Soliman Mohammed Soliman, D.V.M, Ph.D....Ulcerative lymphangitis 8. Neonatal bacterial infections a)Neonatal streptococcal infection b)Shigellosis c)Colibacillosis d)Salmonellosis

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Soliman Mohammed Soliman, D.V.M, Ph.D.Lecturer of Infectious Diseases, Dept. of Medicine & Infectious Diseases

1. TETANUS (LOCKED JAW)

2. GLANDERS

3. STRANGLES

4. EQUINE PURPURA HEMORRHAGICA (PH)

5. RHODOCOCCUS EQUI

6. ABORTION IN MARES (SALMONELLOSIS)

7. DERMATOPHILOSIS

8. ULCERATIVE LYMPHANGITIS

9. EPIZOOTIC LYMPHANGITIS

10. SPOROTRICHOSIS

NEONATAL BACTERIAL INFECTIONS

a) NEONATAL STREPTOCOCCAL INFECTION

b) SHIGELLOSIS

c) COLIBACILLOSIS

d) SALMONELLOSIS

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1. Tetanus (locked jaw)

2. Glanders

3. Strangles

4. Equine purpura hemorrhagica (PH)

5. Rhodococcus equi

6. Abortion in mares (Salmonellosis)

7. Ulcerative lymphangitis

8. Neonatal bacterial infections

a) Neonatal streptococcal infection

b) Shigellosis

c) Colibacillosis

d) Salmonellosis

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Diseases causing nervous manifestation

• Tetanus.

• Listeriosis.

• Borna disease

• Rabies

• Equine viral encephalomyelitis

• Botulism

• Aflatoxicosis

• Plant poisoning

• Chemical poisoning

• Strychnine poisoning

• Hypocalcemia

TETANUS(LOCKED JAW)

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TETANUS (LOCKED JAW)

It is a highly fatal infectious non febrile bacterial disease

of animals and man caused by the toxin of Clostridium

tetani and characterized clinically by hyperaethesia

(excessive sensitivity) and persistent spasms of the

voluntary muscles resulting in death.


Clostridium tetani toxin

Wound with damaged tissues that absorbed toxin

Gram positive

Anaerobic spore forming

Haemolytic toxin

(tetanolysin)

Neurotoxic toxin

(tetanospasmin)

Spores are highly resistant, remained indefinitely in soil

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Epidemiology:

• Wounds have to be deep, lacerated with low tissue oxygenation with presence of pyogenic infection that will ease the the growth and vegetation of spores and toxin production.

• Horse and man are highly susceptible.

• Sheep, goat and cattle are less susceptible.

• Dog and cat are rarely get infected.

• Young animals are more susceptible than adults.

• Cl. tetani present in the soil and manure of the horse in large numbers.

• Mode of infection occurs through deep puncture or lacerated wounds and traumatized tissues (castration, foot wound, dehorning, umbilical infection, etc...).


Pathogenesis:

• Tetanus toxin consists of two chains, the light toxic chain and the heavy chain responsible for receptor binding to the ganglion receptor on motor neuron terminals and is transported to the nerve cell body and its dendritic processes in the central nervous system.

• Toxin also can be blood born , especially w hen produced in large amounts and can be then bind to motor terminals throughout the body prior to transfer to the central nervous system. Bound toxin is not neutralized by antitoxin.

• It blocks the transmission of inhibitory signals in the terminals of inhibitory neurons resulting in spastic paralysis.

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Clinical signs:

• Incubation period is usually 1-3 weeks but depends on site of infection and potency of toxin.

• Bad prognosis and fatal courses is expected in cases of lock jaw , fever, recumbency and presence of the infected wound close to the brain

• Course of tetanus is varied between animals from 5-10 days.

• Hyperesthesia followed by muscular stiffness, tremors and spasms in the head and extend backward along the whole body musculature.

• Erection of ears, prolapse of third eyelid and dilatation of the nostrils.

• Locked jaw, due to spasms of masticatory muscles, stiffness in the neck muscles and rigidity of whole body., Generalized muscle stiffness can result in a saw-horse stance.

• Shallow rapid respiration and altered heart rate.

• Tail is raised, urine retention and constipation.


Diagnosis:

• Depends on the presence of a wound, clinical signs (diagnostic) and detection of drum stick like Cl. tetani bacilli in gram stained wound smear.

• Strychnine poisonning (intermittent or clonic spasms, Occur as outbreak as it added in ration as stomachic.).

• Lactation tetany (hypocalcemia, usually in late pregnancy or after parturition, respond to calcium therapy).

• Acute laminitis and muscular rheumatism, respond well to anti-inflammatory drugs, No ear erection, protrusion of 3rd eye lid or lock jaw..

Differential Diagnosis:

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Management:

BACTERIA

TOXINS

WOUND

SIGNS

Control

Penicillin: high doses 10,000 I.U/kg B.W/ by I/M route for 3-5 days.

Antitetanic serum: 300,000 I.U by I/V or I/M route or S/C every 12 hours 3 times.

Cleaning the wound: By hydrogen peroxide (source of oxygen)

Sedative and muscle relaxant: to reduce spasms and pain

Supportive care: remove shoes, keeping animal in dry, quite, dark place with slinging of animal to prevent falling, back racking, catheterization, tracheal tube to prevent suffocation ..... etc.

those animals which have received antitoxinToxoid may be given subcutaneously to promote an active immune response even in those animals which have received antitoxin


Prophylaxis:

Disinfection of surgical equipment's.

Prophylactic dose of antitetanic serum after operations: 1500 - 3000 I.U.

Vaccination: by formalized, alum adjuvanted tetanus toxoid.

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STRANGLES(Equine Distemper, Shipping Fever of Equines)

STRANGLES

It is a common highly contagious bacterial disease affecting

mainly the upper respiratory tract of equines caused by

Streptococcus equi and characterized clinically by respiratory

manifestations and lymphadenopathy of the upper respiratory

tract lymph nodes.

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STRANGLES

Streptococcus equisubspecies equi type

C haemolytica

Gram positive

Two main strains vary in the pathogenicity

Atypical strain

• It's less virulent and frequently associated with mild form of clinical disease (Atypical Strangles).

The typical strain

• It's highly virulent encapsulated and produce honey mucoid colonies on blood agar.

• It has virulence factors such as hyalouronic acid capsule and M-protein.

STRANGLES

Epidemiology:

• Strangles is worldwide distributed affecting equines, where Horses are highly susceptible but donkeys and mules are less, susceptible

• Strangles is worldwide distributed affecting equines, where Horses are highly susceptible but donkeys and mules are less, susceptible

• It affects all ages but it is common among animals of 1-5 years old (Foals, Weaningles and Yearlings).

• It affects all ages but it is common among animals of 1-5 years old (Foals, Weaningles and Yearlings).

• It's common during periods of stress including inclement weather, poor nutrition, transportation, overcrowding ………..etc

• It's common during periods of stress including inclement weather, poor nutrition, transportation, overcrowding ………..etc

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STRANGLES

Transmission:

• As not a normal inhabitant in the respiratory tract of equines, equines acquired the infection either through direct contact between infected and healthy animals or indirect contact through fomites (feed, water, utensils) of infected animals.

• As not a normal inhabitant in the respiratory tract of equines, equines acquired the infection either through direct contact between infected and healthy animals or indirect contact through fomites (feed, water, utensils) of infected animals.

• Workers may also play a role in transmission of infection between infected and clean premises.

• Workers may also play a role in transmission of infection between infected and clean premises.

• The common sources of infection are discharges (Nasal discharges and pus ) from diseased animals, recovering or asymptomatic carriers or contaminated equipments.

• The common sources of infection are discharges (Nasal discharges and pus ) from diseased animals, recovering or asymptomatic carriers or contaminated equipments.

• Mode of Infection :is by ingestion and inhalation. • Mode of Infection :is by ingestion and inhalation.

STRANGLES

Transmission:

• Significant numbers of recovered animals continue shedding the organism after complete recovery for up to 4-6 weeks and small numbers will maintain the organism for more than 6 weeks as they keep the organism in guttural pouch and chondroid. Infected premises can harbor the infection for up to one year.

• Significant numbers of recovered animals continue shedding the organism after complete recovery for up to 4-6 weeks and small numbers will maintain the organism for more than 6 weeks as they keep the organism in guttural pouch and chondroid. Infected premises can harbor the infection for up to one year.

• Long term asymptomatic carrier animals are very important for maintenance of infection and initiation of outbreaks in free premises.

• Long term asymptomatic carrier animals are very important for maintenance of infection and initiation of outbreaks in free premises.

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STRANGLES

Pathogenesis:

• Infection occurred either via oral or nasal routes.

• The organism adheres to the epithelial cells of the buccal or nasal

mucosa and then rapidly spread to the draining lymph nodes of head and

neck (submandibular, retropharyngeal and parotid lymph nodes) then

clinical signs appear.

• Infection occurred either via oral or nasal routes.

• The organism adheres to the epithelial cells of the buccal or nasal

mucosa and then rapidly spread to the draining lymph nodes of head and

neck (submandibular, retropharyngeal and parotid lymph nodes) then

clinical signs appear.

STRANGLES

Clinical signs:

• The incubation period is 3-14 days. • The incubation period is 3-14 days.

• It depends on the immune status, age, history of previous infection, infecting strain and the infecting dose.

• It depends on the immune status, age, history of previous infection, infecting strain and the infecting dose.

• The course of the disease varied from 1 week in mild cases up to two months in severe cases.

• The course of the disease varied from 1 week in mild cases up to two months in severe cases.

• The morbidity rate may reach up to 100% especially in young ages with about 5-10% mortality rate.

• The morbidity rate may reach up to 100% especially in young ages with about 5-10% mortality rate.

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STRANGLES

Clinical signs:

• There are two forms:• There are two forms:

Typical Strangles

Atypical Strangles

STRANGLES

Clinical signs:


Typical Strangles

• Sudden onset of fever (39.5–40°C) caused by the pyrogenic exotoxin SePE-I, loss of appetite,

• Halitosis, difficulty in swallowing,

• Intermittent moist cough, extension of the head and neck,

• Nasal discharges (started serous, mucopurulent and ends with purulent discharges).

• Sudden onset of fever (39.5–40°C) caused by the pyrogenic exotoxin SePE-I, loss of appetite,

• Halitosis, difficulty in swallowing,

• Intermittent moist cough, extension of the head and neck,

• Nasal discharges (started serous, mucopurulent and ends with purulent discharges).

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STRANGLES

Clinical signs:


Typical Strangles

• Temperature declines in 1-3 days and begins to

raise with the involvement of the sub maxillary

lymph node and/or supra-laryngeal areas,

retropharyngeal and parotid which become hot,

swollen, painful and fill all the sub maxillary space

and may obstruct swallowing and respiration

leading to dyspnea and dysphagia as well as

Pharyngitis and laryngitis.

• Temperature declines in 1-3 days and begins to

raise with the involvement of the sub maxillary

lymph node and/or supra-laryngeal areas,

retropharyngeal and parotid which become hot,

swollen, painful and fill all the sub maxillary space

and may obstruct swallowing and respiration

leading to dyspnea and dysphagia as well as

Pharyngitis and laryngitis.

STRANGLES

Clinical signs:


Typical Strangles

• Once the lymph node abscess has

ruptured or after evacuation of pus,

Symptoms begin to subside and the

affected horse showed rapid clinical

improvement and may takes 3-7 days for

healing of the skin.

• Once the lymph node abscess has

ruptured or after evacuation of pus,

Symptoms begin to subside and the

affected horse showed rapid clinical

improvement and may takes 3-7 days for

healing of the skin.

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STRANGLES

Clinical signs:

Complications

• Occurred in approximately 20% of cases in the form of either:

Chronic guttural pouch empyema

Myocarditis and Aspiration Pneumonia

Conjunctivitis and purulent ocular discharges.

Periorbital abscess and eye lid swelling

Bastard Strangles

Purpura Haemorrhagica & myopathies (Immune-mediated)

Agalactia in lactating mares,

Laryngeal hemiplegia and tracheal compression due to mediastinal abscess.

• Occurred in approximately 20% of cases in the form of either:

Chronic guttural pouch empyema

Myocarditis and Aspiration Pneumonia

Conjunctivitis and purulent ocular discharges.

Periorbital abscess and eye lid swelling

Bastard Strangles

Purpura Haemorrhagica & myopathies (Immune-mediated)

Agalactia in lactating mares,

Laryngeal hemiplegia and tracheal compression due to mediastinal abscess.

STRANGLES

Clinical signs:


Typical Strangles

Atypical Strangles

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STRANGLES

Clinical signs:


Atypical Strangles

• Affected animals shows:

Mild respiratory signs,

Mild lymphadenopathy and

Abscess may not developed.

• Affected animals shows:

Mild respiratory signs,

Mild lymphadenopathy and

Abscess may not developed.

STRANGLES

Clinical signs:

BASTARD STRANGLES

• It's a complication of strangles occurred due to metastatic spread of the infection to lymph nodes and organs other than that of the head.

• Clinical signs varied depending on the site of infection including the retropharyngeal, cervical, tracheobronchial, pre-scapular, mediastinal, and mesenteric lymph nodes.

• Abscess also involve internal organs such as lungs, mesentery, liver, spleen, kidney, brain, spinal cord, vertebrae, joints, endocarditis, also subcutaneous abscess in periorbital, perianal, fascial and inguinal areas.

• Affected horses may show intermittent colic, recurrent pyrexia, inappetance, depression and weight loss.

• It's a complication of strangles occurred due to metastatic spread of the infection to lymph nodes and organs other than that of the head.

• Clinical signs varied depending on the site of infection including the retropharyngeal, cervical, tracheobronchial, pre-scapular, mediastinal, and mesenteric lymph nodes.

• Abscess also involve internal organs such as lungs, mesentery, liver, spleen, kidney, brain, spinal cord, vertebrae, joints, endocarditis, also subcutaneous abscess in periorbital, perianal, fascial and inguinal areas.

• Affected horses may show intermittent colic, recurrent pyrexia, inappetance, depression and weight loss.

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STRANGLES

Diagnosis:

1. Field diagnosis:

depends mainly on history and clinical signs.

2. Laboratory Diagnosis:

Isolation and identification of Streptococcus equi from the respiratory secretions or abscess

PCR and ELISA using SeM protein provide rapid useful method for diagnosis.

Hematological examination revealed leukocytosis with neutrophilia, anemia and hyperfibrinogenemia

1. Field diagnosis:

depends mainly on history and clinical signs.

2. Laboratory Diagnosis:

Isolation and identification of Streptococcus equi from the respiratory secretions or abscess

PCR and ELISA using SeM protein provide rapid useful method for diagnosis.

Hematological examination revealed leukocytosis with neutrophilia, anemia and hyperfibrinogenemia

STRANGLES

Control of an outbreak:

• The objectives are focused on:

1. Prevent spreading of infection to new premises

2. Prevent infection of new arrivals to the new premises

3. Control of the outbreak within infected premises.

• These can be achieved through:

I. Restriction of animal movement.

II. Diseased animals should be segregated from healthy one in a separate place with special staff away from clean areas and don’t deal with clean area.

III. Treatment of diseased cases.

• The objectives are focused on:

1. Prevent spreading of infection to new premises

2. Prevent infection of new arrivals to the new premises

3. Control of the outbreak within infected premises.

• These can be achieved through:

I. Restriction of animal movement.

II. Diseased animals should be segregated from healthy one in a separate place with special staff away from clean areas and don’t deal with clean area.

III. Treatment of diseased cases.

Ensure that all horses are free

from infection at the end of the

outbreak to avoid development of

carriers.

Ensure that all horses are free

from infection at the end of the

outbreak to avoid development of

carriers.

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STRANGLES

Treatment:

• Streptococcus equi is susceptible to a wide range of antibiotics as procaine penicillin 22,000 IU/kg/IM/12hrs, ceftiofur 5 mg/kg/IM/12hrs and potentiated sulphonamides 15 mg/kg/12hrs.

• In cases where abscess appeared it's not preferred to use antibiotics as it will slow the abscess maturation and prolong the course of the disease.

• Affected animals should be kept in clean, dry environment and offered soft palatable feed.

• Reduce fever and inflammation using NSAIDs as phenylbutazone 4.4mg/kg/day or flunixine meglumine 1.1 mg/kg/day.

• Streptococcus equi is susceptible to a wide range of antibiotics as procaine penicillin 22,000 IU/kg/IM/12hrs, ceftiofur 5 mg/kg/IM/12hrs and potentiated sulphonamides 15 mg/kg/12hrs.

• In cases where abscess appeared it's not preferred to use antibiotics as it will slow the abscess maturation and prolong the course of the disease.

• Affected animals should be kept in clean, dry environment and offered soft palatable feed.

• Reduce fever and inflammation using NSAIDs as phenylbutazone 4.4mg/kg/day or flunixine meglumine 1.1 mg/kg/day.

STRANGLES

Treatment:

• Encourage abscess maturation by hot packs and poultices and open mature abscess and cleaning with H2O2 and Povidone iodine.

• In some cases that are dysphagic or unwilling to eat use external feeding using nasogastric tube.

• Temporary tracheotomy may be necessary in some horses with severe dyspnea due to upper respiratory tract obstruction as well as cough sedatives in cases of cough.

• Cases with bastard strangles treated by drainage of the abscess when possible and prolonged antibiotic therapy (Surgical intervention).

• Antistreptococcal serum in dose of 100-150 ml daily till improvement of the case.

• Encourage abscess maturation by hot packs and poultices and open mature abscess and cleaning with H2O2 and Povidone iodine.

• In some cases that are dysphagic or unwilling to eat use external feeding using nasogastric tube.

• Temporary tracheotomy may be necessary in some horses with severe dyspnea due to upper respiratory tract obstruction as well as cough sedatives in cases of cough.

• Cases with bastard strangles treated by drainage of the abscess when possible and prolonged antibiotic therapy (Surgical intervention).

• Antistreptococcal serum in dose of 100-150 ml daily till improvement of the case.

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STRANGLES

Prevention:

• In order to prevent the introduction of strangles into a herd you must apply the followings:• In order to prevent the introduction of strangles into a herd you must apply the followings:

Vaccination

Quarantine and Screening

STRANGLES

Prevention:

1. All new arrivals should be placed in quarantine and screened for Streptococcus equi by bacterial culture or PCR of 3 repeated nasopharyngeal swabs or guttural pouch lavages with one week intervals.

1. All new arrivals should be placed in quarantine and screened for Streptococcus equi by bacterial culture or PCR of 3 repeated nasopharyngeal swabs or guttural pouch lavages with one week intervals.

Quarantine and Screening

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STRANGLES

Prevention:

2. Vaccination:• Most horses develop a solid immunity during recovery from strangles, which persists in over

75% of animals for 5 years or longer.

• Several vaccines are available but the protective immunity is generally poor and short lived.

• Both local and systemic post-vaccinal reactions appear to be common following vaccination.

• The organism is poorly antigenic and the vaccine doesn’t give complete protection (reduces the number and severity of the disease).

2. Vaccination:• Most horses develop a solid immunity during recovery from strangles, which persists in over

75% of animals for 5 years or longer.

• Several vaccines are available but the protective immunity is generally poor and short lived.

• Both local and systemic post-vaccinal reactions appear to be common following vaccination.

• The organism is poorly antigenic and the vaccine doesn’t give complete protection (reduces the number and severity of the disease).

Vaccination

STRANGLES

Prevention:

2. Vaccination:

• Used at the age of 2-12 months for 3 doses at 10 days interval then repeated annually

• Two types of vaccines are available:

a) Inactivated vaccines: it induces short term immunity and may induce abscess at the site of injection and may lead to purpura haemorrahagica.

b) Living attenuated intranasal vaccines: it provides better local immunity at the site of infection.

2. Vaccination:

• Used at the age of 2-12 months for 3 doses at 10 days interval then repeated annually

• Two types of vaccines are available:

a) Inactivated vaccines: it induces short term immunity and may induce abscess at the site of injection and may lead to purpura haemorrahagica.

b) Living attenuated intranasal vaccines: it provides better local immunity at the site of infection.

Vaccination

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EQUINE PURPURA HEMORRHAGICA (PH)

EQUINE PURPURA HEMORRHAGICA

It is an acute, non-contagious, aseptic immune mediated

necrotizing vasculitis, characterized by fever, depression, edema,

and petechial or ecchymotic hemorrhage of the mucosa and

subcutaneous tissues. General edema can result in exudation,

ulceration, crusting and, eventually, sloughing of the skin.

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It is often associated with infection or vaccination against Streptococcus equi subsp. equi (S. equi).

Purpura hemorrhagica can also occur with other infections, including equine influenza, equine viral arteritis, equine herpes

virus type 1, Streptococcus equi subsp. zooepidemicus, Rhodococcus equi and Corynebacterium pseudotuberculosis.


Pathogenesis:

• The exact pathogenesis is not fully understood.

• The disease appears to be caused by the hypersensitivity type III due to deposition of antigen-antibody immune complexes on the wall of blood vessel leading to Vasculitis and oozing of fluids leading to edema.

• Antibodies are often produced against pathogens (commonly, in the horse, Streptococcus equi subsp. equi).

• IgA may be involved in the pathophysiology of disease, where high IgA titers have been reported in horses with Equine Purpura Hemorrhagica.

• The exact pathogenesis is not fully understood.

• The disease appears to be caused by the hypersensitivity type III due to deposition of antigen-antibody immune complexes on the wall of blood vessel leading to Vasculitis and oozing of fluids leading to edema.

• Antibodies are often produced against pathogens (commonly, in the horse, Streptococcus equi subsp. equi).

• IgA may be involved in the pathophysiology of disease, where high IgA titers have been reported in horses with Equine Purpura Hemorrhagica.

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Clinical signs:

• There is no breed or gender predilections for the disease and most affected horses tend to be older than two years.

• There is no breed or gender predilections for the disease and most affected horses tend to be older than two years.

• Signs usually occurred within 2–4 weeks after a respiratory infection and varied from a mild reaction to a severe fatal disease.

• Signs usually occurred within 2–4 weeks after a respiratory infection and varied from a mild reaction to a severe fatal disease.

• Affected animals are often depressed, febrile with tachycardia, tachypnea, stiff and reluctant to move and show urticaria followed by pitting edema of the distal limbs, head, neck and ventrum.

• Affected animals are often depressed, febrile with tachycardia, tachypnea, stiff and reluctant to move and show urticaria followed by pitting edema of the distal limbs, head, neck and ventrum.

• Severe edema may lead to difficulty in breathing and eating, leading to anorexia, lethargy, and weight loss.

• Severe edema may lead to difficulty in breathing and eating, leading to anorexia, lethargy, and weight loss.


Clinical signs:

• General edema can result in exudation, ulceration, crusting, and eventually sloughing of the skin.

• General edema can result in exudation, ulceration, crusting, and eventually sloughing of the skin.

• Some horses may develop colic or diarrhea due to hemorrhage, infarction, edema or necrosis of the intestinal wall.

• Some horses may develop colic or diarrhea due to hemorrhage, infarction, edema or necrosis of the intestinal wall.

• Mortality usually results from severe pneumonia, cardiac arrhythmias, renal failure, gastrointestinal complications, or severe muscle infarctions.

• Mortality usually results from severe pneumonia, cardiac arrhythmias, renal failure, gastrointestinal complications, or severe muscle infarctions.

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Diagnosis:

Based mainly on history of a recent respiratory tract infection and clinical

signs (including edema and mucosal hemorrhage).

Confirmation of the diagnosis requires a skin biopsy taken early in the

disease process and before the administration of corticosteroids.

Histology shows leukocytoclastic vasculitis with the presence of an

inflammatory infiltrate of neutrophils, nuclear fragmentation, extravasation

of erythrocytes, and necrosis of vessel walls.

Based mainly on history of a recent respiratory tract infection and clinical

signs (including edema and mucosal hemorrhage).

Confirmation of the diagnosis requires a skin biopsy taken early in the

disease process and before the administration of corticosteroids.

Histology shows leukocytoclastic vasculitis with the presence of an

inflammatory infiltrate of neutrophils, nuclear fragmentation, extravasation

of erythrocytes, and necrosis of vessel walls.


Treatment:

• It is aimed for:

1. Reducing the inflammation associated with the blood vessel walls,

2. Removing the inciting cause, and

3. Providing supportive care.

• Reducing the inflammation of blood vessel walls using:

Dexamethasone is initially administered at 0.05–0.2 mg/kg SID IV or PO until inflammation is reduced. Prednisolone at 0.5–2.0 mg/kg PO BID to SID can be used as a maintenance dose after the initial dexamethasone treatment.

Non-steroidal anti-inflammatory drugs, such as phenylbutazone or flunixin meglumine for reducing inflammation and providing analgesia.

• It is aimed for:

1. Reducing the inflammation associated with the blood vessel walls,

2. Removing the inciting cause, and

3. Providing supportive care.


Dexamethasone is initially administered at 0.05–0.2 mg/kg SID IV or PO until inflammation is reduced. Prednisolone at 0.5–2.0 mg/kg PO BID to SID can be used as a maintenance dose after the initial dexamethasone treatment.

Non-steroidal anti-inflammatory drugs, such as phenylbutazone or flunixin meglumine for reducing inflammation and providing analgesia.

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Treatment:


Treatment with either penicillin, potentiated sulfas (e.g., trimethoprim-sulfamethoxazole) or cephalosporins (e.g., ceftiofur) is recommended until clinical signs resolve.

• Typical supportive care in the form of:

Bandaging swollen legs, caring for wounds, cold hydrotherapy and intravenous fluid administration.

For horses with or in respiratory distress, tracheotomy may be required.

Dysphagic horses with severe head swelling or pharyngeal inflammation may need enteral feeding via nasogastric intubation.


Treatment with either penicillin, potentiated sulfas (e.g., trimethoprim-sulfamethoxazole) or cephalosporins (e.g., ceftiofur) is recommended until clinical signs resolve.

• Typical supportive care in the form of:

Bandaging swollen legs, caring for wounds, cold hydrotherapy and intravenous fluid administration.

For horses with or in respiratory distress, tracheotomy may be required.

Dysphagic horses with severe head swelling or pharyngeal inflammation may need enteral feeding via nasogastric intubation.

RHODOCOCCUS EQUI

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RHODOCOCCUS EQUI

One of the most serious, life-threatening causes of foal

pneumonia less than 6 months (1 - 5 months) of age.

Affected foals may also has extrapulmonary infection in the

form of colonic, mesenteric abscessation and osteomyelitis.

RHODOCOCCUS EQUI

Rhodococcus equi

Gram positive

Facultative intracellular bacteria

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RHODOCOCCUS EQUI

Transmission and Susceptibiltiy:

• Inhalation of dust particles containing virulent R. equi is the major route of pneumonic infection.

• Inhalation of dust particles containing virulent R. equi is the major route of pneumonic infection.

• Ingestion of the organism is a significant route of exposure but rarely leads to hematogenous acquired pneumonia.

• Ingestion of the organism is a significant route of exposure but rarely leads to hematogenous acquired pneumonia.

RHODOCOCCUS EQUI

Transmission and Susceptibiltiy:

• High-ambient summer temperatures, sandy soil, and dusty conditions favor multiplication and dissemination of the organism in the environment.

• On dry, windy days, R. equi can be isolated from samples of air from endemic farms.

• It is easily cultured from fecal samples of adult herbivores, but its presence in adult manure is likely contamination from ingestion of soil (passive) rather than active replication within the intestinal tract. In contrast, the organism readily multiplies within the intestine of foals up to 3 months of age.

• Foals with pulmonary infections swallow R. equi-laden sputum, which replicates in their intestinal tract. Therefore, manure from pneumonic foals is a major source of virulent bacteria contaminating the environment.

• High-ambient summer temperatures, sandy soil, and dusty conditions favor multiplication and dissemination of the organism in the environment.

• On dry, windy days, R. equi can be isolated from samples of air from endemic farms.

• It is easily cultured from fecal samples of adult herbivores, but its presence in adult manure is likely contamination from ingestion of soil (passive) rather than active replication within the intestinal tract. In contrast, the organism readily multiplies within the intestine of foals up to 3 months of age.

• Foals with pulmonary infections swallow R. equi-laden sputum, which replicates in their intestinal tract. Therefore, manure from pneumonic foals is a major source of virulent bacteria contaminating the environment.

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RHODOCOCCUS EQUI

Age:

• It' is more common in foals between 1 to 5 months of age.

• Foals may acquire pulmonary infections early in the first two weeks and small numbers were reported in horses over 8 months of age.

• It' is more common in foals between 1 to 5 months of age.

• Foals may acquire pulmonary infections early in the first two weeks and small numbers were reported in horses over 8 months of age.

RHODOCOCCUS EQUI

Economic importance:

• It has significant economic losses due to:

1. Mortality,

2. Prolonged treatment,

3. Loss of performance,

4. Cost of surveillance programs for early detection, and

5. Expensive prophylactic strategies.

• It has significant economic losses due to:

1. Mortality,

2. Prolonged treatment,

3. Loss of performance,

4. Cost of surveillance programs for early detection, and

5. Expensive prophylactic strategies.

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RHODOCOCCUS EQUI

Pathogenesis:

• The pathogenicity is linked to the ability of R. equi to survive intracellularly,

which hinges on failure of phagosome-lysosomal fusion in infected

macrophages, and failure of functional respiratory burst upon phagocytosis of

R. equi.

• The pathogenicity is linked to the ability of R. equi to survive intracellularly,

which hinges on failure of phagosome-lysosomal fusion in infected

macrophages, and failure of functional respiratory burst upon phagocytosis of

R. equi.

RHODOCOCCUS EQUI

Clinical signs:

• The disease may be enzootic or sporadic as a slowly progressive infection with acute to subacute clinical manifestation.

• The disease may be enzootic or sporadic as a slowly progressive infection with acute to subacute clinical manifestation.

• Clinical signs of disease are difficult to detect until pulmonary lesions reach a critical mass, resulting in decompensation of the foal.

• Clinical signs of disease are difficult to detect until pulmonary lesions reach a critical mass, resulting in decompensation of the foal.

• Some foals will present with acute respiratory distress and fever, pulmonary lesions includes subacute to chronic suppurative bronchopneumonia, pulmonary abscessation, and suppurative lymphadenitis.

• Some foals will present with acute respiratory distress and fever, pulmonary lesions includes subacute to chronic suppurative bronchopneumonia, pulmonary abscessation, and suppurative lymphadenitis.

• Cough is a variable clinical sign, and purulent nasal discharge is less common. • Cough is a variable clinical sign, and purulent nasal discharge is less common.

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RHODOCOCCUS EQUI

Clinical signs:

• Some of the affected foals may show colic, diarrhea, fever, depression, anorexia and weight loss due to colonic microabscessation, granulomatous or suppurative inflammation of the intestine and mesenteric lymph nodes.

• Immunecomplex polysynovitis may be observed in nearly 1/3 of foals affected with R. equi pneumonia especially the stifle and tibiotarsal joints.

• Some of the affected foals may show colic, diarrhea, fever, depression, anorexia and weight loss due to colonic microabscessation, granulomatous or suppurative inflammation of the intestine and mesenteric lymph nodes.

• Immunecomplex polysynovitis may be observed in nearly 1/3 of foals affected with R. equi pneumonia especially the stifle and tibiotarsal joints.

• Less common sites of extrapulmonary infection include panophthalmitis, guttural pouch empyema, sinusitis, pericarditis, nephritis, and hepatic and renal abscessation. The prognosis for foals with abdominal forms of R. equi is less favorable than pulmonary disease and the mortality is approximately 50%.

• Less common sites of extrapulmonary infection include panophthalmitis, guttural pouch empyema, sinusitis, pericarditis, nephritis, and hepatic and renal abscessation. The prognosis for foals with abdominal forms of R. equi is less favorable than pulmonary disease and the mortality is approximately 50%.

RHODOCOCCUS EQUI

Diagnosis:

• Routine laboratory diagnosis depends mainly on:

I. Bacterial culture of transtracheal wash samples provides the definitive diagnosis of R. equi pneumonia.

II. Identification of pulmonary abscessation, and mediastinal lymphadenopathy via thoracic radiography and thoracic ultrasound..

III. Serologic testing: two serologic tests for identification of antibody against R. equi Agar gel immunodiffusion (AGID) and enzyme-linked immunosorbent assay (ELISA).

• Routine laboratory diagnosis depends mainly on:

I. Bacterial culture of transtracheal wash samples provides the definitive diagnosis of R. equi pneumonia.

II. Identification of pulmonary abscessation, and mediastinal lymphadenopathy via thoracic radiography and thoracic ultrasound..

III. Serologic testing: two serologic tests for identification of antibody against R. equi Agar gel immunodiffusion (AGID) and enzyme-linked immunosorbent assay (ELISA).

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RHODOCOCCUS EQUI

Treatment:

• R. equi exists intracellularly and within granulomatous masses; therefore, most antimicrobial agents are ineffective in vivo.

• R. equi exists intracellularly and within granulomatous masses; therefore, most antimicrobial agents are ineffective in vivo.

• The combination of erythromycin and rifampin has become the treatment of choice for R. equi infections in foals.

• The combination of erythromycin and rifampin has become the treatment of choice for R. equi infections in foals.

• The combination of erythromycin and rifampin has markedly improved survival of foals with R. equi pneumonia. Where:

Their activity is synergistic.

Rifampin is lipid-soluble (able to penetrate abscess material), and is concentrated in phagocytic cells.

Erythromycin is concentrated in granulocytes and alveolar macrophages

• The combination of erythromycin and rifampin has markedly improved survival of foals with R. equi pneumonia. Where:

Their activity is synergistic.

Rifampin is lipid-soluble (able to penetrate abscess material), and is concentrated in phagocytic cells.

Erythromycin is concentrated in granulocytes and alveolar macrophages

Diseases of horse characterized by skin lesions on the lower limbs

Disease Transmission Lesion on the skin Diagnosis

Glanders (P.mallei)

Direct contact and ingestion

Skin form at medial aspect of hock as nodules and ulcers with honey like pus. Lymph node involved

Mallein test C.F.T.

Epizootic lymphangitis Eq. Blastomycosis (Crypt.farciminosum)

Skin affections through wounds

Hock lesions with lymphangitis and lymphadenitis , ulcers ruptured with creamy pus.L.N. involved

Culture of pus smears

Ulcerative lymphangitis (C.pseudotuberculosis)

Infection through skin wound

Around pastern pustules ruptured discharge green pus. Lymphangitis only

Culture of pus

Sporotrichosis(Sporotrichum schenkeii)

Direct contact Nodules around fetlock and lymphangitis only

Smear and culture of pus

Chorioptic mange (Chorioptes bovis)

Direct and indirect contact

Itching and rubbing of pastern area . thickening and wrinkling of skin.

Skin scrapings

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GLANDERS

“Equinia”, “Farcy”, and “Malleus”

GLANDERS

It is a serious fatal zoonotic bacterial disease affecting equines caused by

Pseudomonas mallei and characterized by skin, nasal and pulmonary

forms appeared as skin nodules on the medial aspect of the hocks, which

rupture and discharging honey-like pus accompanied by lymphangitis

and lymphadenitis, Respiratory signs with nasal discharge and deep

ulcerations and stellate scars of the nasal mucosa and septum nasai.

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GLANDERS

Pseudomonas mallei Pseudomonas mallei (Burkholderia mallei)

Soil and water

Gram negative

Aerobic or facultative anaerobic non motile

GLANDERS

Epidemiology:

• Horses, donkeys and mules are the main hosts, with occasional cases occurring in humans and small carnivores, such as dogs and cats.

• The incidence and distribution of glanders have declined over the recent years.

• In humans the disease is severe with an untreated case fatality rate of 95%.

• Glanders is present in some Middle Eastern countries, the Indian sub-continent, South East Asia (Including Indonesia) and parts of China and Mongolia.

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GLANDERS

Transmission:

• Equine generally get infected by ingestion or Inhalation or via contamination of skin abrasions with dirty grooming utensils or harness.

• Environmental contamination (especially food and water troughs and other utensils by nasal discharges and pus from skin ulcers as well as Latently infected horses (carriers) are major source of spread.

• The organism can survive in the environment for up two months in sheltered positions.

• Carnivores become infected by eating infected carcasses.

• Human infection results from contact with infected animal discharges usually by contamination of skin abrasions or cuts.

GLANDERS

Clinical signs:

Acu

te f

orm

Mostly in donkeys and mule.

Ch

ron

ic f

orm

Mostly in horses.

La

ten

t fo

rm

Lesions only occur in the lungs with few clinical signs.

• The disease may be acute, chronic or latent.

• It is usually acute in donkeys and mules, while most cases in horses are chronic.

• Forms of the disease are: Cutaneous, pulmonary, nasal and asymptomatic carrier

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GLANDERS

Clinical signs:

Acu

te f

orm

Mostly in donkeys and mule



1.High fever, coughing

2.Thick nasal discharge

3.Rapidly spread in deep ulceration of the nasal mucosa

4.Sub-mixillary lymph nodes swollen and painful

5.Death in 1-2 weeks.

Mostly in horses

Ch

ron

ic f

orm

GLANDERS

Clinical signs:



1. Onset is insidious, but slowly progressive and may lead to death.

2.The signs include malaise coughing, unthriftiness and intermittent fever.

3.Chronic purulent nasal discharge.

4.Milliary yellow nodules and ulceration of the nasal mucoosa.

5.Lymphangitis and lymphadenitis on the medial aspects of the hocks.

6.Cutaneous lesions (farcy) or skin nodules, most commonly on the legs , which rupture and ulcerate discharging honey-like pus, painful oedema of the legs and swelling of joints.

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La

ten

t fo

rm Lesions only occur in the lungs with few clinical signs.

GLANDERS

Clinical signs:



1.Occasional labored breathing and nasal discharge.

2.The infected animals act as carrier.

GLANDERS

Post-mortem findings :

1. Catarrhal bronchopneumonia with enlargement of bronchial lymph nodes (especially in acute form).

2. Nasal cavity , pharynx, larynx and trachea shows nodules and stellate scars.

3. Lungs are filled with millary, firm rounded, encapsulated grey nodules resembling, tubercles nodules.

4. The same nodules are seen on septum nasi.

5. The nodules may also be seen in liver, spleen and kidneys.

6. Cutaneous lesions, swollen lymphatics with focal abscesses in lymph nodes and vessels are seen also.

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GLANDERS

Diagnosis:

• Depends on the Clinical signs, Postmortem findings and the field test “Mallein test”

• Strangles, ulcerative lymphangitis , epizootic lymphangitis and Sporotrichosis.


• Mallein test:

- Inject 0.1 ml of mallein reagent by intradermopalpeberal route in the skin of the lower eyelid.

- Reading is after 48 hours and positive cases show marked edema of the eyelid, blepharospasm (tonic contraction of the eyelids ) and sever mucopurulent conjunctivitis.

GLANDERS

Management:

• No attempts should be made to treat animals as these can result in subclinical carriers.

• Affected animals should be destroyed and carcasses should be burned or buried.

• Premises should be thoroughly cleaned and disinfected.

• Contact animals should be quarantined and tested.

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DERMATOPHILOSISStreptothricosis, Cutaneous Actinomycosis, Rain rot,

Mud fever and Dew poisoning

DERMATOPHILOSIS

Dermatophilosis is a common pustular and crusting skin disease

of horses

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DERMATOPHILOSIS

Dermatophiluscongolensis

Gram positive

Facultative anaerobic, branching actinomyces

There are different strains differ mainly in hemolytic activity on blood agar, phospholipases, proteases and lipases.

The extracellular products of Dermatophilus(proteases) have proteolytic activities leading to digestion of keratin, which could play an important role in the establishment of the infection.

DERMATOPHILOSIS

Pathogenesis:

• Establishment of infection with D. congolensis appears to depend on a variety of factors, including:

I. The virulence of the strain,

II. The general health of the animal,

III. Skin trauma,

IV. Moisture and high humidity.

• Zoospores germinate, producing hyphae under favorable conditions. Hyphae penetrate the epidermis and spread from the initial area, triggering an inflammatory response.

• Establishment of infection with D. congolensis appears to depend on a variety of factors, including:

I. The virulence of the strain,

II. The general health of the animal,

III. Skin trauma,

IV. Moisture and high humidity.

• Zoospores germinate, producing hyphae under favorable conditions. Hyphae penetrate the epidermis and spread from the initial area, triggering an inflammatory response.

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DERMATOPHILOSIS

Predisposing Factors:

Skin Trauma

and Insects.

Climatic Conditions

Host Factors

DERMATOPHILOSIS


Skin Trauma

and Insects

• As Dermatophilus is unable to infect intact skin but can readily infect traumatized skin, Various insects and ticks play a role as vectors for the transmission of Dermatophilus and as causes of trauma, which makes the skin more susceptible to the infection.

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Climatic Conditions

DERMATOPHILOSIS


• Wet seasons and heavy rains contributes to the infection in

concentrations.

• Wet seasons and heavy rains contributes to the infection in several ways such as increasing the population of hematophagous flies, which cause skin damage and initiate inflammation at feeding sites, and contributing to maceration, which decreases the barrier function of skin.

• Increased temperature and humidity have been hypothesized to play a role as well. Zoospores are attracted by low concentrations of carbon dioxide and repelled by high concentrations.

Host Factors

DERMATOPHILOSIS


Host factors include:

Poor body condition,

Malnutrition,

Stressful conditions, and

Glucocorticoids increased the susceptibility to infection with dermatophilosis.

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DERMATOPHILOSIS

Clinical signs:

• Horses are usually affected on the back, head, and neck, where insects commonly bite, and the legs,which are commonly infected if the horse is kept in moist footing.

• Lesions can be small dry crusts that are easily removed with grooming or rubbing, or they can belarger crusts with yellow-green or gray colored pus underneath them.

• Early in the infection, removal of crusts or touching the horse in the affected area can cause pain.

• Hair attached to the crusts tends to fall out easily as the crusts are removed, producing the typical“paintbrush” look that characterizes this disease.

• Rain soaked skin, or skin that is broken, irritated, or damaged by insect bites or trauma is morelikely to develop the disease.

• Areas of white skin affected with Dermatophilus are also prone to increased photosensitivity(sensitivity to sunlight) which may exacerbate the condition.

DERMATOPHILOSIS

Diagnosis:

• Diagnosis of dermatophilosis is based on suggestive history, typical

clinical signs, and supportive cytology and histopathology.

• Dermatophilus congolensis grows easily on blood agar when incubated at

37° C with increased carbon dioxide.

• Diagnosis of dermatophilosis is based on suggestive history, typical

clinical signs, and supportive cytology and histopathology.

• Dermatophilus congolensis grows easily on blood agar when incubated at

37° C with increased carbon dioxide.

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DERMATOPHILOSIS


• Dermatophilosis should be differentiated from:

I. Dermatophytosis,

II. Demodicosis,

III. Bacterial folliculitis caused by Staphylococcus, and

IV. Generalized granulomatous disease.

• Dermatophilosis involving distal limbs must be differentiated from:

I. Contact dermatitis,

II. Contact photosensitization,

III. Atypical dermatophytosis,

IV. Pastern folliculitis and pastern leukocytoclastic vasculitis.

• Dermatophilosis should be differentiated from:

I. Dermatophytosis,

II. Demodicosis,

III. Bacterial folliculitis caused by Staphylococcus, and

IV. Generalized granulomatous disease.

• Dermatophilosis involving distal limbs must be differentiated from:

I. Contact dermatitis,

II. Contact photosensitization,

III. Atypical dermatophytosis,

IV. Pastern folliculitis and pastern leukocytoclastic vasculitis.

DERMATOPHILOSIS

Treatment:

• One of the most important components of clinical management for horses with dermatophilosis is to keep animals dry. Most horses recover spontaneously within a month of being moved to a dry environment.

• Topical therapy is also important. as Benzoyl peroxide shampoos are antibacterial and keratolytic, helping with the removal of crusts. Topical therapy should be applied at least once weekly.

• Excessive scrubbing should be discouraged because it leads to trauma in the hair follicles and increases the risk of furunculosis.

• One of the most important components of clinical management for horses with dermatophilosis is to keep animals dry. Most horses recover spontaneously within a month of being moved to a dry environment.

• Topical therapy is also important. as Benzoyl peroxide shampoos are antibacterial and keratolytic, helping with the removal of crusts. Topical therapy should be applied at least once weekly.

• Excessive scrubbing should be discouraged because it leads to trauma in the hair follicles and increases the risk of furunculosis.

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DERMATOPHILOSIS

Treatment:

• It is important not to share grooming tools between affected and nonaffected horses to minimize spread of the organism.

• Systemic antimicrobial therapy using erythromycin, penicillin, sulfonamides, and kanamycin. Most often, penicillin G (22,000 IU/kg) is used for short-term treatment, and trimethoprim-potentiated sulfonamides (15-20 mg/kg twice daily).

• Treatment should be extended 7 to 10 days past the clinical resolution of lesions to minimize the likelihood of a relapse.

• It is important not to share grooming tools between affected and nonaffected horses to minimize spread of the organism.

• Systemic antimicrobial therapy using erythromycin, penicillin, sulfonamides, and kanamycin. Most often, penicillin G (22,000 IU/kg) is used for short-term treatment, and trimethoprim-potentiated sulfonamides (15-20 mg/kg twice daily).

• Treatment should be extended 7 to 10 days past the clinical resolution of lesions to minimize the likelihood of a relapse.

DERMATOPHILOSIS

Prevention:

• The most effective method for prevention of equine dermatophilosis is to minimize exposure to excessive moisture and insects.

• Insect repellents (e.g., 2% permethrin, FlyPel) should be applied at least once daily in tropical climates where high humidity and rainfall are present.

• Topical antibacterial therapy with antibacterial shampoos (e.g., benzoyl peroxide) is also helpful to decrease the bacterial load on the skin.

• The most effective method for prevention of equine dermatophilosis is to minimize exposure to excessive moisture and insects.

• Insect repellents (e.g., 2% permethrin, FlyPel) should be applied at least once daily in tropical climates where high humidity and rainfall are present.

• Topical antibacterial therapy with antibacterial shampoos (e.g., benzoyl peroxide) is also helpful to decrease the bacterial load on the skin.

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ULCERATIVE LYMPHANGITISPigeon fever, Dry land distemper

ULCERATIVE LYMPHANGITIS

It is a mild contagious disease of horses caused by

Corynebacterium ovis (C. pseudotuberculosis) characterized by

lymphangitis (inflammation of lymph vessels) and skin ulcers

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Corynebacterium ovis (C. pseudotuberculosis)

Gram positive

Chinese letters rods

facultative anaerobeIntracellular, facultative anaerobe


Corynebacterium ovis (C. pseudotuberculosis)

• In cattle cause bovine farcy.

• In horse cause ulcerative lymphangitis

• In sheep cause caseous lymphadenitis.

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Epidemiology:

S.O.I.:

• The m.o. lives in the ground (soil) where it can survive for long periods of time—more than 8 months in a study of soil samples at environmental temperatures.

• Pus from ruptured nodules.

• Mode of infection by skin abrasions. By direct contact or insects.

• Overcrowding and dirty stables help spreading of the infection .

• Seasonal incidence: Autumn and summer..


Clinical signs:

• Swelling and pain at the site of infection.

• Nodules are formed in S/C tissues of fetlocks causing lameness.

• Rupture of nodules and discharging creamy green pus leaving irregular granulated ulcers.

• Thickness and induration of lymphatic vessels in the area of infection with formation of enlarged, thickened and endurated nodules.

• Healing by scar formation.

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Treatment:

• Surgical treatment of ulcers.

• Systemic inject on of penicillin. Prolonged high doses of procainpenicillin,15-50 mg|kg by intra muscular route.

• Surgical treatment of ulcers.

• Systemic inject on of penicillin. Prolonged high doses of procainpenicillin,15-50 mg|kg by intra muscular route.


Prevention:

1. Quarantine new horses and carefully inspect them for signs of infection.

2. Isolate known infected horses when possible and practical.

3. Control fly populations on your property.

4. Use fly repellents, especially on horses with open wounds or draining abscesses, but also on other horses toprevent transmission. Oil based fly repellents provide longer lasting protection than water-based products.

5. Establish a regular manure management and sanitation program—including removing old hay, feed spills andwet bedding from barns and stables—in the pastures and feedlots to decrease insect populations.

1. Quarantine new horses and carefully inspect them for signs of infection.

2. Isolate known infected horses when possible and practical.

3. Control fly populations on your property.

4. Use fly repellents, especially on horses with open wounds or draining abscesses, but also on other horses toprevent transmission. Oil based fly repellents provide longer lasting protection than water-based products.

5. Establish a regular manure management and sanitation program—including removing old hay, feed spills andwet bedding from barns and stables—in the pastures and feedlots to decrease insect populations.

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Prevention:

6. Wash or sanitize hands after handling infected horses.

7. Don’t use the same items (buckets, pitchforks and other materials) for infected horses and the general horse population.

8. Carefully clean and disinfect areas potentially contaminated by pus from draining abscesses. Bleach and accelerated hydrogen peroxide disinfectants are effective sanitizers after pus and other organic material have been removed.

9. Inspect stalls, paddocks and fields for sharp edges or objects that could cause wounds on your horse’s skin, which might subsequently become infected.

6. Wash or sanitize hands after handling infected horses.

7. Don’t use the same items (buckets, pitchforks and other materials) for infected horses and the general horse population.

8. Carefully clean and disinfect areas potentially contaminated by pus from draining abscesses. Bleach and accelerated hydrogen peroxide disinfectants are effective sanitizers after pus and other organic material have been removed.

9. Inspect stalls, paddocks and fields for sharp edges or objects that could cause wounds on your horse’s skin, which might subsequently become infected.

EPIZOOTIC LYMPHANGITIS(Pseudoglanders, Equine Blastomycosis, Equine Histoplasmosis)

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EPIZOOTIC LYMPHANGITIS

It is a chronic contagious disease of horses characterized by

suppurative lymphangitis, lymphadenitis and ulcers of the skin

and keratitis.


Histoplasma farciminosum, Blastomyces farciminosum, Cryptococcus farciminosum

Fungus

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Epidemiology:

• Occur in outbreaks, spread by spores on contaminated bedding.

• May survive in soil.

• Entry through skin abrasions.

• Occur in outbreaks, spread by spores on contaminated bedding.

• May survive in soil.

• Entry through skin abrasions.


Clinical signs:

• Ulcers at hocks,

• Lymphadenitis :lymph nodes at hocks swell and discharge creamy pus,

• Lymphangitis,

• Pulmonary abscesses: in some cases of generalized form.

• Ulcers at hocks,

• Lymphadenitis :lymph nodes at hocks swell and discharge creamy pus,

• Lymphangitis,

• Pulmonary abscesses: in some cases of generalized form.

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Diagnosis:

• Symptoms.

• Isolation of the causative organism .

• Symptoms.



• Should be differentiated from other diseases causing ulceration and nodules in the lower parts of the limbs with lymphangitis and lymphadenitis.

• Should be differentiated from other diseases causing ulceration and nodules in the lower parts of the limbs with lymphangitis and lymphadenitis.


Treatment:

Surgical approachSurgical approach

Systemic iodides as sodium iodide (50mg|kg intravenously as 3.5%

solution in normal saline in 2 doses,7days apart) or Potassium iodide (

10 gram per 450 kg orally, twice daily for 10 days).

Systemic iodides as sodium iodide (50mg|kg intravenously as 3.5%

solution in normal saline in 2 doses,7days apart) or Potassium iodide (

10 gram per 450 kg orally, twice daily for 10 days).

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SPOROTRICHOSIS

SPOROTRICHOSIS

It is a contagious disease of horses characterized by the

development of cutaneous nodules and ulcers of the limbs and

may or may not be accompanied by lymphangitis.

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SPOROTRICHOSIS

Sporotrichum schenckii(sporothrix schenckii,

sporothrix equi)

Gram positive Fungus

SPOROTRICHOSIS

Epidemiology:

• Slow spread, sporadic cases,

• Spread by contact and contamination of environment.

• Slow spread, sporadic cases,

• Spread by contact and contamination of environment.

Clinical signs:

• Painless nodules at fetlocks ulcerate then heal.

• Lymphangitis in some animals.

• Lesions heal in 3-4 weeks but new crops appear.

• Painless nodules at fetlocks ulcerate then heal.

• Lymphangitis in some animals.

• Lesions heal in 3-4 weeks but new crops appear.

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SPOROTRICHOSIS


• The disease must be differentiated from skin form of glanders, ulcerative and epizootic lymphangitis.

• The disease must be differentiated from skin form of glanders, ulcerative and epizootic lymphangitis.

Treatment:

• as in epizootic lymphangitis.

• Antifungal drugs can be used as Ketoconazole (Nizoral as 30 mg|kg once daily for 2 months, also Amphotericin B ( Fungizone as 0.3 mg|kg per day in one litre of 5% dextrose saline given slowly IV for 30 days).

• as in epizootic lymphangitis.

• Antifungal drugs can be used as Ketoconazole (Nizoral as 30 mg|kg once daily for 2 months, also Amphotericin B ( Fungizone as 0.3 mg|kg per day in one litre of 5% dextrose saline given slowly IV for 30 days).

ABORTION IN MARES (SALMONELLOSIS)

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Specific disease of equines caused by S. abortivo equina

characterized by:

Abortion in mares ,

Septicaemia in foals and

Testicular lesions in males.


Epidemiology:

• Disease of horse and donkey only.

• Infection by ingestion or through coitus (adults).

• Infection in foals is in utero or by ingestion from contaminated udder or

through umbilicus.

• Disease of horse and donkey only.

• Infection by ingestion or through coitus (adults).

• Infection in foals is in utero or by ingestion from contaminated udder or

through umbilicus.

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Clinical signs:

• Mares: abortion (7-8 months) or dystochia , retained placenta and metritis.• Mares: abortion (7-8 months) or dystochia , retained placenta and metritis.

• Stallion: fever , oedema of prepuce and scrotum , hydrocele , epididymitis , orchitis and testicular atrophy.

• Stallion: fever , oedema of prepuce and scrotum , hydrocele , epididymitis , orchitis and testicular atrophy.

• Placenta: oedematous haemorrhagic area of necrosis.

• Foals: picture of septicaemia and arthritis.

• Placenta: oedematous haemorrhagic area of necrosis.

• Foals: picture of septicaemia and arthritis.

P.M. lesions:


Diagnosis:

• Symptoms.


• Serology by agglutination test.

• Symptoms.


• Serology by agglutination test.


• Abortion from viral respiratory diseases as Eq. viral arteritis , eq. viral rhinopneumonitis, in which abortion occur in the course of respiratory disease with fever and serology (S.N.T).

• Septicaemia caused by other causes as E. coli, shigellosis , salmonellosis, by isolation and serology (agglutination).

• Abortion from viral respiratory diseases as Eq. viral arteritis , eq. viral rhinopneumonitis, in which abortion occur in the course of respiratory disease with fever and serology (S.N.T).

• Septicaemia caused by other causes as E. coli, shigellosis , salmonellosis, by isolation and serology (agglutination).

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Control:

• Infected stallion not used for breeding.

• Autogenous vaccine (Bacterin) for mares by 3 doses (7 days apart).

• Hygienic disposal of infected placenta and abortion materials.

• Infected stallion not used for breeding.

• Autogenous vaccine (Bacterin) for mares by 3 doses (7 days apart).

• Hygienic disposal of infected placenta and abortion materials.

Diseases causing sleepy appearance of newborn foals

Disease Age

susceptibility Signs PM Diagnosis

Shigellosis (Actinobacillus equuli)

Newly born foals up to 3 monthsMares are carrier

Fever, recumbency, diarrhea, comatose , death

Pin point kidney abscesses , enteritis and arthritis

- Blood culture - Cervical swab

Foal septicaemia (E. coli, Salmonella & strept.pyogen)


Fever, recumbency, diarrhea, comatose , death

Septicaemia and enteritis

Blood culture

Corynebacterial pneumonia of foals (Rhabdococcus equi )


Septicaemia in newly born and pneumonia in older.

Septicaemia and suppurative bronchopneumonia

Swab from mare cervix

Tyzzer`s disease (Bacillus piliformis)

3-5 weeks old foals Sudden fever and death in few hours. Sign is usually hepatitis and icterus.

Miliary focci in liver and hepato-megaly

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NEONATAL STREPTOCOCCAL INFECTION

SALMONELLOSIS

SHIGELLOSIS

COLIBACILLOSIS

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Streptococcal infection in neonatal foals caused by Strept.

genitalium (Pyogenes equi) and characterized by bacteremia

and localization in joints with purulent poly-arthritis in addition

to umbilical infection.

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Strept. pyogenes equior Strept. genitalium

Gram positive

Infect genital tract of mares


Epidemiology:

• Foals at 2-3 weeks of age are highly susceptible.• Foals at 2-3 weeks of age are highly susceptible.

• Discharges from infected foals are also source of infection.• Discharges from infected foals are also source of infection.

• Infection through umbilicus.• Infection through umbilicus.

• Source of infection is the infected genital tract of mares which discharge the organism and contaminates the environment, infection spread between mares by coitus.

• Source of infection is the infected genital tract of mares which discharge the organism and contaminates the environment, infection spread between mares by coitus.

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Pathogenesis:

Infection through umbilicus

BacteremiaBacteremia

CAUSE

Umbilical arteritisUmbilical arteritis

OmphalitisOmphalitis

OrchitisOrchitis

OmphalophelebitisOmphalophelebitis

Suppurative arthritisSuppurative arthritis


Clinical signs:

• Fever 39.5 C° (Bacteremia).• Fever 39.5 C° (Bacteremia).

• This may be followed by septicemia and death. • This may be followed by septicemia and death.

• Painful swelling of the navel and its surrounding abdominal wall with pus discharging .• Painful swelling of the navel and its surrounding abdominal wall with pus discharging .

• Swelling, in one or more of the joints specially knee, stifle and hock with severe lameness and recumbency

• Swelling, in one or more of the joints specially knee, stifle and hock with severe lameness and recumbency

• Abscesses in joints may ruptured and discharge pus.• Abscesses in joints may ruptured and discharge pus.

P.M. lesions:

• Suppuration of the umbilicus, arthritis, multiple abscesses in liver and kidney.• Suppuration of the umbilicus, arthritis, multiple abscesses in liver and kidney.

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Diagnosis:

• Clinically navel lesions with polyarthritis at age of 2-3 weeks suggest Strept. infection .

• Differential diagnosis from other causes of arthritis and navel ill caused by E. coli, Shigellosis and Salmonellosis infection must be carried out (Strept. infection occurs in younger foals -few days- with septicemia).

• Lab. Examination: for differentiation by

Culturing of pus to detect organism.

Sensitivity to antibiotics .

Synovial fluid examination to detect joint damage.

• Clinically navel lesions with polyarthritis at age of 2-3 weeks suggest Strept. infection .

• Differential diagnosis from other causes of arthritis and navel ill caused by E. coli, Shigellosis and Salmonellosis infection must be carried out (Strept. infection occurs in younger foals -few days- with septicemia).

• Lab. Examination: for differentiation by

Culturing of pus to detect organism.

Sensitivity to antibiotics .

Synovial fluid examination to detect joint damage.


Treatment:

• Penicillin in high doses (20,000 IU per kg BW , IM) for 3-5 days • Penicillin in high doses (20,000 IU per kg BW , IM) for 3-5 days

• Vaccination of mares by mixed bacterin.

• Administration of long acting penicillin to foals at birth on heavily infected premises.

• Disinfection of umbilicus after birth by tincture iodine.

• Parturition stalls and pens must be cleaned and disinfected.

• Vaccination of mares by mixed bacterin.

• Administration of long acting penicillin to foals at birth on heavily infected premises.

• Disinfection of umbilicus after birth by tincture iodine.

• Parturition stalls and pens must be cleaned and disinfected.

Control:

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SALMONELLOSIS

SHIGELLOSIS

COLIBACILLOSIS

SHIGELLOSISActinobacillosis, Equulosis, Sleepy Foal

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SHIGELLOSIS

It is a highly fatal septicemia disease of newborn foals caused by

Shigella equi and characterized by sudden death. Survivals

show arthritis, lameness and enteritis (diarrhea and dysentery).

SHIGELLOSIS

Shigella equuli, Actinobacillus equuli

Gram negative

Normally found in the intestine of horses

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SHIGELLOSIS

Epidemiology and Pathogenesis:

• Shigella equuli is a commensal in the intestine of solipeds.

• The foal acquires the organism from its dam in utero, during or soon after birth, or from its surroundings. i.e.; Intrauterine and Umbilical cord infection.

• Post-natal infection usually occurs via the umbilicus or, less frequently, by the oral route.

• The dams may have a persistent cervical infection.

• Migrating strongyles may help in infection in older foals.

• Shigella equuli is a commensal in the intestine of solipeds.

• The foal acquires the organism from its dam in utero, during or soon after birth, or from its surroundings. i.e.; Intrauterine and Umbilical cord infection.

• Post-natal infection usually occurs via the umbilicus or, less frequently, by the oral route.

• The dams may have a persistent cervical infection.

• Migrating strongyles may help in infection in older foals.

SHIGELLOSIS

Clinical signs:

Peracute Peracute Acute Acute

• Sick at birth with sleepy presentation.

• Fever.

• Acute abdominal pain.

• Prostration, Lethargy.

• Conjunctivitis and painful swellings in the joints and lameness.

• Diarrhea.

• Survivals for 2-7 days may show arthritis, lameness then died after 2-7 day course.

• Sick at birth with sleepy presentation.

• Fever.

• Acute abdominal pain.

• Prostration, Lethargy.

• Conjunctivitis and painful swellings in the joints and lameness.

• Diarrhea.

• Survivals for 2-7 days may show arthritis, lameness then died after 2-7 day course.

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SHIGELLOSIS

Diagnosis:

• Shigella equuli can be isolated by blood culture from the septicemic foal.

• The organism can be isolated from the umbilicus, kidney and the musculoskeletal lesions.

• It can also be isolated from the cervix of some mares by the use of guarded swabs.

• Necropsy Findings:

Acute: Septicemic petechiae. Severe enteritis.

Sub acute: Arthritis. Pinpoint abscess in renal cortices. A. equuli in tissues.

• Shigella equuli can be isolated by blood culture from the septicemic foal.

• The organism can be isolated from the umbilicus, kidney and the musculoskeletal lesions.

• It can also be isolated from the cervix of some mares by the use of guarded swabs.

• Necropsy Findings:

Acute: Septicemic petechiae. Severe enteritis.

Sub acute: Arthritis. Pinpoint abscess in renal cortices. A. equuli in tissues.

SHIGELLOSIS

Treatment:

• Affected foals should be provided aggressive antibiotic therapy, supportive nursing care and nutritional support.

• Affected foals should be provided aggressive antibiotic therapy, supportive nursing care and nutritional support.

• The therapy of choice is a combination of full doses of Ampicillinor penicillin and an aminoglycoside (kanamycin [15 mg/kg IV]).

• Streptomycin is also good

• Therapy should be continued for at least 2 wk and for 4 wk (or more) if the infection has localized in the joints or lungs.

• The therapy of choice is a combination of full doses of Ampicillinor penicillin and an aminoglycoside (kanamycin [15 mg/kg IV]).

• Streptomycin is also good

• Therapy should be continued for at least 2 wk and for 4 wk (or more) if the infection has localized in the joints or lungs.

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SHIGELLOSIS

Control :

• Attention to hygiene and ventilation of stables is very important. • Attention to hygiene and ventilation of stables is very important.

• Avoid the overcrowding.• Avoid the overcrowding.

• Foaling areas should be thoroughly cleaned and disinfected between foalings.• Foaling areas should be thoroughly cleaned and disinfected between foalings.

• The stump of the umbilical cord should be treated with antiseptic.• The stump of the umbilical cord should be treated with antiseptic.

• The foal should obtain an adequate intake of colostrum during the first day of life and If colostrum is not available, 1L of plasma should be administered.

• The foal should obtain an adequate intake of colostrum during the first day of life and If colostrum is not available, 1L of plasma should be administered.

• Cull infected mares with prophylactic antibiotics (kanamycin [15mg/kg IV]) can be administered to newborn foals on premises where there is a disease outbreak.

• Cull infected mares with prophylactic antibiotics (kanamycin [15mg/kg IV]) can be administered to newborn foals on premises where there is a disease outbreak.



SALMONELLOSIS

SHIGELLOSIS

COLIBACILLOSIS

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COLIBACILLOSIS

Escherichia coli

pathogenic strains

Gram negative

COLIBACILLOSIS


• Approximately 25% of cases of septicemia in the foal are caused by E. coli.

• The foal acquires the bacteria from its immediate surroundings at birth.

• The probable routes of infection (umbilical, oropharyngeal or enteric).

• The pathogenesis in the septicemic disease is probably attributable to shock induced by endotoxin released from the disintegrating bacteria.

• The main manifestations of endotoxic shock are pyrexia, hypotension and neutropenia.

• Approximately 25% of cases of septicemia in the foal are caused by E. coli.

• The foal acquires the bacteria from its immediate surroundings at birth.

• The probable routes of infection (umbilical, oropharyngeal or enteric).

• The pathogenesis in the septicemic disease is probably attributable to shock induced by endotoxin released from the disintegrating bacteria.

• The main manifestations of endotoxic shock are pyrexia, hypotension and neutropenia.

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COLIBACILLOSIS

Clinical and pathologic findings:

• The disease is very sudden in onset.

• It affects foals that are 3 – 4 days old the disease and may take a 1 – 2 day course.

• Severe disease may be present before any clinical signs are observed.

• The clinical signs are mainly those of septicemia. Pyrexia may occur in the very early stages of the disease but the temperature is usually subnormal when the foal undergoes a collapse.

• Diseased foals usually suffer from depression, a reluctance to suck, petechiation of mucous membranes, respiratory distress, a progressively weakening pulse and colic.

• The disease is very sudden in onset.

• It affects foals that are 3 – 4 days old the disease and may take a 1 – 2 day course.

• Severe disease may be present before any clinical signs are observed.

• The clinical signs are mainly those of septicemia. Pyrexia may occur in the very early stages of the disease but the temperature is usually subnormal when the foal undergoes a collapse.

• Diseased foals usually suffer from depression, a reluctance to suck, petechiation of mucous membranes, respiratory distress, a progressively weakening pulse and colic.

COLIBACILLOSIS

Clinical and pathologic findings:

• If the foal survives for a few days individual bacteria and bacterial

emboli can localize in the lungs, joints, bones or elsewhere in the body.

• The long-term prognosis for future athletic performance should be

considered guarded for cases with involvement of the joints or bones,

particularly if multiple joints are involved.

• If the foal survives for a few days individual bacteria and bacterial

emboli can localize in the lungs, joints, bones or elsewhere in the body.

• The long-term prognosis for future athletic performance should be

considered guarded for cases with involvement of the joints or bones,

particularly if multiple joints are involved.

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COLIBACILLOSIS

Diagnosis:

• A definitive diagnosis can be made by blood culture.

• E. coli rapidly invades the carcass from the gut, so post mortem specimens

should be taken for bacteriologic examination no later than 1 hr. after

death.

• A definitive diagnosis can be made by blood culture.

• E. coli rapidly invades the carcass from the gut, so post mortem specimens

should be taken for bacteriologic examination no later than 1 hr. after

death.

COLIBACILLOSIS

Treatment:

• Bacterial sensitivities are very useful in determination of the appropriate antibiotic therapy.

• Aminoglycosides (kanamycin15 mg/kg) is the drugs of choice.

• Trimethoprim—sulfamethoxazole, chloramphenicol or cephalosporins may be useful in some cases.

• Newer antimicrobial molecules, such as the highly active fluoroquinolones (enrofloxacin 7.5 mg/kg), are becoming available for therapy in some countries.

• The prognosis for foals with colibacillosis is not good.

• Bacterial sensitivities are very useful in determination of the appropriate antibiotic therapy.

• Aminoglycosides (kanamycin15 mg/kg) is the drugs of choice.

• Trimethoprim—sulfamethoxazole, chloramphenicol or cephalosporins may be useful in some cases.

• Newer antimicrobial molecules, such as the highly active fluoroquinolones (enrofloxacin 7.5 mg/kg), are becoming available for therapy in some countries.

• The prognosis for foals with colibacillosis is not good.

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SALMONELLOSIS

SHIGELLOSIS

COLIBACILLOSIS

SALMONELLOSISparatyphoid disease

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SALMONELLOSIS

Salmonellosis is a septicemic or bacteremic enteritis of the foal

that usually appears a few days later than other infections such

as shigellosis or colibacillosis.

Manifested clinically by one of the following syndrome peracute

septicaemic , acute enteric and chronic enteric forms, may end

to be asymptomatic carrier.

SALMONELLOSIS

Salmonella typhimurium, auatum, Newport, Arizona, enteridites, hiddelberg and

S. abortivo-equina.

Gram negative

Facultative anaerobic, non-spore-forming rods

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SALMONELLOSIS


• Salmonella typhimurium is most common cause in foals.

• The most likely sources of salmonellae for the very young foal are the dam or the immediate surroundings.

• The organism can be introduced by clinical cases, carrier animals, feedstuffs, water supplies, fomites, or other species of domesticated or wild animals, including birds.

• Salmonella may be a recurrent problem on some premises.

• Infection by ingestion.

• Salmonella typhimurium is most common cause in foals.

• The most likely sources of salmonellae for the very young foal are the dam or the immediate surroundings.

• The organism can be introduced by clinical cases, carrier animals, feedstuffs, water supplies, fomites, or other species of domesticated or wild animals, including birds.

• Salmonella may be a recurrent problem on some premises.

• Infection by ingestion.

SALMONELLOSIS


• Carrier horses and other animals play a major role in the transmission of salmonellae.

• Between 10% and 50% of horses are silent carriers of these organisms.

• Stress, including illness and many veterinary procedures, provokes such animals into active shedding of salmonellae. This shedding only stops when the stress subsides and may recommence if the horse is again stressed.

• It is not clear whether salmonellae persist for the lifetime of the carrier.

• Carrier horses and other animals play a major role in the transmission of salmonellae.

• Between 10% and 50% of horses are silent carriers of these organisms.

• Stress, including illness and many veterinary procedures, provokes such animals into active shedding of salmonellae. This shedding only stops when the stress subsides and may recommence if the horse is again stressed.

• It is not clear whether salmonellae persist for the lifetime of the carrier.

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SALMONELLOSIS


After oral infection After oral infection Intestinal wall of terminal ileium and caecum Intestinal wall of terminal ileium and caecum

Mesenteric L. node (progress after that lead to clinical disease)Mesenteric L. node (progress after that lead to clinical disease)

Lowering of resistance due to stressLowering of resistance due to stress

Invasion to the reticuloendothelial system cell (specially liver)

Invasion to the reticuloendothelial system cell (specially liver)

Blood streamBlood stream

Septicaemia

(peracute disease with death)

Septicaemia

(peracute disease with death)

Bacteremia

Less severe, Acute enteritis

Bacteremia

Less severe, Acute enteritis

InfectionClinical disease

(young)

CarrierStress

PassivePicking up infection

only

Latent infection in L. node without passage of organism

in faeces

Active Disseminate organism in faeces

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SALMONELLOSIS

Clinical signs:

• The onset is often sudden and very young foals may die from septic shock within hours before diarrhea develops.

• The initial features are depression, fever, reluctance to suck, weakness, dehydration and cyanotic mucous membranes.

• A persistent watery fetid diarrhea appears as the disease progresses and some cases develop purulent bronchopneumonia with loud rales.

• The spread of infection to other tissues can result in clinical pyoarthritis, nephritis or meningitis.

• The onset is often sudden and very young foals may die from septic shock within hours before diarrhea develops.

• The initial features are depression, fever, reluctance to suck, weakness, dehydration and cyanotic mucous membranes.

• A persistent watery fetid diarrhea appears as the disease progresses and some cases develop purulent bronchopneumonia with loud rales.

• The spread of infection to other tissues can result in clinical pyoarthritis, nephritis or meningitis.

SALMONELLOSIS

Pathologic findings:

• There's severe visceral congestion and petechial hemorrhage in the

serosae.

• A catarrhal enteritis, particularly of the ileum, is often seen.

• The synovias of foals with pyoarthritis contain floccules of pus and those

with pneumonia may have minute pulmonary abscesses together with a

generalized pulmonary edema.

• There's severe visceral congestion and petechial hemorrhage in the

serosae.

• A catarrhal enteritis, particularly of the ileum, is often seen.

• The synovias of foals with pyoarthritis contain floccules of pus and those

with pneumonia may have minute pulmonary abscesses together with a

generalized pulmonary edema.

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SALMONELLOSIS

Diagnosis:

• Laboratory diagnosis in the living animal depends on isolating the agent

from cultures of the blood and feces.

• Fecal material should be obtained directly from the rectum.

• It is important, for epidemiologic reasons, to determine which serotype

(and phage type).

• Laboratory diagnosis in the living animal depends on isolating the agent

from cultures of the blood and feces.

• Fecal material should be obtained directly from the rectum.

• It is important, for epidemiologic reasons, to determine which serotype

(and phage type).

SALMONELLOSIS

Treatment:

• Treatment consists of:

1. Maintaining hydration by the IV and oral administration of fluids containing electrolytes and an energy source such as glucose,

2. Long-term antibiotic therapy based on sensitivity assays, and

3. The administration of intestinal protectants such as bismuth.

4. NSAIDs therapy, for example flunixin meglumine 1 mg/kg IV s.i.d. or b.i.d., may reduce the signs of endotoxemia.

• Treatment consists of:

1. Maintaining hydration by the IV and oral administration of fluids containing electrolytes and an energy source such as glucose,

2. Long-term antibiotic therapy based on sensitivity assays, and

3. The administration of intestinal protectants such as bismuth.

4. NSAIDs therapy, for example flunixin meglumine 1 mg/kg IV s.i.d. or b.i.d., may reduce the signs of endotoxemia.

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SALMONELLOSIS

Treatment:

• Antibiotics as kanamycin, ceftiofur, chloramphenicol, trimethoprim–sulfonamide, and fluoroquinolones are useful.

• The management of the septicemic foal should include strict isolation of the foal and its dam and vigorous disinfection (sodium hypochlorite, phenols or quaternary ammonium compounds) of their surroundings.

• The personnel caring for the affected animals should wear disposable overalls, boots and gloves and, if possible, they should not have contact with healthy horses. The equipment, bedding and feedstuffs, etc. for the sick animals should be kept separate from those for healthy horses.

• Antibiotics as kanamycin, ceftiofur, chloramphenicol, trimethoprim–sulfonamide, and fluoroquinolones are useful.

• The management of the septicemic foal should include strict isolation of the foal and its dam and vigorous disinfection (sodium hypochlorite, phenols or quaternary ammonium compounds) of their surroundings.

• The personnel caring for the affected animals should wear disposable overalls, boots and gloves and, if possible, they should not have contact with healthy horses. The equipment, bedding and feedstuffs, etc. for the sick animals should be kept separate from those for healthy horses.

SALMONELLOSIS

Vaccination:

• Salmonella of modified virulence has been practiced as a vaccine in some

countries and has a good degree of success in controlling acute disease.

• Pregnant mares where there is a disease outbreak or where there is a recurrent

problem can be vaccinated 8 wk and 4 wk pre partum.

• Salmonella of modified virulence has been practiced as a vaccine in some

countries and has a good degree of success in controlling acute disease.

• Pregnant mares where there is a disease outbreak or where there is a recurrent

problem can be vaccinated 8 wk and 4 wk pre partum.

Documents

Soliman Mohammed Soliman, D.V.M, Ph.D....Ulcerative lymphangitis 8. Neonatal bacterial infections a)Neonatal streptococcal infection b)Shigellosis c)Colibacillosis d)Salmonellosis