Category Archives: Chronic Bacterial Infection Granuloma

Pictures Of Chronic Bacterial Infection Granuloma

Posted by on February 1, 2012 No comments

Pictures Of Chronic Bacterial Infection Granuloma

Early TB granuloma showing epithelioid cells and Langhans giant cells

TB granuloma showing epithelioid cells, many Langhans giant cells and central caseation

Milliary TB showing numerous tiny tubercles

Gumma of syphilis showing central caseation-like necrosis

Hutchinson’s teeth in congenital

Lepromatous reaction in the skin

Lepra cells and giant cells containing the lepra bacilli (arrow)

Sarcoid granmuloma formed of epithelioid cells and giant cells without caseation

Rhinoschleroma: lesion showing numerous Mickulicz cells

Aclinomycosis: club-shapet bacilli are seen in the center surrounded by neutrophils & outer layer of chronic inflammatory cells

Intestinal bilharziasis: numerous ova are present in submucosa

Bilharziasis of the liver: ova surrounded by granulaomas are present.

HYDATID DISEASE

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HYDATID DISEASE

Caused by a small tape worm known as taenia echinococcus. It is a parasite of the dog living in its intrestine.

Method of infection: The human is infected by eating raw vegetable contaminated with the excreta of the infected dogs which is full of ova. In the intestine the ova hatch into embryos which penetrate the wall and are carried by the blood stream to distant organs, the most common is the liver and mesentery. From the liver, the embryos may reach other organs as lung, brain, bones, kidneys.

Reaction: The hydatid cyst excites a chronic inflammatory reaction in the surrounding tissues, with histiocytes, eosinophils, foreign body giant cells and fibroblasts.

Complications:

1- Pressure effects: depending on the size and the site of the cyst.

* A cyst in the liver may reach a big size.

* A cyst in the bone is usually small and multilocular. Hydatid cysts of bones leads to rarefaction of the boney tissue resulting in pathological fracture. It is more common in the ends of long bones such as tibia.

2- Rupture of the cyst: leading to the following effects,
a- Secondary cyst may develop:

- In the surrounding tissues e.g. hydatid cyst of the liver may rupture leading to secondary cysts in the peritoneal cavity.

- In distant organs when the brood corpuscles reach the blood stream leading to secondary cysts in the lungs, brain, kidney.

b- Allergic manifestations: due to sensitization of the body against the protein part of the hydatid fluid. This lead to:

- Urticarial eruption

- Anaphylactic shock, occurs if the fluid enters the blood following rupture of the cyst.

3- Secondary infection: with abscess formation.

4- Pathological calcification.

BILHARZIASIS

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BILHARZIASIS

Bilharziasis is an indemic parasite disease in Egypt caused by Schistosoma hematobium and schistosma mansoni.

The infective stage (cercaria) enters the body by piercing the skin. The adult warm lives & matures in the portal vein.

This worm then migrates to lay its ova. The ova deposited become surrounded by bilharzial granulation tissue made of lymphocytes, plasma cells, foreign body giant cells and eosinophils (bilharzial granulation tissue). The lesion ends in fibrosis.

Urinary bladder Bilharziasis

It is caused mainly by S. hemarobium and affects mainly the trigone of urinary bladder and around ureteric orifices.

 

Lesions:

a) Congestion and granularity.

b) Sandy patches: irregular dirty yellowish patch due to shining of heavy deposits of calcified ova through thinned or atrophied mucosa.

c) Bilharzial polypi: rare.

d) Bilharzial ulcers: occur due to continuous piercing of the ova, atrophy of the mucosa or after casting of a polyp.

Complications of urinary bilharziasis:

1 – Terminal hematuria and anemia.

2- Cystitis.

3- Fibrosis of bladder neck leading to urinary retention or around ureteric orifices causing hydroureter and hydronephrosis.

4- Renal stones.

5- Carcinoma of urinary bladder.

Intestinal Bilhanziasis

It is mainly caused by S. mansoni. The rectum is the commonest site, then it diminishes in severity proximally to become very rare in the small intestine.

Lesions: one a more of the following lesions may appear

1- Hyperaemia and granulanity: are not very well apparent because the intestinal mucosa is thick.

2- Bilhazial ulcers: are more common and usually larger than those of the urinary bladder.

3- Sandy patches: are less common.

4- Bilhanzial polypi: are common, particularly in the rectum and sigmoid colon. The mucosa is elevated, then pushed towards the lumen, carrying with it a central vascular core of fibrous tissue containing the ova and bilharzial granulation tissue. The mucosa in thickened due to reactive hyperplasia.

The polyps are usually multiple, sessile or pedunculated. Torsion of a polyp may occur with cut of blood supply leading to necrosis of the polyp which falls down leaving an ulcer.

Complications of intestinal bilharziasis:

1) Bilharzial dysentery with diarrhea, tenesmus, blood and mucous.

2) Intestinal hemorrhage which is prolonged leading to hypochomic anemia.

3) Pericolic bilhazioma which is a tumor-like mass formed of bilharzial granulation tissue and is usually misdiagnosed as cancer colon.

4) Chronic intestinal obstruction is rare due to a localized is band of fibosis.

5) Closed bilharzial lesion in which marked fibrosis blocks the way for the freshly coming ova, which pass into the portal circulation as emboli to produce bilharziasis of the liver.

Bilharziasis of liver

There is often massive fibrosis around major portal tracts leading to portal hypertension.

Portal hypertesion

It is due to fibrosis and arterio-venous shunting. This may be manifested as:

1- Hepatosplenomegaly.

2- Ascites.

3- Varices due to opening of porto-systemic shunts
sites are:

a- At the lower third of esophagus forming esophageal varices.

b- Around the umbilicus forming caput medosa. c- Around the anus forming piles. 4- Hepatic failure.

ACTINOMYCOSIS

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ACTINOMYCOSIS

It a chronic suppurtive granulematous disease caused by filamentous bacteria called actinomyces bovis. These are normal habitants of tonsils and mouth (with bad teeth) & intestine. The infection occurs with lowering of the immunity.

The organisms attack the body leading to formation of multiple abscesses containing colonies of the organism in the affected area which open to skin by discharging sinuses.

The drained pus contains colonies which appear yellowish in colour and called sulpher granules.

Sites of infection:

a- Cervicofacial type (60%).

b- Abdomenal or illocecal type (20%).

c- Pulmonary type of the base of the lung (least common).

Microscopic appearance:

• The organisms appear as filaments having club-shaped ends.

• It is surrounded by pus then another layer of chronic inflammation.

The granuloma heals by fibrosis.

RHINOSCLEROMA

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RHINOSCLEROMA

Is caused by kelbsiella rhinscleromatis.

The granules affect the mucous membrane of the nose or the mucous membrane of the larynx or pharynx.

Infection leads to nodule formation or leads to thickening of the mucous membrane.

Microscopically: the lesion is characterized by the presence of:

a) Mickulicz cells: macrophages with clear cytoplasm containing organism.

b) Russel bodies: plasma cells showing hyaline degeneration.

These are the two characteristic cells along with lymphocytes, many blood vessels and fibroblasts.

It ends in fibrosis in the affected area.

SARCOIDOSIS

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SARCOIDOSIS

 

It is of unknown cause. It is characterized by multiple granulomatous lesions, may affect lymph nodes, lungs, skin spleen, eyes, salivary glands, liver and bones particularly those of the hands and feet. It is more common in young adult.

- The disease most commonly gives rise to enlarged mediastinal and pulmonary hilar lymph nodes often without symptoms.

- Lesion in lung resembles miliary TB by X-ray.

- Lesion in skin.

Microscopically:

The sarcoid lesions consist of tubercle like granuloma composed of epthelioid cells with occasional Langhans giant cells but with fewer lymphocytes than in TB, the giant cells may contain calcium-rich star-shaped inclusion bodies knows as asteroid bodies. Unlike tuberculosis the lesions do not undergo caseation although there may be little central necrosis.

- The disease can cause blindness by involving the uveal tract.

- The disease is occasionally fatal usually as a result of fibrosis of the pulmonary lesions leading to right ventricular heart failure.

Diagnosis:

1- Taking a biopsy to detect the characteristic sarcoid reaction.

Kveim test: which consists of intradermal injection of an extract of sarcoid tissue, usually obtained from an affected spleen of a patient. After about 2 weeks, a skin biopsy from the site of injection is done. If the test is positive, the characteristic sarcoid reaction can be detected in the subcutaneous tissues.

LEPROSY (HANSEN’S DISEASE)

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LEPROSY (HANSEN’S DISEASE)

Definition:

It is a chronic granulomatous inflammatory disease caused by mycobacterium leprae.

It affects primarily the peripheral nervous system and skin. As a result of nerve damage there may be paralysis, deformity, and ulcerations.

 

Method of infection:

Directly from the ulcerated nodules of the nasal discharge. An intimate and prolonged contact with the patient is important. The incubation period is long (years).

The bacilli probably enter via the respiratory tract, disseminate hemtogenously and grow particularly in the dermal nerves.

 

The reaction of the body against the organism:

1-    Cellular reaction: formed of chronic inflammatory cells mainly: histiocytes, lymphocytes, plasma cells and fiberoblasts. The histiocytes engulf the organisms and are changed into lepra cells which appear large, rounded and have vacuolated, cytoptasm.

2-    Vascular reaction: in the form of endarteritis obliterans.

 

Types of leprosy

The type of leprosy depends or the degree of immunity.

I-  Lepromatous leprosy or nodular leprosy:

This type usually develops in patients who failed to develop cell-mediated immunity (C.M.I) to mycobacterium leprae, in which bacilli are present in large numbers in the affected tissues.

II-      Tuberculoid or Maculoanesthetic leprosy: This type usually develops in patients with high degree of cell-mediated immunity in which bacilli are scanty in tissues.

III-   Borderline leprosy:

It is an intermediate, unstable form of the disease.

 I- Lepromatous or nodular leprosy

1- It is the commonest type and most severe one.

This type occurs in patients with low cell-mediated immunity and so the number of bacilli in the affected tissues are large.

2- Cutaneous lesions or dermal lesions:

a)  There are multiple firm nodules. These nodules affect the

face and extensor surfaces of the extremities. On the face the lesion has a bilateral, symmetrical distribution over the forehead, nose, ears and lips. The eyebrows are lost. The face is disfigured giving the characteristic Leonine face.

b)   Coarsening and thickening of the skin over much of the body.

c)   The regional lymph nodes are enlarged.

3- Nervous lesions:

These cause destruction of the peripheral nerves, especially the ulnar nerve which becomes thickened and fibrosed. This results in loss of sensation and paralysis. The extremities become anesthetic in a glove and stocking distribution.

4- Nasal lesions:

Nodules are seen on the nasal mucosa which may ulcerate and the septum is perforated. Nodules may form also in the palate.

5- Trophic Lesions:

These result from cutaneous anesthesia and motor paralysis. Deep ulcers form which end by mutilation of small bones of the fingers. Claw hand deformity may occur due to fibrosis and fixation of the joints.

6-   It is a systemic disease and the bacilli spread by blood stream to larynx, eyes, bones and testes. Their multibacillary lesions cause iritis, osteitis, bone erosions, lanyngeal mucosal thickening with hoarse voice.

7-   Secondary amyloidosis is often a serious complication.

II-  Tuberculoid or maculoanesthetic leprosy:

 

1- It is a mild type.

It occurs in patients with high cell-mediated immunity and so the number of bacilli are scanty in lesions.

2- Cutaneous lesions:

In the form of multiple rounded macules having pale centre and elevated borders. The macules appear on the face, limbs and trunk. Lesions are asymmetrical, fewer and smaller than those of lepromatous leprosy.

3- Nervous lesions and trophic lesions are similar.

N.B. Sever nerve damage results from the destructive effect of the fibrosing granulomas.

4-   Tuberculoid leprosy does not spread systemically and
patients who have strong C.M.I usually undergo self-
cure even without treatment.

 

III-  Borderline leprosy

It appears clinically and pathologically as a mixture of both types.

 

Differences between types of leprosy

1st type 2nd type 3rd type
Nodules in the face Macules with anesthetic center In between
In both types nerve inflammation occurs and spontaneous falling of the terminal phalanges.
Resistance is weak Resistance is relatively high
Characteristic cell under the microscope is the lepra cell which is a macrophage with clear cytoplasm containing organisms.
Lepra cell are mixed with lymphocytes, plasma cells Lepra cells are arranged at the center and surrounded by lymphocytes, macrophages forming tubercles
For infection by leprosy to occur prolonged contact with the patient is needed due to the ulceration of the nodules.

 

Diagnosis of leprosy:

1-       Demonstration of acid fast bacilli in smears from nasal discharage or scrapings of nasal mucosa.

2-       Biopsy of a skin nodule to demonstrate the characteristic tissue reaction.

3-       Lepromin test: is similar to the tuberculin test. It consists of intradermal injection of the extracts of leprosy nodule containing dead bacilli. A small nodule appears at the site of injection when the test is positive.

Causes of death: Renal failure from secondary amyloidosis.

CONGENITAL SYPHILI

Posted by on January 31, 2012 No comments

CONGENITAL SYPHILI

The disease is transmitted from the syphilitic mother to the fetus. Its severity depends mainly on the duration of material infection.

Manifestions of congenital syphilis

1. Early death of fetus leading to abortion.

2.  Premature still-borne child: in which the skin is
macerated and the syphilitic reaction appears in many
organs as liver, spleen, lung and liver which shows
congenital syphilitic cirrhosis.

 

3. Full term alive child showing the following manifestations:

a)   Syphilitic rash: as in secondary stage of the acquired syphilis. It is more common in extremities and buttock.

b)   Mucous patches: in mouth, vagina.

c)   Destruction of the nasal septum with saddle shaped nose due to gumma formation.

d)   Fissuring of the skin of the angle of mouth and anus.

4.  Living child which is apparently healthy but the
following manifestations appear later on:

a)    The permanent teeth show what is known Hutchinson’s teeth in which the central incisors appear small, widely separated, notched and peg shaped.

b)   Gumma which may appear in long bones and nasal septum.

c)   Bilateral interstitial keratitis leading to corneal opacity and blindness.

d)   Deafness due to syphilitic affection of the eighth nerve.

ACQUIRED SYPHILIS

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ACQUIRED SYPHILIS

 

-Primary stage:

Also known as primary sore or chancre appears at the site of infection after an incubation period 3-4 weeks. It appears as very firm or hard pale brownish red in colour, 1cm in diameter, painless nodule which soon ulcerates (in few days) and becomes infectious. The regional lymph nods are enlarged, indurated (hard) and painless.

Sites of chancre:

1-     Genital organs: (are the most common sites) as glans penis, skin of penis, scrotum, labia majora and minora, vagina and cervix.

2-     Extra genital: chancre appears on lips, mucous membrane of mouth, tongue, fingers, and nipple.

End result: after 2-3 weeks the chancre disappears completely without treatment leaving thin or no scar.

 

 

-Secondary stage or stage of generalization:

Affects many tissues of ectodermal origin. It is of maximal infectivity. The manifestations appears few months from the disappearance of the chancre and are in the form of:

1. Skin lesion:

a. Syphilitic rash: which appears as macules (small areas of erythema), papules (small raised patches) and pustules (small lesion filled with pus)

They are symmetrical and polymorphic i.e. many types of them are present at the same time. They are widespread, hot and itchy. The palms of hands and soles of feet are commonly involved.

b.  Alopecia: Loss of hair of scalp either total or patchy due
to syphilitic lesion of the hair follicles.

c.  Leucoderma: White patches of the skin due to loss of
melanin.

 

2. Mucous membrane lesion:

Round or oval grayish white mucous patches appearing full of spirochaetes and highly infectious. In mouth, tongue, and vagina.

 

3. Condyloma lata: which are flat raised papules at the
mucocutaneous junctions (anus, vulva) and are highly
infectious.

 

4- Genralized enlargement of lymph nodes especially epitrochlear and posterior cervical groups.

End result: After 2-4 weeks all the secondary lesions disappear without any trace then pass to the tertiary stage.

 

 

-Tertiary stage:

It appears usually after 2-3 years or even up to 25 years from the primary infection and takes one of two forms of syphilitic reactions:

a. Diffuse syphilitic granulation tissue: appears most commonly in syphilitic aortitis and syphilis of nervous system.

b. Localized syphilitic granulation tissue (gumma):

Gumma is a tumor-like mass of 3-8 cm in diameter. It is firm and rubbery in consistency and cause destruction of tissues in which it develops.

Sites of gumma:

Subcutaneous tissues, testes, liver, tongue, bones as tibia and nasal bones (leading to loss of septum of the nose and perforation in palate).

 

 

Microscopically:

It is formed of large collection of lymphocytes, plasma cells and hisiocytes with some foreign body giant cells, as well as endarteritis obliterans and marked fibrosis. The center of gumma shows caseation like necrosis.

All tertiary lesions tend to heal eventually by fibrosis and marked distortion of the organ and interference with function may result from extensive scarring.

 

Effects of gumma:

1-   Skin and subcutaneous tissue: syphilitic ulcer.

2-   Nose: saddle shaped nose.

3-   Larynx: stenosis and hoarseness of voice.

4-   Tongue: ulcer which is precancerous.

SPYHILIS

Posted by on January 31, 2012 No comments

SPYHILIS

Definition:

It’s a highly infectious, venereal, chronic granulomatous inflammatory disease caused by treponerna pallidum.

 

Methods of infection:

1-     Direct contact during sexual intercourse. The spirochaetes can penetrate an intact mucous membrane but it cannot enter the skin unless there are abrasions. The spirochaetes spread to the regional lymph nodes rapidly and reach the blood stream before the appearance of primary lesion.

2-     Extra genital:

a- The disease can be transmitted by blood transfusion from any infected donor.

b- Contact with extragenital lesion e.g. during kissing (lip and tongue).

3-  Via placenta: from infected mother to the fetus. This
leads to congenital syphilis.

 

Reaction of the body:

The syphilitic reaction appears either in small or large localized granulomatous masses or as diffuse syphilis granulation tissue. The reaction consists of dense accumulation of lymphocytes and plasma cells around increased number of blood vessels (i.e. periarteritis). Few histiocytes, some fibroblasts and occasional foreign body giant cells are

present. In chronic lesions, there is increased amount of fibrous tissue with endarteritis obliterans i.e. narrowing of lumen of arteries due to proliferation of subendothelial connective tissue leading to thickening of the wall.

Endarteritis and periarteritis are important features of syphilis. The histological features are not diagnostic without the demonstration of Tr. Pallidum.

 

Classification or types of syphilis:

a- Acquired syphilis which appears in three stages.

b- Congenital syphilis.