Diseases caused by viruses

Foot and mouth disease (FMD, Aphthous fever)

 FMD is an acute viral and extremely contagious disease of cloven

footed animals such as cattle, sheep, goats, pigs and antelope.
 It is manifested by vesicles and erosions in the muzzle, nares,
mouth, feet, teats, udder and pillar of the rumen.
 There are three main strains of viruses causing FMD, namely A, O
and C.
 Three additional strains, SAT 1, SAT 2 and SAT 3 have been
isolated from Africa and a further strain ASIA-1 from Asia and the Far
East.
Transmission
Direct and indirect contact with infected animals and their
secretions including saliva, blood, urine, faeces, milk and semen,
aerosol droplet dispersion, infected animal by-products, swill
containing scraps of meat or other animal tissue and fomites and
vaccines.

Clinical findings

 Before vesicle formation:

 Incubation is 1 – 5 days or longer
 Morbidity: Nearly 100 %
 Mortality: variable depending on the strain of virus and its virulence
and susceptibility of host; 50 % in young animals, 5 % in adults
 Fever up to 41.7°C
 Dullness
 Lack of appetite
 Drastic drop in milk production.
 Uneasiness and muscle tremors

Vesicle formation:

 Smacking and quivering of lips

 Extensive salivation and drooling
 Shaking of feet and lameness
 The vesicles and later erosions are commonly found on the muzzle,
tongue ,oral cavity, teat and on the skin between and above the
hoofs of the feet.
 In more chronic cases in cattle the hoof become loose and the
animal may walk with characteristic “clicking” sound (Slippering).
  Some strains of FMD, particularly in swine, sheep and goats cause
erosions instead of vesicles.

Postmortem findings

 Necrosis of heart muscle(tiger heart), usually only in young acutely

infected animals.
 Ulcerative lesions on tongue, palate, gums, pillars of the rumen and
feet.

Diagnosis
 Case history and symptoms
 Diagnostic techniques used include
 serologic tests to identify FMD virus infection-associated antigen
(VIA),
 complement fixation (CF) and enzyme-linked immunosorbent assay
(ELISA) tests to detect FMD viral antigen,
 virus isolation (VI) and neutralization (VN),
 electron microscope (EM),
 animal inoculation studies and RT-PCR.

Differential diagnosis

 Vesicular stomatitis,
 allergic stomatitis,
 feedlot glossitis,
 photosensitization,
 bluetongue,
 rinderpest,
 infectious bovine rhinotracheitis,
 malignant catarrhal fever,
 bovine papular stomatitis,
 bovine viral diarrhoea,
 pseudocowpox,
 ovine pox,
 contagious ecthyma,
 footrot,
 mycotoxicosis and increased salt in concentrate.

Transmission

Direct and indirect contact with infected

Animals and their secretions including

 • saliva,
• blood,
• urine,
• faeces,
• milk and semen,
• aerosol droplet dispersion,
• infected animal by-products,
• swill containing scraps of meat or other animal tissue and
fomites and vaccines.

Control, prevention, treatment

• In regions that are normally FMD-free, control of the disease is

typically attempted by culling all animals on infected
premises, and animal movement controls are imposed to
reduce the risk of virus spread
• In both normally FMD-free regions and endemic areas,
vaccination around outbreaks may be used to limit the spread
of the disease
• No treatments for infected animals are available
• The OIE classifies countries and regions as: FMD-free without
vaccination; FMD-free with vaccination; suspended FMD-free
status with or without vaccination; and unrecognized.
• The current global status of FMD distribution shows
geographic areas where FMD prevalence has been high over
long periods of time.
• They are commonly located in economically challenged
countries where veterinary services and resources are
inadequate to control or eradicate FMD.
• Inactivated virus vaccines protect for only 4–6 months against
the specific serotype(s) contained in the vaccine.
• Vaccination is used more in enzootic countries to protect
production animals, particularly high-yielding dairy cattle,
from clinical illness because slaughter of all at-risk individuals
may be economically unfeasible and can cause food
shortages.
• When mass culling is performed, infected carcasses must be
disposed of via incineration, burial, or rendering on or close to
the infected premises.
• Scavengers and rodents should be prevented or killed to
prevent mechanical dissemination of virus.
• Buildings should be cleaned with a mild acid or alkaline
disinfectant and fumigation, and people that have come into
 contact with virus must decontaminate their clothing and
avoid contact with susceptible animals for a period of time.
• In some regions, FMD persistence in wildlife populations, such
as the wild African buffalo, can make the prospect of FMD
eradication very difficult.
• Control measures, such as fencing of wildlife reserves to
prevent contact with domestic livestock, have helped limit the
spread of virus in certain areas.
• There is no specific treatment for FMD, but supportive care
may be allowed in countries where FMD is endemic.

Rinderpest
 is an acute, highly contagious, fatal viral disease of cattle, buffalo
and wild ruminants manifested by inflammation, haemorrhage,
erosions of the digestive tract, wasting and often bloody diarrhoea.
 Some swine species are also susceptible.
 Man is not susceptible to RP virus.

Etiology
 Morbilli virus of paramyxoviridae family.
 Rinderpest virus is sensitive to environmental changes and is
destroyed by heat, drying and great number of disinfectants.

Transmission

 Direct contact with infected animals or their excretions and

secretions and fomites.
 The virus appears in the blood and in secretions before the onset of
clinical signs and this may cause infection in abattoirs and
stockyards.

Clinical findings
1. Incubation: 3 – 10 days or longer
2. Morbidity: Up to 100 % in a susceptible herd
3. Mortality: 50 % and may reach 90 – 95 %
4. High fever (41–42°C)
5. Nasal discharge and excessive salivation
6. Punched out erosions in the mouth .

Rift valley fever (RVF)

 RVF is an acute viral disease of sheep, cattle, goats and humans.

  It is manifested with hepatitis and high mortality in young lambs
and calves, and abortion in adult animals.
 Rift valley fever resembles influenza in humans.
 The disease is of significant importance in Africa.

Etiology

 The disease caused by Phlebovirus of the family Bunyaviridae

Transmission

 Biting insects and mosquitoes.

 Possible direct contact via cornea.
 Human infection occur by handling diseased tissues, and strict
precautions should be instituted to prevent infection with this virus,
such as wearing goggles and gloves.

Clinical findings
Sheep
 Incubation 12 – 48 hours in young animals
 High morbidity and mortality in lambs and calves
 Fever
 Lambs refuse to eat, have abdominal pain and are recumbent.
 Animals seek a shaded area because of photophobia (squinting
and blinking)
 Photosensitization characterized with a thickened head and ears.
 Encrustation around the muzzle
 Vomiting in adult animals
 Congenital malformation of the brain and muscles
 Abortion in ewes during the illness or convalescence

Cattle
 Edematous unpigmented skin showing cracking and sloughing due
to photosensitization
 Salivation and inflammation in the mouth
 Abdominal pain
 Diarrhoea associated with haemorrhagic inflammation of stomachs
and intestine
 Lameness
 Cessation of milk production
 Abortion

Postmortem findings
  Cyanotic visible mucosae
 Necrosis of the liver in lambs (liver may be mottled grey, or reddish-
brown to bright yellow in colour)
 Edematous and haemorrhagic gall bladder
 Haemorrhage of the gastrointestinal tract, serosae, internal organs
and lymph nodes
 Partial erosions may be seen in the ileum, caecum and colon
 Udder is purple but inflammation is not observed
 Haemorrhages in the fetus and haemothorax

DIAGNOSIS

 Abortions and death associated with heavy rainfall and flooding

 Characteristic histological lesions in liver specimens (necrotic
hepatitis)
 Immunohistochemistry, PCR assay, or viral isolation
 Demonstration of seroconversion
 The virus can readily be isolated from tissues of aborted fetuses and
the blood of infected animals.
 The viral titer in these tissues is often high enough to use organ
suspensions as antigen for a rapid diagnosis in neutralization,
complement fixation, ELISA, agar gel diffusion tests, or staining of
organ impression smears.
 Definitive diagnosis of RVFV infection is now routinely performed via
detection of viral nucleic acid by conventional reverse transcriptase-
PCR assay or by real-time (quantitative) PCR assay.
 Virus can be demonstrated in organ sections using
immunohistochemical stains.

Differential diagnosis
 Defect in porphyrin metabolism,
 fungal conditions,
 acute viremias/toxaemias including
 enterotoxaemia,
 bluetongue,
 bovine ephemeral fever,
 Wesselbron disease,
 rinderpest,
 heartwater,
 East Coast fever;
 abortions caused by Brucella, Vibrio, Trichomonas,
 Nairobi sheep disease
 and ovine enzootic abortion.
Control and prevention

 Prediction may provide early warning

 Vaccination of susceptible animals
 Once an outbreak of Rift Valley fever has started, any efforts to
mitigate its course are usually futile.
 Control of vectors,
 movement of stock to high-lying areas,
 and confinement of stock in insect-proof stables are usually
impractical, instituted too late, and of little value.
 Treatment of individual clinically affected animals should be
symptomatic,
 and the high risk of zoonotic transmission to humans via tissues or
fluids should be considered.
 Immunization remains the only effective way to protect production
animals from RVF.
 The mouse neuro-adapted Smithburn strain of RVFV can be readily
produced in large quantities, is inexpensive, and induces a durable
immunity 6–7 days after inoculation in sheep.
 It should typically not be administered for protection of pregnant
animals, because it may cause abortion, congenital defects
 A formalin-inactivated vaccine is safe to use in pregnant animals;
however, it induces short-lived immunity and requires booster
doses.
 Vaccination is often employed as an emergency measure in the face
of an outbreak
 Routinely immunizing lambs at 6 months old, which should afford
lifelong protection, is advisable.
 The offspring of susceptible ewes can be immunized at any age.
 Pregnant ewes and cattle can be vaccinated with a formalin-
inactivated vaccine, which elicits a better immunity in cattle and is
safe in pregnancy.
 Revaccination after 3 months is advisable to induce an immunity
that will last >1 year and to confer colostral immunity to the
offspring.

Rabbies
 This is an acute infectious viral disease of the central nervous
system in mammals.

Etiology

 A member of the Lyssavirus genus of the Rhabdoviridae family.

  These viruses are enveloped and have a single stranded RNA
genome.

Transmission

 It is usually transmitted through the saliva by a bite from a rabid

animal, commonly the dog or jackal.
 Man is infected the same way.

Antemortem findings

 Furious form
 Incubation from 2 weeks to 6 months or longer
 Restlessness
 Aggressive, may attack other animals
 Sexual excitement
 Bellowing
 Paralysis and death

Paralytic form

 Sagging and swaying of the hind quarters

 Drooling and salivation
 The tail is held to one side
 Tenesmus or paralysis of the anus
 Paralysis
 The animal falls to the ground
 Death after 48 hours of decubitus
 Possible inflammation of gastrointestinal mucosa
 Encephalitis (negri bodies)

Diagnosis
 Diagnosis based on clinical signs alone should not be relied on when
making public health decisions.
 When rabies is suspected and definitive diagnosis is required.
 No definitive antemortem test is available for rabies diagnosis.
 Typically, the suspect animal is euthanized and the head removed
for laboratory shipment.
 At the laboratory, the brain (including the brainstem) is removed as
the preferred organ for testing.
 Immunofluorescence microscopy on fresh brain tissue, which allows
direct visual observation of a specific antigen-antibody reaction, is
the current test of choice.
 Molecular testing, including real-time PCR assay, is becoming
standard in modern diagnostic laboratories.
Differential diagnosis

 Indigestion,
 milk fever or acetonemia when first seen,
 foreign body in the mouth,
 early infectious disease,
 poisoning.

Control and prevention

 Rabies vaccination and registration of cats and dogs

 Promotion of responsible animal ownership
 Management of stray populations
 Oral vaccination of wildlife reservoirs
 Education to avoid exposure to suspect animals

Domestic Animal Management

 Notification of suspected cases and euthanasia of dogs with clinical

signs and dogs bitten by a suspected rabid animal
 Decrease of contact rates between susceptible dogs by leash laws,
dog movement control, and quarantine
 Mass immunization of dogs by campaigns and by continuing
vaccination of young dogs
 Stray dog control and euthanasia of unvaccinated dogs with low
levels of dependency on, or restriction by, people
 Dog registration
 Recommended vaccination frequency is typically every 3 years
(unless otherwise indicated), after an initial series of two vaccines 1
year apart.
 Several vaccines are also available for use in cats, and a few for use
in ferrets, horses, cattle, and sheep.
 Because of the increasing importance of rabies in cats, vaccination
of cats is critica

 Disinfection
 As an enveloped virus, rabies virus is inactivated by various
disinfectants (eg, formalin, phenol, alcohol, halogens, mercurials,
mineral acids).
 The virus is extremely labile when exposed to heat or ultraviolet
light.
 Lumpy skin disease

 Acute debilitating pox viral disease of cattle manifested with

sudden appearance of nodules on the skin.

Etiology

 Belongs to the genus Capripoxvirus of the family Poxvirida

Transmission

 Insect vectors by direct and indirect transmission.

 Seasonal and geographic distribution.

Clinical findings

 Incubation: 4 – 14 days
 Fluctuating fever
 Diarrhoea
 Nasal discharge and salivation
 The first lesion appear in the perineum
 Various sized cutaneous nodules may occur throughout the body
 Skin lesions may show scab formation
 Swelling of superficial lymph nodes and limbs, and lameness
 Infertility and abortion
 Secondary infection may lead to joint and tendon inflammation
 Ulcerative lesions in the mucosa of the respiratory and digestive
tract
 Reddish, haemorrhagic to whitish lesions in the lungs
 Edema (interlobular) and nodules in the lungs
 Heart lesion (endocardium)
 Thrombosis of skin vessels followed by cutaneous infarction and
sloughing.

Diagnosis

 Histopathology, virus isolation, or PCR

 Isolation and/or identification of the causal virus.
 The pox virus of lumpy skin disease can be demonstrated by
electron microscopy in the early skin lesions, and can be
distinguished by PCR.

Differential diagnosis

 Allergies,
 screw-worm myiasis,
 urticaria, dermatophilosis (streptothricosis),
  bovine herpes dermophatic infection,
 cattle grubs,
 vesicular disease,
 bovine ephemeral fever, photosensitization,
 besnoitiosis (elephant skin disease), sweating weakness of calves,
 bovine farcy and skin form of sporadic bovine lymphomatosis.

Control and prevention

 Attenuated virus vaccines may help control spread.
 The spread of lumpy skin disease in recent years beyond its
ancestral home of Africa is alarming.
 Quarantine restrictions have proved to be of limited use.
 Vaccination with attenuated virus offers the most promising method
of control and was effective in halting the spread of the disease .
 Administration of antibiotics to control secondary infection and good
nursing care are recommended, but the large number of affected
animals within a herd may preclude treatment.

Infectious bovine rhinotracheitis

 IBR is a highly infectious viral respiratory disease of cattle, goats

and pigs manifested by inflammation of respiratory passages and
pustular lesions on the male and female genital organs.
 Generally four forms of the disease are recognized; the respiratory
form, the genital form(infectious pustular vulvovaginitis), the enteric
form and the encephalitic form.
 The disease caused by bovine herpesvirus 1 (BHV-1), is a member of
the genus Varicellovirus in the subfamily Alphaherpesvirinae, which
belongs to the Herpesviridae family

Transmission

 Respiratory droplet and nasal exudate in the respiratory form of IBR.

 Obstetrical operations, coitus and licking of genitalia of affected
animals in the genital form of disease.
 The virus is distributed world-wide.

Clinical findings

 Respiratory form
 Incubation: 5 – 14 days
 Fever
  Nasal and ocular discharge and red, swollen conjunctiva and nose
(red nose)
 Drop in milk yield
 Breathing through the mouth and salivation
 Hyperaemia of the nasal mucosa and necrotic areas on the nasal
septum
 Secondary bronchopneumonia
 Abortion

Genital form
 Frequent urination and tail elevation
 Edematous swelling of the vulva and pustule formation on reddened
vaginal mucosa
 Mucoid or mucopurulent exudate in the vagina

Enteric form

 Severe oral and stomach necrosis in new born animals

 High mortality

The encephalitic form in calves

 Depression
 Excitement
 High mortality

Postmortem findings

 Acute inflammation of the larynx, trachea and bronchi

 Profuse fibrino-purulent exudate in the upper respiratory tract in
severe cases
 Chronic ulcerative gastro-enteritis in feedlot cattle
 Lung emphysema
 Secondary bronchopneumonia

Diagnosis

 Identification of the agent: The virus can be isolated from nasal or

genital swabs from animals with respiratory signs, vulvovaginitis or
balanoposthitis, taken during the acute phase of the infection.
 For virus isolation, various cell cultures of bovine origin are use.
 For virus DNA detection, the polymerase chain reaction (PCR)
technique is increasingly used in routine diagnosis especially the
real-time PCR.
  Serological tests: The virus neutralisation test and various enzyme-
linked immunosorbent assays
 (ELISA; indirect or blocking) are most widely used for antibody
detection.

Differential diagnosis

 Pneumonic pasteurellosis,
 bovine viral diarrhoea,
 malignant catarrhal fever
 and calf diphtheria

Control and prevention

 There is no direct treatment for this diseases.
 Infected animals should be isolated from the rest of the herd and
treated with anti-inflammatory drugs and antibiotics for secondary
infections if necessary.
 Carrier cattle should be identified and removed from the herd.
 Control of the disease is based on the use of vaccines.
 Since BHV-1 is a ubiquitous, highly contagious virus, vaccination is
recommended as soon as passive immunity in calves has
disappeared, usually around four to six months of age.
 Currently available vaccines for IBR include modified-live-virus (MLV)
vaccines and inactivated or killed-virus (KV) vaccines.

Bovine viral diarrhoea

 This is an infectious viral disease of cattle manifested by an active

erosive stomatitis, gastroenteritis and diarrhoea.

Etiology

 BVDV is a single linear positive-stranded RNA virus in the genus

Pestivirus of the family Flaviviridae.

Transmission

 Direct contact with clinically sick or carrier animals,

 indirect contact with feedstuffs
 or fomites contaminated with urine, nasal and oral secretions or
faeces
  and contact with aborted fetuses.
 Transmission through aerosol droplet dispersion
 or by insect vector may also be a possibility.
 Virus may persist in recovered and chronically ill cattle which are
considered a potential source of infection.

Clinical findings

 Incubation: 1 – 3 days
 Fever
 Congestion and erosions in the mucous membranes of the oral
cavity
 Depression and anorexia
 Cough, polypnea and salivation
 Dehydration and debilitation
 Foul-smelling diarrhoea
 Cessation of rumination
 Reduced milk supply
 Abortion in pregnant cows
 Laminitis
 Congenital anomalies of the brain (cerebellar ataxia) and arthritis in
young calves

Postmortem findings
 Shallow erosions present on the entrance of the nostrils, mouth,
pharynx, larynx, oesophagus, rumen , omasum, abomasum ,
caecum and less frequently in Peyer’s patches in the small intestine.
 Erythema of the mucosa with submucosal haemorrhage in the
abomasum, small intestine, caecum and colon.
 Stripped appearance on the caecal and colon mucosa is similar to
that seen in rinderpest.
 Cerebral hypoplasia and cataracts in calves.

Diagnosis

 PCR is the most sensitive tool for early identification of persistently

infected (PI) calves, so farmers can remove these highly shedding
animals from the herd as soon as possible.
 PCR tests use either blood or tissue (ear notch) samples, can be
completed in a very short period of time and provide very accurate
results.
  Antibody-based tests are used for bulk-milk screening and allow
diagnosis of BVDV infections in large scale screening and eradication
programs.

Differential diagnosis
 Malignant catarrhal fever,
 rinderpest,
 blue tongue and vesicular diseases.
 The latter produce vesicles which are not present in BVD.
 Diseases with no oral lesion nor diarrhoea include
 salmonellosis,
 Johnna’s disease
 and parasitism.

Treatment

 Treatment of BVD is limited primarily to supportive therapy.

 Once identified, infected animals should be culled.

Prevention

 One strategy to minimise BVD transmission is to make infected

cattle less infectious, and this can be achieved by increasing the
antibody titer.
 Cattle that have antibodies at the time that they acquire acute
BVDV infection do not shed as much virus, and they will shed virus
for a shorter period of time.
 On farm there it is important for producers to cull persistantly
infected animals from the herd.
 Blood tests will identify Housing calves in individual hutches as
opposed to group housing will decrease contact and risk of infection,
as will reducing stocking density.
 Strategic vaccination and high-quality colostrum could also decrease
the proportion of susceptible cattle.
 A BVD control programme on farm would aim to prevent fetal
infections, to eliminate reproductive loss and decrease losses due to
transient infections. Control is achieved with a combination of
removal of PI cattle, vaccination and enhanced biosecurity.
 Vaccines for BVD are available.
 The two categories are modified live virus (MLV) vaccines and killed
virus (KV) vaccines.
 MLV vaccines require only one dose during the initial immunization
step.
  KV vaccines are usually more expensive and more than one dose is
required during immunization.

Bovine Leukosis
 Bovine leukosis is a persistent and malignant viral disease of the
lymphoreticular system.
 It occurs in all breeds and in both sexes.
 Bovine leukosis is observed in two forms : a) the sporadic and b) the
enzootic form. The sporadic form is rare and occurs in cattle under
three years of age.
 The enzootic form is most commonly found in adult cattle,
particularly in cull cows.

Etiology

 Bovine leukemia virus (BLV) is a retrovirus which causes enzootic

bovine leukosis in cattle.
 Family: Retroviridae
 Genus: Deltaretrovirus
 Species: Bovine leukemia virus

Transmission
 By small amounts of infected blood (e.g. infected needles,
dehorning),
 vertical transmission from the dam to the calf (3 – 20 % of calves
may become infected)
 and by colostrum or milk (less than 2 %).
 Insect transmission is also a possibility; higher rates of infection
were reported in the summer.

Clinical findings

 Laboured breathing due to heart involvement

 Persistent diarrhoea following infiltration of the abomasum wall by
neoplastic cells
 Marked enlargement of several superficial lymph nodes
 Edema of the brisket and the intermandibular region
 Paralysis of the hind legs due to tumour compression of the spinal
cord
 Protrusion of the eye as a result of tumour invasion of the orbital
cavity
 Debilitation or emaciation
 Pale mucosal surface
 Bloated animal
  Swelling of the neck when thymus is involved
 Cutaneous nodules in the terminal stage

Postmortem findings

 Lymph node enlargement (clay-like consistency)

 Enlargement of spleen (splenomegaly)
 Thin watery blood
 Neoplastic lesions in the heart, intestines (Virtually all of the organs
may be involved.)
 Ventral edema
 Enlarged haemolymph nodes

Diagnosis

 When an animal is in the clinical stages of leukosis, the disease is

diagnosed by the presence of the previously described tumors and/or
general lymph node enlargement .
 If clinical disease is not present, BLV infection is diagnosed by blood
tests (AGID or ELISA) that detect the presence of BLV antibodies.
 Since BLV infection is for life, the presence of BLV antibodies is always
diagnostic for infection with the virus.
 The diagnosis of lymphosarcoma must be made by cytology or
histopathology.
 PCR is a sensitive and specific assay for diagnosis of BLV infection in
peripheral blood lymphocytes

Differential diagnosis
 Lymphadenitis,
 lymphoid hyperplasia,
 hyperplastic haemolymph nodes,
 pericarditis,
 enlarged spleen in septicemic conditions,
 other neoplasms and parasitism.

Treatment and Control of Bovine Leukosis

No viable treatment

 Limit transfer of infected lymphocytes from one cow to another

 There is no treatment for viral infection or for lymphosarcoma in cattle,
although parenteral corticosteroids can transiently decrease the
severity of clinical signs.
 The most commonly recommended eradication protocol is as follows:
 Identify infected animals using a serologic test
 Cull seropositive animals immediately
 Retest the herd in 30–60 days
 Use PCR assay to test young calves and as a complementary test to
clarify test results in herds with a low prevalence of infection
 Repeat testing and cull until the entire herd tests negative
 Cautery or other bloodless methods of dehorning should be used.
 Equipment used for castration, tattooing, or implanting should be
adequately cleaned and disinfected between animals.
 Transmission can be decreased in adult cattle by changing rectal
sleeves in between cows.
 Artificial insemination or embryo may limit transmission.
 Disinfecting equipment that has come in contact with blood or body
tissue
 Using single-use, disposable needles for blood collection and IM
injections
 Use single-use disposable needles for vaccination
 Cleaning handling facilities between animals when contaminated with
blood

Bovine spongiform encephalopathy (BSE, “Mad cow disease”)

 BSE is a progressive and fatal disease of adult cattle characterized

by a progressive degeneration of the central nervous system
causing neurological signs in animals.
 Some scientists suspect that an unusual and atypical virus-like
transmissible agent called a prion is associated with the etiology of
BSE.
 Prion is the term currently used in literature.
 Prion protein (PrP) on reaching brain slowly and progressively
converted into and abnormal form (PrP sc) and this abnormal protein
causes development of lesions including vacuolation in nerve cells.

Transmission

 The ingestion of protein feed supplements prepared from sheep

meat or sheep by products contaminated with scrapie prion .

Clinical findings

 Incubation period 2 – 8 years

 Reduction in milk production
 Weight loss, while maintaining good appetite
 Behaviour changes (nervousness and aggressiveness), kicking in
the milking parlour.
 The progressive degeneration of the central nervous system
causes neurologic signs:
 Apprehension, teeth grinding
  Tremors and abnormal ear position
 Abnormal posture and disorientation
 Incoordination and stiff gait
 Paresis
 Recumbency and death

Diagnosis
 Diagnosis can be confirmed only on the postmortem histological
examination of brain tissue.
 Microscopic lesions include degenerative lesions and vacuolation
of the cerebral cortex, medulla and central grey matter of the
midbrain.

Differential diagnosis

 Rabies,
 listeriosis,
 bovine pseudorabies (mad itch),
 other brain infections in cattle,
 the nervous type of acetonemia,
 hypocalcemia,
 Hypophosphatemia
 and hypomagnesemic tetany.

Prevention

 There is no effective treatment or vaccine for BSE.

 Control relies on import control, feeding regulations, and
surveillance measures.
 Early efforts to control the BSE outbreak focused on culling (killing)
sick animals to prevent them from entering the food chain.
 Ruminant derived protein is prohibited in all ruminant rations.
 The consumption of milk from affected animals by humans or
animals is also prohibited.
 Bovine brain cannot be used for human consumption.
 The mandatory slaughter of all animals manifesting signs of BSE and
compensation awarded to the owner.

Q fever (Queensland fever, Nine mile fever, American Q fever,

Australian Q fever)

 Q fever is a disease of cattle, sheep, goats, donkeys, camels, fowl,

dogs, cats, pigeons and humans.
 It is caused by Coxiella burnetii.
 Q fever is an occupational disease of livestock personnel.
 Farmers and laboratory personnel.
Etiology

 Coxiella burnetii is an obligate intracellular bacterial pathogen,

 small Gram-negative,
 coccobacillary ,
 can survive in air, soil and water for up to a year.

Transmission

 Ticks spread infection to cattle which develop mild disease.

 The faeces deposited on animal hide by ticks may be the source of
infection for humans.
 Q fever is also transmitted by inhalation or dust contaminated with
infected animal secreta or excreta.
 Healthy animals may serve as a carrier and shed the organism in
milk, urine, faeces, placenta and fetal fluids.
 They harbour the infection and no clinical signs are observed.
Contaminated meat and water are further means of infection read.

Clinical findings

 Field cases there are no clinical signs of this disease.

 In the disease produced by the inoculation of cows via the udder the
clinical signs may include:
 Acute mastitis
 Loss of appetite and depression
 Serous nasal and lacrimal discharge
 Difficult breathing
 Atony of the rumen
 Abortion in pregnant cows
 No gross lesions are reported in cattle.

Diagnosis

 Diagnosis is usually based on serology (looking for an antibody

response) rather than looking for the organism itself.
 Serology allows the detection of chronic infection by the appearance
of high levels of the antibody against the virulent form of the
bacterium.
 Molecular detection of bacterial DNA is increasingly used.
 The most obligate intracellular parasites, Coxiella burnetii can be
grown in an axenic culture.

Treatment
  Treatment of acute Q fever with antibiotics is very effective.
 Commonly used antibiotics include doxycycline, tetracycline,
chloramphenicol, ciprofloxacin, and ofloxacin; the antimalarial drug
hydroxychloroquine is also used.
 Chronic Q fever is more difficult to treat and can require up to four
years of treatment with doxycycline and quinolones or doxycycline
with hydroxychloroquine.

Prevention

 Protection is offered by Q-Vax, a whole-cell, inactivated vaccine

developed by an Australian vaccine manufacturing company.
 The intradermal vaccination is composed of killed C. Burnetii
organisms.
 Skin and blood tests should be done before vaccination to identify
pre-existing immunity.

Bovine ephemeral fever (BEF)

 is a disease that affects cattle and occasionally buffaloes

 and is marked by a short fever, shivering, lameness and muscular
stiffness.
 Also commonly known as 3 day sickness,
 BEF is an arthropod-borne virus .
 The disease may cause serious economic losses through deaths,
decline in condition, decreased milk production, lowered fertility in
bulls, occasional abortions and delays in marketing.

Etiology

 An arthropod–borne belongs to Rhabdoviridae family

 and genus Ephemerovirus and species known as ‘ephemeral fever
virus’ or ‘bovine ephemeral fever virus’.
 BEFV forms a bullet- or cone-shaped virions that consist of a
negative, single stranded RNA Genome

Transmission

 The virus is transmitted by an insect vector.

 The particular species linked to the virus are the mosquitoes and
biting midges Culicoides oxystoma and C. Nipponensis.

Clinical findings

There are typically 3 recognized stages of bovine ephemeral virus.

  The acute febrile stage
 appears suddenly and is especially noticeable in dairy cattle.
 Affected cattle are likely to:
 Show signs associated with a fever
 Have a rectal temperature over 40°C
 Shiver (in approximately 50% of cases)
 Stand with their backs arched and heads held low, muzzles
extended, drooling saliva
 Have discharge from eyes and nostrils
 Stop feeding and cud chewing
 Have reduced milk production, especially in dairy cows.

The second stage is muscular stiffness and lameness in 1 or more limbs.

 Some secondary bloat may occur due to general inflammation of the

abdominal cavity and ruminal stasis.
 Lameness may shift between limbs and joints may be visibly
swollen.
 During recovery, most affected animals resume eating and drinking.
 Animals may go down, with heavy animals in good condition being
most affected.
 Some animals remain down due to muscle damage or damage to
the spinal cord from constant struggling.

Postmortem findings

 Post-mortem examination can either show small amounts of fibrin-

rich fluid,
 or occasionally, an excess of pinkish to blood stained fluid in the
heart sac, chest and abdominal cavities, and joint capsules.
 Lesions in the lungs may be present in severe cases.

Diagnosis

o BEF epidemics are diagnosed on the presence of lameness,

muscular stiffness, pain, short fever and rapid spread of the
disease through herds.
o The virus can often be cultured from a blood sample taken
from animals in the early stages of the disease.
o A PCR test can also identify the presence of the virus, and is
most successful when samples are collected in the first few
days of clinical disease.
o Alternatively, 2 blood samples—the first taken during the
fever stage and the second 14 days later—can be collected to
detect the presence of antibodies to the virus.
 Differential diagnosis
 Other acute febrile diseases that often occur under the same
conditions, such as tick fever.

Treatment

 Anti-inflammatory drugs have been shown to reduce the

course of the disease.(Non-steroidal anti-inflammatory drugs).
 Most animals will recover if given water, shade and food.

Control

Vaccination

 There is a modified live vaccine for BEF that provides long-lasting

protection
 While some cattle might still develop mild disease after vaccination,
the severity and duration of illness tends to be much lower than in
unvaccinated cattle.
 The initial vaccine should be administered twice, 2–4 weeks apart,
under the skin of the neck for long-lasting protection.
 An annual booster should be given 8–10 weeks before the BEF
season.

Bacteria diseases

Black quarter

 is an acute infectious disease of cattle and sheep manifested by

severe inflammation of the muscle with high mortality.
 It is caused by Clostridium chauvoeil

Caused

 C. chauvoei
 is Gram-positive,
 rod-shaped,
 anaerobic,
 and motile.
 Black leg is worldwide in distribution.
 Well nourished animals are more frequently affected.
 It is also more commonly seen in grass fed animals than in stall fed
animals.
  Clostridia are soil-borne organisms which cause disease by releasing
toxins.
 Specific antitoxin and antibiotics are rarely effective in the
treatment of this disease.
 An adequate preventive vaccination program may be the most
effective method in protecting the animals from black leg.

Transmission

 The organisms of blackleg are found in the soil.

 During grazing, organisms may enter the digestive tract of a
susceptible animal.
 Clostridium chauvoei is also found in the digestive tract of healthy
animals.
 In sheep the agent is transmitted through wounds at
 shearing,
 docking
 and castration and during lambing in ewes.

Clinical findings

 High fever (41°C)

 Lameness
 Loss of appetite
 Discoloured, dry or cracked skin
 Stiff gait and reluctance to move
 Crepitating swellings often on the hips and shoulder
 In sheep gaseous crepitation cannot be felt before death

Postmortem findings

 Laying on one side with affected hind leg stuck out.

 Commonly seen in cattle
 Bloating of carcass and blood stained frothy exudates from the
nostrils and anus
 Dark red to black muscle of the loin, back or leg
 Spongelike bubbly appearance of the muscles with a peculiar rancid
odour
 Yellowish, gelatinous subcutaneous tissue and associated gas
bubbles
 Blood stained fluid in body cavities

Diagnosis

 Presence of crepitus and swelling of large muscles is

suggestive
  Ultrasonographic examination of affected areas
 Postmortem examination with anaerobic culture of affected
tissues and biochemical identification organisms in tissue
samples.
 Muscle tissue samples should be collected as soon as
possible after death.
 The fluorescent antibody test for C chauvoei is rapid and
reliable.
 Immunohistochemical testing is performed on formalin-
fixed tissue samples.
 A PCR assay is available and has been reported to be
reliable for clinical samples but not for environmental
samples.

Differential diagnosis

 Other acute Clostridial infections,

 lightning strike,
 anthrax,
 bacillary haemoglobinuria,
 lactation tetany,
 extensive haemorrhage
 and acute lead poisoning.

Treatment

 Treatment is generally unrewarding due the rapid

progression of the disease.
 But penicillin is the drug of choice for treatment and
treatment is only effective in the early stages and as a
control measure.

Control

 Administration of a multivalent vaccine containing C chauvoei, C

septicum, and where needed, C novyi.
 Move animals from affected pastures
 Calves 2 months old should be vaccinated twice, 4 weeks apart,
followed by annual boosters before the anticipated danger period
(usually spring or early summer).
 In an outbreak, all susceptible cattle should be vaccinated and
treated prophylactically with administration of penicillin (10,000
IU/kg, IM) to prevent new cases for as long as 14 days.
 Naive ewes should be vaccinated twice, with the second dose 1
month before lambing and then with yearly boosters.
  In outbreaks in flocks of ewes, administration of prophylactic
penicillin and antiserum treatments are recommended.
 Young sheep should be vaccinated before going to pasture.
 Carcasses should be destroyed by burning or deep burial in a
fenced-off area to limit heavy spore contamination of the soil.

Botulism

 Botulism is a disease manifested by progressive muscular paralysis.

 It is seen in humans, animals, birds and fish
 and is caused by various strains of Clostridium botulinum.

Cause

 Clostridium botulinum
 is a gram-positive,
 rod-shaped,
 anaerobic,
 spore-forming,
 motile bacterium with the ability to produce botulinum toxin, which
is a neurotoxin.
 Cl. Botulinum is found in the digestive tract of herbivores.
 Soil and water contamination occurs from faeces and decomposing
carcasses.
 The proliferation of Cl. Botulinum organisms may also occur in
decaying vegetable material.
 Sporadic outbreaks of botulism are reported in most countries.
 Cattle, sheep and rarely swine are susceptible to this disease.
 Dogs and cats are resistant.

Transmission

 Decomposed flesh and bones are the source of infection for

animals.
 Incubation period 12 – 24 hours. However, 2 hours up to 14
days incubation period has been recorded.

Clinical findings

 In cattle and horses

 Restlessness
 Knuckling and incoordination
 Paralysed tongue and drooling of saliva
  Sternal recumbency
 Progressive muscular paralysis from hindquarters to
frontquarters, head and neck

In sheep

 Serous nasal discharge and salivation

Abdominal respiration
 Stiffness upon walking and incoordination
Switching of the tail on the side
 Limb paralysis and death

In pigs

 Lack of appetite, refusal to drink and vomiting

 Pupillary dilatation
 Muscular paralysis

Postmortem findings
 Foreign material in fore-stomachs or stomachs may be suggestive of
botulism.

Diagnosis

 Diagnosis is usually made based on history and typical clinical signs.

 Specific tests to detect the presence of botulism toxins are currently
expensive, complicated and unreliable.
 In the laboratory, C. Botulinum is usually isolated in tryptose sulfite
cycloserine (TSC) growth medium in an anaerobic environment with
less than 2% oxygen.

Differential diagnosis

 Parturient paresis,
 paralytic rabies,
 equine encephalomyelitis,
 ragwort poisoning in horses,
 miscellaneous plant poisoning.
 In sheep – louping ill,
 hypocalcemia and some cases of scrapie.

Treatment

 There is no treatment specifically for botulism.

 If cattle are affected so badly that they cannot stand or signs
progress rapidly, death is inevitable and they should be humanely
euthanased as soon as possible.
  Mildly affected cattle require gold-standard nursing to avoid
secondary complications.

Prevention

Three steps are recommended for the prevention of botulism.

• Vaccinate cattle with botulism vaccine
• Provide supplementary feed with phosphorus and protein, or non-protein
nitrogen, such as urea.
• Remove all carcasses and bones from pasture.

 Prevention is possible through annual herd vaccination.

 There are several vaccines available, , which involve either 2 initial
doses administered 4 weeks apart, or a single initial dose followed
by an annual booster.
 There used to be a formalin-treated toxoid vaccine against botulism
(serotypes A-E).
 Calves can be vaccinated from one month of age.

Malignant edema

 Malignant edema is a bacterial disease of cattle, sheep, goats,

swine, horses and poultry.
 It is caused by
 Clostridium septicum
 and is manifested by wound infection.

Etiology
 Clostridium septicum
 is a gram positive,
 spore forming,
 obligate anaerobic bacterium.

Transmission
 The infection is commonly soil-borne.
 Deep wounds associated with trauma provide ideal condition
for the growth of this agent.
Clinical findings
 Fever 41 – 42°C
 Depression and weakness
 Muscle tremor and lameness
 Soft doughy swelling and erythema around the infection site

Postmortem
 Gangrene of the skin in area of infection site
  Foul putrid odour is frequently present
 Gelatinous exudate in the subcutaneous and intramuscular
connective tissue
 Subserosal haemorrhage
 Accumulation of sero-sanguineous fluid in body cavities
 Muscle tissue is dark-red but has little or no gas

Diagnosis
 Diagnosis is usually at post-mortem and the clinical signs are
reasonably suggestive.
 Culture and isolation of the bacteria can confirm a diagnosis,
however this is not necessarily straightforward as the bacteria
can be difficult to isolate and identify.

Differential diagnosis

 Blackleg.
 In malignant edema the muscle is not involved and the wound site is
noted. Anthrax in pigs.
 Subcutaneous edema in the throat region is present.

Treatment

 Treatment for C. septicum infection includes

 antibiotic administration,
 supportive treatment (e.g. NSAIDs)
 and surgical intervention to allow drainage of the affected area.
 Antibiotic selection,
 include penicillin,
 metronidazole
 or clindamycin.

Prevention

 Low stress cattle handling and using clean needles and

syringes to administer injectable animal health products will
help reduce the risk of wounds and infection.
 Protection against malignant oedema can be achieved by
vaccination using a multivalent clostridial vaccine, which will
also protect against other fatal clostridial diseases.