Large A.medicine 4th Year

JIMMA UNIVERSITY
COLLEGE OF AGRICULTURE AND VETRINARY MEDICINE

SCHOOL OF VETERINARY MEDICINE
Large Animal Medicine (CLIS - 301)
Instructor: Mekonnen Addis (DVM, MSc, Associate professor)
1
Overview
1. Anthrax
2. Blackleg
3. Botulism
4. Tetanus
5. SepticemicPasteurellosis
6. PneumonicPasteurellosis
7. Brucellosis
8. Tuberculosis
9. ContagiousBovinePleuropneumonia
10. Contagious Caprine Pleuropneumonia
11. Colibacilosis
12. Salmonellosis
13. Actinobacilosis
14. Actinomycosis
15. Paratuberculosis
16. Leptospirosis
17. Listeriosis
18. Mastitis
2
Overviewcont…
1. Rabies
2. FootAndMouthDisease
3. Rinderpest
4. PesteDesPetitsRuminants
5. RiftValleyFever
6. Bluetongue
7. LumpySkinDisease
8. SheepPoxandGoatPox
9. ContagiousEcthyma
10. Epizootic Lymphangitis
11. Dermatophytosis
12. Ketosis
13. Parturient Paresis
3
ANTHRAX
 Anthrax is a per acute disease characterized by septicemia and sudden
death, accompanied by exudation of tarry blood from the body orifices

(mouth, nostrils and anus) of the cadaver
 Failure of the blood to clot, absence of rigormortis and splenomegaly
are the most important necropsy findings

Etiology
 B. anthracis
 Bacillus anthracis produces three types of toxins

 Factor-I – Denotes oedema toxin
 Factor-II – Denotes protecting antigen
 Factor-III – Denotes lethal factor
4
ANTHRAX CONT…
 The simple presence of bacteria in the blood is known as bacteremia
. It may be transient, where small quantities of bacteria are in the blood for a limited period of time,
or it can be sustained, where the bacteria persist and multiply in the bloodstream. The sustained form
of
bacteremia
is usually what leads to sepsis, which is the body's immune response to the presence of the bacteria.
 Septicemia
is a serious medical condition characterized by inflammation of the whole body. It is caused by bact
eria which enter the bloodstream, triggering an immune response which results in inflammation and
a slow shutdown of the body's systems for handling infection. This medical condition can be deadly,
especially if the patient is allowed to progress into the stage of shock, and onset can be alarmingly r
apid
 Why is rigor mortis absent in anthrax?
 Answer: Rigor mortis is dependent on ATP in order for it to occur. However the anthrax bacilli have
a toxin called edema factor which is a toxin that inhibits the stiffening of muscles by constantly stim
ulating the release of cyclic adenosine
monophosphate (cAMP), so that the cAMP 5
ANTHRAX CONT…
 Anthrax is worldwide in distribution
 Morbidity rate may be high among all farm animals (Never affect chickens)
 Susceptibility is highest among ruminants, followed by horses and swine
 Anthrax spores can enter the human body through the intestines (ingestion),
lungs (inhalation) or skin (cutaneous)

 Spores can be picked up directly from the soil or from fodder grown on
infected soil, contaminated bone meal or protein concentrates, infected

excreta, blood or other material
 Water can be contaminated by effluent from tanneries, infected carcasses
and by flooding and deposition of anthrax-infected soil
6
ANTHRAX CONT…
 During their vegetative stage, cells of the anthrax agent multiply in the lymph nodes
of susceptible animals
 When cells of B. anthracis escape from the animal’s body and are exposed to
oxygen, they form spores so they are facultative anaaerobes not obligate aerobes
 These spores are highly resistant to heat, cold, chemical disinfectants and long dry
periods
 B. anthracis spores are reported to survive for years (45 years) in the environment
 Environmental persistence may involve a number of factors, including high levels of
soil nitrogen and organic content, alkaline soil (a pH level higher than 6.0) and
ambient temperatures higher than 16 degrees
 Animals are usually infected by ingesting soil-borne spores, such as in contaminated
feed or water
7
ANTHRAX CONT…
Risk factors:
 Host risk factors: Anthrax occurs in all vertebrates but most common in
cattle and sheep and less frequent in goats and horses. Humans occupy
intermediate position between this group and the relatively resistant
species are swine, dogs and cats
 Environment risk factors: Outbreaks of soil-born origin always occur after
a major climate change such as heavy rain after a prolonged drought and
always in warm weather with temperature over 15 oC.
 Pathogen risk factor: When anthrax bacilli are exposed to air, spores are
formed which protract infectivity of the environment for very long periods
8
ANTHRAX CONT…
Pathogenesis: Upon ingestion of spores, infection may occur through:
Intact mucous membranes
Defects in epithelium around erupting teeth
Scratches from tough, fibrous food materials
 After entry, the bacteria are moved to the local lymph nodes by motile
phagocytes
 Then after proliferation in this site the bacilli pass via lymphatic vessels
into the blood stream and septicemia with massive invasion of all body
tissues follows
 B. anthracis produces a lethal toxin that causes edema and tissue damage
 Death results from shock, acute renal failure and terminal anoxia
9
ANTHRAX CONT…
 Clinical Findings: The incubation period after field infection is
probably 1-2 weeks

Only two forms of anthrax occur in cattle and sheep
A. Per acute form:

This is most common at the beginning of an outbreak
Animals are usually found dead without signs
The course of the disease is probably 1-2 hours
Fever, muscle tremor, dyspnea and congestion may be observed
After death discharges of blood from the nostrils, mouth, anus and
vulva are common

10
ANTHRAX CONT…
B. Acute form: The course runs about 48 hours
There is severe depression and listlessness
High body temperature, up to 42oC
Respiration is rapid and deep
Heart rate much increased
Anorexia and ruminal stasis
Pregnant animals may abort
Milk yield is much decreased and blood stained or deep yellow in color
Diarrhea and dysentery are common
There is local edema of the tongue
Edematous lesions in the throat, sternum, perineum and flanks

11
ANTHRAX CONT…
Necropsy findings: The common postmortem findings in anthrax are:
A striking absence of rigor mortis
The dead body assumes characteristic ‘sawhorse’ attitude
All natural orifices exude dark, tarry blood that does not clot
Bloating and putrefaction are rapid
Diagnosis:
If there is a good reason to suspect anthrax, the carcass should not be opened
Peripheral blood or local edema fluid is collected by needle puncture and
inoculated in to guinea pigs or mice – Death

Culture
1
ANTHRAX CONT…
blood that does not clot
1
ANTHRAX CONT…
The following diseases may confuse with anthrax (cause sudden death):
 Lightening strike - evidenced by singeing of hair and history of electrical
storms
Electrocution - requires careful examination for source of electric current
Acute blackleg – confined to young animals and crepitating swelling
Other clostridial infections
Acute Leptospirosis – sporadic, hemoglobinuria
Peracute lead poisoning – accompanied by nervous signs
Hypomagnesemic tetany - accompanied by nervous signs
Animals dying of acute bloat – show gaseous distention and exudation of
blood from the orifices as in anthrax.

1
ANTHRAX CONT…
Treatment: In early stages before showing clinical signs
 Penicillin (10,000 units/kg body weight twice daily)
 Streptomycin (8-10 g/day in two doses IM for cattle)
 Oxytetracycline (5mg/kg body weight per day)
It is desirable to prolong the treatment to at least 5 days to avoid a recrudescence
Control:
 Placing of the farm in quarantine
 Infected carcasses, beddings, and soil contaminated by discharges should be
immediately burned or buried. Burial should be at least 2 meters deep with ample
supply of quicklime added
 Immunization with live attenuated strains vaccine
15
BLACKLEG
 Synonyms: Black Quarter / Quarter Ill
 Blackleg, the clostridial myositis of skeletal muscles characterized by:
Inflammation of skeletal and cardiac muscles
Severe toxemia
A high mortality
Etiology: Cl. Chauvoei (gram-positive, spore-forming, rod-shaped)

Epidemiology
 When blackleg occurs a number of animals are affected within a few days
It is enzootic in areas subjected to flooding
The case fatality rate approaches 100%
16
BLACKLEG CONT…
Source of infection
Blackleg is a soil-borne infection
 Portal of entry is through alimentary mucosa after ingestion of contaminated feed
 Contamination of soil and pasture occur from infected feces or decomposition of
dead animals
 True Blackleg develops when spores which are lodged in normal tissues, are
caused to proliferate by mechanisms such as trauma or anoxia
 In sheep the disease is almost always wound infection
Infection of skin wounds at fighting, hearing, docking and the navel at birth
cause local lesions
17
BLACKLEG CONT…
Risk Factors
 Environment factors: Some outbreaks in cattle have occurred
following excavation of soil
Disturbance in soil may expose and activate latent spores

 Animal factors
True blackleg is a disease of cattle and occasionally sheep
 In cattle disease is largely confined to young stock between ages of
6 months and 2 years

In field condition, the disease occurs most frequently in rapidly
growing cattle on a high plane of nutrition

18
BLACKLEG CONT…
 Economic Importance: Blackleg is a cause of severe financial loss to cattle raisers in
many parts of the world
 Pathogenesis: Toxin produced by the organism results in a severe necrotizing myositis
locally in skeletal muscles and systemic toxemia which is usually fatal
Clinical Findings
 Severe lameness Due to myositis
 Characteristic edematous and crepitant swellings develop in the hip, shoulder, chest,
back, neck, or elsewhere Due to the gas produced by the growing bacteria
The animal is very depressed & completely anorectic(loss of appetite)
 Ruminal stasis
High temperature (41oC)

19
BLACKLEG CONT…
 In the early stages, the swelling is small, hot and painful to the touch but later on it
becomes cold and painless as the blood supply to the area diminishes
 As the disease progresses, the swelling enlarges and becomes spongy and gaseous
 The skin is discolored, becomes dry and cracked
 Lesions are usually confined to the upper part of one limb
 occasionally lesions are also present on the base of tongue, heart muscle and
diaphragm
 Many animals die without signs having been observed
Necropsy Findings
 Dead animal has a characteristic position, lying on the side with affected hind limb
stuck out stiffly
20
BLACKLEG CONT…
 Bloating and putrefaction occur quickly
 Incision of affected muscle reveals dark, discolored, swollen tissue with rancid odor and
an excess thin, sanguineous fluid and bubbles of gas
Blackleg, cow
 All body cavities contain excess fluid with fibrin and blood stained
Diagnosis
 In typical cases a definite diagnosis can be made on clinical signs and necropsy findings
 Field diagnoses are confirmed by laboratory demonstration of Cl. chauvoei in affected
muscle Bacteriology & FAT
21
BLACKLEG CONT…
Differential diagnosis
Other acute clostridial infections
Lightening strike
Anthrax in the case of anthrax there is fluid without fibrin becouse digested by plasmin
but in the case of bleckleg fluid whith exxes fibrin
Bacillary hemoglobinuria
Treatment
Multiple parenteral injections of penicillin
Control
Movement of cattle from the affected pasture is advisable
Vaccination

22
BLACKLEG CONT…
The Clostridial vaccines are the ones we commonly refer to as “7-way”
or “8-way” vaccines type which protects against:
Cl. chauvoei Blackleg
Cl. septicum and Cl, sordelli Malignant edema
Cl. novyi Black disease
Cl. perfringens types B, C and D Enterotoxaemia
Cl. hemolyticum Red water / Bacillary Hemoglobinuria
23
BOTULISM
 Disease: botulism
 Agent: botulinum toxin
 Cl. botulinum produce seven different types of neurotoxins: A through G
that bind to neuromuscular junctions

Etiology
 Cl. botulinum, a spore forming, gram positive anaerobe which proliferates
only in decaying animal or plant material

Epidemiology
 Botulism has no geographical limitations
 Occurs most often in areas where sheep and cattle suffer a phosphorus or
protein deficiency on range Pica

24
BOTULISM CONT…
 In recent times heavy mortalities occurred in cattle often in feedlots,
fed on poultry litter containing carcasses of dead birds
Transmission
Ingestion – Organism, Spores & Neurotoxins
Wound contamination
Inhalation
Animal risk factors

Botulism is most common in birds, particularly chicken
Cattle, sheep and horses are susceptible
Pigs, dogs and cats appear to be resistant

25
BOTULISM CONT…
Environment risk factors
 Outbreaks are most likely to occur during drought periods when feed is sparse,
phosphorus intake is low and carrion is plentiful
Pathogenesis
 Toxins of Cl. botulinum are neurotoxins & produce functional paralysis
 Toxin interferes with secretion of acetylcholine, the chemical mediator of nerve
impulse transmission
 Then a true flaccid paralysis develops and the animal dies of respiratory
paralysis
 Toxicoinfectious botulism is described as the disease in which Cl. botulinum is
present in tissues and produce toxin there. Toxins are liberated from lesions and
cause typical botulism
26
BOTULISM CONT…
Clinical Findings
 Signs appear 3-17 days after animals gain access to toxic material
 The incubation period being shorter when toxin is high
 The disease is not accompanied by fever
 Peracute cases die without prior signs of illness
 The characteristic clinical picture is progressive muscular paralysis
 Muscle weakness and paralysis commence in the hindquarters and
progress to forequarters, head & neck

 The onset is marked by very obvious muscle tremor and fasciculation,
sufficient to make the whole limb tremble

27
BOTULISM CONT…
In most cases the disease in subacute in which there is:
 Restlessness, incoordination, stumbling and ataxia
 Inability to rise or lift the head
 Affected animals lie in sternal recumbency
with head on the ground or turned into the flank

 In some cases, tongue paralysis and hangs from mouth
 Unable to chew, swallow and drools saliva
 Paralysis of chest muscles leads to a terminal abdominal type of respiration
Clinical Pathology
In peracute cases toxin can be detected in blood by mouse inoculation test
Examine the feed culturally and for the presence of toxin.
28
BOTULISM CONT…
An animal with botulism exhibiting paralysis and excess salivation due to impaired
swallowing
29
BOTULISM CONT…
Diagnosis
 It is seldom possible to establish diagnosis by demonstrating presence of toxin in
suspected feed
 Filtrates of stomach and intestinal contents tested for toxicity to experimental animals
 Feeding of suspect material to susceptible animals
 Occurrence of pica at pasture is of diagnostic significance
 Parturient paresis in cattle
 Hypocalcaemia in sheep
 Many other diseases of nervous system
30
BOTULISM CONT…
Treatment
Specific or polyvalent antitoxic serum
Purgatives
Laxatives are foods or drugs taken to loosen the stool and stimulates evacuation of the bowels
Magnesium sulfate ( Epsom salt)
 CNS stimulants
These treatments may be supported by feeding by stomach tube
Control
Correction of dietary deficiencies by supplementation with phosphorus or protein
Prompt disposal of carcasses
Avoid spoiled feedstuff and or poor quality silage
Vaccination with type specific or combined toxoids
31
TETANUS
 Tetanus is a highly fatal, infectious disease of all species of domestic animals
characterized by hyperesthesia, tetany and convulsions
 Etiology: Cl.tetani
 Epidemiology: Tetanus occurs in all parts of the world
 Source of infection: Cl.tetani organisms are present in feces of animals,

especially horses, and in soils contaminated by these feces
 Transmission: Portal of entry is usually through deep puncture wounds. The
spores lie dormant for some time and produce illness only when tissue
conditions are favor their proliferation
 Diseases results due to toxin produced in the gut or ingested preformed in feed
32
TETANUS CONT…
Animal Risk Factors
 Horses are the most susceptible and cattle the least
 Puncture wounds of the hooves are the common sites of entry in horses
 Introduction in the genital tract at parturition is the usual portal of
entry in cattle
 High incidence of tetanus occurs in young pigs following castration
and in lambs following castration, shearing, docking and vaccination

Importance
 Tetanus is important because of its high mortality rates and
very long convalescence (period of recovery) in survivors

33
TETANUS CONT…
Pathogenesis
 Tetanus bacilli remains localized at the site of introduction and do not
invade surrounding tissues

 They start proliferating and produce neurotoxin only when there is
lowering of local tissue oxygen tension

 This may occur immediately after introduction if the trauma is severe or
may be delayed for several months until subsequent trauma to the site
causes tissue damage
 The toxin reaches the CNS by passing up peripheral nerves
 Death occurs by asphyxiation due to fixation of muscles of the respiration
34
TETANUS CONT…
Clinical Findings
 Muscle stiffness accompanied by tremor
 Trismus with restriction of the jaw movements – lock jaw
 Prolapse of the third eyelid (nictitating membrane) - pathognomonic sign
 Stiffness of the hind limbs leading to unsteady, straddling gait
 The tail is held stiffly when backing or turning
 Sharp lifting of muzzle
 Anxious and alert expression
 An erect carriage of ears, retraction of the eyelids and dilation of nostril
 Exaggerated response to normal stimuli
35
TETANUS CONT…
Calf with tetanus exhibiting rigid limbs due to muscle spasm
36
TETANUS CONT…
 Mastication is prevented by tetany of the masseter muscles and saliva drools
 Constipation is usual and urine is retained
 Great difficulty in walking leads the animal to fall
 Titanic (gigantic) convulsions begin
 Opisthotonus is marked Spasm in which head, neck and spine are arched
backwards
 Sweating is profuse and temperature rises to 42oC
Diagnosis
 Fully developed tetanus is so distinct clinically that it is seldom confused with
other diseases
 The muscular spasms, the prolapse of the third eyelid and recent history of injury
and surgery are characteristic findings

37
TETANUS CONT…
Treatment
 Elimination of the organism is attempted by parenteral administration of
penicillin in large doses
 Tetanus antitoxin is usually administered but is of little value once signs have
appeared
 Relaxation of muscle tetany is attempted with chlorpromazine and acetyl
promazine are widely used
 Intravenous or stomach tube feeding is important
 The management of tetanus cases depends largely on keeping the animal alive
through the critical stages
 Keeping the animal calm becouse animal have alert appreance

38
TETANUS CONT…
Control
 Many cases of tetanus could be avoided by proper skin and instrument
disinfection at castrating, docking and shearing times

 For short term prophylaxis, passive immunity can be achieved by
injection of antitoxin
 In enzootic areas, all susceptible animals should be actively immunized
with “toxoid”, an alum-precipitated, formalin treated toxin

 Prevention of tetanus in newborn lambs is also best effected by
vaccination of ewes in late pregnancy

 Annual booster vaccination is important
39
SEPTICEMIC PASTEURELLOSIS
 Pasteurellosis in farm animals is broadly divided in to two:
 Septicemic Pasteurellosis (Hemorrhagic Septicemia)
 Pneumonic Pasteurellosis (Shipping Fever)
♦ Pasteurella and Mannheimia organisms are β-hemolytic, gram-negative, aerobic, non motile,
non spore forming cocco bacilli in the family Pasteurellaceae
♦ This family tends to inhabit the mucosal surfaces of the GI, respiratory, and genital tract of
mammals
♦ Many are known as opportunistic secondary invaders
♦ An opportunistic infection is an infection caused by bacterial, viral, fungal, or protozoan

pathogens that take advantage of a host with a weakened immune system or an altered
microbiota (such as a disrupted gut flora). Many of these pathogens do not cause disease in a
healthy host that has a normal immune system. A compromised immune system, however,
presents an "opportunity" for the pathogen to infect
40
SEPTICEMIC PASTEURELLOSIS
Causes of opportunistic infection: Immunodeficiency or immunosuppression can be
caused by:
 Malnutrition
 Fatigue
 Recurrent infections
 Advanced HIV infection
 Chemotherapy for cancer
 Genetic predisposition
 Skin damage
 Antibiotic treatment leading to disruption of the physiological microbiome, thus allowing
some microorganisms to outcompete others and become pathogenic Medical procedures

 Ageing
 Leukopenia (i.e. neutropenia and lymphocytopenia)
41
SEPTICEMIC PASTEURELLOSIS CANT…
Septicemic pasteurellosis
¨ Primarily caused by P. multocida
 Septicemic pasteurellosis occurs in outbreaks during periods of
environmental stress
 The causative organism persists on tonsillar and nasopharyngeal
mucosae of carrier animals
Normal flora commensals
 Spread occurs by ingestion of contaminated food stuffs, the infection
originating from clinically normal carriers, clinical cases or by ticks and

biting insects
42
SEPTICEMIC PASTEURELLOSIS CONT…
The disease is an acute septicemia and clinically it is characterized by:
 A sudden onset of fever (41-42oC)
 Profuse salivation
 Submucosal petechiation
 Severe depression
 Death in about 24 hours
 Localization may occur in subcutaneous tissue, resulting in

development of warm, painful swellings about the throat, dewlap,
brisket or perineum
 Severe dyspnea occurs if respiration is obstructed
43
Necropsy Findings
Generalized petechial hemorrhages particularly under the serosae
Edema of lungs and lymph nodes
Subcutaneous infiltration of gelatinous fluid
Diagnosis
Bacteriological examination Gram-negative
Culture
ELISA
Treatment
Oxytetracycline & Sulfadimidine are highly effective
Control
Killed vaccine - Gives solid immunity for at least 12 month

44
A buffalo calf clinically affected with Heart of an animal that died of

haemorrhagic septicaemia. Note the haemorrhagic septicaemia showing
dull appearance and rough coat and the ecchymotic and petechial haemorrhages on
prominent submandibular swelling the subepicardial adipose tissue
45
PNEUMONIC PASTEURELLOSIS
 Synonym: Shipping Fever
 Etiology: Mannheimia haemolytica and occasionally P. multocida
 Shipping fever is characterized by acute bronchopneumonia with toxemia,
exudative pneumonia and fibrinous pleuritis
Epidemiology
 Pneumonic pasteurellosis is a common disease worldwide
 The disease is most important in cattle that have been recently introduced in
Economic importance to feedlots and exposed to stress
 Pneumonic is responsible for the largest cause of mortality in feedlots and the
costs of treatment is considerable

46
PNEUMONIC PASTEURELLOSIS CONT…
Host risk factors
It most commonly occurs in young growing cattle from 6 months to 2 years
of age. But all age groups are susceptible

The disease occurs most commonly in outbreaks 7-10 days after cattle have
arrived in feedlot following stressful transportation

Environmental risk factors
 Feeding corn silage as the major roughage in the first month after arrival is
associated with increased mortality

 Mixing of cattle from different sources
 Vaccinating cattle against respiratory disease on arrival
 Transportation and assembling of yearling beef calves

47
Deprivation of feed and water followed by confinement in unfamiliar surroundings
Drafty or humid and poorly ventilated barns
Exposure to inclement weather, transport and fatigue
Transmission: Occurs by inhalation of infected droplets
Pathogenesis
 A combination of a viral infection of upper respiratory tract and /or devitalizing
influences from transportation, starvation, weaning, rapid fluctuations in ambient
temperature, mixing of cattle from different origins and excessive handling after
arrival in feedlots, can all collectively promote an increase in the total numbers and
virulence of Mannheimiae in nasopharynx which are then inhaled in to alveoli and
not effectively cleared - disease

48
Clinical findings
 The disease develops within 10-14 days after stress
 Affected cattle are depressed and respirations are shallow and rapid
 Cough becomes more pronounced and frequent when urged to walk
 Mucopurulent nasal discharge, crusty nose and ocular discharged are common
 Apparently healthy cattle may have temperature of 40-41oC
 Auscultation reveal rapid shallow respiration and increased breath sounds
 Loud breath sounds (bronchial tones) are audible over the anterior and ventral parts of lungs
 As the disease progresses the breath sounds become louder and extend over a greater area,
crackles become audible followed by musical wheezes in few days
 Pleuritic friction rubs may be audible and in severe cases dyspnea is marked
49
Animal died of pneumonic pasteurollosis
50
Clinical pathology
 Nasal swabs from clinical cases yield pure culture of Mannheimiae
 Levels of plasma fibrinogen are elevated and parallel increase in
temperature are more reliable indication of the presence of lesion

Necropsy findings
 Marked consolidation of lungs
 A catarrhal bronchitis, bronchiolitis and a serofibrinous pleurisy
 The cut surface consists of several colors due to hemorrhage, necrosis and
red and gray consolidation

 Coagulation necrosis of pneumonic lungs
 Pleural adhesions
51
Diagnosis
 Clinical findings
 Most common in young beef calves recently stressed
Bacteriological examination Gram-negative
Culture
ELISA
 Pneumonic pasteurellosis should be differentiated from:
 Viral interstitial pneumonia
 Bovine respiratory syncytial virus pneumonia
 Lung worm pneumonia
 Aspiration (drenching) pneumonia
 IBR
 CBPP
52
Treatment
 Oxytetracycline
 Penicillin
 Sulfonamide
 Severely affected or those relapse require treatment daily or three times daily for up to 3-
5 days
Control
 Adoption of good management techniques when calves are still on the range
 The use efficacious vaccines
 Care in handling and transportation of cattle
Avoid all sorts of stressors

53
BRUCELLOSIS
 Brucellosis is an infectious bacterial disease localize to the
reticuloendathelial system and genital tract
 The disease is characterized by abortions in females and epididymitis and orchitis
in males
Etiology
 Brucellosis results from infection by various species of Brucella, a Gram negative,
facultative intracellular coccobacillus or short rod in the family Brucellaceae
 Brucellosis is usually caused by B. abortus in cattle, B. melitensis or B. ovis in
small ruminants, B. suis in pigs and B. canis in dogs
 More recently many strains of Brucella organisms have been isolated from marine
mammals, and these are tentatively designed as B. maris
54
BRUCELLOSIS CONT…
 RES is component of the immune system, comprised of phagocytic cells
 Phagocytic cells capable of engulfing substances, such as bacteria and viruses, rendering them incapable of
causing harm to the body. They also ingest abnormal cells and old cells, thus clearing the body of their har
mful presence
 Phagocytic cells are derived from the bone marrow stem cells and become monocytes,
which circulate in the blood
 Most of these monocytes migrate to different tissues inside the body. When they are no longer in the blood
circulation, they are called macrophages
 Macrophages are found mostly in the lymph nodes, liver, spleen, brain and subcutaneous tissues
 Macrophages are given specific names depending on the organs in which they reside
 They are called Kupffer cells when they are found in the liver. In the brain they are known as microglia.
When found in the lymph nodes, bone marrow, and spleen, they are named reticular cells. Tissue
histiocytes
or fixed macrophages are the names used when they are located in the subcutaneous tissues, and while in th
e lungs they are known as alveolar cells 55
BRUCELLOSIS CONT…
Transmission
 Direct or indirect contact with infected animals
 Ingestion is the most common rout of entry
 Through conjunctiva, genital mucosa, skin and respiratory systems
 Aborted fetuses, placenta and post abortion uterine fluids
 Ingestion of milk from infected cattle and goats (calves and kids)
 Venereal transmission of B. suis, B. ovis and B. canis is common
Pathogenesis
Following exposure, Brucella penetrates infected mucosal surfaces
The epithelium covering the ileum Peyer’s patches are the preferential site for
entry
56
BRUCELLOSIS CONT…
 Peyer's patches are organized lymphoid nodules, named after the Swiss
anatomist, Johann Conrad Peyer
 They are aggregations of lymphoid tissue that are usually found in the lowest
portion of the small intestine, the ileum and they differentiate the ileum from
the duodenum and jejunum. The duodenum can be identified by Brunner's
glands. The jejunum has neither Brunner's glands nor Peyer's Patches
 Following entry, Brucella organisms either in free in intracellular environment
or in phagocytic cells localize in the regional lymph nodes
 From the regional lymph nodes, Brucella disseminates hematogenously and
localize in the reticuloendothelial system and the reproductive tract
 There is preferential localization to the pregnant uterus

57
BRUCELLOSIS CONT…
 Brucella prefers the uterus due to a factor called erythritol, a four carbon sugar
alcohol in a gravid uterus that stimulates their growth
 The amount of erythritol in the uterus is very high during the third trimester of
pregnancy Brucella infection
 Infection of the uterus results in abortion
 The likely mechanism of abortion are:
Interference with fetal circulation due to the existing placentitis
The effect of endotoxin
Fetal stress resulting from inflammatory response in fetal tissue
 Clinical findings: The primary clinical manifestations of brucellosis are related to
the reproductive tract

58
BRUCELLOSIS CONT…
In Females
 Third trimester abortions
 Retained placenta - Once expelled will have a leathery appearance
 Endometritis
 Birth of dead or weak calves - Respiratory distress and lung infections
 Females usually abort only once, presumably due to acquired immunity
 Brucella melitensis infections in goats and sheep are similar to B. abortus in cattle
except that acute mastitis develops in goats infected with B. melitensis
 Abortions in swine can occur at any time in gestation
 Abortions in dogs with B. canis occur around 50 days of gestation
 Brucella ovis infections in sheep only rarely result in abortions in ewes

59
BRUCELLOSIS CONT…
In Males
Epididymitis and orchitis are the most common presenting signs
Lesions are usually unilateral but may be bilateral
Brucella ovis infections in rams mainly affect the epididymis, being testicular lesions
uncommon
In bulls infection with B. abortus frequently involves the testicle
In dogs infected with B. canis develop scrotal swelling as a result of fluid
accumulation in tunica. Scrotal dermatitis may develop because of constant licking of
scrotum
Infection of the male genital tract results in decreased fertility and in some cases,
sterility
60
BRUCELLOSIS CONT…
Extragenital manifestations
 Swine infected with B. suis may develop arthritis, especially in large joints of
limbs or lumbar spondylitis

 Dogs infected with B. canis can develop meningoencephalitis, osteomyelitis,
discospondylitis, and anterior uveitis (inflammation of the middle layer of the

eye)
 Chronic infections with B. abortus in cattle can result in hygromas
 Horses infected with B. abortus develop “poll evil” or “fistulous withers” and
present with fistulous tracts originating from atlantar or supra-spinous bursas,

respectively
61
BRUCELLOSIS CONT…
Brucellosis in humans
 Brucellosis in humans is also known by many names including undulating fever,
Malta fever, Mediterranean fever, Gibraltar fever
 Brucellosis in humans is primarily of a disease of the reticuloendothelial system
Concerned with blood cell formation and destruction
 A mild lymphadenopathy, splenomegaly and hepathomegaly may be detected
 The onset of signs occurs within 2 to 3 weeks after exposure
 Most cases of human brucellosis are caused by ingestion of unpasteurized dairy
products or meat from infected animals and close contact with their secretions
 May be transmitted through direct contact with blood, placenta, foetus or uterine
secretions
62
BRUCELLOSIS CONT…
 In humans, brucellosis can be caused by B. abortus, B. melitensis, B. suis and
rarely, B. canis
 Worldwide, B. melitensis is the most prevalent species causing human brucellosis
 Brucellosis induces inconstant fevers, sweating, weakness, anaemia, headaches,
depression and muscular and bodily pain
 The popular name undulant fever originates from the characteristic undulance
("wave-like" nature) of the fever, which rises and falls over weeks in untreated
patients
Economic significance
 Brucellosis occurring worldwide in domestic animals creates a serious economic
problem in livestock production

63
BRUCELLOSIS CONT…
The economic losses due to brucellosis can be summarized as follows:
Loss of calves due to abortion
Reduced milk yield (by 20-25 %)
Culling of valuable cows because of breeding failure
Endangering animal export trading of a nation
Loss of man-hours and medical costs
Government costs for research and eradication programs
Diagnosis
 Gram stains of stomach contents from aborted fetus and placenta reveals large
numbers of gram-negative coccobacilli
 Cultured tissues or milk samples on solid media

64
BRUCELLOSIS CONT…
Guinea pigs inoculation
Tube agglutination, plate agglutination or rose Bengal plate test of blood
Complement fixation test and ELISA
Milk is screened with the Brucella milk ring test (MRT)
PCR
Treatment:
As a general rule, treatment of infected animals is not attempted because of:
High
 treatment failure rate
High
 cost
High
 potential problems for eradication programs
Indemnity program from government
Tetracycline and dihydrostreptomycin have been used

65
BRUCELLOSIS CONT…
Combination antibiotic therapy has the best efficacy
Dihydrostreptomycin and tetracycline for a 2 to 4 weeks period
Control and Prevention:
Education about risk of transmission
Wear proper attire if dealing with infected animals/ tissues
Gloves, masks, goggles
Avoid consumption of raw dairy products
Immunize in areas of high prevalence
Use of vaccines, most notably B. abortus strain 19
Eradicate reservoir
Identify, segregate, and/or cull infected animals
Test and slaughter
66
TUBERCULOSIS
 The disease is caused by Mycobacterium and characterized by progressive
development of tubercles in any of the organs in most species
 TB a significant zoonosis
 It can spread to humans through aerosols and by ingestion of raw milk
 In developed countries, eradication efforts significantly reduced prevalence but
reservoirs in wildlife made complete eradication difficult
 TB is still common in less developed countries and economic losses occur in cattle
and African buffalo due to:
 Deaths
 Chronic disease
 Trade restrictions
67
TUBERCULOSIS CONT…
Etiology
M. bovis is the specific cause of TB in cattle
M. tuberculosis – human
M. leprae
M.avium
Unique characterstics of Mycobacterium
 High content of mycolic acid (waxy material) in cell wall
 Slow growth rate
Mycobacterium multiplies once every 20 hours (Others 20minutes)
 Does not grow outside of a host except in cultured media
 Obligate aerobes
68
Epidemiology
All species including humans and all age groups are susceptible to M. bovis
But cattle, goats and pigs are the most susceptible
Sheep and horses showing a high natural resistance
Source of infection
Infected cattle are the main source for the cattle
Organisms are excreted in:
 Exhaled air, sputum, feces, milk, urine
 Vaginal and uterine discharges
 Discharges from open peripheral lymph nodes
All secretions and excretions

69
Methods of transmission
Inhalation is the almost invariable portal of entry in housed cattle and in those
at pasture
Infection by ingestion is more likely at pasture when feces contaminate feed,
drinking water and feeding troughs
Drinking of infected milk by young animals
Intrauterine infection at coitus
Infected semen and instruments
Infected cups of milking machines
Feeding tuberculosis cattle carcasses to pigs

70
Environment risk factors
The disease is more common and serious in housing and zero grazing practices
The closer the animals are packed together, the greater is the chance of disease
transmitted
In beef cattle degree of infection is much lower because of the open range
condition they are kept
Host risk factors
Zebu cattle are thought to be much more resistant to TB than European cattle
In pigs incidence is much lower because they are slaughter at early age
Goats are quite susceptible if kept with infected herds of cattle
71
Sheep are considered to be resistant

In horses the disease occurs rarely due to limited exposure and natural resistance

Pathogen risk factors
The organism is moderately resistance to heat, desiccation and many disinfectants


Readily destroyed by direct sunlight


Pathogenesis
Spreads in the body by two stages, the primary complex and post primary

dissemination
The primary complex consists of lesions at the point of entry & in LNs

72
 A visible primary focus develops within 8 days of entry of bacteria
 Calcification of lesions commences 2 weeks later
 The developing necrotic focus is soon surrounded by granulation tissue and
lymphocytes The pathognomonic “tubercle” is established

 Bacteria pass from primary focus to a regional lymph node and, cause a
similar lesion to develop there

 Post-primary dissemination from the primary complex may take the form of:
 Acute miliary tuberculosis with discrete nodular lesions in various organs
or
 Chronic organ tuberculosis caused by endogenous or exogenous re
infection of tissues rendered allergic to tuberculoprotein

73
Tubercle may be variated size One/joined
If cut feels like cutting sand center of cheese-like form
 Tubercle are commonly seen on the lung, spleen, retropharyngeal lymph nodes,
bronchiale lymph nodes, mesenteric lymph nodes
Tubercles
74
Clinical Findings
 Progressive emaciation
 Capricious appetite and fluctuating temperature
 Hair coat may be rough or sleek (shiny)
 Animal tends to be more docile and sluggish
 Pulmonary involvement is characterized by chronic cough
 The cough:
Is never load or paroxysmal (bursting)
Is low, suppressed and moist
Is easily stimulated by squeezing pharynx or by exercise
Is most common in the morning or in cold weather

75
 Dyspnea with increased rate and depth of respiration
 Enlargement of mediastinal LN and persistent ruminal tympany
 Rarely tuberculous ulcers of small intestine cause diarrhea
 Retropharyngeal LN enlargement causes dysphagia & noisy breathing
Clinical pathology
 There is universal dependence on tuberculin test for diagnosis and
policy of slaughtering all positive reactors
 Sputum and discharges may be examined by inoculation into
guinea pigs
76
1: Submental lymph nodes
2: Submandibular lymph nodes
3: Supraclavicular lymph nodes
4: Retropharyngeal lymph nodes
5: Buccal lymph nodes
6: Superficial cervical lymph nodes
7: Jugular lymph nodes
8: Parotid lymph nodes
9: Retroauricular lymph nodes
& occipital lymph nodes

77
Tuberculin Test
The basis of all TB eradication schemes is the tuberculin test
 Tuberculin is an extract of tubercle bacilli
A special purified protein derivative (PPD) is used for culturing the bacilli
M. tuberculosis or M. bovis
Tuberculin is prepared by killing and filtering off the bacilli from the culture medium
To the liquid which remains trichloracetic acid is added
This precipitates tuberculo-protein which is poured into cylinders to form sediment
The sediment is centrifuged, diluted to a standard strength and bottled
The delayed-type hypersensitivity response of the host, responsible for much of the pathology of TB, is
fundamental to the tuberculin skin test that is widely used for diagnosis in large animals
In a reactor, the antigen stimulates a local infiltrate of inflammatory cells and causes skin swelling that can be
detected by palpation and measured by calipers
78
There are different types of tuberculin test
1. Single Intra dermal (SID) Test
This test is applied by intra dermal injection of 0.1 ml (2000 IU) of tuberculin into a
skin-fold on a cervical fold (center of the lateral aspect of the neck) or the anal (caudal
fold) at the base of the tail
The reaction is read between 48 and 96 hours after injection
A positive reaction constitutes a diffuse swelling at the site of injection
Measured by callipers which are device for measurement of skin thickness
The mammalian tuberculin is not sufficiently specific to differentiate between
reactions due to infection with M. bovis, M. avium, M. tuberculosis and M.
paratuberculosis
79
Intra dermal tuberculin test on skin-fold on a cervical fold : Methods:
Shave the hair, measure the thickness of cowhide with caliper (cutimeter)
 PPD tuberculin is injected intradermally and observation after 72 hours
Result: Fever, Swelling, Redness and hardness
Increasing of cowhide thickness > 60% Positive ≥4

mm
< 60% test on skin-fold

Intra dermal tuberculin Negative
on a cervical fold
80
Caudal Fold Tuberculin Test
 PPD tuberculin is injected intradermally (between the layers of skin) of the caudal
tail fold, under the animal’s tail
81
2. Short Thermal Test
 0.1 ml Intra dermal tuberculin is injected into the neck of cattle, with a rectal temp of
not more than 39oC at the time of injection and for 2 hours later
If the temp at 4, 6, 8 hours after injection rises above 400C, animal is classed as a
positive reactor
Temp peak is usually obtained at 6-8 hrs and is generally over 410C
3. Stormont test
The test is performed similarly to SID test in the neck with a further injection at the
same site 7 days later
An increase in skin thickness of 5 mm or more 24 hours after the second injection
is a positive result
82
4. Comparative intra dermal tuberclin test test
 Avian and mammalian tuberculin are injected simultaneously into two separate
sites on the same side of the neck, 12cm apart and one above the other and the
test is read 72 hours later
 The greater of the two reaction indicates the organism responsible for the sensitization
Necropsy findings
 Tuberculous granulomas may be found in any lymph nodes but particularly in
bronchial and mediastinal lymph nodes and in many organs
 In the lung, miliary abscesses may extend to suppurative bronchopneumonia
 The pus has characteristic cream to orange color; the consistency varying from thick
cream to crumbly cheese
83
Diagnosis
Microbiological culture of bodily fluids
CFT, FAT, direct bacterial agglutination and hemagglutination tests
Tuberculin test
Microscopic examination of blood (FNA = fine needle aspirate) - Acid Fast Staining
Culture: Culturing usually takes 8 to 16 weeks

PCR: Used to detect the presence of DNA that is specific to the organism of interest
Johne’s disease
Aspiration pneumonia
TRP
CBPP
Actinobacillosis
84
.
Treatment
 Usually failed because :
Cell wall of bacteria is thick
Bacteria can live by intracellular
Drugs penetration is slow
Animals: Not attempted
Humans: isoniazid and rifampicin
TB requires much longer periods of treatment (around 6 to 24 months)
Control
Test and slaughter policy
Removal of the infected animals, prevention of spread of infection and avoidance of further
introduction of the disease

85
 Hygienic measures to prevent spread of infection should be instituted as soon as the
first group of reactors is removed
Sanitation using disinfectant liquids such as cresol/phenol
 Feed troughs, water troughs and drinking cups should be cleaned and thoroughly
disinfected with hot, 5% phenol or equivalent cresol disinfectant
 Isolation of suspect animals
 New animal From TB free places
 It is most important that calves reared as herd replacements be fed TB free milk
 Farm attendants should be checked as they may provide a source of M. tuberculosis and
M. bovis
 Use of TB free semen (AI)
 Vaccination with Bacillus – Calmette - Guerin (BCG) vaccine

86
CONTAGIOUS BOVINE PLEUROPNEUMONIA
 CBPP is a highly infectious septicemia characterized by localization in the
lungs and pleura

 It is one of the major plagues in cattle causing heavy losses in many parts of
the world
Etiology
 Mycoplasma mycoides mycoides (small colony type)
Not communicable to other species
Natural hosts are bovine
Organisms are pleomorphic (various shape – cocci, bacilli, spiral…)
Quickly inactivated in environment
Does not survive in meat or meat products

87
CONTAGIOUS BOVINE PLEUROPNEUMONIA CONT…
 Principal method of spread is by inhalation of infective droplets from
active or carrier cases

 Introduction of carrier animals
 Inhalation of infected droplets of coughing animal
 Close contact
 Organism present in saliva, urine, fetal membranes and uterine
discharges
 Humans are not susceptible
 Transplacental infection reported

88
M. mycoides var. mycoides is sensitive to all environmental influences including, disinfectant,
heat and drying
Organisms do not survive outside the animal body for more than a few hours
Six meters is usually sufficient separation between animals to prevent infection
Animal risk factors
CBPP only occurs in cattle
There is no difference in susceptibility between Bos indicus and Bos taurus
Bos indicus cattle, also called zebu, are adapted to hot climates. Bos taurus are the typical
cattle of Europe, north-eastern Asia, and parts of Africa which are adapted to cooler climates
A strong immunity develops after natural disease
89
Economic Importance
 Enormous losses are experienced each year from deaths of animals and loss
of production during convalescence
Pathogenesis
 CBPP is an acute lobar pneumonia and pleurisy developing by localization
from initial septicemia

 An essential part of the pathogenesis of the disease is thrombosis in pulmonary
vessels
 Death results from anoxia and presumably from toxemia
 Approximately 50% of animals that become infected go through mild form of
the disease and often recognized as clinical cases

90
Clinical Findings
 The incubation period is 3-6 weeks (occasionally up to 6 months)
 Fever (400C), a fall in milk yield, anorexia, cessation of rumination and depression
 Animals stand apart or lag behind a traveling group
 Coughing at first only on exercise and chest pain
 Disinclined to move due to thoracic pain, standing with elbows out, the back
arched and the head extended
 Respirations are shallow, rapid and with expiratory grunting
 Auscultation reveals:
Pleuritic friction sounds in the early stage of acute inflammation,
Dullness, fluid sounds and moist crackles in the later stage of effusion
91
CBPP: Severe respiratory

disease
92
 Edematous swellings of the throat and dewlap
 Recovered animals may be clinically normal. But in some animals an inactive
sequestrum forms in the lung. The sequestrum with a necrotic center of sufficient
size to produce a toxemia which can result in unthriftiness, a chronic cough and
mild respiratory distress on exercise
 These sequestra commonly breakdown when the animal is exposed to

environmental stress and cause an acute attack of the disease
 In fatal cases death occurs after several days to 3 weeks
Necropsy Findings
 The post mortem lesions of CBPP include thickening and inflammation of lung
tissues with extensive fibrin accumulation

93
 Large amounts of straw-colored fluid (up to 10 litters) in the thoracic cavity
 Interlobular septa greatly distended with serofibrinous exudates giving rise to the
classical “marbled” appearance of the affected lungs
 Encapsulated sequestra containing necrotic tissue
 Consolidation and grey and white hepatization of lungs
Diagnosis
 History of contact with infected animals
 Clinical signs and clinical findings
 Necropsy findings (Post mortem lesions)
 Cultural examination
 Serological tests (CFT, ELISA and hemagglutination)

94
Marbling and hepatization

95
A sequestrum is a piece of dead tissue that has become separated during the process
of necrosis from normal/sound one
96
Treatment
 Tylosin (10mg/kg every 12hrs for six injection)
 Spiramycin (10-50mg/kg for 3 days )
Control
 Any measure which brings animals together should be avoided
 Prevention of entry of CBPP into a free area
 Strict quarantine of infected and in contact animals must be maintained
 Infected animals should be removed as soon as possible
 Eradication by test and slaughter of reactors
 Vaccination
97
CONTAGIOUS CAPRINE PLEUROPNEUMONIA
 CCPP is classical, highly contagious and serious respiratory lethal
disease of goats
 CCPP is caused by Mycoplasma mycoides var capri (large colony)
 The disease is readily transmitted by inhalation
 The organism does not survive long outside the host body
 Infection is usually brought into the flock by a carrier or infected
animals
 CCPP is not transmissible to sheep or cattle experimentally or naturally
 Infectivity is high with a morbidity of 100%
 The illness is acute severe with mortality of 60 – 100%

98
CONTAGIOUS CAPRINE PLEUROPNEUMONIA CONT…
Clinical Findings
 The incubation period of CCPP is 6 – 10 days
 Cough, dyspnea, lagging behind, lying down a lot
 Fever (40.5 – 41.50 C)
 Mouth breathing, tongue protrusion & frothy salivation
 Death occurs in 2 – or more days
Diagnosis
 Clinical signs and clinical findings
 Cultural examination
 Serological tests (CFT, ELISA and hemagglutination)

99
CONTAGIOUS CAPRINE PLEUROPNEUMONIA CONT…
Treatment
 Tylosin (9 – 10 mg per kg)
 Oxytetracycline (15 mg per kg) are highly successful
Control: Control depends on:

 Isolation of affected animals
 Vaccination
 Revaccination at interval of 6 months
10
COLIBACILLOSIS
 One of the most common diseases of newborn farm animals is colibacillosis
There are two different types of the disease
 Enteric colibacillosis: Manifested primarily by varying degrees of diarrhea,
dehydration and death in a few days if not treated
 Septicemic colibacillosis: Manifested by septicemia and rapid death after onset
Etiology: Escherichia coli (E. coli)
 Escherichia coli (E. coli) are a Gram negative rod (bacillus) in the family
Enterobacteriaceae
 Most E. coli are normal commensals found in the intestinal tract
 Pathogenic strains of this organism are distinguished from normal flora by their
possession of virulence factors such as exotoxins

101
COLIBACILLOSIS CONT…
E. coli are serotyped based on the O (somatic lipopolysaccharide), H (flagellar) and K
(capsular) antigens - 700 serotypes
Enterovirulent E. coli strains (EEC) cause poisoning or diarrhea within the intestine by
producing toxins or intestinal inflammation
There are six groups of E. coli strains that comprise EEC
EHEC (enterohemorrhagic E. coli)
ETEC (enterotoxigenic E. coli)
EPEC (enteropathogenic E. coli)
EIEC (enteroinvasive E. coli
EAEC (enteroadherent E. coli
EAggEC (enteroaggregative E. coli)

102
Epidemiology:
 Colibacillosis occurs commonly wherever farm animals are maintained
Morbidity and mortality rates

 In dairy calves
 Morbidity may reach 75% but is usually about 30%
 Case fatality vary 10 to 50%
 In beef calves
 Morbidity from 10 to 50%
 Case fatality from 5 to 25%
 Population mortality rate in calves vary from a low of 3% in well managed
herds to a high of 60% in problem herds

103
Host risk factors
 Most common in animals under 3 days of age but it may occur as early as 12-18
hours after birth and occasionally in calves up to several days of age
 Diarrhea caused by enterotoxigenic E. coli occurs in calves mainly during the 1 st few
weeks of life, rarely in older calves, and never in adults
 The mechanism of this age related resistance may be related to development of
resistance to colonization of small intestine as the calf becomes older
 The disease is more common in piglets born from gilts than from sows. This
suggests that immunity develops with increasing in age of sows and is transferred to
piglets
 Newborn farm animals are born agammaglobulinemia – so what?

104
 They must ingest colostrum and absorb colostral immunoglobulins (Igs)
within hours to obtain protection against colibacillosis

 Passive transfer of maternal Igs to colibacillosis in calves is achieved by
provision colostrum soon after birth

 Colostral Igs are absorbed for up to 24 hours after birth in calves
Maximum efficiency during the first 6-12 hrs
Decreases rapidly from 12 to 24hrs
The intestinal tract of calves is permeable to Igs only up to 24 hours after

birth
 Calves should ingest 80-100g of colostral IgG1, and ideally up to 150g,
within a few hours after birth

105
 An antibody (Ab), also known as an immunoglobulin (Ig), is a large Y-shaped protein produced by B-
cells that is used by the immune system to identify and neutralize foreign objects such as bacteria,
parasites and viruses
 The antibody recognizes a unique part of the foreign target, called an antigen
 Antibodies are secreted by a type of white blood cell called a plasma cell
Description
Found in mucosal areas, such as the gut, respiratory tract and urogenital tract, and prevents colonization

by pathogens. Also found in saliva, tears and breast milk.
It has been shown to activate basophils and mast cells to produce antimicrobial factors.
Binds to allergens and triggers histamine release from mast cells and basophils, and is involved in allergy. Also

protects against parasitic worms.
Provides the majority of antibody-based immunity against invading pathogens. The only antibody capable of
crossing the placenta to give passive immunity to the fetus.
106
Environmental and management risk factors
 There is a relationship between adverse climatic conditions and colibacillosis
 Overcrowding is commonly followed by an outbreak of enteric colibacillosis
 Irregular feeding practices resulting in dietaric diarrhea contribute to a higher
incidence of enteric colibacillsis in calves

 Dairy calves fed milk substitutes are more prone to enteric colibacillosis than
those fed whole cow milk. Extreme heat treatment of liquid skim milk to prepare
milk substitutes results in denaturation of whey proteins
 Poor housing and hygienic practices
 As size of herds increased and livestock production more intensified the quality of
hygiene and sanitation, particularly in housed animals, assumes major importance
107
The virulence attributes of enterotoxigeric E. coli include:


Adhesions in their pilli or fimbriae which allow them to adhere to intestinal


villous epithelial cells and prevent elimination
The production of heat-stable enterotoxins


Source of organism and its ecology and transmission
The major source of infection is feces of infected animals and all inanimate objects

contaminated by feces: bedding, pails, boots, tools, clothing, feed and water
Normal calves, which are subliminally infected and adult cows serve as reservoirs

Ingestion is the most likely portal of infection in calves, piglets and lambs

108
Pathogenesis of septicemic colibacillosis (coliform septicemia)
Results from EIEC invading tissues and systemic circulation via the intestinal
lumen, nasopharyngeal mucosae, tonsillar crypts or umbilical vessels
These strains are able to escape phagocytosis and induce tissue damage by the
release of cytotoxins
Calves and piglets deficient in colostral Igs are highly susceptible to septicemia
The clinical findings and lesions in septicemic colibacillosis are attributable to
the effects of endotoxin which causes shock
Effects of endotoxin in cattle include: hypothermia, decreased systemic blood
pressure, changes in blood counts, alteration in blood coagulation,

hyperglycemia followed by hypoglycemia and depletion of liver glycogen
109
Pathogenesis of enterotoxigenic colibacillosis
Any factor which results in an increase of the pH in the lumen allow proliferation of
the organism where as lowering the pH may reduce the severity of colibacillosis
ETEC possess ability to colonize and proliferate in the upper part of small intestine
and to produce enterotoxins which causes increase in net fluid secretion

Production of enterotoxin by E. coli results in net secretion of fluid and electrolytes
from systemic circulation into the lumen of the gut

This results in varying degrees of diarrhea, dehydration, electrolyte imbalances,
acidosis and hypocalcaemia

When acidosis is severe there will be circulatory failure, shock and death. If the
disease is progressive the acidosis becomes more severe
110
Clinical Findings: Septicemic colibacillosis
 It is most common during the first 4 days of life
 Illness is acute, the course varying from 24-96 hours
 Affected animals are depressed and weak; anorexia is complete and marked
tachycardia
 Initially temperature is high but became subnormal when the calf becomes
weak and moribund

 Oral mucous membrane is dry and cool
 If the calf survives the septicemic state, clinical evidence of post septicemic
localization may appear in about 1 week

 This include arthritis, meningitis, ophthalmitis and pneumonia
111
Clinical Findings: Enterotoxigernic colibacillosis
 It is most common form of colibacillosis in calves from 3 to 5 days of age
 It can occur in calves as early as 1 day of age and only rarely up to 3 weeks
 Clinical severity varies depending on the number and kind of organisms
causing the disease

 In this form of the disease outstanding signs include severe weakness,
coma, subnormal temperature, cold clammy skin, pale mucosae, wetness

around mouth, slowness and irregularity of heart, mild convulsive
movement and periodic apnea (brief pause in breathing)
 Prognosis for these calves is poor - they commonly die in 2-6 hrs after onset
of signs
112
There is diarrhea in which the feces are profuse and watery to pasty, usually pale
yellow to white in color, streaked with blood flecks and very foul smelling
Defecation is frequent and effortless, and tail and buttocks are soiled
Temperature is normal in initial stages but becomes subnormal as the disease
worsens
Weakness from the effects of rapid and severe dehydration
Abdomen may be slightly distended due to distension of fluid filled intestines
Mild to moderately affected calves may be diarrheic for few days, and recover
spontaneously without treatment

However, 15-20% of affected calves become progressively worse over 3-5 days,
gradually become weak, lose desire to suck and obviously clinically dehydrated
113
Diagnosis
 Isolation of the organism from intestines and feces of affected animals
 The laboratory tests to identify enterotoxigenic strains include:
Direct fluorescent antibody technique
ELISA
DNA gene probes
 Total and differential leukocyte count
Treatment: Considerations for treatment of acute neonatal diarrhea include:
1. Alteration of the diet
 Diarrheic calves are commonly treated with oral fluids and electrolytes and left
with the cow

114
 It is a common practice to reduce milk intake of diarrheic dairy calves for up to 24
hours or until there is clinical improvement
 This is because lactose digestion is impaired and resting of intestine for few days
would prevent osmotic diarrhea caused by fermentation of lactose in the large intestine
 So it is necessary to provide these animals with readily absorbable substances such as
oral glucose electrolyte mixtures
2. Fluid and electrolyte replacement

 Dehydration, acidosis and electrolyte imbalance are corrected by potential and oral use
of simple or balanced electrolyte solutions
3. Management of outbreaks
 Isolation of affected animals from other susceptible calves
115
Control
Reduction
 of degree of exposure of newborn calves to the infectious agents
The emphasis is that newborn are born into a clean environment
Barns, pens and paddocks used as parturition areas must be clean
Provision
 of optimum nutrition to pregnant dam
Vigorous newborn animal
Adequate quantities of colostrums
Ensure that
 colostrums is ingested in liberal quantities soon after birth
Increase specific
 resistance of newborn by vaccinating pregnant dam or new born
The pregnant dam is vaccinated 2-4 weeks before parturition to stimulate specific
antibodies to E. coli - antibodies passed on the newborn

116
SALMONELLOSIS
 Salmonellosis is an economically important disease of all animal species worldwide
 Both salmonellosis and the Salmonella genus of microorganisms derive their names after
Daniel E. Salmon (1850–1914), an American Veterinary surgeon
Etiology
 Genus Salmonella, family Enterobateriaceae
 Salmonella is a motile enterobacteria with flagella which grade in all directions

(peritrichous)Gram-negative, facultative rod-shaped bacterium, non-spore-forming,
predominantly
 Currently, there are two recognized species: S. enterica and S. bongori
 The genus salmonella is further divided into over 2300 serotypes based on flagellar (H)
antigens
 Salmonella can be classified into three main groups based on their association with human and
animal hosts
117
SALMONELLOSIS CONT…
1.Serotypes which have specificity to the human host: S. typhi and S. paratyphi
2.Serotypes adapted to specific animal hosts: S. dublin in cattle, S. abortusequi in
horses, S. abortusovis in sheep and S. choleraesuis in pigs
3.Serotypes which cause disease in humans and animals (unadapted): S.
typhimurium is the best example
Serotypes that most commonly cause clinical salmonellosis in farm animals are:
Cattle: S. typhimurium, S. dublin, S. newport


Sheep and goats: S. typhimurium, S. anatum


Pigs: S. typhimurium, S. choleraesuis


Horses: S. typhimurium, S. anatum, S. Newport, S. Enteritides & S. arizona


118
Epidemiology
 The epidemiology of salmonellosis as a disease of animals and zoonosis is complex
 Epidemiological patterns differ greatly between geographical areas depending on
climate, population density, land use, farming practices, food harvesting and
processing technologies and consumers habit
 Salmonellosis occurs universally and in all species
Morbidity and case fatality
 The morbidity rate in outbreaks of salmonellosis in pigs, sheep and calves is high,
reaching 50% or more
 In all species the case fatality rate reaches 100% if treatment is not provided
119
 Salmonellae are spread by direct and indirect means
 Farm animals may be infected in many ways:
By animals-to-animal transmission
By contaminated animal feed &water
 By a contaminated environment: soil, birds, rodents and insects
 The bacteria may also be disseminated during transport of animals and
during holding of infected animals in lairage

 Mixing of young susceptible calves and their transportation is an
efficient mechanism for rapid dissemination of salmonellae

120
The carrier state
Because salmonellae are facultative intracellular organisms that survive in
macrophages, they can evade the bactericidal effects of antibody and complement
Thus persistence of infection in animals and in the environment are important
epidemiological features of salmonellosis
Host risk factors
Transport, intercurrent disease, anesthesia and surgery, dosing with antibiotics or
anthelmintics, acute deprivation of food or parturition are predisposing causes to

salmonellosis
Infection of newborn calf may be from the dam because many cows which are
latent shedders become active shedders at parturition

121
Environment and management risk factors
Intensification contributes significantly to the increased infection rate
Temperature and wetness are most important as salmonellae are susceptible to drying
and sunlight
Contaminated feedstuffs are important in spreading infection
Housed animals are more susceptible to infection from purchased feed contaminated
with animal byproducts

Whereas pastured animals are more susceptible to infection from animal product
based fertilizers

Salmonellae are facultative intracellular organisms which survive in macrophages and
can evade the bactericidal effects of antibodies and complement

122
 They are relatively resistant to various environmental factors as compared to other
organisms in the family
 Salmonellosis is a significant cause of economic loss in farm animals because of:
Diagnosis and treatment of clinical cases
Deaths
Diagnostic laboratory costs
Costs of cleaning and disinfection
Pathogenesis
 After oral infection, invasion of the host takes place through intestinal wall in the
terminal ileum and cecum and progresses to mesenteric LNs
123
Progress beyond mesentric LNS and development of the disease is determined by:
 Immune status and age of the host
 Exposure to stress
 Virulence of the strain organism
 Virulence of the organism is influenced by:
 The presence of adhesion (pili and flagellae)
 The production of cytotoxin, endotoxin, lipopolysaccharide and
 The inflammatory response they initiate in the intestinal wall
In young animals and adults whose resistance is lowered, spread beyond the mesenteric
lymph nodes occurs and infection is established in liver cells, from this site the
infection invades the bloodstream

124
Clinical findings
 Abortion is a common manifestation of salmonellosis in cattle
 The pathogenesis is based on the growth of the organisms in the placenta,
seeded there from a primary lesion in other maternal tissues
 Salmonellosis is most satisfactorily described as three syndromes classified
according to the severity as :
1. Septicemia:
 It is characteristic form of the disease in newborn foals, calves and young pigs
up to 4 months of age
 Affected animals show profound depression, dullness, prostration, high fever
(40.5-42oC) and death in 24-48 hours

125
2. Acute enteritis
It is the common form in adult animals of all species
There is high fever (40-41oC)
There is severe fluid diarrhea and sometimes dysentery with tenesmus
The feces have putrid smell and contain mucous, blood and fibrous casts
There is complete anorexia, rapid pulse rate and respiration is rapid and shallow
Pregnant animals usually abort
The animal loses weight and strength rapidly, becomes recumbent and dies in 2-5 days.
Case fatality without treatment reaches 75%
Newborn animals those survive septicemic state develop severe enteritis with diarrhea
at 12-24 hours after illness

126
3. Chronic enteritis
 Is a common syndrome in pigs and occurs occasionally in cattle and adult horses
 There is intermittent or persistent diarrhea with occasional passage of blood,
mucous and firm fibrous casts
 Intermittent moderate fever (39 oC) and loss of weight leading to emaciation
Necropsy findings
1. Septicemic form: There may be extensive submucosal and subserus petechial
hemorrhages
2. Acute enteric form: There is inflammation as mucoenteritis and hemorrhagic
enteritis, mesenteric lymph nodes are enlarged, abomasitis with multiple mucosal
erosions and petechiation
127
3. Chronic enteric form
Discrete areas of necrosis on the wall of the cecum and colon
The wall is thickened
Mesenteric lymph nodes and spleen are swollen
Diagnosis
Clinical signs and clinical findings
Bacterial culture (Fecal culture)
DNA probes
Serological tests (ELISA)
Indirect tests- differential white cell count

128
Treatment
Treatment is recommended for all sick animals
The choice of drugs depends on a test of sensitivity in each case
The drug of choice is trimethoprim-sulfadoxine parenterally until
clinical recovery occurs
Ampicillin and amoxicillin are also highly effective
Gentamicin, Ampicillin and chloramphenicol
Administration of electrolyte solutions by the oral route has gained
popularity for the ease of administration and relative safety

129
Control
 If possible purchase animals when they are older, this gives time to develop
immunity
 Introduce only those animals guaranteed not to be carriers
 Identify carrier animals and either cull them or treat them vigorously
 Restrict the movement of animals and limit the infection to the smallest group
 Vigorous disinfection of buildings
 Heat treatment of feed
 Disposal of infective materials should be carried out with great care
 Immunization (Vaccination) - A killed bacterin or A live attenuated vaccine
130
ACTINOBACILLOSIS
Synonym: Wooden tongue
Actinobacillosis is an infectious disease
 In cattle characterized by inflammation of the tongue and less commonly
pharyngeal lymph nodes
In sheep characterized by inflammation in the lips and cheeks, with occasional
extension to mucous membranes of turbinate and soft tissues of the heads and necks
Etiology
Actinobacillosis is caused by gram-negative coccobacilli in the genus Actinobacillus
and species A. lignieresii
A. lignieresii is a normal inhabitant of the oral cavity and rumen of ruminants
131
ACTINOBACILLOSIS CONT…
Epidemiology
Infection in soft tissue results from damage to oral mucosa
Infection in cattle occurs through ulcerating or penetrating lesions to the tongue
The disease in cattle is worldwide in distribution, usually of a sporadic occurrence in
individual farms
High prevalence of the diseases is recorded in cattle grazing “burnt-over” peat pastures
These pastures contain much gravel and ash likely to cause oral injury
Pathogenesis
Localization of the organism is followed by an acute inflammatory reaction
This results in the development of granulomatous lesion
132
Spread to regional lymph nodes is usual
Lingual involvement in cattle causes interference with prehension and mastication due
to acute inflammation in the early stage and distortion of the tongue in the later stages
Clinical findings
Swelling on the submandibular region
Affected animals being unable to eat for about 48 hours
Excessive salivation and gentle chewing
On examination the tongue is swollen, and hard, particularly at the base, the tip
appearing normal
Manipulation of the tongue causes pain and resentment (hatred)
133
 Nodules and ulcers are seen on the sides of the tongue
 In the later stages, acute inflammation is replaced by fibrous tissue and the
tongue becomes shrunken and immobile which causes considerable

interference in prehension
 Visible and palpable enlargement of submaxillary and parotid LNs
Actinobacillosis on the mandible and tongue
134
Diagnosis
Purulent discharges commonly contain “sulfur bodies” which are granular in nature
and on microscopic examination, consists of club like rosettes with central mass of
bacteria
Examination of smear or culture of pus for the presence of the organism is advisable
Salivation, chewing and anorexia of lingual form in cattle may resemble early rabies
or foreign body in the mouth (choke)
Enlargement of lymph nodes with tongue unaffected, may resemble TB and
tuberculin test necessary for differentiation
135
Treatment
 Sulphonamides, penicillin, streptomycin and other broad spectrum antibiotics
 Potassium iodide and sodium iodide given IV as a 10% solution for both
sheep and cattle are commonly used
 Incision of the swelling and evacuation of the pus and local application of
potassium iodide and sodium iodide
Prevention and control
 Quick treatment of affected animals and prevention of contamination of
pasture and feeding troughs
 Isolation or disposal of animals with discharging lesions
136
ACTINOMYCOSIS
Synonym: Lumpy jaw
Actinomycosis is a bacterial disease characterized by rarefying osteomyelitis of the
bones of the head, particularly the mandible and maxilla
Etiology: Actinomyces bovis
Epidemiology
Actinomycosis is recorded from most countries of the world
The disease is common only in cattle
A. bovis is a common inhabitant of the bovine mouth
Infection occurs through wounds to bucal mucosa by sharp pieces of feed or foreign
material
Infection may also occur in young cattle when teeth are erupting
137
ACTINOMYCOSIS CONT…
Pathogenesis
In the jaw bones a rarefying osteomyelitis is produced
The lesion is characteristically granulomatous
The effects of the disease on animals are purely physical
Involvement of the jaw results in interference with prehension and mastication
Involvement of the alimentary tract leads to interference with ruminal
movement and digestion
Clinical findings
Actinomycosis of the jaw commences as a painless, bony swellings on the
mandible or maxilla, at the level of central moral teeth

138
Swellings are very hard, immovable and painful to the touch
They break through the skin and discharge sticky honey-like pus
Teeth embedded in the affected bone become painful resulting in difficult mastication
and consequently loss of condition
Excessive swelling of maxilla leads to dyspnea
The most common form of actinomycosis of soft tissues is involvement of esophageal
groove with spread to the lower esophagus and anterior wall of the reticulum
The syndrome of such involvement is one of impaired digestion with periodic
diarrhea, passage of undigested feed material, chronic bloat and allotriophagia (pica)
A morbid impulse to eat unnatural foodstuffs such as, ice, dirtclay, laundry
startch, gravel, plaster or hair

139
Submandibular swelling due to actinomycosis
Rarefaction of the bone due to actinomycosis
140
Necropsy findings
 Rarefaction of the bone and the presence of loculi and sinuses containing whey-like
pus with small gritty granules
 Extensive fibrous tissue reaction around the lesion
 Granulomatous lesions containing pockets of pus are found in the esophageal
groove, lower esophagus and reticulum
Diagnosis
 Clinical signs and clinical findings are suggestive
 Smears of the pus stained with gram’s stain
 Gram positive filament of the organisms most readily found in the center of the
crushed granules
141
Foreign body or accumulation of dry feed jammed between teeth and cheek
Syndrome of indigestion by visceral actinomycotic lesions resembles that caused
by chronic peritonitis.
Treatment
Sulfanilamide
Sulfapyridine
Sulfathiazole
Streptomycin
Iodides
Local surgical incision

142
PARATUBERCULOSIS
Synonym: Johne’s disease
Paratuberculosis is a chronic, contagious granulomatous enteritis
characterized in cattle by persistent diarrhea, progressive weight loss,

debilitation and eventually death
The etiologic agent is believed to be capable of infecting and causing
disease in all other ruminants (sheep, goats, llamas, deer) and in captive
and free-ranging wildlife
The infection has also been recognized in omnivores and carnivores
such as wild rabbits, foxes, weasels, as well as nonhuman primates
 Distribution is worldwide
143
PARATUBERCULOSIS CONT…
 Etiologic: M. paratuberculosis
 Pathogenesis
 M. paratuberculosis is excreted in large numbers in feces of infected animals and in
lower numbers in their colostrum and milk
 It is resistant to environmental factors and can survive on pasture for >1 year;
survival in water is longer than in soil
 The infection is usually acquired through the fecal-oral route
 Introduction of the disease into a non infected herd is usually through herd
expansion or replacement purchases via sub clinically infected carriers
 Infection is acquired early in life often soon after birth but clinical signs rarely
develop in cattle <2 year old because progression to clinical disease occurs slowly
144
 Infection is acquired by ingestion of the organism when nursing on
contaminated teats, consumption of milk, solid feed, or water contaminated by

the organism, or licking and grooming behavior in a contaminated
environment
 After ingestion, and uptake in the Peyer’s patches of the lower small intestine,
this intracellular pathogen infects macrophages in the GI tract and in

associated lymph nodes
 The organisms multiply and eventually provoke a chronic granulomatous
enteritis that interferes with nutrient uptake and processing leading to

cachexia
 This may take months to years to develop - chronic

145
Clinical Findings
Weight loss and diarrhea
In cattle, diarrhea may be constant or intermittent
Diarrhea typically does not contain blood, mucus, or epithelial debris and is
passed without tenesmus
Over weeks or months, the diarrhea becomes more severe, further weight loss
occurs, coat color may fade, and ventral and intermandibular edema may
develop due to a protein-losing enteropathy
This leads to low concentrations of total protein and albumin in plasma
In dairy cattle and goats, milk yield may drop or fail to reach expected levels
146
Animals are alert, and temperature and appetite are usually normal, although
thirst may be increased
The disease is progressive and ultimately terminates in emaciation and death
In infected herds, the mortality rate may be low for a number of years, but up to
50% of animals may be infected sub clinically with associated production losses
Lesions:
Thickened and corrugated intestine with enlarged and edematous neighboring
lymph nodes
Serosal lymphangitis and enlargement of mesenteric and other regional lymph
nodes are usually apparent
147
JOHNES DISEASE - M. PARATUBERCULOSIS
148
Diagnosis
 Demonstration of M. paratuberculosis in the faeces by microscopy,
culture, DNA probes and PCR

 Ziehl-Neelsen stains of tissue samples for acid-fast bacteria
M. Paratuberculosis
 Necropsy by finding the pathognomonic lesions of the disease in the
intestines Corrugated intestine

Finding evidence of cellular immune response to infection (skin testing)
Detecting antibody to M. paratuberculosis antigens (ELISA, AGID)
149
Treatment: No satisfactory treatment is known
Control
 Good sanitation and management practices aimed at limiting the exposure of
young animals to the organism
 Newborns should be birthed in areas free of manure
 Animals testing positive should be sent to slaughter
 Because intrauterine infection can occur, calves from dams that have or
develop signs of the disease should be culled
 Herd replacements should be obtained from herds free of the disease and the
replacements themselves should be tested prior to introduction to the new herd

150
What is the public health risk associated with this disease (Zoonotic Risk)?
♦ Paratuberculosis has not been demonstrated as a zoonosis. However, the
organism that causes Johne’s disease (M. paratuberculosis) has been found
on occasions in patients with Crohn’s disease. Crohn’s disease is a chronic,
painful, diarrhoeal infl ammatory disease of the intestinal tract in humans
that resembles Johne’s disease
♦ There are conflicting data on the involvement of the causative organism in
Crohn disease, a chronic granulomatous enteritis of unknown cause in

people. However, M paratuberculosis is consistently detected by PCR in
people with Crohn disease. This fact, coupled with its broad host range,
including nonhuman primates, indicates that paratuberculosis should be
considered a zoonotic risk until the situation is clarified
151
LEPTOSPIROSIS
 Leptospirosis is an infectious disease caused by the genus Leptospira that are transmitted
directly or indirectly from animals to animals (humans)
Etiology:
 L. interrogans
 Aerobic or microaerophilic, motile, finely coiled bacteria
Epidemiology
 Leptospirosis occurs worldwide but is most common in temperate and subtropical areas
with high rainfall
Reservoirs
 Rodents, livestock (cattle, horses, sheep, goats, swine), canines and wild mammals
 Many animals have prolonged leptospiruria without suffering from the disease themselves
152
LEPTOSPIROSIS CONT…
Modes of Transmission
 By direct or indirect contact of nasal, oral or eye mucosal membranes and
abraded (traumatized) skin with urine or carcasses of infected animals

 Urine: Indirect exposure through water, soil, or foods contaminated by urine
from infected animals is the most common route

 Inhalation of droplet aerosols of contaminated fluids
 Person-to-person transmission is considered extremely rare
 They can be transmitted from human to human by sexual intercourse,
transplacentally from the mother to the fetus and via breast milk to a child
 Urine from a human patient suffering from leptospirosis should be
considered infectious
153
Incubation period
 The incubation period is usually 7 – 10 days, with a range of 2 – 30 days
Period of Communicability or Infectious Period
 An outbreak occurs during the rainy season because of widespread contamination by infected
rodent urine in flood water
 Rodents are displaced from their burrows and drains by the water
 High humidity and heavy rainfall intensify the outbreak
 Rats distribute more virulent leptospires through their urine into the environment than other
animals
 Rodents were the first recognized carriers of leptospirosis
 Rodents are the only major animal species that can shed leptospires throughout their lifespan
without clinical manifestations

154
Clinical Findings
 Abrupt onset of fever, chills, conjunctival suffusion, headache, myalgia and
jaundice
 A mild, influenza-like illness
 Weil’s syndrome characterized by jaundice, renal failure, haemorrhage and
myocarditis with arrhythmias
 Meningitis/meningoencephalitis
 Pulmonary haemorrhage with respiratory failure
Diagnosis
 Direct Evidence
1. Demonstration of leptospires by microscopy

155
 Dark-field microscopy Thin, coiled, rapidly moving Mos
 Phase contrast microscopy
2. Culture
3. PCR
 Indirect Evidence: Detection of antibodies to leptospira
1. Agglutination test
2. Indirect fluorescent antibody test (IFAT)
3. Indirect haemagglutination test (IHA)
4. Complement fixation test (CFT)
5. ELISA
156
Treatment
 Penicillin
 Amoxycillin, Erythromycin & Doxycycline
Prevention
 Prevent contamination of living, working and recreational areas by urine of infected animals
 Control rodent populations in areas of human habitation
 Domestic animal owners should take necessary precautions to minimize their animal’s
potential contact with wildlife (do not feed pets outside or allow animals to roam
unsupervised)
 Do not allow animals to urinate in or near ponds or pools
 Keep animals away from gardens, playgrounds and sandboxes and other places children may
play
157
 Among domesticated animals, vaccination of swine, cattle and dogs
 Chlorination is seldom useful, as virulent leptospires withstand up to 4 ppm
in potable water
 Filtered water is not safe
 Using boiled or ultraviolet irradiated water is advisable
 Water tanks must be sealed if possible
 Food articles must be stored in properly fitting containers
 Bathroom and kitchen waste pipes must be blocked at night
 Try avoiding walking in flood water. If you have to, wear gum boots
 Heavy drinking and smoking predispose damage to the liver and the
kidneys which in turn become vulnerable to leptospiral infection

158
 Protected water supply to all
 Proper collection, transport, treatment and secured disposal of garbage
 Drinking boiled water
 Disinfections of contaminated work areas
 Providing proper protective clothing, shoes and gloves, to high-risk occupational
groups
High risk groups
1.Dairy farmers and milkers
2. Slaughter-house workers
3. Meat inspectors
159
4. Veterinarians and meat carriers in food industries
5. People who work habitually in wet occupations (rice farmers, sugar cane harvesters, drainers,
sewer workers, miners)
“rice field fever”, “sugar cane cutter fever”
6. Adventure travellers (cave exploration, white water rafting, water sports)
Hence,
All the people involved in high-risk activities should wear protective clothing and need to adopt
a reasonable standard of hygiene
Impervious knee-high boots, aprons, gloves, face masks or eye protection should be used
wherever indicated
Immunization of high risk groups worth important
Chemo prophylaxis: Doxycycline can prevent leptospirosis, if given before and during exposure.
160
LISTERIOSIS
 Listeriosis is a zoonotic infectious but not contagious disease caused by the
bacterium L. monocytogenes, far more common in domestics animals,

especially ruminants, than in human beings
 The causative bacterium lives in the soil and in poorly made silage and is
acquired by ingestion
 The disease is usually sporadic, but can occur as farm outbreaks in ruminants
Etiology
 Genus – Listeria
 Species - L. monocytogenes (of more public health importance), L. innoucla, L.
ivanovi, L. seeligeri and L. welshimeri
 A Psychrophilic bacterium – contaminate foods kept in a refrigerator

161
LISTERIOSIS CONT…
L. monocytogenes is a rod-shaped aerobic and gram positive pathogenic bacterium
that invades the cytoplasm of living cells
In human listeriosis is a serious infection caused by eating foods contaminated with
the L. Monocytogenes. This disease affects primarily pregnant women, newborn
and adults with weakened immune systems
Symptoms
Fever
Muscle ache
Nausea & diarrhea
 Influenza-like early on
Miscarriage, still birth, premature delivery or infected newborn

162
LISTERIOSIS CONT…
 Intrauterine or cervical infections in pregnant animals may result in
spontaneous abortion
 Lethargy
 Neural listeriosis resulting in salivation, droopy ear and Irritability

 If infection spreads to the nervous system: headache, stiff neck, confusion, loss of balance, or
convulsions, meningitis and encephalitis
 Listeria can cause pneumonia and sepsis
Transmission
 L. Monocytogenes is found in soil and water
 Normally orally through contaminated food
 Many animals carry the bacterium without symptoms

163
LISTERIOSIS CONT…
Neural
Listeriosis
Salivation
Droopy Ear
164
LISTERIOSIS CONT…
 L. monocytogenes has been associated with raw foods

Raw milk
Soft-ripened cheeses
Raw meats
Raw and smoked fish
Vegetables
 It can grow in cans and at temperatures as low as 3°C
 It is resistant to dehydration and temperature
 If acquired at birth, the incubation period is 7 to 28 days
 The average incubation period is 31 days; with a range from 11 to 47
days extremes
165
LISTERIOSIS CONT…
Pathogenesis
 An intracellular pathogen
 Phagocytosis by monocytes
 Lysis of phagosome
 Proliferation in the cytoplasm
Diagnosis
 Signs of fever, stiff neck and Irritability
 Culturing the organism from the blood, cerebrospinal fluid and stool
 Microroscopy
Gram positive bacilli

166
LISTERIOSIS CONT…
Treatment
Listeriosis is a serious disease requiring prompt treatment
A combination of antibiotics is given intravenously
Successful treatment has been achieved by parentral application of penicillin or ampicillin
When infection occurs during pregnancy, antibiotics must be given promptly to the mother
to prevent infection of the fetus or newborn
Newborns with Listeriosis receive the same antibiotics as adults
The duration of antibiotic treatment is at least 2 weeks
Even with prompt treatment, some infections result in death
Prevention
Thoroughly cook raw food from animal sources
167
LISTERIOSIS CONT…
Wash raw vegetables thoroughly before eating
Separate uncooked foods from cooked foods and ready-to-eat foods
Avoid unpasteurized milk or food
Wash hands, knives, and cutting boards with hot soapy water for at least 20 sec after handling
uncooked foods
Results with vaccines have been equivocal, which together with the sporadic nature of the
disease, lead to questions about the cost-benefit of vaccination
In an outbreak, affected animals should be segregated
If silage is being fed, use of the particular silage should be discontinued
Spoiled silage should be avoided
Corn ensiled before being too mature and grass silage containing additives are likely to have
a more acid pH, which discourages multiplication of L monocytogenes

168
MASTITIS
Mastitis is the inflammation of the udder
 Mastitis is physical, chemical and bacteriological changes in the milk, and
Pathological changes in the glandular tissues

There are two types of mastitis:
 Clinical mastitis: there are observable clinical signs – cardinal signs of
inflammation and changes in milk

Sub – clinical mastitis: there are no clinical signs
 Sub – clinical mastitis is said to exist when the following conditions are met:
Absence of signs of inflammation
No detectable changes in the colour, consistency and composition of milk
Increased somatic cell count
Increased PH
169
♦ The Somatic Cell Count (SCC) is a main indicator of milk quality. The majori
ty of somatic cells are leukocytes (white blood cells) - which become present
in increasing numbers in milk usually as an immune response to a mastitis-ca
using pathogen.
♦ The
SCC is quantified as the number of cells per ml of milk. In general terms:

♦ An individual cow SCC of 100,000 or less indicates an 'uninfected' cow, wher
e there are no significant production losses due to subclinical

mastitis
♦ A threshold SCC of 200,000 would determine whether a cow is infected with
mastitis. Cows with a result of greater than 200,000 are highly likely to be inf
ected on at least one
quarter 170
Etiology
Many infectious agents are implicated as causes of mastitis and are divide into:
1. Causes of contagious mastitis

Example: Streptococcus agalactiae, S. aureus
2. Causes of environmental mastitis
Example:. E. coli, Str. dysgalactiae, Str. uberis
 1 and 2 are also known as major pathogens
3. Normal teat flora

Example: S. hyicus, S . epidermidis, Corynebaterium bovis
These are also referred to as minor pathogens
171
Source of Infection
1. Contagious Mastitis
 Results when bacteria are transferred from infected gland to healthy one by:
Contaminated milking equipment
Nursing calves
The hand of dairy employees
Example: Str. agalactiae, S. aureus, Mycoplasma species

2. Environmental Mastitis
Results when bacteria with reservoirs of infection of the environment gain
entrance to the gland and causes the disease

Such category of mastitis occurs at an increasing rate when contagious mastitis is
brought under control

172
Thus clinical mastitis caused by environmental pathogens becomes most
prevalent in well-managed herds

Contaminated bedding, water, fecal material or fomites may harbor and nurture
bacterial populations causing disease if introduced in mammary gland

Example: E . coli, Klebsiella spp, Enterobacter species, Serratia, Pseudomonas
and Proteus species
Environmental Risk Factors
Season: Most cases in summer, especially if wet
Milking practices: Efficiency of milking personnel, milking machine and too high
milking speed
Management system: If hygiene & bedding are neglected in housed cattle
prevalence of environmental mastitis can be disastrous

173
Host Risk factors
Age: Incidence increases with age, peaking at 7 years
Stage of lactation: Most new cases in first 2 months
Milk yield: High yielding cows more susceptible
Breed: Incidence greater in Holstein Friesians
Skin lesions on teats
Other diseases: like retained fetal membrane (RFM) causes higher prevalence

Bacterial viability
Colonizing ability
Susceptibility to antibiotics
Seasonal prevalence of individual bacteria
174
Economic losses
Decreased milk production
Discarded milk
Treatment costs
Replacement of dead and nonproductive cows
Zoonotic potential
Mastitis contaminated milk can provide mechanism of spread of diseases to
humans TB, Brucellosis, Streptococcal sore throat

Clinical Findings
Include abnormalities of the milk, abnormalities of the glands and systemic
reactions
175
Clinical Forms of mastitis according to severity:
1. Peracute: Severe inflammation with swelling, heat and pain of quarter, and
marked systemic reactions
2. Acute: Severe inflammation without marked systemic reaction
3. Subacute: Mild inflammation with persistent abnormality of the milk

4. Chronic: Recurrent attacks of inflammation with little change in the milk
5. Subclinical: There is evidence of inflammation High somatic cell count
in milk, without any visible abnormality of the milk or udder
Abnormalities of the milk
Discoloration: may be in the form of blood staining or wateriness
Clots or flakes
176
Abnormalities of the udder
Abnormalities of size and consistency of quarters seen and felt
Palpation and inspection of udder revealed fibrosis, swelling and atrophy
Systemic reaction
A systemic reaction comprising toxemia, fever, tachycardia, ruminal stasis,
depression, anorexia and recumbency may or may not be present depending

on the type and severity of infection
Clinical Pathology and diagnosis

Bacteriological culturing of milk
Cell counts in milk - direct microscopic & SCC
The California Mastitis Test
177
Mastitis – Inflammation of the udder
178
Treatment
 Parenteral Treatment: This is advisable in all cases of mastitis in which there is
marked systemic reaction

To prevent or control development of septicemia or bacteremia
To assist in the treatment of infection in the gland
 Udder Infusions (IMI)
Are preferred methods because of convenience & efficiency
Strict hygiene is necessary to avoid introduction of bacteria, yeast and fungi into
treated quarters
Complete emptying of quarter before infusion is essential
After an intramammary infusion emptying the gland and thus losing of antibiotic
should be avoided as long as possible Treat immediately after milking
179
Intramammary infusion
Emptying the gland
180
Control of mastitis
Pre milking udder washing
Post milking teat dipping
Dry cow therapy (DCT)
Prompt treatment of clinical cases
Culling of chronic mastitic cows
Proper maintenance and use of milking machines
Clean, dry yards and calving sites
Clean, dry passage and proper ventilation
Tail clipping
Fly control
181
“Learn Today, Do Tomorrow”
THANK YOU ALL FOR YOUR ATTENTION!
182
RABIES
Rabies can be defined as an invariably fatal neurologic disease affecting most warm-blooded
animals
It is manifested by motor irritation with signs of mania and an attack complex, inability to
swallow and progressive paralysis beginning in the pelvic limbs, moving to the trunk and
thoracic limbs
Rabies is the oldest and most feared of animal & human diseases
Death is almost always inevitable once an animal or human shows clinical signs
According to a report by WHO in 1998, rabid dog bites were the sources for more than 33,000
human deaths each year worldwide
Etiology
Family: Rhabdoviridae; Genus: Lyssavirus
Disease Agent: Rabies virus

183
RABIES CONT…
The virus is truly neurotropic and one of the largest RNA viruses
The virus is relatively fragile and susceptible to most standard disinfectants
There are two types of rabies virus:
 Fixed viruses: Refer to laboratory strains of low virulence
 Street viruses: Refer to isolates of rabies virus from naturally infected field cases
Epidemiology
Rabies occurs in most countries of the world except Australia and New Zealand
which have never had the disease
Rabies does not presently occur in the Scandinavia, Great Britain, Ireland, Scotland
and the British Islands
184
RABIES CONT…
 All warm-blooded animals are susceptible to the disease and there is no
variation in susceptibility with age

 Variation in susceptibility between species is noticeable:
Foxes, cotton rats and coyotes are extremely susceptible
Cattle, rabbits and cats are highly susceptible
Dogs, sheep and goats are moderately susceptible
Transmission
 Source of infection for rabies is almost always an infected animal
 Method of spread is almost always by the bite of an infected animal
 Rarely contamination of skin wound by fresh saliva as well as ingestion of
virus (if the dose is large enough) can spread rabies

185
RABIES CONT…
 Traditionally the dog and, to a minor extent cat, are considered as the main source
animals
 Foxes, skunks, wolves, coyotes, vampire, insectivorous and fruit-eating bats may be
major source of infection
 Domestic livestock are rarely a source of infection for humans
 Spread of the disease is quite seasonal and the highest incidence is seen in late
summer and autumn, because of large scale movement of wild animals at mating time
and in pursuit of food
Zoonotic Implication
 Rabies is not of major economic importance in farm animals, although there may be
high fatalities in individual farms. The prime importance is its transmissibility to

humans, veterinarians being at special risk
186
RABIES CONT…
Pathogenesis
Infection of bite wound

Virus multiplies locally in myocytes for weeks or months

Virus travels up peripheral nerve to CNS

Virus multiplies in CNS Encephalitis

Virus moves out through the peripheral and cranial nerves

Salivary glands Skin Mucosal surfaces Gut Most other organs

Saliva is infective for several days/ up to 2weeks/ before clinical signs appears
Death
187
RABIES CONT…
Clinical Findings
 Destruction of the spinal neurons by rabies virus is responsible for the clinical
sign of paralysis seen in rabies

 When the virus invades the brain, there is irritation which produces manias,
excitement and convulsions

 The incubation period varies with:
 The amount of virus transmitted
 Virus strain
 Site of inoculation (bites closer to the head have a shorter incubation period)
 Host immunity
 Magnitude (severity) of the wound
188
RABIES CONT…
 The incubation period of rabies in cattle is about 3 weeks (vary from 2 weeks to
several months)
 Incubation period of 5 and 6 months are reported in cattle and dogs respectively
 Rabies can be divided into three forms, the initial (prodromal form), the paralytic
(dump) and the excitative (furious) forms

 Early signs of rabies are non-specific and include anorexia, depression, mild
ataxia and rise in body temp due to muscular activity. Following this early signs,
1.The initial (prodromal form): Clinical signs are often nonspecific and include:
 Apprehension, restlessness, anorexia or an increased appetite, vomiting, a slight
fever, dilation of the pupils, hyper reactivity to stimuli and excessive salivation
 Animals often have behavior and temperament changes, and may either become
unusually aggressive or uncharacteristically affectionate

189
RABIES CONT…
2. The paralytic (dumb) form: This form of rabies in cattle is characterized by
Swaying of the hindquarters while the animal walks
Flaccidity or deviation of the tail to one side
Decreased sensation
Drooling of saliva
Voiceless attempts to bellow
Tenesmus with paralysis of the anus
Bulls have paralysis of the penis
Then paralysis follows, animal goes down and unable to rise
Death 48 hours after recumbency and a total course of 6-7 days
190
RABIES CONT…
3. The excitative (furious) form
 The animal has tense, alert appearance
 Hypersensitive to sounds and movements
 Violently attack other animals or inanimate objects
 Loud bellowing with hoarse sound and actions are exaggerated
 Sexual excitement with bulls attempting to mount even inanimate objects
 Termination is characteristically sudden
 Severe signs may be evident for 24 – 48 hours, then the collapses
suddenly, dying within few hours

 The course vary from 1 to 6 days
191
RABIES CONT…
Diagnosis
Dogs or other animals, suspected of rabies because of abnormal behavior, should be
kept in isolation for 10 days
The animal is classified as non-rabid if it is alive after this period
The recommended laboratory procedures include the following three tests and it is
recommended to use two tests for all specimens
Fluorescent Antibody Test (FAT): The test is done on impression smears from the brain
Mice Inoculation: Negative specimen on FAT and still suspicious are inoculated into
experimental mice. Mouse brain is harvested as soon as signs appear and subjected to
FAT
Detection of Negribodies: It is histological detection of Negribodies in tissue section
192
RABIES CONT…
There many diseases that resemble rabies:
Lead poisoning in cattle
Lactation tetany
Avitaminosis A
Polyencephalomalasia in sheep and cattle
Listeriosis in sheep and cattle
Pregnancy toxemia in sheep
Treatment
 Treatment is not recommended after signs are evident
 Immediate and thorough washing of all wounds and scratches with soap and water is the
most important measure for preventing rabies in veterinarians and animals after exposure
193
RABIES CONT…
Control
 The major goal of rabies control in animals is reduction and or elimination of human
rabies
 The most rational approach for this is reducing the prevalence and incidence in animals
 In the developed countries this has been accomplished by vaccination of dogs and cats
 In farm animals there are two useful techniques for rabies control: prevention of
exposure and vaccination.
1. Prevention of exposure can be achieved by:
 Destruction of wild fauna
 Muzzling, restraint and vaccination of dog and cat
 Keeping animals indoors
2. Vaccination
194
FOOT AND MOUTH DISEASE
 FMD is an extremely contagious viral disease of all cloven-hooved animals
 It is characterized by fever and vesicular eruptions in the mouth, on the feet and
teats
Etiology
 Family of Picornaviridae
 Genus: Aphthovirus
 Species: FMD virus
 FMD virus has 7 serotypes namely A, O, C, SAT-1, SAT-2, SAT-3 and Asia-1
 There are a number of immunologically and serologically distinct subtypes
within each serotype

 So far about 80 subtypes have been identified
 There is no cross immunity between the serotypes

195
FOOT AND MOUTH DISEASE CONT…
Epidemiology
 FMD affects all cloven-hooved domestic and wild animals
 The disease is enzootic in Africa, Asia, South America and parts of Europe
 The disease is not reported in Japan, Australia and New Zealand
 A, C and O are prevalent in all continents where the disease occurs
 SAT-1 is found in Africa and Asia
 SAT-2 and SAT-3 are limited in Africa
 Asia-1 is found only in Asia
 Overall, types O and A occur more frequently than the others
 The morbidity rate in outbreaks can approach 100%
 Case fatality rate is usually very low 2% in adults and 20% in young animals
 Violent form in exotic animals may cause case fatality rate of up to 50% in adults
196
Methods of Transmission
 The disease spreads from one animal to another by inhalation and ingestion
 In the tropics the most important method of spread is by direct contact between
animals moving freely as trade or nomadic cattle

 Air-borne spread is common and the speed and direction of the wind are very
important factors
 In most favorable circumstances, infection can be wind-borne as far as 250 KM
 All secretions may be infective before the animal is clinically ill
 Vesicular fluid has maximum virus concentration
 Up to 50% of infected cattle, sheep and goats may become carriers but there is
no carrier state in pigs
197
FMD is spread from one herd to another either:
1. Directly
 By movement of infected animals
 Possibly by infected humans ???
2. Indirectly
 Inanimate objects
 Uncooked and unprocessed meat products
 Animal products other than meat
 Milk and milk products
Host Risk Factors
 FMD is most important in cattle and pigs
 Sheep and goats can also be affected

198
 Elephants, hedgehogs and wild ruminants are susceptible to FMD and act as reservoirs for
domestic animals
Environmental and Pathogen Factors
 FMD virus is resistant to common disinfectants
 The virus persists:
Over a year in infected premises
For 10-12 weeks on closings and feed
Up to a month on hair and in bull semen stored at -79oC
The virus is susceptible to:
Changes in pH away from neutral
Sunlight
Boiling
199
Economic Importance
 FMD is probably the world’s most important animal disease in economic losses
 Losses occur in many ways :
 Loss of production (meat and milk)
 Expense of eradication
 Interference with movement of livestock and meat between countries (trade barrier)
Zoonotic Implications
Humans are slightly susceptible to FMD. Vesicles may develop in the mouth and on
hands (only 40 human cases are reported)
Pathogenesis
Once infection gains access to the blood, virus is disseminated to many epidermal sites
carried by mononuclear cells

200
 But gross lesions develop only in the mouth and feet and to less extent, on the teats
 After the end of viremia, animal recovers but the virus may persist in pharyngeal area for
months or even years
 Bacterial complications aggravate lesions particularly of the feet and teats, leading to severe
lameness and mastitis
 In young animals the virus frequently causes necrotizing myositis
 Clinical Findings
 The incubation period is 3-6 days (vary from 1-7 days)
 Fall in milk yield and high fever (40-41oC)
 Severe dejection (sadness) and anorexia
 Acute painful stomatitis
 Abundant salivation - ropy
201
 Smacking of lips and animal chews carefully
 Vesicles appear on the bucal mucosa, dental pad and tongue
 Vesicles rupture in 24 hours leaving a raw of painful surface
 Concurrently with the oral lesions, vesicles appear on the feet in the clefts and coronet
 Rupture of vesicles causes acute discomfort and animal become grossly lame
 The animal is often recumbent with marked painful swelling of the coronet
 Bacterial complication interferes with healing and causes severe involvement of
deeper structures
 Vesicles on the teats cause severe mastitis
 Very rapid loss of condition and fall in milk yield
 Abortion and sterility
202
Diagnosis
 Tissue culture
 Complement fixation test (CFT)
 ELISA
 Guinea pig inoculation
 Large animal inoculation
 DNA probes
 PCR
Differential Diagnosis
 Vesicular stomatitis
 Vesicular exanthema
 Swine vesicular disease

203
Treatment
 Good nursing care
 Treatment with mild disinfectants and antimicrobial drugs
Control
 Rapid identification of outbreaks, quarantine and slaughter of all
affected and exposed animals are effective to prevent the disease

 Vaccination
 The vaccine must be type specific. Killed trivalent (O, A and C)
vaccines are in general use

 Immunity lasts only for 6-8 months
204
RINDERPEST
Rinderpest is an acute, highly contagious viral disease of ruminants and swine characterized by
high fever, necrotic stomatitis, diarrhea and high mortality
Etiology
Family: Paramyxoviridaehe ,Genus Morbillivirus and Species: RP virus
The virus occur as many strains with considerable variation in virulence
But all strains are immunologically identical
That means, vaccination for one strain confer protection against all other strains.
The virus is quite fragile
RP virus is antigenically related to:
 PPR virus in sheep and goats
 Canine distemper virus in dogs
 Measles virus in humans

205
RINDERPEST CONT…
Epidemiology
 Historically, rinderpest (cattle plague) has been among the most devastating of cattle
diseases
 Rinderpest still occurs enzootically in equatorial and north east Africa, in parts of the
Middle East and Asia
 All ruminants and pigs are susceptible to the disease
 Natural infection occurs commonly only in cattle and buffalo
 But in some outbreaks, sheep and goats do become infected
 Wildlife are often affected during outbreaks and infection spread to them from infected
cattle
 Commonly affected wildlife includes buffalo, bushbuck, waterbuck, warthogs, eland,
giraffe and kudu

206
RINDERPEST CONT…
Morbidity and Case Fatality
Morbidity rate often approaches 100%
Mortality rates range from 25-90%
Method of Transmission
Close contact between infected and non-infected animals is necessary for the spread, because
the virus does not survive long outside the host
All secretions and feces of infected animals are infectious throughout the course of the disease
Transmission occurs through contaminated feed or by inhalation of aerosol
Host Risk Factors
Cattle and buffalo of all ages are susceptible
Amongst races of cattle, European breeds are more susceptible than zebu cattle
207
RINDERPEST CONT…
Environmental and Pathogen Risk Factors
 The highest virus concentration is seen at the highest temperature reaction
 So the risk of transmission of the disease is greatest during the febrile stage
 The virus is very susceptible to external influence and does not persist outside the host body
for more than a few hours
 It is readily destroyed by heat, drying and most disinfectants
Pathogenesis
 The virus is inhaled in infected droplets, penetrates epithelium of the upper respiratory tract
and multiplies in the tonsils and regional lymph nodes
 Then it enters the blood in mononuclear cells and disseminated to other lymphoid organs, the
lungs and epithelial cells of mucous membranes
 RP virus has high degree of affinity for lymphoid tissue and alimentary mucosa
208
RINDERPEST CONT…
There is striking destruction of lymphocytes in tissues causing leucopenia
The focal, necrotic stomatitis and enteritis, which are characteristic of the disease, are
the direct result of viral infection and replication in epithelial cells in the alimentary tract
Death is usually from severe dehydration resulting from diarrhea
In less acute cases, death may be from activated latent parasitic or bacterial infections
which are exacerbated by immunosuppression as a result of destruction of lymphoid
organs by the virus
Clinical Findings
The incubation period of RP is 3 to 15 days
Sudden onset of fever, depression and anorexia
The nose is dry and mucous membranes congested
209
RINDERPEST CONT…
 Oral erosions where necrotic foci have sloughed
 Purulent lacrimation is a constant sign
 Diarrhea is severe and blood may be present
 Dehydration and emaciation lead to death
 Bovine virus diarrhea (BVD)
 Malignant catarrhal fever (MCF)
 Arsenic poisoning
 Coccidiosis
 Infectious bovine rhinotracheitis (IBR)
Diagnosis
Virus isolation
210
RINDERPEST CONT…
Detection of viral antigens by FAT or AGID
Detection of rising titers of antibody
Histopathologic (Necsopsy)evaluation
 Oral erosions with red floor
 Edema and congestion of abomasums
 Ulcers and hemorrhagic to necrotic Peyer’s patches
 Lymph nodes have necrotic germinal centers
 Carcass emaciated, dehydrated and soiled with fetid feces
 Zones of hemorrhage and erythema running transversely across the colonic
mucosa produces a characteristic striped appearance, the so called ‘zebra

stripes’
211
RINDERPEST CONT…
Prevention and Control
 Since there is only one known serotype and protection after infection
or vaccination is life-long, vaccination of cattle with a live cell culture

attenuated virus is an effective means of control of rinderpest
 Control of epidemics in areas where the disease is not endemic
involves:
Quarantine
 Slaughter of infected animals and contact animals
Disinfection of premises
212
PESTE DES PETITS RUMINANTS
PPR is an acute, highly contagious viral disease of shoats
It is characterized by fever, anorexia, stomatitis, diarrhea, oculonasal purulent discharge and
respiratory distress
Etiology
PPR is caused by a Morbillivirus in the family of Paramyxoviridae
The virus is related to rinderpest virus, canine distemper virus and measles virus
Epidemiology: The disease occurs in goats and less often in sheep
Morbidity and Case Fatality Rate
Infection rates in goats and sheep in enzootic areas are generally high (> 50%)
The disease is more severe in goats than in sheep
Is rapidly fatal in young animals
Case fatality rate much higher in goats (55-85%) than in sheep (less than 10%)
213
PESTE DES PETITS RUMINANTS CONT…
Methods of Transmission
 Close contact with infected animals or contaminated fomites
A fomite is any inanimate object or substance capable of carrying infectious organisms, such as

germs or parasites, and hence transferring them from one individual to another
 Large amounts of virus are present in all body secretions and excretions
 Infection occurs mainly by inhalation
 Infection could also occur through the conjunctiva and oral mucosa
Risk Factors
 Goats are more susceptible than sheep
 Kids over 4 months to under 1 year of age are most susceptible
 Risk of outbreak greatly increased when:
 A new stock is introduced
 Animals are returned unsold from markets 214

Pathogenesis
 Virus penetrates the retropharyngeal mucosa, sets up viremia and specifically damages
The respiratory
The alimentary and
Lymphoid systems
Infected cells undergo necrosis. In respiratory mucosa and lungs there is also
proliferation of cells
Virulent strains cause death from severe diarrhea and dehydration, particularly in
young goats
In others death is hastened by concurrent diseases such as pneumonic pasteurellosis
and coccidiosis
215
Clinical Findings
 Signs appear 3-6 days after contact with infected animal
 Severe respiratory distress is a common feature of PPR
 High fever (above 400c)
 Dullness, sneezing and serous discharge from eye & nose
 A day or two later, discrete necrotic lesions develop in mouth and extend over the
entire oral mucosa forming diphtheritic plagues

 There is profound halitosis and the animal is unable to eat
 Nasal and ocular discharges become mucopurulent
 Exudates dry up, matting the eyelids & partially occluding the external nares
 Diarrhea is profuse and may be mucoid or blood tinged
 Dyspnea and coughing occur later
216
Clinical Pathology and Diagnosis
Leucopenia occurs in association with destruction of lymphocytes
Hemoconcentration may be seen due to severe dehydration
Antibody detection tests are done on herd basis and include:
ELISA
Immuno-electrophoresis
Neutralization
Complement fixation tests
differential diagnosis of PPR are:

Heart water
Contagious ecthyma
217
Treatment
 Supportive Rx – Fluid therapy with antibiotics to prevent secondary
bacterial infection
Control
 The disease is effectively prevented by not introducing new stock from
unknown sources
 Animals returned from markets should be segregated
 The tissue culture rinderpest vaccine is effective for the control of PPR
 Kids and lambs should be vaccinated at 3-4 months of age

218

Opportunities to eradicate PPR
1. Thye virus has a single serotype

2. The virus doesn’t has reservoir host other than small ruminants
3. There is a live attenuated vaccine which gives lifelong immunity
4. The disease doesn’t result in carrier state
219
RIFT VALLEY FEVER
RVF is an acute, febrile disease of cattle, sheep and humans characterized:
In lambs and calves by hepatitis and high mortality
In adult sheep and cattle by abortion
In humans by an influenza-like disease
Etiology
Family: Bunyaviridae
Genus: Phlebovirus
 Species: arbovirus
Epidemiology
Generally found in eastern and southern Africa where sheep and cattle are raised
Source of Infection
 A pronounced viremia occurs in infected animal for about a week and facilitates spread by
biting insects
220
RIFT VALLEY FEVER CONT…
Aedes and culex mosquito
In humans infections are most likely to occur via skin abrasions in persons handling
infective materials
Environmental Risk Factors

Incidence varies with size of vector population and is greatest in heavy rainfall
Animal Factors
Cattle, sheep, camels, domestic buffalos, monkeys, human and rats are highly
susceptible
Goats moderately susceptible
Pigs, rabbits and poultry are not susceptible
Economic Importance: Abortion account for major economic loss

221
Pathogenesis
 The disease is an acute hepatic insufficiency in the form of focal necrosis caused by
destruction of liver cells by rapidly multiplying virus
Clinical Findings
 Incubation period of about 12 hours
 Sudden onset of high fever and incoordination
 Collapse and sudden death within 36 hours
 In adult sheep and cattle abortion is the outstanding sign
Clinical Pathology: Severe leucopenia is a common finding
Necropsy Findings
 Extensive hepatic necrosis is characteristic
 Venous congestion and petechiation in the heart

222
Diagnosis
Serum neutralization
ELISA
Hem agglutination
AGID
CFT
Bluetongue in sheep
Ephemeral fever in cattle
Enterotoxaemia
223
Control
Prevent introduction of RVF into free countries
Importation of all susceptible species from Africa should be prohibited
Importation of infective insects and infected biological should be prohibited
 A person's chances of becoming infected can be reduced by taking measures to decrease
contact with mosquitoes and other blood-sucking insects through the use of mosquito
repellents and bed-nets
In enzootic area control depends on the use of vaccines
 Both killed and live attenuated vaccines are available
 Attenuated virus vaccines are not recommended in pregnant ewes because the
vaccines are abortigenic, causing fetal death and some anomalies
 Attenuated vaccines provided good protection for cattle which lasts at least 28
months
224
BLUETONGUE
 Bluetongue is a disease of sheep and occasionally cattle
 The disease is characterized by catarrhal stomatitis , rhinitis, enteritis and lameness
Etiology:
 Family: Reoviridae
 Genus: Orbivirus
 Species: Bluetongue virus /BTV/
Epidemiology
 Bluetongue is transmitted mainly by culicoides
 BTV is found in Africa, the middle East, the Americas and Australia
 Distribution and intensity of infection is determined by the climate, geography and altitude as
they affect the occurrence and activity of the vector and by the presence of susceptible hosts as
well
225
BLUETONGUE CONT…
The disease is spread only by insect (culicoides) bites
 BTV has been found in semen of infected bulls and infection transmitted by
insemination from infected bulls

Economic Importance
 Adults either lose their fleece or develop a break in the staple of the fleece (wool)
 Pregnant ewes commonly abort
 Severe loss of condition and prolonged convalescence
 Costs to treat clinical diseases
 Reduced wool quality
 Suboptimal productions following infection
226
BLUETONGUE CONT…
Pathogenesis
Following infection, there is viremia detectable by day 3 and peak viremia,
associated with fever and leucopenia, 6-7 days after infection

With viremia there is localization of virus in vascular endothelium
Destruction of vessel walls leads to ischemic lesions in epithelium which are the
characteristic lesions of bluetongue

The virus penetrates placental barrier and congenital infection occurs readily
Clinical Findings
¨Incubation period is less than a week (2-4 days)
¨Severe febrile reaction with max temp 40.5 - 41 0C
¨Fever continues for 5 to 6 days
¨Nasal discharge and salivation with reddening of bucal and nasal mucosae
227
BLUETONGUE CONT…
 Saliva is frothy
 Swelling and edema of lips, gums, dental pad and tongue
 Excoriation of buccal mucosa and saliva becomes blood stained with offensive mouth
odor
 Necrotic ulcers develop on the lateral aspects of the tongue which may be swollen and
purple in color
 Respiration is obstructed, strenuous and increased in rate
 Diarrhea and dysentery may occur
 Foot lesions, including laminitis and coronitis - lameness and recumbency
 Marked rapid loss of condition
 Severe conjunctivitis with profuse lacrimation
 Death in most fatal cases occurs about 6 days after the appearance of signs
 A partial or complete loss of fleece is common and causes great financial loss
228
BLUETONGUE CONT…
Diagnosis
1. Virus isolation: commonly in cell culture, developing chick embryos or less
commonly by inoculation of blood into susceptible sheep
2. Detection of specific antibodies: Sera are usually tested with:

 Complement fixation
 AGID
 Competitive and blocking ELISAs
3. More rapid virus but specific BTV detection tests are being developed
including:
 In situ nucleic acid hybridization
 PCR
229
BLUETONGUE CONT…
 FMD
 Contagious ecthyma and ulcerative dermatosis
 Sheep pox
Control
 Prevent exposure to night flying insect vectors:
Spraying with repellents
Housing at night
Avoidance of low marshy areas
 Vaccination
Modified live vaccines are available and should be based on the local strains and
serotypes
230
LUMPY SKIN DISEASE
LSD is an acute to chronic viral disease of cattle that is characterized by skin
nodules
Etiology
Family: Poxviridae
Genus Capripoxvirus
Species: Neethling poxvirus
The virus is closely related anitgenically to sheep and goat pox viruses
Epidemiology
LSD used to be confined to sub- Saharan Africa
Morbidity rates reach 80% during epizootic
Mortality rates average 2%

231
LUMPY SKIN DISEASE CONT…
Transmission
Primarily by biting insects particularly mosquitoes (Culex and Aedes)
Flies ( Stomoxys, Biomyia, Culicoides, Glossina and Musca )
Epidemics During rainy seasons

Direct contact A minor source of infections.
Virus can be present in:
 Cutaneous lesions
 Saliva and Nasal discharge
 Milk and semen
Virus can survive in desiccated crusts for up to 35 days
No carrier state
Spread Often related to movement of cattle

232
Animal Risk Factors
All ages and types of cattle are susceptible to lumpy skin disease
Pathogen Risk Factors
Virus is resistant to environmental influence
Exotic breeds are much more susceptible than zebu types
Economic Importance:
Loss of production
Severe emaciation
Lowered milk production
Abortion
Loss of fertility
Damage to hides
233
Pathogenesis
After an initial viremia which is accompanied by febrile reaction, localization in the skin
occurs, with development of inflammatory nodules
Clinical Findings
Incubation period is 2 - 4 weeks
Fever lasting about a week, lacrimation, nasal discharge, salivation and lameness
Multiple nodules appear suddenly a week later
Nodules are round and firm, and vary from 1 to 4 cm in diameter
Nodules vary in number from a few to hundreds
Nodules are intradermal and, in most cases confined to the skin area
Nodules on the conjunctiva causing severe lacrimation
Pneumonia is common where lesions occur in respiratory tract 234

Diagnosis
Clinical: LSD suspected with a contagious disease with:
Characteristic skin nodules
Fever
 Emaciation
Lacrimation
Laboratory tests
Direct immunofluorescent staining
Virus neutralization
ELISA
Cross reactions may occur with other poxviruses
235
Treatment
 The use of antibiotics or sulfonamides is recommended to prevent secondary
infection
Control
 Control of cattle movement from infected to uninfected territory is an
important measure
 Vaccination
 The vaccine is administered to all animals over 6 month’s age
A freeze- dried, living attenuated vaccine
236
SHEEP POX AND GOAT POX
In sheep pox
 Typical pox lesions occur particularly under the tail
 A malignant form with a general distribution of lesions occurs in lambs
Goat pox virus causes a similar disease in sheep and goats
Etiology: Three viruses have to be taken into account:
SPV, the causative capripoxvirus (Family poxviridae) affects only sheep
SGPV, a highly contagious pox, is infectious to goats and sheep, antigenically distinct from
SPV. Both SPV and SGPV are capripoxviruses
KSGPV, identified in Kenya infects sheep and goats, is genomically identical to LSD virus
Epidemiology
Sheep pox is restricted in its distribution to the Middle Eastern countries
237
SHEEP POX AND GOAT POX CONT…
 Sheep pox is the most serious of all the pox diseases often causing death in 5%
of those affected
Transmission
 Contact with infected animals and contaminated articles
 Spread by inhalation also occurs
Animal Risk Factors

 The goat pox virus affords solid protection in sheep against both goat pox and
sheep pox
 But sheep pox vaccine does not protect goats against goat pox
 Imported breeds may show greater susceptibility than the native stock to sheep
pox
238
Importance
 In ewes severe losses may occur if the udder is invaded because of secondary
occurrence of acute mastitis

 The mortality rate in adults is low usually about 5%
 Sheep pox is a potent threat to countries such as Australia which have big sheep
population and where the disease does not occur

Pathogenesis
 During an initial viremia, the virus is deposited in most tissues including the skin
 The development of pox lesions is characteristic of the disease
 Virus is present in greatest quantities between the 7 th and 14th day after inoculation
 Skin lesions typically begin with small red spots followed by papules
239
Exudates causes these papules to become vesicles
Pus forms in the vesicles so that they become pustules
These pustules either: Burst or Become desiccated
The larger ones may leave a pocket mark which can be a deep lesion with permanent
scarring
Clinical Findings
1. Sheep pox in sheep
Incubation period ranges from 2 to 14 days
The disease can occur in two forms: malignant and benign
A.The malignant form: Is the more common type in lambs & is characterized by:
Marked depression and prostration
A high fever and discharges from the eye and nose

240
Sheep and Goat Pox Crusty pox lesions on tail

241
 Affected lambs may die during this stage before typical pox lesions develop
 The lesions commence as papules, then nodular, vesicular, pustular and finally
scabs
 Skin lesions seen on unwooled skin (under tail & lips) and on the bucal,
respiratory, digestive and urogenital tract mucosae

 In peracute case mortally may be as high as 80%. But the mortality rate is
usually about 50%

 The benign form: Common in adults:
 Only skin lesions occur, particularly under the tail
 There is no systemic reaction
 Skin lesions in sheep may cause intense irritation and or pain leading to self
mutilation
242
2. Goat pox in sheep is more severe than sheep pox in sheep and lesions occur:
On the lips and oral mucosae
On the teats and udder
3. Goat pox in goats
It is very similar clinically to sheep pox in sheep
Morbidity of 90% and mortality of 4% occur in susceptible goat flocks
Young kinds suffer from systemic disease
In adult goats the disease in mild
Diagnosis
Lesions are characteristic of pox disease
Direct fluorescent antibody test
Virus can be cultured in tissue cultures
243
Indirect FAT
Immunodiffusion technique
Bluetongue
Contagious ecthyma (orf)
Necropsy Findings: In the malignant form, pox lesions extend in to:
The mouth and pharynx
Larynx and vagina
Lesions appear also in the trachea with catarrhal pneumonia
Occasionally reach the abomasums and intestine and are accompanied by hemorrhagic enteritis
White nodules may be found in many organs
244
Control
In free areas
Prohibition of importation of animals from infected areas
If infection is introduced:
Destruction of affected flocks
Quarantine of affected premises
In enzootic areas:
Vaccination is the basis for control
A large variety of commercial vaccines are available. Most of them appear to give
excellent protection for periods greater than 1year
245
CONTAGIOUS ECTHYMA
 Synonyms: Orf, Sore Mouth
 Contagious ecthyma is a zoonotic disease
 It induces acute pustular lesions in the skin of goats, sheep and wild
ruminants worldwide
 Young animals are the most susceptible to contracting the disease
 Kids and lambs can contract sore mouth after a few weeks of birth
 However, sore mouth outbreaks in young animals are most frequent during
post weaning
 Etiology
 Sore mouth is caused by a pox virus (a parapoxvirus)
 The virus is epitheliotropic, which means that it has an affinity for the skin
246
CONTAGIOUS ECTHYMA CONT…
Epidemiology
 Outbreaks occur more frequently during periods of extreme temperatures such as late
summer and winter
Clinical findings
 Susceptible animals usually develop the first signs of the disease 4 to 7 days after
exposure that persists for 1 to 2 weeks or for longer periods
 The disease initially presents itself as papules (elevation of the skin) that progresses to
blisters (fluid-filled pouches) or pustules before encrusting
 These lesions are found in the skin of the lips
 They can spread around the outside and inside of the mouth, face, lips, ears, vulva,
lets, scrotum, teats, and feet, usually in the interdigital region
 Extensive lesions on the feet can lead to lameness in adults and young animals
247
 During the course of the disease, blisters eventually break down to release more of
the virus and later develop into wet pus-like (suppurative) scabs
 These lesions can persist for 3 weeks and can become a site for the development of
secondary bacterial infections
 Scab tissues are extremely painful, to the point of preventing sick animals from eating
 Because infected kids present lesions on their gums and lips, does and ewes can
acquire lesions on their udder
 The lesions on the udder are due to direct contamination during nursing that causes
mastitis (inflammation of the mammary gland) in does and ewes
 Severe to moderate enlargement of the lymph nodes, arthritis, and pneumonia
resulting from sore mouth has been reported

248
Orf lesion
249
Transmission
The infection is spread by direct and indirect contact from infected animals or by contact
with infected tissue or saliva containing the virus
Diagnosis
Diagnosis is based on the characteristics and location of the lesions, as well as a herd history
of previous outbreaks
A definitive diagnosis is based on viral isolation and an immunologic test
Treatment
Lesions can be treated with a single application of 3 percent iodine solution
In severe cases of secondary bacterial infection, the usage of a systemic antibiotic is
recommended
For infected kids, be sure they are fed artificially

250
 Treat the lesions on the teats (nipples) of the does and ewes to prevent the
development of mastitis
 Minimize transportation stress
 Always quarantine new animals before introducing them to the rest of the herd
 In case of an outbreak, separate sick animals in a pen for treatment
 Always feed and treat sick animals after feeding the herd
 Incinerate gloves and all tissues that come in contact with lesions extracted from
sick animals
 The virus can persist in animal tissue for a long period of time, becoming a
source of contamination
251
 Always wear gloves when handling sick animals and vaccines as humans can
contract the disease

 Avoid the consumption of milk from does and ewes that present lesions on the
teats and udder

 A systematic vaccination of the entire herd is recommended only during
outbreaks
 There are two vaccines available for use
 The vaccines are modified versions of live viruses and are administered topically
 A small dose of the vaccine is brushed over light scarifications of the skin on the
inside of the thigh

 In flocks where there is a prevalence of the disease, lambs should be vaccinated
at the age of 1 month with a booster 2 to 3 months later

252
EPIZOOTIC LYMPHANGITIS
 Epizootic lymphangitis is an economically important disease in some areas of the
world, particularly where large numbers of horses, donkeys, or mules are

assembled
Etiology
 A dimorphic fungus, Histoplasma capsulatum var. farciminosum. This organism
has also been known as Histoplasma farciminosum

 H. capsulatum var. farciminosum exists as yeast in tissues and a mycelium in the
environment
Species Affected
 Epizootic lymphangitis mainly affects horses, donkeys, and mules. Infections
have also been reported in camels, cattle, and laboratory animals such as mice
and rabbits.
253
EPIZOOTIC LYMPHANGITIS CONT…
Geographic Distribution
Epizootic lymphangitis is endemic in the Middle East, India, the Far East, and parts of
Africa. In Africa, infections are most common in the north, but have also been seen in other
parts of the continent
 Sporadic cases have also been reported from other parts of the world
Transmission
The skin form results from wound contamination by organisms in the soil
Flies in the genera Musca and Stomoxys are thought to spread the conjunctival form
Flies may also spread the skin form by feeding on infected open wounds
The pulmonary form, which is rare, probably develops when an animal inhales the organism
spread is possible via fomites such as grooming or harness equipment
254
Clinical Findings
The incubation period is usually several weeks
Lesions are common on the skin and lymphatics, particularly on the extremities,
chest wall, face and neck

The first symptom is a painless, freely moveable, intradermal nodule,
approximately 2 cm in diameter
This nodule enlarges and eventually bursts
More often, the skin ulcers grow, with cycles of granulation, partial healing, and
renewed eruptions
The surrounding skin becomes hard, variably painful, and swollen
The infection also spreads along the lymphatics, causing cordlike thickening of
the lymphatic vessel and further skin involvement

255
Epizootic lymphangitis
Epizootic-lymphangitis.epizootic-lymph
256
These cycles of eruption and granulation gradually resolve, leaving only a scar
Sometimes spreads to the underlying joints and results in severe arthritis
Occasionally, conjunctivitis, keratoconjunctivitis, a serous or purulent nasal discharge, or
pneumonia may also be seen
The lymph nodes may be enlarged, but fever is uncommon
Diagnosis
Epizootic lymphangitis should be suspected in Equidae with skin nodules or ulcers and
cycles of granulation, partial healing and renewed eruptions
Diagnosed by detecting H. capsulatum var. farciminosum in tissue sections or smears of
lesions
On a Gram stained slide, the organism is a Gram positive, approximately 2– 5 cm diameter,
pleomorphic, ovoid to globose structure

257
Organisms can also be detected in haematoxylin and eosin stained tissue samples
H. capsulatum var. farciminosum can be cultured from lesions
Mycobiotic agar is the recommended medium; other media that may be used
include Sabaraud’s dextrose agar enriched with 2.5% glycerol, brain heart
infusion agar with 10% horse blood
Mycelial colonies develop in approximately 2–8 weeks at 26°C
The colonies are dry, granular, wrinkled, and yellow to dark brown. Aerial forms
are rare
Antibodies have been detected by indirect and direct FAT, ELISA,
hemagglutination, and skin hypersensitivity tests
Inoculation of samples into immunosuppressed mice can also be used for
diagnosis
258
 Glanders, strangles, ulcerative lymphangitis and sporotrichosis
Public health
 Rare cases of human infections have been reported
Treatment
 NaI, KI and surgical excision combined with antifungal drugs
Prevention
 Both killed and live attenuated vaccines have been tried in some endemic areas
 Strict hygienic precautions are necessary to prevent the spread of this disease
 In endemic areas, care should be taken to prevent spread the organism on grooming equipment
or harnesses, and bedding should be burned
 In non–endemic areas, affected animals must be destroyed

259
DERMATOPHYTOSIS
 Synonyms: Ring worm
 Is a superficial fungal infection of the skin, hair or nails characterized by redness of the
skin, small papular vesicles, fissures and scaling
Etiology
 The infection is generally limited to the top layer of skin
 Dermatophytosis is an infection of keratinized tissue (skin, hair, and claws) by one of the 3
genera of fungi collectively called dermatophytes— Epidermophyton, Microsporum
and Trichophyton
 Dermatophytes, are the pathogenic members of the keratinophilic (keratin digesting) soil
fungi
 Microsporum and Trichophyton are human and animal pathogens
 Epidermophyton is a human pathogen
260
DERMATOPHYTOSIS CONT…
Dermatophytoses are referred to as ringworm as a result of its classic circular, scaly
patches (ring) that resemble a worm lying below the skin surface (worm)
The fungi feed on dead skin and hair cells causing a round, red lesion with a ring of
scale around the edges and normal skin in the center
Epidemiology
These pathogenic fungi are found worldwide, and all domestic animals are susceptible
Dermatophytes grow best in warm and humid environments and are, therefore, more
common in tropical and subtropical regions
Transmission
Direct or airborne contact with symptomatic or asymptomatic host hairs or skin scales
Fomites such as brushes and clippers can be important in transmission
261
Clinical Signs
 The incubation period is 1 to 2 weeks
 Grow only in keratinized tissues such as hair, nails and the outer layer of skin
 The fungus usually stops spreading where it contacts living cells
 Mucus membranes are not affected
 Pruritus is the most common symptom
 The skin lesions are usually characterized by inflammation that is most severe at
the edges, with erythema, scaling and occasionally blister formation

 Central clearing is sometimes seen, particularly in tinea corporis; this results in
the formation of a classic “ringworm” lesion.

 On the scalp and facial hair, there may be hair loss
262
multiple lesions of dermatophilosis, head
263
Diagnosis
 Clinical signs are characteristic of the disease
 Wood's Lamp can be used to shine UV light onto the lesion and it will fluoresce
in 50% of cases
 Light microscopy: a scraping or swab of the affected area is placed on
a microscope slide. A single drop of 10% KOH solution is then added to the

specimen. The KOH dissolves the skin cells but leaves the dermatophyte cells
intact, permitting visualization of cells of many dermatophyte
 Fungal cultures: Sabouraud's Dextrose agar can be used to culture the
dermatophyte at room temperature for a month

 A biopsy can also be taken and examined histologically
 Signs will include epidermal hyperplasia and inflammation

264
Treatment:
Antifungal
 Drugs (Griseofulvin, Fluconazole, Amphotericin B Injection, Itraconazole)
Wash
 the patch daily with soap and water and use the medication as directed
Control and prevention:
The
 affected animal should be isolated and hair should be clipped around the lesions
Infected
 animals should be treated and the premises and fomites should be disinfected
Gloves and
 protective clothing should be used during contact, with infected animals
Do
 not share harness, combs, brushes, hats, scarves, towels, socks or shoes
Wear
 shoes in public places
Wear
 shoes or flip-flops at gyms, locker rooms, and pools
Keep
 your skin and feet dry and clean
Avoid
 touching pets with bald spots
265
KETOSIS
 Synonyms: Acetonemia of cattle and Pregnancy toxemia of sheep
 Ketosis is due to increased hepatic utilization of fatty acids
 Biochemically ketosis is characterized by:
Ketonemia and ketonuria
Hypoglycemia
Low levels of hepatic glycogen
Etiology
 Maintenance of adequate concentrations of glucose in the blood is the prime function
of the mechanisms involved in the regulation of energy metabolism
 Ruminant absorbs very little dietary carbohydrates as hexose sugars because they are
fermented in the rumen to short chain fatty acids: acetate (70%), propionate (20%)
and butyrate (10%) 266
KETOSIS CONT…
 Consequently glucose needs in ruminants are met by gluconeogenesis
 Ketosis is caused by the cows’ demands for carbohydrate exceeding that of
available from the feed

 Factors that decrease energy supply to ruminants increase the
demand for glucose increase utilization of body fat as an energy
source increase ketone production and ketonemia
 Whenever the glucose level in the blood plasma is low as in starvation or on a
low carbohydrate diet or when glucose is not utilizable as in diabetes, the

concentration of free fatty acids in plasma rises
 Ketosis is common in heavily producing cows in post calving periods,
because high-yielding cows in early lactation are in negative energy balance
267
KETOSIS CONT…
The following types of ketosis are recognized in cattle:
1. Alimentary ketosis: Excessive amounts of butyrate in silage reduced food intake because
of poor palatability
2. Starvation ketosis: Occurs in cattle in poor body condition and fed poor quality foodstuffs.
This in turn leads to deficiency of propionate and protein
3. Primary (Production ) ketosis: Occurs in cows with good body condition and that have
high lactation potential and fed with good quality ration. High body condition and high
dietary protein may lead to excessive lipid mobilization. High protein diets mean greater
butyric acid production in the rumen
4. Secondary ketosis: Diseases cause decreased food intake: abomasal displacement,
traumatic reticulitis, metritis and fluorosis
5. Ketosis due to specific nutritional deficiencies: Deficiency of cobalt and phosphorus

268
KETOSIS CONT…
Ovine ketosis
 The most important etiological factor in pregnancy toxemia in sheep is a decline in
plane of nutrition during the last 2 months of pregnancy (particularly ewes carrying
twins)
 The disease in sheep can be divided as to the cause as follows:
1. Primary pregnancy toxemia: This is the most common manifestation and results in
most flocks from a combination of:
 A fall in plane of nutrition in later half of pregnancy
 Management procedure in late pregnancy such as shearing, drenching and docking
 Cold inclement weather and absence of shelter
 When ewes are bred too early and pasture is not sufficient
 Stress such as transport in late pregnancy and change in environment
269
KETOSIS CONT…
2. Fat ewe pregnancy toxemia

Occurs without a stress induction in ewes that are very well fed and in over fat
condition in late pregnancy

Fat ewes experience voluntary fall in food intake in late pregnancy due to
reduction of rumen volume by the pressure of intra-abdominal fat and

developing fetus
3. Starvation pregnancy toxemia

Occurs in excessively thin ewes and it is relatively uncommon
4. Secondary pregnancy toxemia

 Occurs as a sporadic disease as a result of intercurrent diseases such as foot rot
and heavy worm infestation, Haemonchus conturtus Affect feed intake
270
KETOSIS CONT…
Economic importance
Loss of production while the disease is present
Failure to return to full production after recovery
Pathogenesis
The principal metabolic disturbances observed, hypoglycemia with low level of hepatic
glycogen and ketonemia may both exert an effect on the clinical syndrome
In many cases severity of clinical syndrome is proportional to the degree of
hypoglycemia and ketonemia, and this together with rapid response to glucose treatment
in cattle, suggests that hypoglycemia is the predominant factor
Nervous signs in some cases of bovine ketosis are thought to be caused by
 Production of isopropyl alcohol (a product of aceto-acetic acid in rumen)
 A requirement of nervous tissues for glucose is also a factor

271
KETOSIS CONT…
Clinical Findings: Two forms of the disease are described in bovine
1. The wasting type: This is the more common of the two
 decrease in appetite and milk yield over 2 – 4 days
 The cow first refuses to eat grain, then silage but may continue to eat hay
 Appetite may be depraved and body weight is lost rapidly
 Feces are firm and dry
 Moderate depression and disinclined to move
 Temperature, pulse and respiratory rates are normal
 There is a characteristic odor of ketones in the breath and milk
 Milk yield falls and never fully regained and the loss may be as high as 25%

272
KETOSIS CONT…
2. The nervous type: Signs are bizarre and begin suddenly and include:
Walking in circles, straddling or crossing of legs
Head pushing and apparent blindness
Vigorous licking of skin and in animate object
Depraved appetite and chewing movements with salivation
Clinical pathology and diagnosis

Hypoglycemia (Blood glucose level reduced)
Ketonemia and ketonuria
Increased plasma free fatty acid
Levels of 80-1300 mg/dl of ketones in urine indicates ketosis
Changes in leukocyte count eosinophilia & lymphocytosis
273
KETOSIS CONT…
Treatment
1. Dietary correction: The only rational treatment for ketosis is:
To relieve the need for glucose formation from tissues
Allow ketone body utilization to continue normally
2. Replacement therapy
In injection of 500ml of a 50% solution of glucose (dextrose) effects marked improvement but
relapses commonly occur unless repeated treatments are used
Propylene glycol or glycerin can be administered as a drench or they or salts of propionic acid
in feed given excellent results and overcome repeated IV injections
3. Hormonal therapy
Glucocorticoids dexamethasone
Vitamin B12 and cobalt

274
KETOSIS CONT…
Control
Keep cows neither starved nor over fat at calving
Cows that are housed should receive exercise daily
Ration should contains adequate cobalt, phosphorus and iodine
Ground maize has a particular quality in providing readily available glucose
in a ration and is a logical preventive feed

Control of clinical ketosis is integrally related to adequate nutrition of cows in
the dry and lactating periods
275
 Synonyms: Milk Fever, Hypocalcemia
 Parturient paresis is an acute- to - peracute flaccid paralysis and/or somnolence
of lactating dairy cows/sheep

 Usually occurs within 72 hours of parturition and late pregnancy
 Is seen most often in high producing cows/sheep
 It should be considered as an emergency and prompt therapy with calcium
solutions is required
Etiology
 Hypocalcemia occurs when rapid onset of milk production results in acute
depletion of serum calcium

 Hypocalcemic paresis are ultimately fatal unless treatment is instituted
276
Epidemiology
 Parturient paresis is a disease of high producing dairy cattle
 About 5% to10% of adult dairy cows are affected
 Jersey cattle are most susceptible and have much higher incidence
 This may be associated with higher milk production per unit body weight
 Most cases of parturient paresis occur within first 48 hours after calving
 Heifers are very seldom affected; there is gradual increase in incidence with
parity
 Most cases of parturient paresis occur in animals older than 5 year age
 It is uncommon in beef cattle
277
Pathogenesis
 Onset of lactation at parturition results in a sudden loss of calcium in milk
 Several times the amount of calcium present in the entire plasma pool may be lost in
initial production of colostrums
 When calcium homeostatic mechanism is unable to meet this demand then
hypocalcemia occurs
 During dry period, calcium demand is relatively low. Therefore intestinal absorption
and bone resorption of calcium is relatively inactive
 Some degree of hypocalcaemia occurs in nearly all cows at the onset of lactation
 Approximately 24 hours of elevated vitamin D stimulation is required to improve
intestinal transport of calcium

278
 An increased rate of bone resorption requires 48 hours of parathyroid hormone
(PTH) stimulation
 If these adaptations to calcium demand are prolonged clinical hypocalcemia may
develop
Hypocalcemia affects muscular contraction in different ways:

1. Ca++ has membrane stabilization effect on peripheral nerves. So hypocalcemia results
in lack of membrane stabilization hyperesthesia and tetany
2. Ca++ is required for release of acetylcholine at neuromuscular junction. So

hypocalcemia results in inability to release acetylcholine blocking of nerve
impulse transmission paralysis
3. Ca++ is directly required by muscle cells for contraction
279
So hypocalcemia results in paralysis of various muscle types:
Paralysis of skeletal muscles Recumbency

Lack of smooth muscle tone GI stasis and bloat
Decreased contractility of cardiac muscle and lowered stroke volume
Poor peripheral perfusion and inability to shiver or generate heat by muscular
activity lead to hypothermia and depression of consciousness

Clinical Findings: There are three discernible clinical stages
1. Stage one
The animal is still able to stand but shows signs of hypersensitivity and excitability
Head bobbing, ear twitching and fine tremors over the flank
When standing appear restless and shuffle hind feet
Bellowing, open mouth breathing & protrusion of tongues
280
2. Stage two
 The cow is unable to stand but able to be in sternal recumbency
 Depression, anorexia and dry muzzle
 Subnormal body temperature with cold extremities
 Tachycardia with decreased intensity of heart sounds
 Arrested parturition and retained fetal membranes due to uterine inertia
Absence of effective uterine contractions during labor

 Sternal recumbency with head turned into the flank is a characteristic posture
3. Stage three
 Continued loss of consciousness to the point of coma
 Animals have complete muscle flaccidity
 Unresponsive to stimuli and unable to maintain sternal recumbency with severe bloat
 Cardiac output worsen, pulse undetectable & high heart rate (120 beats/minute)
281
Milk fever or parturient paresisis a disease that infects hypocalcemia dairy
282
Clinical pathology and diagnosis
 Diagnosis are usually based on clinical signs
 Pretreatment blood samples should be taken so diagnosis can be confirmed with
serum Ca++ levels

Differential diagnosis for recumbency in postpartum cow includes:
 Toxic mastitis, toxic metritis and traumatic injury
 Toxic conditions cause a similar depression of consciousness and are the most
difficult to distinguish from hypocalcemia

Treatment
 Intravenous injection of calcium borogluconate salt.
 A rule of thumb for Ca++ administration is 1 gram of Ca++ per 45 kg body weight
 Most solutions are available as a single dose 500ml bottles (to 11 gram of Ca ++ )
283
 Calcium is directly cardio toxic and any Ca++ containing solution should be
administered slowly (over 10 to 30 minutes) with continuous cardiac auscultation

 If severe dysrhythmias or bradycardia develops administration should be stopped
 Administration is resumed slowly when the heart beat has returned normal
 Oral Ca++ administration avoids risks of cardio toxic side effects and can be used in
mild cases of disease

Hypocalcemic cows show immediate characteristic signs of response to therapy:
 As neuromuscular function returns tremors begin in muscle of flank and spread to
entire body
 Improved cardiac function Stronger heart sounds and decreasing pulse rate
 Return of smooth muscles function Eructation and defecation
 Muzzle Full of individual droplets of sweat
284
 The use of dietary cation-anion difference has revolutionized the prevention of
parturient paresis
 Cation have a positive charge & anions have a negative charge
 The key to this method is providing an excess of anions over cations in the diet
by adjusting the diet, adding of anionic salts (of sulfate or chloride) or

combination of both
 Anionic salts that can be added include magnesium sulfate, calcium sulfate,
ammonium sulfate etc.

 Feeding anionic salts not only prevented milk fever but also have been shown to
increase lactation and reproductive efficiency

 One drawback of this method is poor palatability
285

Large A.medicine 4th Year

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JIMMA UNIVERSITY

COLLEGE OF AGRICULTURE AND VETRINARY MEDICINE

Large Animal Medicine (CLIS - 301)

Instructor: Mekonnen Addis (DVM, MSc, Associate professor)

death, accompanied by exudation of tarry blood from the body orifices

are the most important necropsy findings

 Bacillus anthracis produces three types of toxins

 Factor-II – Denotes protecting antigen

 Factor-III – Denotes lethal factor

 Susceptibility is highest among ruminants, followed by horses and swine

lungs (inhalation) or skin (cutaneous)

infected soil, contaminated bone meal or protein concentrates, infected

and by flooding and deposition of anthrax-infected soil

 Environmental persistence may involve a number of factors, including high levels of

Defects in epithelium around erupting teeth

Scratches from tough, fibrous food materials

probably 1-2 weeks

A. Per acute form:

Animals are usually found dead without signs

The course of the disease is probably 1-2 hours

Fever, muscle tremor, dyspnea and congestion may be observed

vulva are common

High body temperature, up to 42oC

Respiration is rapid and deep

Heart rate much increased

Anorexia and ruminal stasis

Pregnant animals may abort

Diarrhea and dysentery are common

There is local edema of the tongue

Edematous lesions in the throat, sternum, perineum and flanks

The dead body assumes characteristic ‘sawhorse’ attitude

Bloating and putrefaction are rapid

Peripheral blood or local edema fluid is collected by needle puncture and

inoculated in to guinea pigs or mice – Death

 Lightening strike - evidenced by singeing of hair and history of electrical

Acute blackleg – confined to young animals and crepitating swelling

Other clostridial infections

Acute Leptospirosis – sporadic, hemoglobinuria

Peracute lead poisoning – accompanied by nervous signs

Hypomagnesemic tetany - accompanied by nervous signs

Animals dying of acute bloat – show gaseous distention and exudation of

blood from the orifices as in anthrax.

 Penicillin (10,000 units/kg body weight twice daily)

 Streptomycin (8-10 g/day in two doses IM for cattle)

 Oxytetracycline (5mg/kg body weight per day)

It is desirable to prolong the treatment to at least 5 days to avoid a recrudescence

 Placing of the farm in quarantine

 Infected carcasses, beddings, and soil contaminated by discharges should be

 Immunization with live attenuated strains vaccine

 Blackleg, the clostridial myositis of skeletal muscles characterized by:

Inflammation of skeletal and cardiac muscles

Etiology: Cl. Chauvoei (gram-positive, spore-forming, rod-shaped)

It is enzootic in areas subjected to flooding

The case fatality rate approaches 100%

Blackleg is a soil-borne infection

 Portal of entry is through alimentary mucosa after ingestion of contaminated feed

 Contamination of soil and pasture occur from infected feces or decomposition of

caused to proliferate by mechanisms such as trauma or anoxia

 In sheep the disease is almost always wound infection

cause local lesions

following excavation of soil

Disturbance in soil may expose and activate latent spores