Pathology

Pathology

In humans, the parasite matures into the adult worm in the intrahepatic biliary radicles, where it may reside for many years. The intrahepatic bile ducts are dilated, with epithelial hyperplasia and periductal fibrosis. These changes may lead to dysplasia, causing cholangiocarcinoma – the most serious and dreaded complication of this parasitic infestation. The eggs or dead worms may form a nidus for stone forma - tion in the gallbladder or common bile duct, which becomes thickened and much dilated in the late stages. Intrahepatic bile duct stones ar e also caused by the parasite producing mucin - rich bile. The dilated intrahepatic bile ducts may lead to chol - angitis, liver abscess and hepatitis. Pathology

The bacillus inhabits the colder parts of the body; hence, it is found in the nasal mucosa and skin in the region of the ears, foramen. The disease is transmitted from the nasal secretions of a patient, the infection being contracted in childhood or early adolescence. After an incubation period of several years, the disease presents with skin, upper respiratory or neurologi cal manifestations. The bacillus is acid fast but weakly so when compared with Mycobacterium tuberculosis. The disease is broadly classified into two groups: leproma tous and tuberculoid. In lepromatous leprosy , there is wide spread dissemination of abundant bacilli in the tissues, with macrophages and few lymphocytes. This is a reflection of the poor immune response, resulting in depleted host resistance from the patient. In tuberculoid leprosy , on the other hand, the patient shows a strong immune response with scant bacilli in the tissues, epithelioid granulomas, numerous lymphocytes and giant cells. The tissue damage is inversely proportional to the host’s immune response. There are various grades of the disease between the two main spectra called dimorphous or borderline variant. Summary box 6.12 Mycobacterium leprae : pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF

Leprosy is a chronic curable infection caused by M. leprae It occurs mainly in tropical regions and resource-poor countries The majority of cases are located in the Indian subcontinent Transmission is through nasal secretions, the bacillus inhabiting the colder parts of the body It is attributed to poor hygiene and insanitary conditions The incubation period is several years The initial infection occurs in childhood Lepromatous leprosy denotes a poor host immune reaction Tuberculoid leprosy occurs when host resistance is stronger than the virulence of the organism

Pathology

There are two types: ulcerative and hyperplastic. In both types, there may be marked mesenteric lymphadenopathy . /uni25CF Ulcerative type: The organism colonises the lymphat ics of the terminal ileum, causing transverse ulcers with typical undermined edges. The serosa is usually studded with tubercles. Histology shows caseating granuloma with giant cells ( Figure 6.36 ). This pathological entity , referred to as the ulcerative type, denotes a severe form of the dis ease in which the virulence of the organism overwhelms ★ Burrill Bernard Crohn , 1884–1983, gastroenterologist, Mount Sinai Hospital, New Y ork, NY , USA, described regional ileitis in 1932 along with Leon Ginzburg and Gordon Oppenheimer. ulcers lead to multiple strictures that may present later with luminal narrowing and intestinal obstruction. /uni25CF Hyperplastic type: This occurs when host resistance has the upper hand over the virulence of the organism. There is a marked inflammatory reaction causing hyper - plasia and thickening of the terminal ileum because of its abundance of lymphoid follicles, thus resulting in nar - rowing of the lumen and obstruction. Macroscopically , this type ma y be confused with Crohn’s disease. Ileocaecal right iliac tuberculosis ( Figure 6.37 ) may present with a - fossa mass and features of intestinal obstruction. As a result of fibrosis, there is shortening of the bowel with the cae - cum being pulled up into a subhepatic position with resul - tant widening of the ileocaecal angle beyond 90°. Summary box 6.23 - Tuberculosis: pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF - /uni25CF /uni25CF

Figure 6.36 Histology of ileocaecal tuberculosis showing epithelioid cell granuloma (black arrows) with caseation (star) (courtesy of Dr AK Mandal, New Delhi, India). Increasingly being seen in non-endemic areas, mostly among immigrants from endemic areas Two types are recognised – ulcerative and hyperplastic The ulcerative type occurs when the virulence of the organism is greater than the host defence and forms strictures The opposite occurs in the hyperplastic type and presents with a mass Small bowel strictures are common in the ulcerative type, presenting with obstructive symptoms, while the hyperplastic type mainly affects the ileocaecal area and presents with a right iliac fossa mass and obstructive symptoms In peritoneal tuberculosis, the parietal and visceral peritoneum is studded with tubercles Localised areas of ascites (loculated) depicts peritoneal involvement Encasement of bowel in a /f_i brotic sac (cocoon) may be seen in the plastic type of peritoneal tuberculosis, which presents with obstruction The lungs and other organs, particularly of the genitourinary system, may also be involved simultaneously

Pathology

Following ingestion of contaminated food or water, the organ ism colonises the Peyer’s patches in the terminal ileum, causing hyperplasia of the lymphoid follicles followed by necrosis and ulceration. The microscopic picture shows erythrophagocyto sis with histiocytic proliferation ( Figure 6.40 ). If the patient is left untreated or inadequately treated, the ulcers may lead to perforation and bleeding. The bowel may perforate at several sites, including the large bow el. Daniel Elmer Salmon , 1850–1914, veterinary pathologist, Chief of the Bureau of Animal Industry , Washington, DC, USA. Johann Conrad P eyer , 1653–1712, Professor of Logic, Rhetoric and Medicine, Scha ff hausen, Switzerland, described the lymph follicles in the intestine in 1677. e Widal , 1862–1929, Professor of Internal Pathology , and later of Clinical Medicine, The Faculty of Medicine, Paris, France. Georges Fernand Isidor A typical patient is from an endemic area or has recently visited such a country and su ff ers from a high temperature for 2–3 weeks. The patient may be toxic with abdominal distension from paralytic ileus and may have melaena due to haemor - rhage from a typhoid ulcer; this can lead to hypovolaemia. Blood and stool cultures confirm the nature of the infection and exclude malaria. Although obsolete in some parts of the world, the Widal test is still done on the Indian subcontinent. The test looks for the pr esence of agglutinins to O and H antigens of Salmonella Typhi and Paratyphi in the patient’s serum. In endemic areas, laboratory facilities may sometimes be limited. Certain other tests have been developed that identify sensitive and specific markers for typhoid fever. Practical and cheap kits are available for their rapid detection that need no special expertise and equipment. These are MultiTest Dip-S-Ticks to detect immunoglobulin G (IgG), Tubex to detect immunoglobulin M (IgM) and TyphiDot to detect IgG and IgM. These tests are particularly valuable when blood cultures are negative (as a result of prehospital treatment or self-medication with antibiotics) or facilities for such an investigation are not available. In the second or third week of the illness, if there is severe generalised abdominal pain, this indicates a perforated typhoid ulcer unless otherwise proven. The patient, who is already very ill, deteriorates further with classical features of peritonitis. An erect chest radiograph or a lateral decubitus film (in the very ill, as they usually are) will show free gas in the peritoneal cav - ity . In fact, any patient being treated for typhoid fever who shows a sudden deterioration accompanied by abdominal signs should be considered to have a typhoid perforation until proven otherwise. - - -

Figure 6.40 Histology of enteric perforation of the small intestine showing erythrophagocytosis (arrows) with predominantly histiocytic proliferation (courtesy of Dr AK Mandal, New Delhi, India).

Diagnosis of bowel perforation secondary to typhoid /uni25CF /uni25CF /uni25CF /uni25CF

The patient presents in, or has recently visited, an endemic area The patient has persistent high temperature and is very toxic Positive blood or stool cultures for Salmonella Typhi and the patient is already on treatment for typhoid After the second week, signs of peritonitis usually denote perforation, which is con /f_i rmed by the presence of free gas seen on a radiograph

Pathology

In humans, the parasite matures into the adult worm in the intrahepatic biliary radicles, where it may reside for many years. The intrahepatic bile ducts are dilated, with epithelial hyperplasia and periductal fibrosis. These changes may lead to dysplasia, causing cholangiocarcinoma – the most serious and dreaded complication of this parasitic infestation. The eggs or dead worms may form a nidus for stone forma - tion in the gallbladder or common bile duct, which becomes thickened and much dilated in the late stages. Intrahepatic bile duct stones ar e also caused by the parasite producing mucin - rich bile. The dilated intrahepatic bile ducts may lead to chol - angitis, liver abscess and hepatitis. Pathology

The bacillus inhabits the colder parts of the body; hence, it is found in the nasal mucosa and skin in the region of the ears, foramen. The disease is transmitted from the nasal secretions of a patient, the infection being contracted in childhood or early adolescence. After an incubation period of several years, the disease presents with skin, upper respiratory or neurologi cal manifestations. The bacillus is acid fast but weakly so when compared with Mycobacterium tuberculosis. The disease is broadly classified into two groups: leproma tous and tuberculoid. In lepromatous leprosy , there is wide spread dissemination of abundant bacilli in the tissues, with macrophages and few lymphocytes. This is a reflection of the poor immune response, resulting in depleted host resistance from the patient. In tuberculoid leprosy , on the other hand, the patient shows a strong immune response with scant bacilli in the tissues, epithelioid granulomas, numerous lymphocytes and giant cells. The tissue damage is inversely proportional to the host’s immune response. There are various grades of the disease between the two main spectra called dimorphous or borderline variant. Summary box 6.12 Mycobacterium leprae : pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF

Leprosy is a chronic curable infection caused by M. leprae It occurs mainly in tropical regions and resource-poor countries The majority of cases are located in the Indian subcontinent Transmission is through nasal secretions, the bacillus inhabiting the colder parts of the body It is attributed to poor hygiene and insanitary conditions The incubation period is several years The initial infection occurs in childhood Lepromatous leprosy denotes a poor host immune reaction Tuberculoid leprosy occurs when host resistance is stronger than the virulence of the organism

Pathology

There are two types: ulcerative and hyperplastic. In both types, there may be marked mesenteric lymphadenopathy . /uni25CF Ulcerative type: The organism colonises the lymphat ics of the terminal ileum, causing transverse ulcers with typical undermined edges. The serosa is usually studded with tubercles. Histology shows caseating granuloma with giant cells ( Figure 6.36 ). This pathological entity , referred to as the ulcerative type, denotes a severe form of the dis ease in which the virulence of the organism overwhelms ★ Burrill Bernard Crohn , 1884–1983, gastroenterologist, Mount Sinai Hospital, New Y ork, NY , USA, described regional ileitis in 1932 along with Leon Ginzburg and Gordon Oppenheimer. ulcers lead to multiple strictures that may present later with luminal narrowing and intestinal obstruction. /uni25CF Hyperplastic type: This occurs when host resistance has the upper hand over the virulence of the organism. There is a marked inflammatory reaction causing hyper - plasia and thickening of the terminal ileum because of its abundance of lymphoid follicles, thus resulting in nar - rowing of the lumen and obstruction. Macroscopically , this type ma y be confused with Crohn’s disease. Ileocaecal right iliac tuberculosis ( Figure 6.37 ) may present with a - fossa mass and features of intestinal obstruction. As a result of fibrosis, there is shortening of the bowel with the cae - cum being pulled up into a subhepatic position with resul - tant widening of the ileocaecal angle beyond 90°. Summary box 6.23 - Tuberculosis: pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF - /uni25CF /uni25CF

Figure 6.36 Histology of ileocaecal tuberculosis showing epithelioid cell granuloma (black arrows) with caseation (star) (courtesy of Dr AK Mandal, New Delhi, India). Increasingly being seen in non-endemic areas, mostly among immigrants from endemic areas Two types are recognised – ulcerative and hyperplastic The ulcerative type occurs when the virulence of the organism is greater than the host defence and forms strictures The opposite occurs in the hyperplastic type and presents with a mass Small bowel strictures are common in the ulcerative type, presenting with obstructive symptoms, while the hyperplastic type mainly affects the ileocaecal area and presents with a right iliac fossa mass and obstructive symptoms In peritoneal tuberculosis, the parietal and visceral peritoneum is studded with tubercles Localised areas of ascites (loculated) depicts peritoneal involvement Encasement of bowel in a /f_i brotic sac (cocoon) may be seen in the plastic type of peritoneal tuberculosis, which presents with obstruction The lungs and other organs, particularly of the genitourinary system, may also be involved simultaneously

Pathology

Following ingestion of contaminated food or water, the organ ism colonises the Peyer’s patches in the terminal ileum, causing hyperplasia of the lymphoid follicles followed by necrosis and ulceration. The microscopic picture shows erythrophagocyto sis with histiocytic proliferation ( Figure 6.40 ). If the patient is left untreated or inadequately treated, the ulcers may lead to perforation and bleeding. The bowel may perforate at several sites, including the large bow el. Daniel Elmer Salmon , 1850–1914, veterinary pathologist, Chief of the Bureau of Animal Industry , Washington, DC, USA. Johann Conrad P eyer , 1653–1712, Professor of Logic, Rhetoric and Medicine, Scha ff hausen, Switzerland, described the lymph follicles in the intestine in 1677. e Widal , 1862–1929, Professor of Internal Pathology , and later of Clinical Medicine, The Faculty of Medicine, Paris, France. Georges Fernand Isidor A typical patient is from an endemic area or has recently visited such a country and su ff ers from a high temperature for 2–3 weeks. The patient may be toxic with abdominal distension from paralytic ileus and may have melaena due to haemor - rhage from a typhoid ulcer; this can lead to hypovolaemia. Blood and stool cultures confirm the nature of the infection and exclude malaria. Although obsolete in some parts of the world, the Widal test is still done on the Indian subcontinent. The test looks for the pr esence of agglutinins to O and H antigens of Salmonella Typhi and Paratyphi in the patient’s serum. In endemic areas, laboratory facilities may sometimes be limited. Certain other tests have been developed that identify sensitive and specific markers for typhoid fever. Practical and cheap kits are available for their rapid detection that need no special expertise and equipment. These are MultiTest Dip-S-Ticks to detect immunoglobulin G (IgG), Tubex to detect immunoglobulin M (IgM) and TyphiDot to detect IgG and IgM. These tests are particularly valuable when blood cultures are negative (as a result of prehospital treatment or self-medication with antibiotics) or facilities for such an investigation are not available. In the second or third week of the illness, if there is severe generalised abdominal pain, this indicates a perforated typhoid ulcer unless otherwise proven. The patient, who is already very ill, deteriorates further with classical features of peritonitis. An erect chest radiograph or a lateral decubitus film (in the very ill, as they usually are) will show free gas in the peritoneal cav - ity . In fact, any patient being treated for typhoid fever who shows a sudden deterioration accompanied by abdominal signs should be considered to have a typhoid perforation until proven otherwise. - - -

Figure 6.40 Histology of enteric perforation of the small intestine showing erythrophagocytosis (arrows) with predominantly histiocytic proliferation (courtesy of Dr AK Mandal, New Delhi, India).

Diagnosis of bowel perforation secondary to typhoid /uni25CF /uni25CF /uni25CF /uni25CF

The patient presents in, or has recently visited, an endemic area The patient has persistent high temperature and is very toxic Positive blood or stool cultures for Salmonella Typhi and the patient is already on treatment for typhoid After the second week, signs of peritonitis usually denote perforation, which is con /f_i rmed by the presence of free gas seen on a radiograph

Pathology

In humans, the parasite matures into the adult worm in the intrahepatic biliary radicles, where it may reside for many years. The intrahepatic bile ducts are dilated, with epithelial hyperplasia and periductal fibrosis. These changes may lead to dysplasia, causing cholangiocarcinoma – the most serious and dreaded complication of this parasitic infestation. The eggs or dead worms may form a nidus for stone forma - tion in the gallbladder or common bile duct, which becomes thickened and much dilated in the late stages. Intrahepatic bile duct stones ar e also caused by the parasite producing mucin - rich bile. The dilated intrahepatic bile ducts may lead to chol - angitis, liver abscess and hepatitis. Pathology

The bacillus inhabits the colder parts of the body; hence, it is found in the nasal mucosa and skin in the region of the ears, foramen. The disease is transmitted from the nasal secretions of a patient, the infection being contracted in childhood or early adolescence. After an incubation period of several years, the disease presents with skin, upper respiratory or neurologi cal manifestations. The bacillus is acid fast but weakly so when compared with Mycobacterium tuberculosis. The disease is broadly classified into two groups: leproma tous and tuberculoid. In lepromatous leprosy , there is wide spread dissemination of abundant bacilli in the tissues, with macrophages and few lymphocytes. This is a reflection of the poor immune response, resulting in depleted host resistance from the patient. In tuberculoid leprosy , on the other hand, the patient shows a strong immune response with scant bacilli in the tissues, epithelioid granulomas, numerous lymphocytes and giant cells. The tissue damage is inversely proportional to the host’s immune response. There are various grades of the disease between the two main spectra called dimorphous or borderline variant. Summary box 6.12 Mycobacterium leprae : pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF

Leprosy is a chronic curable infection caused by M. leprae It occurs mainly in tropical regions and resource-poor countries The majority of cases are located in the Indian subcontinent Transmission is through nasal secretions, the bacillus inhabiting the colder parts of the body It is attributed to poor hygiene and insanitary conditions The incubation period is several years The initial infection occurs in childhood Lepromatous leprosy denotes a poor host immune reaction Tuberculoid leprosy occurs when host resistance is stronger than the virulence of the organism

Pathology

There are two types: ulcerative and hyperplastic. In both types, there may be marked mesenteric lymphadenopathy . /uni25CF Ulcerative type: The organism colonises the lymphat ics of the terminal ileum, causing transverse ulcers with typical undermined edges. The serosa is usually studded with tubercles. Histology shows caseating granuloma with giant cells ( Figure 6.36 ). This pathological entity , referred to as the ulcerative type, denotes a severe form of the dis ease in which the virulence of the organism overwhelms ★ Burrill Bernard Crohn , 1884–1983, gastroenterologist, Mount Sinai Hospital, New Y ork, NY , USA, described regional ileitis in 1932 along with Leon Ginzburg and Gordon Oppenheimer. ulcers lead to multiple strictures that may present later with luminal narrowing and intestinal obstruction. /uni25CF Hyperplastic type: This occurs when host resistance has the upper hand over the virulence of the organism. There is a marked inflammatory reaction causing hyper - plasia and thickening of the terminal ileum because of its abundance of lymphoid follicles, thus resulting in nar - rowing of the lumen and obstruction. Macroscopically , this type ma y be confused with Crohn’s disease. Ileocaecal right iliac tuberculosis ( Figure 6.37 ) may present with a - fossa mass and features of intestinal obstruction. As a result of fibrosis, there is shortening of the bowel with the cae - cum being pulled up into a subhepatic position with resul - tant widening of the ileocaecal angle beyond 90°. Summary box 6.23 - Tuberculosis: pathology /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF - /uni25CF /uni25CF

Figure 6.36 Histology of ileocaecal tuberculosis showing epithelioid cell granuloma (black arrows) with caseation (star) (courtesy of Dr AK Mandal, New Delhi, India). Increasingly being seen in non-endemic areas, mostly among immigrants from endemic areas Two types are recognised – ulcerative and hyperplastic The ulcerative type occurs when the virulence of the organism is greater than the host defence and forms strictures The opposite occurs in the hyperplastic type and presents with a mass Small bowel strictures are common in the ulcerative type, presenting with obstructive symptoms, while the hyperplastic type mainly affects the ileocaecal area and presents with a right iliac fossa mass and obstructive symptoms In peritoneal tuberculosis, the parietal and visceral peritoneum is studded with tubercles Localised areas of ascites (loculated) depicts peritoneal involvement Encasement of bowel in a /f_i brotic sac (cocoon) may be seen in the plastic type of peritoneal tuberculosis, which presents with obstruction The lungs and other organs, particularly of the genitourinary system, may also be involved simultaneously

Pathology

Following ingestion of contaminated food or water, the organ ism colonises the Peyer’s patches in the terminal ileum, causing hyperplasia of the lymphoid follicles followed by necrosis and ulceration. The microscopic picture shows erythrophagocyto sis with histiocytic proliferation ( Figure 6.40 ). If the patient is left untreated or inadequately treated, the ulcers may lead to perforation and bleeding. The bowel may perforate at several sites, including the large bow el. Daniel Elmer Salmon , 1850–1914, veterinary pathologist, Chief of the Bureau of Animal Industry , Washington, DC, USA. Johann Conrad P eyer , 1653–1712, Professor of Logic, Rhetoric and Medicine, Scha ff hausen, Switzerland, described the lymph follicles in the intestine in 1677. e Widal , 1862–1929, Professor of Internal Pathology , and later of Clinical Medicine, The Faculty of Medicine, Paris, France. Georges Fernand Isidor A typical patient is from an endemic area or has recently visited such a country and su ff ers from a high temperature for 2–3 weeks. The patient may be toxic with abdominal distension from paralytic ileus and may have melaena due to haemor - rhage from a typhoid ulcer; this can lead to hypovolaemia. Blood and stool cultures confirm the nature of the infection and exclude malaria. Although obsolete in some parts of the world, the Widal test is still done on the Indian subcontinent. The test looks for the pr esence of agglutinins to O and H antigens of Salmonella Typhi and Paratyphi in the patient’s serum. In endemic areas, laboratory facilities may sometimes be limited. Certain other tests have been developed that identify sensitive and specific markers for typhoid fever. Practical and cheap kits are available for their rapid detection that need no special expertise and equipment. These are MultiTest Dip-S-Ticks to detect immunoglobulin G (IgG), Tubex to detect immunoglobulin M (IgM) and TyphiDot to detect IgG and IgM. These tests are particularly valuable when blood cultures are negative (as a result of prehospital treatment or self-medication with antibiotics) or facilities for such an investigation are not available. In the second or third week of the illness, if there is severe generalised abdominal pain, this indicates a perforated typhoid ulcer unless otherwise proven. The patient, who is already very ill, deteriorates further with classical features of peritonitis. An erect chest radiograph or a lateral decubitus film (in the very ill, as they usually are) will show free gas in the peritoneal cav - ity . In fact, any patient being treated for typhoid fever who shows a sudden deterioration accompanied by abdominal signs should be considered to have a typhoid perforation until proven otherwise. - - -

Figure 6.40 Histology of enteric perforation of the small intestine showing erythrophagocytosis (arrows) with predominantly histiocytic proliferation (courtesy of Dr AK Mandal, New Delhi, India).

Diagnosis of bowel perforation secondary to typhoid /uni25CF /uni25CF /uni25CF /uni25CF

The patient presents in, or has recently visited, an endemic area The patient has persistent high temperature and is very toxic Positive blood or stool cultures for Salmonella Typhi and the patient is already on treatment for typhoid After the second week, signs of peritonitis usually denote perforation, which is con /f_i rmed by the presence of free gas seen on a radiograph