Actinobacillosis (Wooden Tongue)

I. Definition
➢ Inflammation of soft tissue of head specially tongues.
➢ It is a chronic infectious disease of ruminants, caused by actinobacillus ligniersi,
characterized by inflammation of soft tissue of the head especially tongue (localized
firm swelling of dorsum), less commonly pharyngeal lymph nodes, facial skin, nares
and esophageal groove. It is sporadic and self-limiting disease.
II. Etiology
➢ Actinobacillus ligniersi (normal commensal organism in the oral flora of the cattle),
Gram negative coccobacilli or pleomorphic rods, grow on blood and serum
containing media.
III. Epidemiology
1. Distribution:
➢ The disease in cattle is worldwide in distribution and usually of sporadic reported in
Egypt.
2. Animal susceptibility:
➢ Cattle, buffaloes (mature and of dairy breed are more susceptible).
3. Mode of infection:
➢ Source of infection: Pus or infected discharges are the main source of infection.
4. Mode of transmission:
➢ The disease is transmitted by ingestion of contaminated food and water with the
presence of oral mucosa injury (wounds or abrasions).
IV. Pathogenesis:
➢ Local infection by the organism causes an acute inflammatory reaction in the tongue
and development of granulomatous lesions in which necrosis and suppuration occur,
often with the discharge of pus to the exterior. Spread to regional lymph nodes is
usual.
➢ Lingual involvement in cattle causes interference with prehension and mastication
due to acute inflammation in the early stages and distortion of the tongue at a later
stage.
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V. Clinical signs
➢ In cattle, actinobacillosis mainly affects the tongue (‘wooden tongue’), the lymph
nodes of the head and neck. The characteristic lesion is a granuloma of the tongue,
with discharge of pus to the exterior. Infection usually begins as an acute
inflammation with sudden onset of: inability to eat or drink for several days
➢ Drooling saliva
➢ Rapid loss of condition
➢ Painful and swollen tongue
➢ Nodules and ulcers on the tongue.
➢ Animals may occasionally die from starvation and thirst in the acute stages of the
disease. As the infection becomes chronic, fibrous tissue is deposited and the tongue
becomes shrunken and immobile and eating is difficult.
VI. Diagnosis
➢ Field diagnosis: It depends on clinical signs of disease as fever, tongue protrusion,
salivation and history of feeding on hard food objects beside the epidemiology of the
disease.
➢ Laboratory diagnosis:
A) Samples: Pus, smear or biopsy from the lesion, parts of lesion on ice or formalin,
blood and serum.
B) Laboratory procedures:
➢ Direct examination of stained smears after staining with Gram stain.
➢ Culture of the suspected material on blood agar.
➢ Histopathological findings.
➢ Serological diagnosis.
VII. Treatment
➢ Treatment can involve surgical debridement and flushing with iodine.
Administration of potassium iodide orally (6 to 10 g a day for 10 days) or
intravenous injection of sodium iodide at 10 % (8 g for 100kg) are effective to stop
the acute signs of the disease within two days.

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➢ Systemic antibacterial agents, such as ceftiofur, penicillin, ampicillin, florfenicol,
and tetracyclines may be effective and are primarily recommended in severe cases of
actinobacillosis or in cases refractory to sodium iodide therapy.
➢ Surgical debulking of lesions, especially if they interfere with airflow, may be
useful. This is particularly true when large granulomatous masses are present that do
not respond to medical therapy.
VIII. Control
➢ Isolation or disposal of animals with discharging lesions is essential, although the
disease does not spread readily unless predisposing environmental factors cause a
high incidence of oral or skin lacerations.

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 Actinomycosis (LumpyJaw)
I. Definition
➢ A localized, chronic, progressive, granulomatous abscess that most frequently
involves the mandible, the maxillae, or other bony tissues in the head caused by
Actinomyces bovis and characterized by rarefying osteomyelitis and chronic
granulomatous inflammation in cattle.
II. Causes
➢ Actinomycosis is caused by Actinomyces bovis.
➢ Gram +ve rod shaped anaorobes pleomorphic, non sporulating, non-motile
➢ Present in the mucosa of the mouth and pharynx.
➢ In addition to this organism, association of bacteria like Corynebacterium
pyogenes and Staphylococcus are also seen
III. Epidemiology
➢ Actinomycosis generally affects cattle between 2 to 5 years.
➢ It is a sporadic disease .
➢ A. bovis common inhabitant of the bovine mouth.
➢ Infection ---through wounds to buccal mucosa.
➢ Infection ----through dental alveoli ---more in young cattle
➢ Infection of alimentary tract ---laceration by sharp foreign bodies.
IV. Pathogenesis
➢ After infection of jawbones ---rarefying osteomyelitis
➢ Characteristically granulomatous lesions
➢ Interfere prehension and mastication.
➢ Purulent centers surrounded by granulation tissue displaces normal tissue
➢ The yellowish pus from abscess are referred to as 'sulphur granules’.
V. Clinical signs
➢ Painless, bony swelling ---mandible or maxilla at the level of the central molar teeth
➢ Enlargement ---diffused or discrete.
➢ lesions ---lateral surfaces of bones ---common
➢ Swellings ---very hard---immoveable ---later painful.

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➢ Discharge through one or more openings.

➢ Pus is small in amount ---consists of sticky, honeylike fluid containing minute, hard,
yellow-white granules.
➢ Teeth in affected bone ---painful and difficult mastication.
➢ Loss of condition.
VI. Treatment
➢ The affected areas are treated with iodine solutions.
➢ A common method to achieve this is to give the cattle sodium iodide orally on a
regular treatment schedule.
➢ Antibiotics such as tetracyclines are also used, alone or with iodine; simultaneous
use is considered more aggressive.
➢ Surgical debridement.

VII. Diagnosis
A) Field diagnosis: Clinical signs.
B) Lab diagnosis:
➢ Culture of the organism from the lesion.
➢ Smear of discharging pus.
➢ A Gram stain of purulent material will reveal gram-positive, club-shaped rods and
filaments (sulfur granules).
➢ Radiology of the head is also useful.

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➢ Biopsy sample can be taken with a trephine and submitted for histopathology.
VIII. Prevention
➢ Because A bovis is part of the normal oral flora in ruminants, control focuses on the
avoiding of course, stemmy feeds or feeds with plant awns that might damage the
mucosal epithelium. When multiple cases occur in a herd, it is not from the
contagious nature of the pathogen but from the widespread exposure to a risk factor
(ie, coarse feed).

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 Anthrax (Splenic fever, Charbon).
I. Definition
➢ Anthrax is an peracute, acute, subacute or fatal infectious, soil -borne, disease of
mammals including humans, caused by Bacillus anthracis and characterized by
septicemia and sudden or rapid death, with exudation of tarry blood from the body
orifices, failure of blood to clot, absence of rigor mortis and splenomegaly. Anthrax
is a notifiable disease.
II. Cause
➢ Bacillus anthracis is the only important pathogen of animals and humans in the
genus Bacillus.
➢ In animal tissues it develops a prominent protective capsule of polyglutamic acids.
➢ When material containing anthrax bacilli is exposed to the air, central spores are
formed which protects the infectivity in the environment for very long periods.
➢ Three types of proteins (toxins) which are lethal, produce edema and have
antiphagocytic activity are produced.
III. Epidemiology
1- Distribution:-
➢ Anthrax is a worldwide disease, although its prevalence and public health
significance tend to be much higher in less developed tropical areas as in Africa
and Asia. Only a few countries are free of infection.
2- Transmission:-
➢ Occur by streams, insects, dogs, other carnivores, wild birds and by fecal
contamination from infected animals.
➢ Introduction of infection into a new area is usually through contaminated products
such as bone meal, fertilizers, hides, hair, and wool.
➢ The mode of infection is usually by ingestion and less commonly by aerosol or skin
abrasions, biting flies and other insects that transmit the infection mechanically.
3- Susceptible hosts:-

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➢ The disease occurs in all mammals, but the susceptibility of domestic animals
decreases in the following order: sheep, cattle, goats, buffaloes, camels, horses,
pigs, dogs and cats.
➢ Humans are usually susceptible to pulmonary, skin and intestinal infections.
➢ Birds are not susceptible.
4. Factors influencing susceptibility:-
➢ All sexes, ages and breeds are susceptible except a few breeds in sheep and pigs are
naturally resistant such as dwarf pigs and Algerian sheep.
➢ Most cases develop during dry hot summers.
5. The economic importance of the disease:-
➢ The economic losses result from animal deaths, quarantine enforcement, costs of
preventive measures and dead animal disposal programs in addition to the zoonotic
importance of the disease.
IV. Pathogenesis
➢ The spores usually enter through injuries of the alimentary tract, skin, or mucous
membranes and germinate at the site of entry.
➢ The bacilli proliferate and form capsules that protect them against phagocytosis, but
do not protect against specific antibodies.
➢ The elaboration of the toxic edema factor causes local edema which protects the
bacilli against anthracidal and tissues.
➢ The organism continues to multiply rapidly in the edematous fluid and passes via the
lymphatic vessels into the local lymph nodes, then into the blood stream and
septicemia with massive invasion of all body tissues occurs.
➢ The organism produces three types of toxins which contain the lethal factor (LF),
the protective factor (PF) and edema factor (EF),
➢ The combined effects of the LF and PF act the central nervous system causing fatal
respiratory failure.
➢ Death may be attributed to respiratory distress, terminal anoxia, shock and acute
renal failure.

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➢ During the clinical course blood and bacteria may exude from the body openings
and if necropsy is performed, blood escapes from the vessels.
V. Clinical signs
➢ The IP varies from 1-14 days,
➢ the morbidity and mortality of domestic farm animals are between 2-80 %,
and the course of the disease varies from 10-48 hours and sometimes death may
occur after 1-2 hours.
1. In cattle and sheep:-
➢ The peracute form of the disease is more common at the beginning of an outbreak.
➢ Characterized by sudden or rapid death without previous illness.
➢ In rare cases, the animal shows signs of fever, muscle tremors, dyspnea, collapse
and terminal convulsions with death occurring in 1-4 hours. After death, discharges
of blood from the nostrils, mouth, anus and vulva are common.
➢ The acute form of the disease is characterized by high fever, and complete
cessation of rumination, feeding, and lactation. Bloating, depression, rapid and
labored respiration, diarrhea or dysentery may develop.
➢ Sometimes feces, urine and milk may be stained with blood,
➢ Hemorrhagic congestion of the visible mucous membranes,
➢ Pregnant animals may abort.
2. In equines:-
➢ The clinical forms vary according to the mode of infection.
➢ When infection is by ingestion, there is septicemia with enteritis and colic.
➢ When infection is by insect transmission, a hot painful edematous subcutaneous
swelling appears about the throat, lower neck, floor of the thorax and abdomen,
prepuce and mammary gland and there is a high fever and severe depression and
dyspnea .
3. In camel:-
➢ The disease may take sub-acute or chronic form,
➢ Characterized by edema.
4. In carnivores:-

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➢ When affected they frequently show swelling of the throat. great depression, high
fever and blood stained feces.
VI. Postmortem lesions
➢ Before a necropsy is performed on an animal that has died ,it is essential that anthrax
should be ruled out to prevent contamination of the environment and ensure proper
disposal of the carcass.
➢ Blood exudes from all body orifices and sometimes through the skin, bloating and
decomposition of the carcass occurs rapidly and in most cases.
➢ rigor mortis is absent.
➢ If the carcass is accidentally opened, signs of septicemia are present such as blood
stained fluid in all body cavities and widespread hemorrhages throughout the
carcass,
➢ Unclotted or poorly clotted blood oozes from the cut blood vessels,
➢ The spleen is often enlarged with a dark semi fluid pulp and occasionally a ruptured
capsule.
VII. Diagnosis…
1- Field diagnosis:- The clinical diagnosis of anthrax is made on the basis of typical
signs .
2- Laboratory diagnosis:-
A) Specimens:-
➢ Should be collected from fresh carcasses or at the time of death and submitted on
ice and packed in a non-breakable container, sealed and labeled "Suspected
anthrax",
➢ Swabs from exuded blood or blood taken by syringe and blood smears
➢ Aspirated fluid from localized lesions
➢ Pieces of one ear (the cut must be cauterized).
B) Laboratory diagnosis depends on:-
➢ Demonstration of capsulated bacilli in peripheral blood .
➢ Confirmation by laboratory isolation and identification.

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➢ Isolation of the organism from specimens on blood agar and incubated on blood
agar plates at 37 °C for 24 hours.
Identification by:-
➢ Microscopic examination of blood and culture smears by Gram stain, revealing gram
positive rods,
➢ Microscopic examination of blood smears for demonstration of capsular material
stained with Giemsa or Loffler's methylene blue. The capsule is purplish and the
bacilli are stained pink.
➢ Culture characteristics, as rough, flat, gray colonies without hemolysis or weak
hemolysis may be observed. In general B. anthracis is identified by characteristic
colony rods, centrally located spore formation, non-motile and aerobic.
➢ Guinea pig and mouse inoculation with blood or tissue suspension. The animals
begin to die within 24 hours and large capsulated rods
demonstrated in smears from their spleen and blood.
➢ Ascoli's test is a one of precipitin test used for detection of anthrax
VIII. Treatment …
➢ Anthrax is a notifiable disease.
➢ Antibiotics should be given to unvaccinated individuals.
➢ Penicillin, tetracycline and streptomycin are effective if administered before the
onset of lymphatic spread or septicemia, estimated to be about 24 hours.
➢ Penicillin is recommended twice daily at a dose of 10000 IU/kg b.w. I/M for 4 – 5
successive days.
➢ Antibiotic treatment is also known to lessen the severity of the disease in individuals
who acquire anthrax through the skin.
IX. Prevention & Control…
➢ Because anthrax is often fatal in domestic animals, a preventive strategy should be
adopted involving annual vaccination of susceptible animals (usually cattle, sheep
and goats) in areas prone to the disease .
➢ This is usually done two to four weeks before the onset of known period of
outbreaks.

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➢ When animals show clinical signs of the disease, antibiotic treatment is
recommended.
➢ Other measures to be adopted in addition to immunization and treatment are
enforcement of quarantine regulations ,
➢ Prompt disposal of dead animals, bedding and contaminated materials ,
➢ Control of scavengers, and observation of general hygiene by people who have
come in contact with diseased or dead animals .
➢ The non-encapsulated Sterne strain vaccine is used .
➢ This live attenuated vaccine produces immunity against anthrax .
➢ A single vaccination produces immunity lasting for an average of nine months.
➢ Annual vaccination of susceptible animals is sufficient to control outbreaks of
anthrax.

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 Edematous Skin Disease (ESD)
I. Synonyms
➢ Ulcerative lymphangitis, Pseudo tuberculosis.
II. Definition
➢ It is a mild contagious disease of buffaloes and cattle caused by Corynbacterium
pseudotuberculosis "C.ovis", and characterized by cutaneous nodules, cutaneous
edematous swellings, skin ulcerations, and lymphadenitis "suppuration of superficial
lymph nodes".
III. Cause
➢ Corynbacterium pseudotuberculosis is the correct name used by microbiologists
today in replace of C.ovis.
➢ C.pseudotuberculosis has two serotypes. Serotype I is mostly nitrate negative &
responsible for causing CLA in sheep & goats. In Egypt, serotype II reducing nitrate
& it was shown to be the cause of ESD in buffaloes.
➢ All strains producing powerful exotoxin phospholipase D (PLD) which are
antigenically similar.It was found that exotoxin from nitrate negative bacteria was
lethal for mice within 48 hours post-inoculation. In contrast, exotoxin of seroype II
failed to kill mice. However, in guinea pigs nitrate- positive strains(serotype II) were
more lethal than nitrate- negative strains.
IV. Epidemiology
1. Distribution:- Worldwide distribution and occurs regularly in Egypt.
2. Susceptible host :- Buffaloes are mainly susceptible and also cattle.
3. Mode of transmission :-
➢ Spread of infection results from contamination by pus drained from infected animal
also presence of skin wound, abrasions especially in lower limbs, contaminated
bedding and grooming utensils and insects (Hippobosca equina) also can transmit
the infection.
4. Factors influencing infection :-
➢ Bad hygiene as overcrowded, dirty, muddy, unhygienic stables are predisposing
factors to infection.
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5. The economic importance :-
➢ Decrease the capacity of the animal, marked losses in production in addition to costs
of treatment.
V. Clinical signs: IP is long, low morbidity and mortality, long course.
➢ Fever, decrease appetite, decrease milk production,
➢ formation of S/C edematous swellings or cutaneous nodules of 5-7 cm in diameter
or abscess formation along the course of corded lymph vessels on chest, abdomen,
and legs or spread all over the body. (stage I or skin form).
➢ Edematous swellings of legs render the affected leg, swollen, hot, painful resulting
in locomotion disturbance and lameness, the swelling may rupture and discharge
serosanginous fluid or creamy green pus (stage II), with necrosis or ulcer formation
(stage III which may be attributed to immune complex reaction).
➢ Septicemia and toxemia may result in respiratory manifestation with rapid
respiration, coughing, dyspnea and urinary manifestation with hemoglobin urea
followed by deplitating, recumbency and death.
VI. Diagnosis…
1. Field diagnosis: Clinical signs, history, epidemiology.
2. Lab. Diagnosis:
➢ Specimens from pus, lymph nodes, swabs or biopsy from lesions.
➢ Stained smear to see gram +ve diphthroid Chinese- letter bacilli.
➢ Culture characters on specific media.
➢ Serological test… CFT, FAT, IH, and neutralization test.
➢ Hematological and serum biochemical analysis.
➢ Animal inoculation as mouse protection test and skin sensitivity test as well as
inoculation in susceptible calves. Crude cell wall lipid is dermo-necrotic when
injected I/D into rabbit or guinea pigs.
VII. Treatment …
➢ Systemic antibiotics as large dose of penicillin 50.000 IU/Kg b.wt. for 5-7 days or
tetracycline, gentamicin, cephalosporin and antipyretic, and anti-inflammatory, and
antihistaminic, diuretics, fluid therapy and vitamins.
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➢ Local applicaton of iodine or icthyol ointment (5-10%) on closed lesion, open lesion
are completely evacuated from pus and irrigated daily with antiseptics as Betadin
until healing.
VIII. Prevention & Control…
➢ Isolation and treatment of infected animals.
➢ Good hygiene and management practices.
➢ Vaccination… by Bacterin or toxoid or vaccination of male calves at 6 months by
BCG which give non- specific immunity. Although the disease is present in Egypt,
there is no available vaccine produced up till now for field application.

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 Shipping Fever Pneumonia
I. Synonyms
➢ Haemorrhagic septicemia,
➢ Stockyand pneumonia,
➢ pneumonic pasteurollosis.
II. Definition …
➢ It is an acute infectious respiratory disease of cattle, buffalo, sheep, goat, and pigs
caused by pasteurella hemalytica, and characterize by .. septicemia, fever, signs of
bronchopneumonia and high mortality rate.
III. Etiology…
➢ Posteurella hemolytica,
➢ Gram – ve cocobacilli, non matile, non-spore forming, aerobic, and fermentative.
IV. Epidemiology…
1. Distribution: is common in Europe, and North America, north and South of Asia,
and recorded in Egypt.
2. Susceptible host: Cattle, Buffalo, sheep.
3. Mode of transmission
➢ Nasal discharge of infected animal is main source and infection transmitted by
inhalation of infected droplets, the spread of infection among animals in pasture is
slower than in stable.
4. Seasonal incidence: in winter in which cold weather.
5. Economic importance:
➢ Losses from marked decrease in milk and meat production cost of treatment and
eradication of the disease.
V. Clinical signs…
➢ IP 10 – 14 days post exposure to stress, morbidity and mortality rate is high. Course
is short and animal may recover within 2-4 days.
Signs…
➢ Sudden death is very young calves due to septicemia.

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➢ Fever (40 - 42C), depression, anorexia, reluctance to move, marked decrease in
milk production,
➢ Shallow rapid respiration, moist painful cough
➢ if animal is urged to walk, dyspnea with respiratory grunt, extended head and neck,
open mouth breathing,
➢ Salivation or froth in lips, S/C emphysema, mucopuralent nasal discharge "crusty
nose", ocular discharge
➢ Pain or palpation of intercostals region over the pneumonic lung.
➢ On auscultation there is evidence of bronchopneumonia, in early stages there are
increase in vesicular sound and bronchial tones, as the disease regress there are
moist or dry roles and pleuritic friction sounds.
➢ Sever cases may show hemorrhagic diarrhea accompanied respiratory signs.
VI. P.M. Lesions…
➢ There are bilateral fibrinous bronchopneumonia, the affected lung is meaty, friable,
slightly swollen, firm, contain microabscess and fibrin deposits on visceral and
parietal pleura, increased amount of yellow or yellow red pleural fluid, catarrhal or
suppurative bronchitis, and fibrinous pericarditis. In chronic cases dorsal aspect of
lung have bullous emphysema or interstitial edema, discolored lung, which varies
from area to area.
VII. Diagnosis…
1. Field diagnosis … signs and epidemiology.
2. Lab. diagnosis .
➢ Specimens from nasal or tracheal swabs, part of lungs and its lymph node, or smear
from heart blood or spleen.
➢ Examination of the organisms in the blood smear.
➢ Culture of suspected materials on specific media.
➢ Haematological profile show increase in plasma fibrinogen, leucopenia, and
neutropenia,
➢ Serological test as ELISA.

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➢ Radiograph or ultrasonography to detect degree of consolidation and abscess
formation.
VIII. Treatment…
➢ Specific therapy … antibiotic for 3-5 successive days at least, by using long acting
oxytetracydine "20 mg/kg B.wt" I/M, alone or with combination with
sulphamethazine "150 mg/kg B.wt I/V or orally". Trimethoprim "22 mg/kg".
➢ - Gentamycin alone "2.2 mg/kg B.wt I/M" alone or in combination with penicillin or
erythromycin (5.5 mg/kg B.wt I/M), penicillin – dihydro – streptomycin (20000 –
30000 IU/Kg B.wt penicillin and 20 mg/kg B.wt of dihydrostreptomycin I/M) and
also can uses lincomycin – spectinomycin (11 mg/kg B.wt).
➢ - Can also make mass medication by sulphamethazin as 100 mg/kg in water for 5-7
days or oxytetracycline as 3-5 my /Kg B.wt in thefeed or tylosin for 7 days for all
animals may be indicated.
➢ Symptomatic treatment… as antipyretic as analgin, anti-inflammatory as
dexamethazone or phenylbutazone in pregnant cows and flunixin meglumine (0.5-1
mg/Kg B.wt) as a single dose or once every other day and antihistaminic,
bronchiodilator as aminophyllin or atropine, diuretics, fluid therapy.
IX. Prevention and control…
➢ Proper management… avoids any stress factors and avoid sudden change in climates
and isolates the infected cases in well-ventilated area and early treated.
➢ Biological prophylaxis… animal should be vaccinated by pasteurella hemolytica
killed vaccine, and also vaccinates against other respiratory bacterial or viral agents.
➢ Chemoprophylaxis… Antibiotics or sulphonamides may be used and mass
medication in water or feed.
➢ During outbreaks… isolation of infected animals and treated, and hygienic disposal
of carcasses of dead animals, destruct all possible sources of infections, cleaning and
disinfections of the farm and vaccination of apparently clinical normal animals.

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 Contagious bovine pleuropneumonia (CBPP –lung plague)
I. Definition …
➢ Contagious bovine pleuropneumonia (CBPP) is a contagious bacterial disease of
cattle and water buffalo caused by Mycoplasma mycoides subsp. Mycoides (M.
mycoides). it attacks the lungs and the membranes that line the thoracic cavity (the
pleura) causing fever and respiratory signs such as laboured or rapid respiration,
cough and nasal discharges.
II. Causative agent of CBPP
➢ Mycoplasma mycoides subsp.
III. Transmission and spread
➢ Transmission of the disease occurs through direct contact between an infected and a
susceptible animal which becomes infected by inhaling droplets disseminated by
coughing. Since some animals can carry the disease without showing signs of
illness, controlling the spread is more difficult.
➢ There is no evidence of transmission through fomites (inanimate objects such as
clothing, implements or vehicles) as the organism does not persist in the
environment.
IV. Pathogenesis
➢ After infection by inhalation, the organism produces local inflammation in the
bronchi and bronchioles, followed by initial septicemia and localization in other
sites including kidney and brain, in lung causing acute lobar pneumonia and
pleurisy. Thrombosis in pulmonary vessels is evident, probably prior to the
development of pneumonic lesions, and death results from anoxia and toxemia. If
the animal survives, it may become a carrier. Recovery from CBPP leads to lifelong
immunity.
V. Clinical signs
Acute Infections
➢ Inculpation period: 10 days to 6 months.
➢ loss of appetite and fever

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➢ Respiratory signs, such as rapid respiratory rate, cough and nasal discharges and
painful, difficult breathing.
➢ In many cases, the disease progresses rapidly, animals lose condition, and breathing
becomes very laboured, with a grunt at expiration.
Chronic Infections
➢ Less obvious signs of pneumonia
➢ Coughing with exercise
➢ Extreme weight loss; recurrent mild fever
➢ Recover after several weeks
➢ Calves infected when they are born
➢ Arthritis in several joints
➢ May not show signs of pneumonia
➢ Healthy appearing animals may spread CBPP
➢ Depressed, thin Reluctant to move
VI. Diagnosis
A) field diagnosis
➢ Case history.
➢ Epidemiology
➢ Clinical signs
B) Lab diagnosis
➢ For the isolation and growth of M. m. mycoides SC, nasal swabs, bronchoalveolar
lavage and blood may be taken from live animals and tissue samples from edge of
pulmonary lesions, broncho-pulmonary lymph nodes, pleural fluid.
➢ Isolation of m.o.
➢ Biochemical Tests.
➢ Serological Tests.
➢ Antigen Detection Systems (a monoclonal antibody-based sandwich ELISA )
➢ Molecular Diagnosis

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➢ based on PCR have been developed for the rapid detection, identification and
differentiation of members of the M. mycoides cluster and the specific identification
of M. m. mycoides SC.
VII. Treatment
➢ Treatment Tetracyclines, macrolides and fluoroquinolones are reported to be useful
in treatment, but individual drugs may differ in their effects. Complete elimination
of mycoplasmas is reported to be rare. The degree of risk from treated animals is
still uncertain; however, treatment is controversial, and some countries do not permit
antibiotics to be used. Antibiotics are reported to be ineffective in chronic cases.
What is being done to prevent or control the disease?
➢ The main problems for control or eradication are the frequent occurrence of
subacute or unapparent infections and the persistence of chronic carriers after the
clinical phase.
➢ In most continents, control strategies are based on the early detection of outbreaks,
control of animal movements and a stamping-out policy. This has successfully
eliminated the disease from North America and Europe.
➢ In Africa control of the disease is currently based mainly on vaccination campaigns.
➢ Surveillance of the disease through slaughterhouse inspection is a very efficient
method of detecting clinical cases.
➢ Treatment of affected animals with antibiotics can result in healthy looking animals
that are still infected and able to spread the disease, so it is not recommended.
➢ Vaccination with an attenuated strain of the bacteria is used to reduce the level of
infection. Vaccine is produced following the guideline in the OIE Manual of
Diagnostic Tests and Vaccines for Terrestrial Animals.

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 Caseous Lymphadenitis
I. Definition:
➢ Chronic debilitating infectious disease of sheep and goats, caused by
corynebacterium pseudotuberculosis, characterized by suppurating, necrotizing
inflammation of one or more lymph nodes (abscessation of lymph node).
II. Etiology
➢ Corynebacterium pseudotuberculosis. It produces an exotoxin, phospholipidase D,
which functions as a sphingomyelinase and is an immunodominant antigen.
III. Epidemiology
1. Distribution: Caseous lymphadenitis occurs in the major sheep-producing
countries in the world.
2. Animal susceptibility: Sheep and goats of all ages but adults are more affected
than young because repeated exposure to infection at shearing. CL is more serious in
goats than in sheep.
3. Predisposing factors:
Dirty condition at shearing time, faulty shearing, dipping where the organism still
lives for 24 h in sheep dip, abrasions, wounds from fighting or grass seeds.
4. Mode of infection
Source of infection: The discharges from ruptured abscessed superficial lymph
nodes.
5. Mode of transmission:
Infection of an animal is facilitated by the presence of skin wounds, but the
organism can invade through intact skin. Transmission is by direct contact with
infective discharges or mediated by contaminated shearing equipment, contaminated
shearing shed boards
IV. Pathogenesis
➢ After infection m.o invade local lymph nodes multiply resulting in initial diffuse
inflammation and multiple abscess formation which coalesce with each other and
undergo encapsulation the infected lymph node become consists of central necrotic
mass of connective tissue in the center surround by capsule from connective tissue

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 inflammatory cells and capillaries, the cells of inner layer of connective tissue
capsule is killed by bacterial toxins and thus add a new layer of suppuration to the
central necrotic mass and a new capsule, these process repeated resulting in onion
ring appearance of the lesion.
V. Clinical signs:

➢ Sheep: Signs may be divided to superficial or cutaneous form and subclinical or

visceral form.
➢ Superficial form: There is enlargement of one or more of the superficial lymph
nodes. The abscesses commonly rupture and thick green to caseated pus.
➢ Internal or Visceral form: In cases in which systemic involvement occurs, chronic
pneumonia, pyelonephritis, ataxia, and paraplegia may be present depending on the
site of infection. The debilitating disease of adult ewes commonly referred to as 'thin
ewe syndrome' is often associated with the occurrence of internal abscesses.

VI. Diagnosis
➢ Field diagnosis: It depends on clinical signs as suppurative lymphadenitis of
superficial lymph nodes especially after shearing, docking, castration beside
postmortem lesions, epidemiology of the disease and field allergic skin test.
➢ Laboratory diagnosis:
A) Samples:
➢ Pus, biopsy of lymph nodes, parts of lymph nodes, blood and serum.
B) Laboratory procedures:

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➢ Examination of pus smears after staining with Gram stain to detect Gram positive,
polymorphic rods organism.
➢ Culture on blood agar, incubation for 1-2 days at 37 C, colony appear as small pin
point and off-white faintly hemolysis.
➢ Detection of toxins by inoculation of suspected materials I/D into rabbits, resulting
in dermal necrosis. G. Pig inoculation I/V by pus, death after 4-10 days, with
absecessation of lung and liver while I/P injection produce orchitis with abscess
formation.
➢ Detection of antitoxins by IHT, ELISA, CFT or agglutination tests.
➢ Hematological and serum biochemical analysis.

VII. Treatment
➢ There is no treatment
➢ The treatment is not satisfactory due to suppuration and cell wall lipids of organism
VIII. Control
Proper management:
➢ Isolation and culling of infected sheep.
➢ Sanitary care during shearing, castration or docking and use skin disinfection and
disinfection of surgical instrument.
➢ Avoid contamination of dipping fluids so, dipping of lamb firstly, and then adult due
to decrease chance of lamb infection.
There is no vaccination.

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