form (Dunlop) shows sudden fever, dyspnea (due to pulmonary edema) with frothy exudate from nostril (Fig. 59). Sweating and cough followed by death within few hours.

3. Subacute cardiac form (Dikkop) is characterized by long course of the disease. The cardiac form shows edematous swelling of the head, lips, eyelids and neck with a prominent obliterating of the supraorbital fossa and jugular groove (Fig. 60).

Abdominal pain and paralysis may be seen. The death is may be due cardiac failure.

4. Mixed form is characterized by a combination of pulmonary and cardiac forms.

Lesions

The pulmonary form shows hydrothorax and edema of the lung (subpleural, interalveolar and alveolar) (Fig. 61). Moreover, froth plugs the respiratory passage (Fig. 62). On cut section, the lung oozes a clear frothy fluid.

Microscopically, edema of the interlobular stroma is observed. Fibrin and proteinaceous material is recognized in the edematous fluid, which contain few leukocytes. In some cases, leukocytes may be present in sufficient numbers to suggest bronchopneumonia).

Cardiac form: Hydropericardium and ascites beside subendocardial and subepicardial petechial hemorrhages and inflammatory edema are seen (Fig. 63). The draining lymph nodes appear soft and swollen. The spleen, liver, and kidneys are congested.

Edema around pharynx, which causes esophageal paralysis, may be recorded. Hemorrhages are common in gastric mucosa.

Microscopically, focal necrosis in the myocardium usually associated with hemorrhages is seen. Edema of the adventitia of arterioles is observed. Depletion of lymphocytes from spleen and lymph nodes beside increase of reticuloendothelial and plasma cells may be seen.

Fig. 59: Horse near to death due to acute respiratory form showing severe nasal frothy discharge.

Fig. 60: : Horse infected with  subacute cardiac form showing prominent obliterating of the supraorbital fossa and jugular groove.

Fig. 61: Horse infected with  acute respiratory form form showing hydropericardium and hydrothorax.

Fig. 62: Horse infected with  acute respiratory form showing frothy exudate in trachea.

Fig. 63: Heart of horse infected with subacute cardiac form showing petechial hemorrhages.

Disease caused by Rotaviruses

Rotaviruses cause enteric diseases with signs characterized by diarrhea, vomiting and abdominal pain. The viruses affect mainly newborn animals and young age. The virus consists of double layered icosahedral capsid enclosing a core of double stranded RNA.

Neonatal calf diarrhea

It is a serious disease of calves occurs during the first 2 weeks. The essential etiologic factor is rotavirus associated with enteric bacteria as E coli. The diseased animal suffered from diarrhea, which lead to dehydration and death (Figs. 64, 65 & 66).

Fig. 64: Calf infected with neonatal calf diarrhea showing diarrhea and dehydration.

Fig. 65: Calf infected with neonatal calf diarrhea showing diarrhea and dehydration and recumbency.

Fig. 66: Calf infected with neonatal calf diarrhea showing widening and flattening of intestinal villi, besides leukocytic infiltration in lamina propria. H&E.

Virus Diarrhea and mucosal Disease

It is an acute infectious disease of cattle, which caused by pestivirus and characterized by diarrhea and erosions on the digestive tract.

Cause

It is caused by RNA pestivirus. Antigenically related viruses cause the two syndromes.

Susceptible hosts

Cattle and buffalo are the only susceptible hosts. Young animals without maternal immunity and less than 2 years of age are most susceptible to the disease.

Mode of transmission and pathogenesis

The disease is transmitted by direct and indirect contact, particularly through ingestion and inhalation of infected saliva, oculonasal discharge, urine and feces. The virus is present in two forms, cytopathogenic BVDV (cpBVDV) and noncytogenic BVDV (noncpBVDV) according to its effect on tissue culture. Moreover, the cpBVDV has 80kDa protein. The cattle postnatally infected with cpBVDV between 6 months to 2 years develop bovine viral diarrhea with high morbidity and low mortality. Meanwhile, mucosal disease with low morbidity and high mortality developed in cattle infected intra-uterine with noncpBVDV and become tolerant. The disease develop when the virus undergoes transformation to cpBVDV BY RNA recombination

Signs:

The diseased cattle show fever, anorexia, depression and diarrhea (Fig. 67). Moreover, excessive salivation with stringy mucus hanging from the muzzle to ground is characteristic.

Erosion and ulcers are seen on muzzle and nose. The conjunctiva may be congested and the animal is emaciated and dehydrated.

Abortion and still birth are recorded in pregnant animals. Congenital cerebral hypoplasia, cataract, micorphthalmia and others malformation are seen in calves born to infected dam. Calves born alive may be persistently infected and later develop mucosal disease.

Gross appearance

The diseased animals are dehydrated and emaciated. The lesion usually restricted to the gastrointestinal tract.

Erosions or well circumscribe ulcers of irregular shape are seen on inside the lips, gums, check, dental pad, posterior part of the hard palate, and on the lateral surface of tongue (Fig. 68). Ulcers are seen also on muzzle and external nares.

The pharynx shows ulcer, which may be extended, to larynx. The esophagus shows ulcer and erosion. Rumen and omasum show ulcer and erosion (Fig. 69)beside erosions in the folds of the fundus and submucosal hemorrhage and edema of the abomasum wall.

Congestion and erosions are noticed in small intestine, cecum and colon particularly the areas above Payer’s patches. Necrosis is seen in lymph node and spleen.

In cattle with chronic mucosal disease, chronic ulcer are seen on the oral cavity and on skin particularly perineum, skin horn junction and around hooves

Microscopic appearance

Erosions are represented by necrosis of the cells of stratum spinosum and granulosus with intact basal cell layer followed by necrosis of the upper layers their removal leading to ulcer are seen on buccal cavity and esophagus (Figs. 70 & 71). No vesicles are seen.

The abomasum shows atrophy and cystic changes of the gastric glands, besides edema and erosion and occasional hemorrhage are common in the lamina propria and submucosa (Fig. 72). The intestine showed catarrhal and necrotic inflammation (Figs 73 & 74)

Focal areas of necrosis and erosions of the epithelium particularly over Payer's patches are seen in small and large intestine. The lymphoid follicles and lymph nodes show necrosis of lymphocytic elements (Fig. 75 8).

Fig. 67: Calf infected with BVD showing diarrhea and dehydration.

Fig. 68: Calf infected with BVD showing necrosis and ulceration of tongue and esophagus.

Fig. 69: Rumen of calf infected with BVD showing necrosis .

Fig. 70: Tongue of calf infected with BVD showing erosions are represented by necrosis of the cells of stratum spinosum and granulosus with intact basal cell layer. H&E

Fig. 71: Esophagus of calf infected with BVD showing ulceration of the epidermis besides infiltration of the lamina propria with inflammatory cells. H&E

Fig. 72: Abomasum of calf infected with BVD showing erosion. H&E

Fig. 73: Intestine of calf infected with BVD showing increase number of goblet cells, congestion of blood vessels and infiltration of lamina propria with inflammatory cells. H&E

Fig. 74: intestine  of calf infected with BVD showing necrosis of lining epithelium beside infiltration of lamina propria with inflammatory cells (necrotic enteritis). H&E

Fig. 75: Bayer's batches showing    necrosis of lymphocytic element. H&E

Rift Valley Fever

It is an acute arthropod transmitted viral disease of sheep and cattle characterized by hepatitis and high mortalities among lamb and calves and abortion in pregnant ewe and cow.

Cause and hosts

It is caused by negative sense single stranded RNA virus. The virus is a member of Bunyaviridae. The virus develops in cytoplasm and bud into the smooth surfaced membrane in or adjacent to the Golgi region.

Sheep and cattle are usually highly susceptible. Buffaloes, goat and camels can be infected and show symptoms of varying intensity. Human may be infected through handling the infected animals or the virus in the laboratory.

Route of infection

Infection occurs through biting of arthropod vectors (Aedes and Culex).

Signs

The signs appear after short incubation period of 20 to 72 hours. The acute form usually seen in calves and lambs and less in adult sheep and the diseased animals die within 24 hours.

The lambs may be refusing to eat and move, exhibit signs of abdominal pain. The animal becomes recumbent and unable to move shortly before death.

The adult sheep may be die without any signs or show vomiting, mucopurulent nasal discharge and diarrhea. The pregnant ewes usually abort during illness or convalescence.

Cattle may suffer from fever, anorexia, profuse salivation, diarrhea, abdominal pain and a storm of abortion in pregnant animals. Moreover, erosion on the buccal mucosa and encrustation around the muzzle besides necrosis of skin of udder and scrotum are seen. The mortality rate in cattle is not high.

Lesions

The main and characteristic lesions are seen in liver. The liver is enlarged, mottled, and show subcapsular gray foci of Centro-lobular necrosis (Figs. 76 & 77). The gall bladder is distended with bile beside thickened edematous wall and subserosal hemorrhages. Some cases showed abomasal and intestinal hemorrhages.

Fig. 76: Liver of sheep infected with rift valley fever showing congestion and subcapsular necrosis.

Fig. 77: Liver of sheep infected with rift valley fever showing subcapsular hemorrhage necrosis and yellowish coloration.

Microscopically, the gray foci represented by necrosis of the hepatocytes near the central veins. The paracentral location suggested that the necrosis is due to hypoxia (Fig. 78).

The affected liver cells show more eosinophilic cytoplasm and fragmented nuclei (Councilman bodies). Intranuclear inclusion bodies (May be due to degenerative changes not due to viral particles). Congested hepatic blood vessels beside lymphocytic infiltration of the portal areas are seen.

The visible mucous membranes are cyanotic particularly over the head and neck beside congestion of subcutaneous blood vessels. The mammary glands may be purple in color.

Hemorrhagic gastroenteritis and hyperemic and edematous lungs with sub pleural hemorrhages are seen (Fig. 79 & 80). Ulceration of the intestinal mucosa particularly terminal portion of the ileum, cecum, and initial part of colon are seen.

Spleen is enlarged with subcapsular hemorrhages. The malpighian bodies are indistinct due to lymphocytic depletion. Red pulps show congestion and infiltration with neutrophils. Kidneys are enlarged and show microscopic evidence of nephrosis.

Moreover lymph nodes are enlarged, moist and congested. Necrosis of the lymphoid elements, congestion and edema beside infiltration with neutrophils, is seen.

Hemorrhages may also be found in the peritoneum, pleura, pericardium, endocardium, adrenals, and thymus.

Fig. 78: Liver of sheep infected with rift valley fever showing hepatic coagulative necrosis represented by pyknotic nucleus. The surrounding hepatocytes showing fatty changes. H&E

Fig. 79: Abomasum of sheep infected with rift valley fever showing hemorrhages.

Fig. 80: Small intestine of sheep infected with rift valley fever showing petechial hemorrhages on serosa.

Rabies, Lyssa, Hydrophobia

It is highly fatal viral disease of all warm-blooded animals including man. It is primarily a disease of carnivores. Moreover, it is the cause of a lethal encephalomyelitis and ganglionitis in many areas of the world.

Cause and susceptible host

The disease is caused by  an enveloped RNA rhabdovirus. The virus is neurotropic, but has an affinity for salivary glands. There are two strain of virus; street strain and fixed strain. All warm-blooded animals human and birds are susceptible. Vampire bat, wild carnivores, wolves are important reservoir.

The incubation period is varied according to the site of bite and amount of saliva. It varied from two weeks to several months or even year.

Route of transmission and pathogenesis.

The virus is present in saliva of rabid dogs up to five days before signs appear.

The infection occurs through bite of a rabid dog. The virus present in saliva of affected dogs up to 5 days before clinical signs appeared. Following inoculation of rabies virus, the virus enters myocytes where it can replicate. Then the virus moves through the muscle into the axoplasm of the peripheral nerve. Then the virus moves centripetally to the dorsal root ganglion then to spinal cord to brain.

The virus replicate in the nerve cells causing its degeneration and necrosis besides necrosis of endothelial cells. The irritation of nerve cells lead to excitability manifested by furious form. Moreover, degeneration led to paralysis. Due to the paralysis of deglutition muscles the animal not able to swallowing and the saliva dribbles from mouth. Paralysis of respiratory muscles leads to death. Perivascular cuffing was seen due to degeneration of vascular endothelium.

Moreover, the virus spread along the nerve that supply salivary glands, reach them and excreted through saliva.

Signs

Cattle, sheep and sheep

The affected animals bellow and bleat beside tenasmus and paralysis of the anus, knuckling of hind quarters and  terminate with paralysis. Moreover, the diseased animals may attack other animals or bit itself (Fig. 81)

Dog and cat

The disease takes two forms; furious form or dumb form.

In furious form the diseased animals are highly excitable, biting animals, human and even inanimate objects and run aimlessly with dribbling of saliva. The eyes appeared red beside lose of corneal reflex.

In dumb form, the animal does not obey orders, rarely bites and not recognize its owner. The lower jaw showed paralysis besides dribbling of saliva. Death occurs in 3 to 4 days after onset of signs and usually within 10 days.

Horse usually express signs of colic besides mania.

Gross appearance

The gross lesions of the infected central nervous system are limited to the nervous system and represented by meningeal congestion and petechial hemorrhages.

Microscopic appearance

The lesions are mainly in brain and characterized by non-suppurative encephalitis, besides meningitis, perivascular cuffing with round cells.

The presence of intracytoplasmic inclusion bodies (Negri bodies) (Fig. 82&83), which initially developed as aggregation of stand of viral nucleocapsid in neurons and peripheral ganglia are characteristic. The inclusion body occurred either in the cell body or in dendrites.

In rabid dogs, Negri bodies are found mainly in hippocampus but in cattle, Negri bodies are seen in Purkinjie cells of the cerebellum where they are likely to be elongated.

Diffuse gliosis (babe’s nodules) and neuronal degeneration may found in the brain.

Other lesions such as catarrhal gastritis and inflammation of the respiratory mucosa and salivary gland were seen.

Fig. 81:Clinical signs of donkey infected with rabies. The diseased animals may attack  or bit itself

Fig. 82: Brain of animal infected with rabies showing intracytoplasmic eosinophilic inclusion body (Negri body) in neurons. Moreover, some neurons are degenerated, others showing satellitosis and neuronophagia besides gliosis. H&E

Fig. 83

PRION

They are infections agents that cause a group of diseases (spongiform encephalopathy) in humans and animals which include scrapie, bovine spongiform encephalopathy, transmissible mink encephalopathy, chronic wasting disease of mule deer and elk, spongiform encephalopathy of cats, kuru, Creutzfeldt-Jakob disease and Gerstmann- Straussler syndrome. The incubation period is long (months to decades). The course lasts weeks to years, slowly progressing to death. Lesions are mostly restricted to the CNS which restricted to the CNS which shows neuronal vacuolation (spongiform degeneration), astrocytosis, and often amyloid plaques. Immunosuppression potentiation does not alter the incubation period, course or duration of the disease. Immune B-cell and T-cell functions are intact.

Prions are filterable, resistant to most physical and chemical virucidal treatments (ultraviolet radiation, ionizing radiation, ultrasonication, proteases, nucleases, heat, formaldehyde, chloroform and ether). It may be an abnormal isoform of protein. The animals, susceptible to prion disease, bear a gene (PrP gene) which encodes for normal prote- in called prion protein (PrP) or cellular prion protein (Pr Pc) which attaches itself to the outer leaflet of plasma membrane lipid bilayer.

An abnormal isoform of PrP (usually called scrapie PrP “Pr Psc”, or scrapie-associated fibril protein “SAF”) is generated in case of spongiform encephalopathies and accumulates in and around neurons as large aggregates of polymerized macromolecular fibrils, comparable to amyloid protein. These fibrils are resistant to  proteases whereas normal PrP is not. Both Pr Pc and Pr Psc are transcribed from the same gene. Mutation of the PrP gene results in different strains Pr Psc in the same host which may control the disease incidence, breed and species susceptibility and incubation period.

Passage of prion through an alternate host alters the prion (passage of sheep-scrapie though mink causes the prion to lose its pathogenicity for mice, passage of goat scrapie through monkeys causes the prion to lose its pathogenicity for sheep). It is possible that the various spongiform encepalopathies are each caused by a variant strain of scrapie agent. T

he disease, in cattle, was caused by ingestion of meat and bone meal from scrapie-infected sheep. The disease may be inherited in humans (Gerstmann-straussler syndrome) with mendelian dominent pattern, resulting in different mutations within the PrP gene giving rise to different prion diseases.

Scrapie of Sheep

(Ovine Spongiform Encephalopathy)

 Is a disease of sheep and goats, deriving its name from the continuous scraping of the skin against objects due to pruritus. The infectious agent “Prion” causes spongiform encephalopathy of sheep, goats, other animals and humans. It is transmitted from ewes to lambs, early in life and prenatal. Lateral transmission (via the oral, nasal and parental routes) is believed to occur among adult sheep from the persistent contaminated environment for a long time. The incubation period (1 – 5 years) restricts the signs to adult sheep. The animals become restless with startlet look, wild fixed eye with dilated pupil. The sheep may hold its head down and wag it as if hunting a fly. Stiffness of the forelegs grinding teeth, twitching muscles of lips, shoulders and thighs and epileptiform seizures of brief duration are noted. Intense pruritus leads to rubbing against objects and loss of wool (Fig. 84). Finally the animal shows recumbency, paralysis and death.

Microscopic lesions are limited to the medulla oblongata, pons, midbrain and spinal cord in the form of large vacuoles in the cytoplasm of neurons. Astrogliosis and perivascular cuffing with lymphocytes are encountered. The affected neurons are prevalent just anterior to the calamus scriptorius and in reticular formation, beside the medial vestibular and lateral cuneate nuclei. Amyloid plaques (prion protein) are found in the molecular and granular layers of the cerebellum. Neutral fat can be demonstrated in the white matter.

Fig. 84: Sheep showing loss of wall due to intense pruritus leads to rubbing against objects

Fig. 85:Sheep infected with scrapie showing large vacuoles in the cytoplasm of brainstem neurons

Fig. 86: Cattle Infected with bovine spongiform encephalopathy showing locomotor disturbances

Bovine Spongiform Encephalopathy

BSE is a progressive neurological fatal disease of adult domestic cattle, which closely resembles sheep scrapie.

 It is caused by a prion, identical with the cause of scrapie. Fibrils, comparable to  scrapie-associated fibrils (SAF) are seen in the brain of infected cattle. Meat and bone meal, from scrapie-infected sheep, induced the disease in cattle. Inoculation of brain homogenates, from natural cases, transmitted the disease.

The affected cattle show locomotor disturbances, exhibit apprehension and aggression when handled. Hind-leg ataxia and loss of condition over 1 – 4 months (Fig. 86) end with death, mostly of 2 – 5 year old dairy cows.

There are no abnormalities in gross pathology and the significant necropsy findings are histological changes in the brain that comprise bilaterally symmetric intracytoplasmic vacuolation of neurons and gray matter neuropil "spongiosis" similar to the lesions seen in scrapie (Figs. 87& 88).

Fig. 87:  Microscopic lesions present in a the brain of a cow with bovine spongiform encephalopathy . Note vacuolization within the cytoplasm of nerve cells.

Fig. 88:  Microscopic lesions present in a the brain of a cow with bovine spongiform encephalopathy . Note vacuolization within the cytoplasm of nerve cells.