Bacterial Diseases

Bacterial Diseases:-

Hemorrahgic septicemia(H S):

Also known as pasturelosis, stockyardis disease, shiping fever, barbon disease. This is No 1 bacterial disease in Pakistan. H.S is an acute ,septicemic bacterial disease of cattle and buffalo. It is characterised by high temp, severe depression, pneumonia and swelling at throat region/ neck.

Etiology:

            Pasturela Multocida is the causative agent of this disease. It has four types. Type A: It causes

•                            Bovine pneumonic pasturelosis in cattle and buffalo.
•               Mastits, pneumoing in sheep and gaot.
•               Rhinits and pneumonia in Pig.
•               Fowl cholera in poultry.

Type B: it causes Hemorrhagic septicemia in Asia.

Type D: causes rhinitis in pig

Type E: causes Hemorraghic septicemia.

Predisposing Factor:

• Over work that cause fatigue,
• Poor body condition,
• Moonsoon rain,
• Transportation stress
• close confinement

Epidemiology:

            H. S is present in all tropical and subtropical areas. Mostly it occurs in Rushia,  Africa, Australia, India, Pakistan, Indionasia, Malayasia, Phelpine and Thiland.

 Buffalo is most susceptible than cattle.

Animal of all age are susceptible but more susceptible age is 6-24 months.

 Mortality and Morbidity rate vary from 50-100%.

Out breaks of this disease is often associated with wet humid wheather during rainy season.

Pathogensis:

            Pasturela Mulltocida normally commensel of upper respiratory tract and may invade tissue of immunosupressed animal. Exogenus transmission occurs through direct contact or through aerosol route.
2 factors are important in pathogensis .

1. adhesion of bactera to mucosa (fimbrae).
2. To avoid from phagocytosis (capsule).

             Severe septicemia may occur which is associated with capsular material of bactera. The effect of septicemia are more severe in respiratory tract, heart and gastrointestinal tarct.

Clinical Findings:

  Four type of clinical findings.

1. Oedematous form
2. Pulmonary form
3.  Alimentary  form
4. Septicemic form                                                                                                               

1. Edematous form:

•  Swelling on neck/throat region.
• High temperature upto 106-107 F.
• Off feed
• Severe depressed
•  Perfuse salivation
• Dyspnea
• Some time death may occur in severe cases.

2.  Pulmonary form:

• No swelling on neck
• Temperature remain 104-105F
• Open mouth breathing
• Protrude and cyanotic tongue
• Dyspnea which may lead to death.

3. Alimentary form:

• Diarrhea
• Loss of appetite
• Increase thirst
• Dehydration

4. Septicemic form:

•  Increase temperature
• This form is of very short duration, endotoxin produce and circulate in blood. Animal die in short period of time

Diagnosis:

• History and clinical sign
• Observe throat swelling
• Open mouth breathing
• Tongue cyanotic
• Observe month( june, july and august.

Differential diagnosis:

1. Black Quarter:

•    clostridium infection, thigh muscle and shoulder muscle involve.
•    Lameness
•    Swelling of quarter
•    This is soil born disease.

     2. Anthrax:

• Bleeding from natural orifices

     3.Wooden tongue:

Treatment:

Use bacteriostate drugs instead of bacteriocidal in this disease.

Drug of choice is Sulphonamides calve 100ml large animal 200ml I/V

Or

Tribersin (sulphmetnzine 150mg/kg + chloramphenicol 10mg/kg) for 3-4 days.

Give fluid therapy.

Use antipyretic .

Use bronchodilators

Mastitis:-

It is an infectious but consider as managemental disease. Mastitis is characterized by inflammation of parenchymal cells of udder.

Inflammation of mamory gland is called as mamilitis. Complication of mamalitis is mastits.

Etiology:-

Staplococcus aureus is gram +ve bacteria and other bacteria like streptococcus agalacae, corynobacterium, E. coli, enterococci, mycoplasma bovis, klebshiela etc.

Mastitis is actually contagious and environmental disease.

Managemental problems:-

            Poor bedding, housing, hot, humid area favour pathogens present in wood dust, rice straw.

Mortality is negligible but morbidity is very high and more economic loss.

Subclinical mastitis has more economical losses because no signs so no treatment.

Physio-chemical changes in mastitic milk are taste, consistency. Only can be diagnosed by tests.

Clinical signs:-

Subclinical mastitis:-

Anthrax: 

It is also known as spleenic fever, carbuncles, wool sorter’s disease, hide porter’s disease and malignant pustular dermatitis.

It is per acute disease characterized by septicemia and sudden death accompanied by the exudation of tery blood from the natural orifices after death.

Etiology:

This disease is caused by bacteria bacillus anthracic. Bacillus anthracic is Gram +ve , spore forming, non-motile capsulated, aerobic bacteria. Spore are very resistant to chemical disinfectant. These spore may survive in the soil for years and for ten years in the culture. The organism produces medusa head appearance on nutrient agar. The spores remain resistant to 100^oC for five minutes.

Epidemiology:

Anthrax is world wide in distribution but incidences are more common in hot-humid climate. Infection remains in the soil and suitable climate supports the occurrence. The morbidity and mortality rate is very high.

Pathogenesis:

After ingestion of the spores or entry through abrasions in the epithelium or through scratches caused by fibrous food materials. The bacteria are moved to the local lymph nodes by motile phagocytes. After proliferation in this site the bacilli pass via the lymphatic vessels in to the blood stream and septicemia takes place followed by massive invasion of all body tissues. During multiplication it releases lethal toxins that cause edema, tissue damage, and haemorraghes. Death occur due to shock, renal failiure and terminal anoxia mediated by CNS.

Clinical findings:

      Incubation Period: 2-10 days

Four types:

1.  Per acute
2.  Acute
3.  Sub-acute
4. Chronic

1. Per-acute:

•       Death occurs without showing any signs.

2. Acute:

• Temp 104 ^oF
•  Increase heart beat
• Rapid and deep respiration
• Mucosae congested and hemorrhagic
• Diarrhea and dysentery

3. Sub-acute and Chronic forms:

• Edema
• Loss of appetite
• Blood in milk for weeks

Postmortem findings:

• Carcass should not be opened if confirmed
• Terry blood from natural orifices
• Increase spleen size

Diagnosis:

• On the basis of signs
• History
• Ascoli’s test for anthrax

Differential diagnosis:-

Black Quarter: 

• there will be frothy bleeding from nostrils. But in anthrax there is terry blood from natural orifices.

Treatment:

Pencilline 10000 IU/kg I/M twice daily is drug of choice

Oxytetracycline 8-10 mg/day

Black Quarters:-

            It is also known as black leg, quarter ill and symptomatic anthrax.It is manifested by severe toxemia and high mortality.

Etiology:-

            It is caused by clostridium shovei which is gram +ve, rod shape, anaerobic and spore forming bacteria. The spores of this bacterium are highly resistant to heat. Spores can tolerate the temperature up to 120^oc or may live for many years in the soil. This bacterium have four type of exotoxins  α, β, γ and epsilon toxins.

Epidemiology:-

            Bollinger was scientist who first who identify this disease. Black quarter is an enzootic disease of tropical countries of world. This disease occurs after heavy rainfall and flood. Animal of 6-24 months are more susceptible for this disease. While cattle is more susceptible than other animals. Animal having good body condition are more susceptible to this disease.

Transmission:-

            This disease comes under the heading of soil born infections. It is spread by infected carcass. It may also be transmit due to contaminated feed, water, wound or trauma in large animals. In small animal it may be transmitted during shearing, docking, castrating or kidding/lambing.

Pathogenesis:-

            Spore may enter through injured mucosa of alimentary tract then it moves to the blood where it produces toxins and causes septicemia. Then it is engulfed by macrophages and reaches to muscles and causes hemorrhages due to injured capillaries. Toxins produce systemic reaction and local lesions and local lesions. Aspirate toxemia cause death in animals. In immune animals there is permanent damage of affected part.

Clinical signs:-

1.      Incubation period: 2-6 days

2.      Increase temperature 106-107 ^oF

3.      Swelling of affected part………. Swelling is hot and painful with passage of time swelling will cold and painless.

4.      Bubble formation by toxins.

5.      Necrosis

6.      Animal will feel restlessness

7.      Dull, depress

8.      Loss in appetite

9.      Abdominal pain and increase thirst

10.   Skin become dry and rough

11.  Death occur within 3-4 days

12.  In severe cases there may be lemeness and rupter of skin, discoloration of skin and fowl smelling.

Diagnosis:

            O n the basis of signs and symptoms

            FAT ( florescent antigen test)

Differential diagnosis:-

            Antrax:- at the death there will be bleeding in natural orifices. But in Black Quarter there will be frothy bleeding from nostrils.

Treatment:-

            Pencilline is drug of choice 20 I.U twice daily

            NASAIDs or steroids 1ml/10kg

            Antihistaminic drugs (Avil)

            Fluid therapy

            Multivitamins (never use ca in high fever because it leads to tachycardia.)

Controls:-

            Vaccination in April

            Deep burial of carcass 6-7 feet.

            Avoid animal grazing on contaminated pasture.

            Never open the carcass


Tetanas:
       It is also known as lock jaw, saw horse disease.

Etiology:
       Tetanus is caused by clostridium tetani. It is a G +ve, motile anaerobic bacteria. It is normal habitat in carnivors. It has three strains H, A and O. and produces three types of toxins.

1. Tetanospasmin (neurotoxin)
2. Tetanolysin (haemolysin)
3. Fibrolysin

Epidemiology:

           Tetanus occurs in all species of animals. All age of animals such as horses, mules, sheep, goats and cattle are susceptible but equines are more susceptible among all. Sometimes outbreaks are observed in young animals. Morbidity rate is high and mortality rate is 80%.

Pathogenesis:

             The bacteria enter through deep punctured wounds in case of retain placenta, porlapse, shearing, docking and vaccination. When there is low O₂ in these tissues, this will help the spores of clostridium to germinate, grow and produce toxin. Tetanospasmin or neurotoxin is released by cellular autolysis. It is absorbed and disseminated in to bold to produce neurotoxic effect through absorption by peripheral nerve endings. It affacts centrally in the spinal cord and brain and peripherally on motor nerves to produce spastic paralysis. Flaccid paralysis also occurs due to local invasion of the nerves. Death occurs due to apnea as a result of fixation of respiratory muscles.

Clinical findings:

• Incubation period few days to few weeks.
• Suddenly progressive stiffness.
•  Prolapsed of  3^rd eye lid with the passage of time.
•  Erection of ears
• Saw-horse posture.
• Animal standed with extended feet.
• Death occur due to asphyxia

Diagnosis:

•  on the basis of history
•  clinical signs
• stiff legs and locked jaw.

Differential diagnosis:

Milk fever: 

             In milk fever there quick response of ca therapy but in tetanus there is no such effect of calcium.

Strychnine poisoning: 

              History of accident feeding, absence of wounds,

Treatment:

Pencilline 10000IU/kg twice

 Chlorpromazine 0.2mg/kg as muscle relexant

 Mgso₄

Homeopathic treatment:

Camphora-10 drops every 20 minutes. After camphora administer belladonna every hour.

Lpetospirosis:

Etiology:

           Leptospirosis is caused by leptospira, which is more than 212 serotypes. In old books it is serotype in new one it is serovars. The pathogenic specie is L. enterogen. It affects all ruminents, canine and feline family as well as in human beings. This disease is of two types

1. Host adapted
2.  Non host adopted

Non host adopted:

L. pomona is specific for dogs if it infect in cattle that infection will be non host adapted infection. The cattle will be incidental or accidental host.

Host adapted:

L. hardjo is specific for cattle. If cattle get infected from this then it will be host adapted infection. Non host adapted form of infection is more severe than host adapted infection.

Transmission:

          This is more fragile bacteria; it grows in moist, marshy and rainy areas. It can servive upto 6 month. It destroyes with in 30 min if the area is dry. PH from 6-8 is gud growth for its growth. It cannot servive in less than 10 C and more than 40 C. it shed through urine, semen, aborted fetus. Sheding occur after 6 month of recovery from disease.

Pathogensis:

             It enters through skin, ingestion and direct contact and multiplies in epithelial cells and extra cellular fluid. Then it enter into blood and produces hemolysin and cause hemolysis. its predilection site is liver and kidney. In kidney it causes glumerulonephritis. It also causes abortion in 2^nd trimester of pregnancy.

This is No# 1 occupational hazzard in newzeland. 34% veterinarians are infected with Leptospira. No vaccine available for human.

Clinical Findings:

Three types

1. Acute
2. Subacute
3. Chronic

Acute:

•  I.P= 4-7 days
• Temperature upto 107 F
•  Milk production drop
•  Anorexia
• Anemia
• White spotted kidney
• Dyspnea
•  Abortion in 1^st week

Subacute:

•  Less severe
• Abortion in 3-4 weeks
• Increase temperature upto 105 F

Chronic:

• Abortion and other signs

Occult:

• Only abortion
• Increase antibody titer

 L. pomono causes acute and subacute form it secretes hemolysin and causes homolysis.

L. hadjo cause chronic form it cannot secrete hemolysin but causes abortion.

Differential diagnosis:

1. Bacillary Hemoglubinuria:

No abortion and is caused by clostridium hemoluticam, clostridium novyae. No milk drop syndrome spountaneosly.

2. Bebasiosis:

Ticks are present.

3. PPH:

Due to the deficiency of Phosphorus. No temperature.

Diagnosis:

Culture tests.

Treatment:

Streptomycin, ox tetracycline are drug of choice.

Conrol:

         Vaccine is available for dog, buffalo and cattle. Pentavalent vaccine for cattle and buffalo. L. Pomona, L. hardjo, icterohemorrhagica, kirschneria and grippotyphosa.

Tetravalent vaccine is for dog.

Bacillary Hemoglubinuria:

     It is caused by clostridium hemolyticum, clostridium  navyae type D. spore forming anaerobic soil born rod shaped G +ve bacteria. It is normally present in the soil and liver. All clostridail pathogens live in soil as well as in liver. They can survive up to 1 year outside the body of animal. This was observed on the bone of dead animal which was died one year ago.

Clostridium Navyae type D produce two types of toxin.

1. Necrotoxins
2. Β- hemolytica

Type A, B; C and D are toxin producer. All are pathogenic except type C which is non pathogenic. Type B cause black disease, necrotic hepatitis in sheep and goat.

Necrotoxins:

It causes necrosis.

Β-hemolytica:

it causes rupture of blood vessels, breakdown of RBCs.

This disease is prevalent in autumn and summer.

Transmission:

Transfer through direct ingestion from there it goes to epithelial cells of liver (predilection site). If damage of parenchyma it causes anerobic condition and start its activity and cause localize necrosis.

Clinical Findings:

•   Ip 1-7 days
•  Sudden death without signs.
• Sudden increase temperature up to 106-107F.
• Sudden decrease in milk production
• Animal feel abdominal pain due to liver damage
• Edema of braskit
•  Dark brown color feces
•  Hypoxia and severe anemia
•  Death
• Abortion in later stages.

Treatment:

•  G +ve medication.
• Pencillin drug of choice for all clostridium pathogens
•  Amoxicilline

Control:

• Vaccination 4-6 week before prevalence
• In calf and newborn vaccinate at six month and then annually
• Twice in year if the disease is more prevalent
• Affected carcass should be properly disposed off.

Actionmycosis (Lumpy Jaw):

Actinomycosis is sporadic disease therefore rarely animal transmission

Viral diseases:

PPR ( Peste Des Petits Rumenitis):- 

        Also called as Goat Plaque in India KATA, Psedu rinder pest. Pakistan is free from PPR.

Characteristics:-

        Acute, subacute disease of goat & sheep. High rise of temp, erosions, stomatitis, conjunctivitis & gastroenteritis.

Etiology:-

       Family: Paramaxovaridae

       Genus: Morbilli virus

Epidemiology:-

        Common in rainy and cold dry seasons in middle east counties. In Pakistan this was common in October.

Morbidity rate: up to 90%                     Mortality rate: 50-80%

Pathogenesis:-

        After inhalation of virus, the virus enter into the pharyngeal and mandibular lymph node. There it multiplies and enter into the blood and develop viremia in 3 days. After this virus goes into the lymph nodes of different organ mucosa and GIT mucosa cause leucopenia and immune suppression and follow the necrosis. The virus shedding continuous in acute phase and subsides in few days and body temp of animal become normal.

Transmission:-

           The virus spread through direct contact. It is present in tears, nasal and cough secretions and excretions.

Clinical findings:-

·         Incubation period: 3-10 days

·         Temp upto 106-107 F

Animal become anorectic, dull depress. Erosion of mucosa of mouth and nasal passage become evident after 5 days of infection, that develops the procure salivation, necrotic stomatitis, halitosis (bad smell) serous nasal discharge become mucopurulent  resulting in perfuse catarrhal exudates which crust over and occuled the nostrils. Animal feels difficulty in respiration. There is severe conjunctivitis. After 3 days of infection the sign of gastroenteritis appear. The animal shows perfuse watery diarrhea that leads to death of animal with in 3-5 days. If animal is pregnant then there may be chances of abortion.

Reson of Abortion:

           ACTH is stress hormone that converts placental progesterone into estrogen. That causes expulsion (before time) of fetus.

Diagnosis:-

·         On the basis of history, clinical signs.

·         Samples of secretions

·         ELIZA and PCR

     

Treatment:-

·         Antibiotic therapy to stop secondary bacterial infection.

·         Supportive therapy (multi vitamin)

     

Prevention and control:-

·         Separation of affected animal from healthy one.

·         Cull the affected animal.

    

Differential Diagnosis:-

·         Rinder Pest (RP):- Disease of cattle and buffalo.

·         Foot And Mouth Disease (FMD):-   Hoofs are also involved.

·         Blue Tongue (BT):- Tongue of animal become blue and inflammation of coronary band (coronitis).

·         ORF:- Only upper and lower lips are involved, no diarrhea.

Rinder Pest:-

         Also called cattle plaque, bovine typhus and peste of bovine.  In India known as Mata.

Characteristics:-

         RP is contagious viral disease of cattle and buffalo. Characterized by high fever, oral erosions, diarrhea, lymphoid leucosis, high mortality.

Etiology:-

      Family: paramyxo viridae

      Genus: Morbilli virus

Epidemiology:-

              Common in rainy and cold dry seasons in middle east counties. In Pakistan this was common in October. Pakistan is free from RP certified by OIE (office of international disepizootics).

Transmission:-

       No vertical transmission, no arthropod transmission. The virus spread through direct contact. It is present in tears, nasal and cough secretions and excretions.

Pathogenesis:-

        After inhalation or ingestion virus enter in to the pharyngeal and mandibular lymph nodes and starts multiplication there. The virus enters in to the blood and develops viremia in 3 days. Lymphoid organs, mucosa of GIT and respiratory tract, that leads to leucopenia and immune suppressions and follows the lymphoid leukosis. The shedding of virus take place in acute form of stage. The virus is excrete through all secretions and excretions.

Clinical findings:-

·         Incubation Period: 3-9 days

·         Four forms

A)    Peracute:

·         Sudden rise in temp

·         Congestion of mucosa

·         Respiratory distress

·         Death of animal in 2-3 day

B)    Acute:

·         high fever 106-107 without oral lesions (Prodromal fever).

·         Dull, depression.

·         Sudden fall in milk production.

·         Inflammation of buccal mucosa, oral cavity, vagina and vulva, bulbi salivation.

·         Perfused eye discharged that become purulent accompanied by blephrospasm of  orbicular muscles of eye.

·         Serous nasal discharge that become mucoprulent

·         Discreet gryeish raised necrotic lesions  of 1-5mm in diameter develop appear. First of lower lip the cheek mucosa at the comissure and lower side of tongue . later on these lesions spread on all mouth. Similar lesions found in mucosa of nasal  cavity, vagina and vulva. Skin lesion effecting the premium, sebutum and flank very less common. There is severe dearrhea and some animal show dysentery with tenesmiss (feces with pain) that lead to dehydration and death of animal.

C)    Sub acute

·         Temp 103-104 oF

·         Course of disease 2-3 weeks.

·         Persistant diarrhea may lead to loss of weight and weakness

·         Necrotic and oral lesions appear and heal during course of disease

D)    Atypical

·         Animal do not exhibit typical clinical signs and symptoms.

·         Animal become weak, dull vigourless.

    

Diagnosis:-

·         On the basis of history

·         Clinical signs

·         Post Mortem lesions (zebra stripping in colon of intestine)

·         ELIZA, PCR.

·         Collection of secretion or excretion.

Treatment:-

·         Antibiotics to check secondary bacterial infections

·         NASIDs

·         Fluid therapy (ringer lactate, normal saline).

·         Vitamin therapy

Differential Diagnosis:-

          FMD:- Lesions develop in cloven hoofs.

          Blue Tongue:-   coronitis and blue color of tongue.

          Salmonellosis:-  Diarrhea is present

          Paratyberculosis (jhone’s disease) shooting diarrhea.

 Foot And Mouth Disease:-

          It is also called Apathies fever. In Pakistan it is known as Mun Khur.

Characteristics:-

 FMD is a contagious disease characterized by pustules in mouth  and in cloven hoofs.

Etiology:-

         Family:- Picorna Varidae

         Genus:- Aptha virus

         Serotypes: 7 in number. A, O, C, SAT-1, SAT-2, SAT-3 and Asia-1. In Pakistan A,O,C and 

ASIA-1 serotypes are present.

Epidemiology:-

         After BSE, FMD in is more severe disease in the world. This virus is shorty and hardy and in Pakistan it is common in may-june and December- January.  FMD is resistant in Equines. Japan, Newzeland and Australia are FMD free countries.

Transmission:-

      Transboundary , by inhalation and ingestion. This virus can travel 250 km in air. It can live for 60 days in frozen meat, 2 years in dried milk, 30 days in hair and 60 days in cloths. Kill in acidic PH.

Pathogenesis:-

      After ingestion and inhalation the virus enter into pharynx mucosal epithelium and launched in epithelial cells of mucosa and multiplies in cytoplasm them move in to lymphatic the  in to blood and cause viremia.

Clinical signs:-

·         Incubation period: 21days signs appear in 7-8 days

·         High temp.

·         Appearance of pustules and vesicles in mouth and foot pads.

·         Ropy strings (hyper salivation)

·         Sometimes pustules on the teats

·         FMD cause indirect abortion.

Diagnosis:-

·         On the basis of history and clinical sign.

Treatment:-

·         FMD serum. (5ml in S.A and 50 ml in L.A)s/c

·         Antibiotic to check secondary bacterial infections

·         Supportive therapy

Control and Prevention:-

·         Apthization (took the ingesta from the mouth of infected animal and rub on the mouth to other animals to create immunity in other animals.)

Vaccination:-

 In Pakistan

      Water base vaccine:  In the month of May and November

       Oil base vaccine: once a year.

Differential diagnosis:-

    Rinder Pest (RP):-   Diarrhea and no lesions in the cloven hoofs

    Blue Tongue:-   Color of lesions is bluish and coronitis.

    Vesicular Stomatitis:- stomatitis.

Blue Tongue:-

               BT is an important economically infectious disease but non contagious disease.

Etiology:-

          Family:- Reoviridae

          Genus:- Orbivirus

           Serotypes:- 24 in number

Epidemiology:-

           Morbitidy:- 50-75%

           Mortality:- 2-30%

This disease is common in sheep, less common in cattle and rare in goat.  Cattle are reservoir and sheep get infection from cattles.

Transmission:-

             This disease is transmitted by Culicides (biting fly) which cause BT disease. This fly is available in wet and humid areas of fecal area breed.

Pathogenesis:-

            This virus replicate in  the midgut of biting fly. In 6-10 days  the virus is ready for transmit. The female fly only feed once in life. Male do not transmit the disease.

The fly bite on skin and swelling occur and transmit to lymph node and cause lymphatics and enter in to blood (3 days takes to reach in blood) and viremia occur. After 6 days of infection virus localized in the blood vessels and damage endothelial wall of blood and hemorrhages, necrosis and bloodage.

Clinical findings:-

·         Incubation period:- less than 6 days

·         Viremia

·         Temp 104-106 oF

·         Redness of mucus membrane

·         Swelling, edema, hemorrhages, necrosis bluish appearance called Blue Tongue

·         Saliva lesions on lateral site of tongue.

·         Animal become off feed.

·         Coronitis

·         Animal emaciated 6 days.

Diagnosis:-

·         On the basis of history

·         Clinical signs

Treatment:-

·         Only symptomatic  treatment

·         Antiseptic like KMno4

Control:-

         Separate the affected animal

Bovine Viral Diarrhea:-

           BVD is acute, subacute  inappearent infection of cattle and buffalo.

Characteristics:-

           BVD is characterized by increase temp, diarrhea and erosion of mouth, esophagus, rumen, abomasum and intestine.

Etiology:-

          Family:-  Flaviviridae

          Genus:-  Peste virus

BVD is two types. Type 1 and Type 2 and each type is further divided into

1.      Cytopathic

2.      Non cytopathic

Type 2 is more severe than type 1.

Epidemiology:-

       Mostly occur in cattle and buffalo but less common in small ruminants. Succeptible age of this disease is 6-24 months. Animal less than 6 months are less succeptible.

Pathogenesis:-

       Virus acquired by both oro- nasal routes. Initially virus flows in oral and nasal mucosa where it start multiplication and enter in to blood and cause viremia then through blood virus goes into different body organs. BVD is an immunosuppressive in which both B and T lymphocytes are suppressed. The  transplacental spread disease depend upon the age of fetus and time of gestation. During 1^st 30 days of gestation this virus causes  Early Embryonic Mortality (EEM) and dam reverse to estrous. During 30-90 days it cause abortion, mummification and congenital abnormalities and after 120 days of gestation the fetus can mount and active immune response and usually born normal at the time of birth. But remains carrier throughout whole life.

Clinical Findings:-

         Incubation period:-    1-121 days

a). Acute:-

              This form is basically epidemic in nature. Sudden high rise in temp 106. Temp may be biphasic in nature. Initially there is high rise of temp for 4-7 days. After few days of normal temp then 2^nd rise of temp. There is mucopurulent nasal discharge, moist cough, muzzle become rough, dry and crested. Mucopurulent ocular discharge also seem that may lead to conjectivitis and finally corneal opacity.  Animal shows involuntary movement of eye balls. (nystagmous).

b). Mild Form:-

·         Fever persists for very short duration.

·         Temporary loss of milk production

·         Diarrhea

·         Oral lesions

·         Anorexia

·         Enlargement of super facial lymph nodes

c). Chronic Form:-

·         Prolong course of disease

·         Growth retard

·         Loss of body condition

·         Emaciation

·         Skin become rough and dry

·         Intermittent diarrhea

·         In some cases animal shows signs of nose bleeding

·         Elongated distorted hooves

·         Arch back condition seen in few cases

·         Death is not common in this form.

Diagnosis:-

• On the basis of history
• Clinical signs
• ELIZA and PCR
• Neutralization

Treatment:-

·         Antibiotics to stop 2ndry bacterial infection

·         Multivitamins

·         Ringer lactate for emaciated animal

·         Vit A and vit K. vit A plays vital role in healing of epithelium

·         NSAIDs

Rabies:-

          Also known as “Drop Jaw” disease. Rabies is infectious disease but not a contagious disease.

Etiology:-

          Family:-  Rhabdoviridae

          Genus:-  Lyssa virus

Epidemiology:-

            Occur in almost all over the world except Australia and Newzeland. This disease is caused by bite of variety of animals e.g. rats, squirrel, bats foxes, cat and dog. Vampire bat is most susceptible host of rabies.

Transmission:-

          Rabies virus enters through saliva of infected animal. When host bite the animal the saliva transfer in to the body of infected animal. No oro-fecal transmission is reported.

Site of multiplication is Neuro muscular junction.  Virus enters into the wound and start replicate in striated muscles, from striated muscles it moves into CNS (Spinal Cord) with the speed of 2-4mm/day. When virus moves into the spinal cord then there is no force to stop the movement of this virus. Severity of disease depends upon position of bite. In the start it is paralytic form when it enters into CNS it becomes furious.

In America and other developed countries there is paralytic form while in Africa and Asia there is furious form.

Two forms of Lyssa virus.

1). Fixed virus: cultivated on cell culture in lab for vaccine purpose.

2). Street virus: it is present in infected animals.

Properties of  virus:-

                       Lyssa virus is very fragile, it is disinfected by carbolic acid and phenolic disinfectants.

 Types of Rabies:-

     1). Paralytic/Dump rabies  

     2). Furious rabies

Chorea: condition in which there is no coordination in limbs.

Dyarthrea: paralysis of facial muscle.

Clinical findings:-

 Incubation Period: 10-15 days

 In cattle 15 days

In horse 12 days

In sheep 10 days

Coarse time:-

 In cattle 3.7 days

In horse 5.5 days

In sheep/goat 3.2 days

·          In paralytic form

        Ø  Salivation

        Ø  Paralysis (drop jaw)

        Ø  Paralysis of involuntary muscles

        Ø  indigestion

        Ø  Death due to failure of respiratory muscles.

·          In furious form

  Ø  Pressing of heads

  Ø  Males shows more sexual excitement

  Ø  Death is due to convulsions

Diagnosis:-

ELIZA is the bet confirmatory test for rabies virus.

Control:-

          Prophylactic vaccination.

        Pre-exposure. In human at 0-day 1ml, 7^th day 1ml, 28^th day 1ml,and annual vaccine.

If  you are infected after vaccination then only 2 shots at 0-day 1ml, and 3^rd day 1ml.

If not vaccinated then 5 shots at day 0-day 1ml, 3^rd day 1ml, 7^th day 1ml, 14^th day 1ml, 28 day 1ml.

In animals vaccinate at the age of 4 months and then annul booster pre- exposure.

In post exposure 5 shots with double dose.

Vaccine schedule of rabies:

 Two types of protocol

a)      Pre- exposure

b)      Post exposure

Pre- exposure:-

           0-day, 7^th day, 21^st day, and annual booster

Post exposure:-

If already vaccinated then at 0-day and 3^rd day.

If not vaccinated then vaccinate at 0-day, 3^rd day, 7^th day, 14^th/21^st day and 28^th day.

WHO recommended protocol of post exposure:

0.1ml of vaccine                    on 8 different sites on day 0

0.1ml of vaccine                   on 4 different sites on day 7^th.

0.1ml of vaccine                    on 1 site on 28^th day.

0.1ml of vaccine                    on 1 site on day 90.

Vasicular Stomatitis:-

                        Also called as sour mouth, pseudo FMD, mouth thrush and sporadic aptha.

It is an infectious viral disease of cattle, horses and pigs that is characterized by vesicular leions containing serous fluid on the mouth, foot  interdigital space, udder and teat that persist for short period of time.

Etiology:-             

         This virus belongs to family Rhabdoviridae genus vesicular virus. Two distinct antigenically types

     a)      Indiana            b) New jersy.

New jersy is most virulent and most common type. Indiana has 3 sub types

    1)      Fort lupton

    2)      Algaoes

    3)      Cocal

This virus is bullet shape.

Epidemiology:-

                  This virus is endemic in central America and some region of south .

America. This disease is also present in India. All breed of cattle, horses, donkey and pigs are succeptible. The outbreaks mostly seen in horses and cattle. Calf is less succeptible than cattle. Sheep and goat are resistant to this disease.

Transmission:-

a)      Through direct contact

b)      Contaminated food, water and equipments

c)      Mechanical transmission insect, fly and mosquitoes

d)     Reservior host for this virus is pigs, ferrals(wild cat) raccon and bear.

     

Pathogensis:-

                        Virus enters through abresion of skin or mucus memberane due to the bite of insect fly or mosquitoies. The vesicle formation at the site of infection. These vesicles joint together and form big vesicle in that way virus spread to new leions. Secondary leions at distinctory places may develop but still it is unclear that how virus transmission occur.

      

Clinical Findings:-

                        Incubation period 3-15 days

       In cattles:-

a)      Mild rse in body temperature.

b)      Vesicles form on the dorsal surface on tongue.

c)      Dental pads,lips and buccal cavity.

d)     The viescle joint together and form big vesicle these vesicles quickly ruptures and result irritation that may lead to perfuse ropy salvition. Animal become anorectic in case of milking animal decrease in production. Leions on foot and udder rarely except milking cow.

In Horses:-

a)      Similar with cattle.

b)      Fever, deptession, inappetenc, salivation

c)      Effected horses may rub their lips with trough. In that way vesicle rupture and form big shallow ulcers. Leions also develop on the coronary band that lead to the laminitis in horses.

Diagnosis:-

       On the basis of history, clinical finding and different microbiological tests ELIZA, PCR.

Rota and corona virus causes winter dysentry.

Treatment:-

a)      No specific treatment

b)      Only supportive therapy

c)      Antibiotic to check secondary infections

d)     NASIDs, best antiseptic for oral leions is KmnO4 and for foot is CuSo4 for dipping.

Contageous Ecthyma:-

                       Also called ORF, Scabies mouth, sour mouth, contageous pustular dermatitis.

This is the disease of sheep and goat confusing with PPR.

Etiology:-

 It is caused by Poxviridae family

Genus:- Parapox. It has furthur 3 sub types

1)       Parapox ovis

2)      Parapox 1

3)      Parapox 2

Parapox ovis:- This type cause contageous ecthyma

Parapox 1:-  this type cause disease in bovines.

Parapox 2:- this type cause pseudo pox.

            Epidemilolgy:-

                        This virus present in all over the world. Morbidity 100%     Mortality 5-10% . death occur when leions move into respiratory system.

            Transmission:-

                        Invasion is through skin trap through direct or indirect contact.

            Pathogensis:-

            When skin breaks the virus enter from that skin where it multiplies and spread continously and uniformly form macule, papule, vesicle, pustule and scab formation. These will form on mucocutaneous junctions. Lambs and kids are more succeptible at the age of 2-3 months. This disease is also observed at the age of 17 days. This disease is self cure and recover in 4-5 weeks.

          Clinical Signs:-

•  No leion in the mucus memberane
• Macule, Papule, vesicle, Pustule and scab
• Temperature may rise or not.
• Size of scab 0.5mm in diameter. Scab is not easily peeld off.
• Leions on the mucocutaneous junction. Very less chances of leions on ear, nose or commissures.
• Salivation, no diarrhea,

            Zoonotic point:-

                        Leions form on the arms and face of affected person bbut these are self limiting.

            Treatment:-

a)      No treatment

b)      Mild disinfectants to check the secondary infection.

Bovine Ephemral Fever:-

            Also called 3-day sickness, bovine epizootic fever,  in some countries also called as stiffnes sickness.

            Bovine ephemarl fever is an arthropod transmited viral disease of cattle and buffalou.

This disease is characterized by increase temperature, muscle trmers, stiffness, lameness (shutling)

Etiology:-

            Virus belongs to rhabdoviridae family and genus ephemro virus having only one sero type.

Epidemilology:-

            BEF is an enzootic disese in east indies, Africa, Australia, Pakistan, Turkey and cyprus. All breeds of cattle are succeptible at the age of 6-24 months. Animal of age over 24months or under 6 monthsare least succeptible. This disease is not reported in sheep, goat, cat and dog. This disease is transmitted through sand fles. Out breaks are commonly seen in summer season because this virus travels rapidly by winds.

Pathogensis:-

            Blood sucking insects acquire virus from infected animal. The virus goes into the body cavity of insect. The multipication starts into body of insect. Virus comes into the saliva of insect and it transmit it to the healthy animal. The virus goes into the blood and cause viremia and starts multiplication in mesodermal joints, muscles and lymphnodes.

Clinical Signs:-

a)      Incubation Period= 2-4 days. Some time it may long upto 10 days.

b)      Increase body temp upto 105-106 ^oF

c)      Animal become dull, depress and anorectic, sharp fall in milk.

d)     Shivering and muscle tremour also noticed.

e)      Limbs of affected cattle become stiff hard and pain full and animal can  not more or if move with great difficulty with arch back posture. Severly effected cattles may lay down with extended ridge hind limb. Lameness due to acute laminitis, lameness move from leg to leg with in few hours. In some cases lameness persist afterdisappearence of clinical signs. Salivation nasal discharge and lacrimation also noticed in some cases. Few cases that shows the typical posture as in milk fever the S-shaped neck or post parturent hematuria. This generalized enlargment of super facial lymphnodes.

Post disease complications:-

1)      Fall in milk production

2)      Delay to next estrus

3)      Pneumonea due to prolonged recumbency

4)      Prone to mastitis

5)      Animal unfit for drought purpose.

Diagnosis:-

      On the basis of history and clincal signs

      Virus neutralization test,

      FAT, PCR

Treatment:-

            Phenyl Butozone 8mg/kg repeat after 8 hours.

            Flunixin meglumine