Know about the bacterial disease

1. Part I | Morbid Anatomy | Dr. Ahmed Alsaidya Page | 1
Ahmed M.A. Alsaidya , PhD
Lecturer , Department of Pathology and Poultry Diseases
College of Veterinary Medicine, University of Mosul, Mosul, Iraq
https://orcid.org/
https://www.researchgate.net/profile/
Morbid Anatomy | Part I | 4th
year 2019
Actinobacillosis (Wooden tongue)
It is a chronic suppurative inflammatory 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.
Etiology :
Actinobacillus ligniersi (normal commensal organism in the oral flora of the cattle),
• Gram negative coccobacilli or pleomorphic rods.
• form sulfur granules as white or yellow-white cheesy accumulation of the
organism.
Predisposing factor : Oral mucosa injuries by fibrous feed materials or by foreign
bodies and during oral manipulation by hand of owner or veterinarian.
Pathogenesis :
• The organisms are present in the mouth and upper respiratory tract.
• Local infection by the organism causes an acute inflammatory reaction in the
tongue and the subsequent 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.
• Visceral involvement is recorded.
Clinical signs :
• Incubation period is unknown, morbidity and mortality rate is low and course of
the disease is long.
• The onset of glossal actinobacillosis is usually acute, the affected animal being
unable to eat for a period of about 48 hours. There is excessive salivation and
gentle chewing of the tongue.

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• On palpation the tongue is swollen and hard, particularly at the base, the tip often
appearing to be normal.
• Nodules and ulcers are present on the side of the tongue and there may be an
ulcer at the anterior edge of the dorsum.
• In the later stages when the acute inflammation is replaced by fibrous tissue, the
tongue becomes shrunken and immobile and there is considerable interference
with prehension.
Macroscopic & Microscopic appearance :
The organism A. lignieresi invades the injured areas in the mouth, pharynx or
intestines etc., to enter different kinds of tissues (especially soft tissues) to produce the
lesions. The granulomas developing in these organs contain several colonies of the
organisms. Grossly, these are firm, hard and the colonies of the organisms look like
yellowish white specks on the cut surfaces of the granulomas. Finger like clubs or
projections abutting the bacterial colonies are surrounded by cellular granulation tissue
consisting of epithelioid cells, a few giant cells and leucocytes. Fibroblasts form masses
of fibrous tissue beyond these infiltrating inflammatory cells. The granulomatous
growth of the tissue marked by inflammation and abscessation in this infection contains
foci of pus having clubs radiating from the centres of the masses called rosettes.
Microscopically, these rosettes are surrounded by giant cells, epithelioid cells and
neutrophiles.
The organisms can be found between these clubs and stain blue in the sections
staind by Ziehl-Neelsen's method. The clubs stain Red with carbol fuchsin , and these
clubs stain Pink with eosin and hematoxyline .
Diagnosis :
1. Clinical signs
2. History of the disease
3. Demonstration of organisms in the tissue sections
4. Demonstration of the Rosettes
5. Culture and identification of the organisms
Differential diagnosis :
1. Actinomycosis
2. Nocardiosis
3. Staphylococcus infection
4. Tubercullosis

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Actinomycosis (Lumpy Jaw )
It is a chronic infectious debilitating disease of cattle mainly, caused by
actinomyces bovis, characterized by rarefying osteomyelitis of jaw bones. and
formation of bony cavities filled with pus in head bones particularly the mandible and
maxilla.
Etiology :
• Actinomyces bovis is the primary cause
• Actinomyces bovis is common inhabitant (flora) of the mouth and digestive tract,
Gram positive, grow in branching filaments (crushed preparation of sulfur
granules from pus or tissues), coccoid, or filament rods have distinct cell walls.
Pathogenesis :
• The diseases caused by Actinomyces bovis, which is a soil born bacteria
• Trauma to the oral mucosa and eruption of teeth allow the organisms to inter the
osseous tissue .
• The lesions in the tissues of animals infected with A. bovis are of a
granulomatous kind and the organisms are found embedded in the granulation
tissue or found as granules in the pus of suppurative lesions. The swollen lesions
may discharge sticky honey like exudates containing minute hard yellowish
white granules called sulphur granules.
• In the jawbones a rarefying osteomyelitis is produced.
• The lesion is characteristically pyogranulomatous, necrosis and loss of the bone ,
with scare formation and multiple fistulae are characteristic.
• Involvement of the jaw causes interference with prehension and mastication.
• Rarely, localization occurs in other organs, caused apparently by hematogenous
spread from these primary lesions.
Lesions :
 large mass of granulomatus and osteoid growth protroded skin
 The discharge of pus is small in amount and consists of sticky, honey-like fluid
containing minute, hard, yellow white granules (Sulfur granules).
 Granulomatous lesions containing pockets of pus may be found in the esophageal
groove, the lower esophagus and the anterior wall of the reticulum.
 Spread from these lesions may cause a chronic, local peritonitis.
 Suppurative osteitis is found in the maxillae. A mass of granulation tissue with
soft purulent centres is found in the medullary cavity of the maxillae. Several
sulphur granules are seen in such purulent centres.
 The bone adjacent to these growths becomes absorbed and rarefied and the
formation of a new bone on its outside forms what is called lumpy jaw. Sinuses
leading to the surface of the skin with discharge of pus develop in such affected
areas (maxillary region).

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Microscopically, the stained sections of the lesions of actinomycosis show a
granular center as a mass of Gram positive filaments matted together to form a
mycelium(rosettes like) . This mycelium is surrounded by a zone of shiny and radiating
clubs , followed by layer of neutrophils surrounded by giant cells , epithelioid cells
and finally fibrous connective tissue.
The colonies of actinomyces may become calcified in cases of long standing.
Diagnosis : its depended on
1. Clinical signs
2. Gross and microscopic lesions , using gram stain to identified the G+ organisms
in tissue
3. Demonstration of the organism in smears of fresh unfixed material stained by
Grams stain
4. Demonstration of the (Mycelium ) or Rosettes with shiny , refractile , radiating
clubs in the fresh pus .
Differential diagnosis :
1. Actinobacillosis
2. Nocardiosis
3. Staphylococcus infection.

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Black Leg
(Black Quarter)
Definition
It is a highly fatal and febrile bacterial disease caused by Clostridium
chauvoei in ruminants (particularly cattle) and characterized by swollen and
emphysematous or crepitating lesions of the muscles and subcutaneous
tissues in some region in the bodies such as the shoulder or the hind quarter
of the affected animals.
(The infectious myositis is the most marked lesion.)
.
Etiology
Cl. chauvoei , Gram positive, spore-forming bacteria and may have central
or subterminal spores ,The organisms exist in the soils and are also found in
large numbers in the local muscle lesions and exudates around such lesions.
Susceptible animals
Although blackleg has been found in cattle as young as
2 months old, most losses occur in cattle between
6 months and 2 years of age. Occasionally, losses are seen in adult cattle.
Generally, the best conditioned animals are affected, with most losses
occurring where there is an abundance of feed.
Pathogenesis
Toxins and neuraminidase produced by the causative bacteria are believed to
play a significant role in pathogenesis of diseases. The bacteria enters by
ingestion and then gains entrance to the body through small punctures in the
mucous membrane of the digestive tract.
Bacterial spores are eaten in contaminated feed or soil. The spores then enter
the bloodstream and lodge in various organs and tissues, including muscles.
Here they lie dormant until stimulated to multiply, possibly by some slight
injury to the animal. The injury reduces blood flow to the area, thereby
reducing the supply of oxygen to the tissues.
In the absence of oxygen, the spores germinate and multiply. As they grow,
the bacteria produce toxins which destroy surrounding tissues. The toxins are
absorbed into the animal’s bloodstream which makes the animal acutely sick
and causes rapid death.

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Clinical signs
It occurs as an acute disease usually with a fatal ending. Animals are found
dead without showing signs of illness.
There is a characteristic extension of the limbs a short time after death of the
affected animals. Lameness is noticed in the sick animals. High temperature
,increased pulse rate are seen in the sick animals. Sheep reveal myositis,
lameness and depression in the cases of Cl. Chauvoei infection.
Lesions
The local lesions occur mainly in some muscular parts of the body and
these lesions are found in the shoulders, hind quarters, neck, back and loins
etc. Lesions of black quarter do not occur below the hock or knee in the
ruminants.
These lesions in the muscles are hot, painful insensitive and (painless).
Blackened, soft, emphysematous and necrotic muscles infiltrated with gas
bubbles produce a crackling sound as heard from application of pressure on
them.
Affected animals die within 24 to 40 hours. A large amount of blood
stained fluid or dirty red exudate escapes from the oedematous tissues.
Bubbles of gas are found in the exudate. The affected muscles are dry,
black or of dark colour with dissection of the muscle by infiltrating gases
because of bacterial growth.
An odour of rancid is emitted by the muscular lesions and the adjoining
lymph nodes are swollen. Serous cavities contain blood tinged fluid and
internal organs show degenerative changes.
Microscopically
the affected muscles show spherical spots (gases) separating muscle
bundles and fascia. The muscles show areas of necrosis and collections of
neutrophils and lymphocytes along the muscle septa.
Gram-positive bacteria are seen singly or in small irregular clumps in the
muscles. The skin over the affected muscles shows dryness, cracks and
discolouration .

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Diagnosis
It is based on the clinical symptoms and the characteristic crepitating lesions
in the muscle of the black quarter cases. Culture from needle biopsy is done
to isolate the causative bacteria. The organisms of black quarter can be seen
in the smears of the exudate and can also be isolated in cultures of the
infected materials.
Differential diagnosis
Other acute Clostridial infections, lightning strike, anthrax, bacillary
haemoglobinuria, lactation tetany, extensive haemorrhage and acute lead
poisoning.

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Tuberculosis
It is a chronic granulomatous infectious disease of man and animals caused by
certain organisms within the genus Mycobacterium, and characterized by the
development of tubercles nodules in different organs.
Bovine tuberculosis is a chronic bacterial disease of cattle that occasionally
affects other species of mammals. This disease is a significant zoonosis that can spread
to humans, typically by the inhalation of aerosols or the ingestion of unpasteurized
milk. In developed countries, eradication programs have reduced or eliminated
tuberculosis in cattle, and human disease is now rare; however, reservoirs in wildlife
can make complete eradication difficult.
Causes:
Is caused by an aerobic, acid-fast, rod-shaped organism, the organism can
multiply only if plentiful oxygen is available. So in closed caseous lesions, the bacilli
do not proliferate. But if the lesions were to open up into a bronchus, the organism
proliferates rapidly.
There are several strains of M. tuberculosis are found that can be distinguished
culturally, and by their pathogenicity to animals. These are:
1-The human strain ( Myco. Tuberculosis) infective to humans and animals.
2-The bovine strain (Myco.bovis) infective to man and animals.
3-The avian strain( Myco. Avium) infective to fowls and some animals.. They are
Gram. positive.
Mycobacterium bovis is the main cause of tuberculosis in animals such as cattle,
buffalo, camels, sheep, goats, horses, pigs and dogs.
Route of infection: source of infection is an affected animals the common routes of
infection are:
a-Aerogenous or inhalation(droplet infection, dust inhalation)
b-Enterogenous or ingestion( by contaminated materials may be milk or pasture by
sputum, urine, or feces from infected animals)
Pathogenesis
Mycobacterium infection occurs by airborne transmission or ingestion of droplet
contains viable organisms produced by sputum of infected animals. The bacilli adhere
to the lining epithelium, where they induce local infiltration of neutrophils. The
neutrophils are able to engulf the bacilli but are not able to kill them. The neutrophils

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rapidly totally disappear from the infected area due to their destruction and can not be
seen in the lesion.
The macrophages arrive to the site of infection and phagocytize the bacilli. The
intracellular organisms resist destruction by macrophages. The mechanism by which
intracellular survival may be due to prevention of phagosome. lysosome fusion, or
direct cytotoxic effect of some cell wall component to macrophages or prevent
acidification of phagolysosome. Accumulation of mycobacterium stimulates an
inflammatory response, which mature into a granulomatous lesion.
Following the formation of the primary lesion at the site of entry in organs, the
bacilli carried to regional lymph node either freely or in macrophages through the
lymph where tubercles are formed. The lesions in organ and regional lymph node called
primary complex
Infection spread to next lymph node and lymphatic until reach the circulation,
localized in an organ or various organs in large numbers
Postprimary infection can occur in animal under stress, the resistance of the body is
lowered activation of infection from old encapsulated lesions resulting in formation of
daughter tubercle or get entry to general circulation and localized in various organs.
Gross lesion
Tubercle bacilli produce characteristic lesions no matter where they localize in
tissue. Lesions in tuberculosis are either proliferative (focal or diffuse) or with
exudation. The proliferative is more common forming microscopic tubercles, which
later diffuse to be seen by naked eye.
A. The proliferative form seen either as tubercles, miliary form or caseous form
1. Tubercle or nodular form is the classical form of lesions. The tubercle is 1. 2 cm in
diameter, first gray and translucent but soon becomes yellowish. Large tubercles are
dry, grayish. white and contain caseous masses calcified foci
2. Miliary tuberculosis is generalized form of tubercle. The lesions are characterized by
the presence of numerous number of recent tubercle 2. 3 mm in diameter,
approximately of the same age and shape
3. Caseous form is characterize by a small or large areas of tissue necrosis
Microscopically,
The tuberculous lesions are basically proliferative except in serous membrane is
exudative.
The tissue reactions to mycobacterium bacilli start as a small aggregates of
neutrophils that phagocytize the bacilli. The neutrophils die and totally disappear from
the area.
After that the macrophages arrive and phagocytize the bacteria. The bacilli kill
macrophage. Numerous monocytes and histocytes are attracted to the area under the
effect of cytokines, metabolic products and disintegration of bacilli. The mononuclear
cells become enlarged and pale with large vesicular nuclei and foamy cytoplasm
(epithelioid cells).
Fusion of more than one epithelioid cell or by mitotic division of the nucleus of

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one cell without division of the cytoplasm resulted in formation of Langhan’s giant
cells. Lymphocytes, migrating from the adjacent blood vessels, form a dense zone
around epithelioid cells. Under the effect of bacterial toxin, unsaturated fatty acids and
perhaps also a vascular condition of the tubercle the tubercle undergoes degenerative
changes and caseous necrosis
Old tubercles are encircled with fibrous tissue. Encapsulated. The necrotic
portion may calcify or liquefy old tubercles. Calcification is a characteristic in some
species of animals (cattle, sheep, and goats) while it is rarely or not observed (buffalo,
pig, dog, and fowl).
The disease mainly occurs in thoracic cavity, particularly lungs and related lymph
nodes.
Diagnosis :
1-Clinical :-Tuberculosis can be difficult to diagnose based only on the clinical signs. In
developed countries, few infections become symptomatic; most are diagnosed by
routine testing or found at the slaughterhouse.
2-Laboratory tests
In live cattle, tuberculosis is usually diagnosed in the field with the tuberculin
skin test. In this test, tuberculin is injected intradermally; a positive test is indicated by a
delayed hypersensitivity reaction (swelling). The tuberculin test can be performed using
bovine tuberculin alone, or as a comparative test that distinguishes reactions to M. bovis
from reactions to environmental mycobacteria. False negative responses are sometimes
seen soon after infection, in the late stages of the disease, in animals with poor immune
responses and in those that have recently calved.
Differential diagnosis
The differential diagnosis includes contagious bovine pleuropneumonia, Pasteurella or
Corynebacterium pyogenes pneumonia, aspiration pneumonia (which is often
secondary to chronic wasting disease in cervids), traumatic pericarditis, caseous
lymphadenitis or melioidosis in small ruminants, and chronic aberrant liver fluke
infestation.

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Johne's Disease
(Paratuberculosis)
It is a bacterial disease caused by an acid-fast organism known as
Mycobactrium paratuberculosis (also called M.johnei). Cattle, sheep, goats
and deer are affected by this disease. The organisms seem almost entirely
confined to the lesions in organs like mesenteric lymph nodes and intestinal
mucous membrane of the infected animals.
Evidence of Johne's disease is found in the animals of at least 18 months of
age and it is usually seen between the age of 3 to 6 years.
Ingestion of food and water contaminated with the faeces or infected
material produces this disease in healthy animals. Young cattle are more
susceptible to infection than old ones. Parturition, lactation and other factors
lowering resistance of animals frequently accelerate the disease process in
the infected aminals.
infection is transmitted by ingestion of contaminated food and water and JD
is marked by a long incubation period in the affected animals.
Signs
Faeces in the infected animals is thin, watery, and mixed with gas bubbles.
Affected animals are emaciated, dull and their bony eminences or ribs are
very prominent with a little subcutaneous fat or adipose tissue in the
gelatinized form.
All affected animals suffer from this disease for months or years and usually
die of it. Progressive emaciation and persistent diarrhoea are important
features of paratuberculosis.
Pathology
Gross Appearances
The main lesions are as follows :
1. Emaciated carcasses with prominent ribs or bony eminences (hide bound
condition of the skin).
2. The lesions are more common in the ileum in the region of Peyer's patches
or near the ileo-caecal valves. Caecum, colon and rectum also show lesions.
3. The small intestinal mucous membrane may be severely thickened (4 to 5
times of its normal thickness) and is also corrugated.
The corrugations in the mucosae, run into longitudinal or transverse
directions like the convolutions of the brain. The crests of the folds may
show hyperaemia.

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The intestinal mucous membrane is smooth to touch, shiny in appearance or
covered with grey green slime. The mucous membrane of the intestine is
intact with no necrosis or ulceration in animals (e.g., cattle).
The mesenteric and colic lymph nodes are swollen and oedamatous. The
characteristic observation of JD cases is chronic enteritis with persistent
diarrhoea in the affected animals.
Microscopic Appearance
Proliferation of plasma cells and endothelioid cells is noticed in the mucosae
of the intestinal lesions. There are no changes in the muscular coat of the
intestine.
There is a disappearance of the normal cells and glands of the intestine with
increasing number of proliferated plasma cells etc., in the mucosae causing
swelling or distortion of the villi.
The changes like necrosis and caseation are not noticed in the intestine
affected with Johne's disease in cattle.
The disease process in JD stops at a stage called symplasma stage which is
marked by a partial fusion of the cytoplasm in the
endothelioid calls and appearance of clefts or channels.
The nuclei of the cells are found free in such clefts. The microscopic
sections of the small and large intestines reveal lamina propria of the mucosa
to be packed with epithelioid cells. These epithelioid cells have foamy
cytoplasm and are often multinucleated. Such cells also cause thickening of
the submucosae but the muscularis mucosae and the muscularis are left
intact.
Nests of epithelioid cells are also found in the mesenteric lymph nodes.
Acid-fast rods indistinguishable from M. paratuberculosis are seen in the
epithelioid cells of the sections of intestines and mesenteric lymph nodes
stained by Ziehl-Neelsen's method. Necrosis and calcification are noticed in
the nodular lesions in the sheep and goats.
Diagnosis
It is based on the following facts:
1. Symptoms and lesions with detection of acid-fast organisms in clumps in
the smears from the affected tissues ( intestinal mucosae mesentric lymph
nodes or faecal material stained by Ziehl-Neelsen's stain).
Smears are prepared from mucosal material pinched from rectum. Films of
moist faeces are made on the clean glass slides and stained by Z.N. method
to look for acid-fast bacteria.
2. Performance of Johnin Test

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The process is similar to double intradermal test with tuberculin to detect
tuberculosis. 0.2 m1 of Johnin (or avian tuberculin) is injected into the
dermis on the side of the neck. A diffuse hot and painful swelling appears in
72 hours after the injection of Johnin. The test is very useful to eradicate JD
from herds of cattle.
3. Cultural Examination
Suitable preparations of faecal material are sown on to tubes of serum Dubos
agar and reading is taken after 8 – 12 weeks.