Pathology Education Instructional Resource - User contributions [en]

Cytologically Yours

2025-04-10T13:44:10Z

Peter Anderson:

Welcome to '''Cytologically Yours''', an online library of teaching materials from the University of Alabama at Birmingham, Department of Pathology. It is maintained and curated under the direction of [https://scholars.uab.edu/2122-peter-anderson] Dr. Peter Anderson.

== Cases of the Week ==
The following are a collection of interesting cytology cases seen at our institution.

* [[Cytologically Yours: CoW: 20131125|Current Case of the Week]]
* [[Cytologically Yours: CoW|Cases of the Week Index]]

== Unknowns ==
The following cases are compiled by the Cytopathology Fellows for conference discussion every month.

* [[Cytologically Yours: Unknowns: 2014#May|Current Unknowns]]
* [[Cytologically Yours: Unknowns|Unknowns Index]]

== HSOM Systemic Pathology Virtual Microscopy Slides ==
Virtual Microscopy slides for HCOM Systemic Pathology Modules. Slides curated by Dr. Peter Anderson and by Dr. Jennifer Gordetsky (currently at the Department of Pathology, Vanderbilt University).

=== Breast ===
<gallery heights="250px" widths="250px">
File:IPLab7IDC1b.jpg|</gallery>
* Normal Breast
<peir-vm>IPLab7IDC_Normal_Breast</peir-vm>

* Breast - Benign
* Fibroadenoma
<peir-vm>IPLab7Fibroadenoma</peir-vm>
* Fibrcystic Change
<peir-vm>UAB-Histology-00118</peir-vm>
*Phylloides Tumor
<peir-vm>UAB-Histology-00118</peir-vm>
*Myofibroblastoma
<peir-vm>UAB-Histology-00118</peir-vm>

* Breast - Malignant
* Lobular Carcinoma
* Paget Disease and DCIS
*Invasive Ductal Carcinoma

{{Cytologically Yours}}

Cytologically Yours

2025-04-10T13:42:21Z

Peter Anderson: /* HSOM Systemic Pathology Virtual Microscopy Slides */

Welcome to '''Cytologically Yours''', an online library of teaching materials from the University of Alabama at Birmingham, Department of Pathology. It is maintained and curated under the direction of [https://scholars.uab.edu/2122-peter-anderson] Dr. Peter Anderson.

== Cases of the Week ==
The following are a collection of interesting cytology cases seen at our institution.

* [[Cytologically Yours: CoW: 20131125|Current Case of the Week]]
* [[Cytologically Yours: CoW|Cases of the Week Index]]

== Unknowns ==
The following cases are compiled by the Cytopathology Fellows for conference discussion every month.

* [[Cytologically Yours: Unknowns: 2014#May|Current Unknowns]]
* [[Cytologically Yours: Unknowns|Unknowns Index]]

== HSOM Systemic Pathology Virtual Microscopy Slides ==
Virtual Microscopy slides for HCOM Systemic Pathology Modules. Slides curated by Dr. Peter Anderson and by Dr. Jennifer Gordetsky (currently at the Department of Pathology, Vanderbilt University).

=== Breast ===
<gallery heights="250px" widths="250px">
File:IPLab7IDC1b.jpg|</gallery>
* Normal Breast
<peir-vm>IPLab7IDC_Normal_Breast</peir-vm>

=== Breast - Benign ===
* Fibroadenoma
<peir-vm>IPLab7Fibroadenoma</peir-vm>
* Fibrcystic Change
<peir-vm>UAB-Histology-00118</peir-vm>
*Phylloides Tumor
<peir-vm>UAB-Histology-00118</peir-vm>
*Myofibroblastoma
<peir-vm>UAB-Histology-00118</peir-vm>

=== Breast - Malignant ===
* Lobular Carcinoma
* Paget Disease and DCIS
*Invasive Ductal Carcinoma

{{Cytologically Yours}}

Cytologically Yours

2025-04-09T19:31:12Z

Peter Anderson: /* HSOM Systemic Pathology Virtual Microscopy Slides */

Welcome to '''Cytologically Yours''', an online library of teaching materials from the University of Alabama at Birmingham, Department of Pathology. It is maintained and curated under the direction of [https://scholars.uab.edu/2122-peter-anderson] Dr. Peter Anderson.

== Cases of the Week ==
The following are a collection of interesting cytology cases seen at our institution.

* [[Cytologically Yours: CoW: 20131125|Current Case of the Week]]
* [[Cytologically Yours: CoW|Cases of the Week Index]]

== Unknowns ==
The following cases are compiled by the Cytopathology Fellows for conference discussion every month.

* [[Cytologically Yours: Unknowns: 2014#May|Current Unknowns]]
* [[Cytologically Yours: Unknowns|Unknowns Index]]

== HSOM Systemic Pathology Virtual Microscopy Slides ==
Virtual Microscopy slides for HCOM Systemic Pathology Modules. Slides curated by Dr. Peter Anderson and by Dr. Jennifer Gordetsky (currently at the Department of Pathology, Vanderbilt University).

=== Breast ===
<gallery heights="250px" widths="250px">
File:IPLab7IDC1b.jpg|</gallery>
* Normal Breast
<peir-vm>IPLab7IDC_Normal_Breast</peir-vm>

* BENIGN
* Fibroadenoma
<peir-vm>IPLab7Fibroadenoma</peir-vm>
* Fibrcystic Change
<peir-vm>UAB-Histology-00118</peir-vm>
*Phylloides Tumor
<peir-vm>UAB-Histology-00118</peir-vm>
*Myofibroblastoma
<peir-vm>UAB-Histology-00118</peir-vm>

* MALIGNANT
* Lobular Carcinoma
* Paget Disease and DCIS
*Invasive Ductal Carcinoma

{{Cytologically Yours}}

Cytologically Yours

2025-04-09T19:22:41Z

Peter Anderson:

Welcome to '''Cytologically Yours''', an online library of teaching materials from the University of Alabama at Birmingham, Department of Pathology. It is maintained and curated under the direction of [https://scholars.uab.edu/2122-peter-anderson] Dr. Peter Anderson.

== Cases of the Week ==
The following are a collection of interesting cytology cases seen at our institution.

* [[Cytologically Yours: CoW: 20131125|Current Case of the Week]]
* [[Cytologically Yours: CoW|Cases of the Week Index]]

== Unknowns ==
The following cases are compiled by the Cytopathology Fellows for conference discussion every month.

* [[Cytologically Yours: Unknowns: 2014#May|Current Unknowns]]
* [[Cytologically Yours: Unknowns|Unknowns Index]]

== HSOM Systemic Pathology Virtual Microscopy Slides ==
Virtual Microscopy slides for HCOM Systemic Pathology Modules. Slides curated by Dr. Peter Anderson and by Dr. Jennifer Gordetsky (currently at the Department of Pathology, Vanderbilt University).

=== Breast ===
<gallery heights="250px" widths="250px">
File:IPLab7IDC1b.jpg|</gallery>
* Normal Breast
<peir-vm>IPLab7IDC_Normal_Breast</peir-vm>

* = BENIGN =
* Fibroadenoma
<peir-vm>IPLab7Fibroadenoma</peir-vm>
* Fibrcystic Change
*Phylloides Tumor
*Myofibroblastoma

* = MALIGNANT =
* Lobular Carcinoma
* Paget Disease and DCIS
*Invasive Ductal Carcinoma

{{Cytologically Yours}}

Cytologically Yours

2025-04-09T19:05:10Z

Peter Anderson: /* Breast */

Welcome to '''Cytologically Yours''', an online library of teaching materials from the University of Alabama at Birmingham, Department of Pathology. It is maintained and curated under the direction of [https://scholars.uab.edu/2122-peter-anderson] Dr. Peter Anderson.

== Cases of the Week ==
The following are a collection of interesting cytology cases seen at our institution.

* [[Cytologically Yours: CoW: 20131125|Current Case of the Week]]
* [[Cytologically Yours: CoW|Cases of the Week Index]]

== Unknowns ==
The following cases are compiled by the Cytopathology Fellows for conference discussion every month.

* [[Cytologically Yours: Unknowns: 2014#May|Current Unknowns]]
* [[Cytologically Yours: Unknowns|Unknowns Index]]

== HSOM Systemic Pathology Virtual Microscopy Slides ==
Virtual Microscopy slides for HCOM Systemic Pathology Modules. Slides curated by Dr. Peter Anderson and by Dr. Jennifer Gordetsky (currently at the Department of Pathology, Vanderbilt University).

* Current Resident Writeup
* Resident Writeups Index

=== Breast ===
<gallery heights="250px" widths="250px">
File:IPLab7IDC1b.jpg|</gallery>
* Normal Breast
<peir-vm>IPLab7IDC_Normal_Breast</peir-vm>

== Normal Breast ==
<peir-vm>IPLab7IDC_Normal_Breast</peir-vm>

* [[BENIGN]]
* [[Fibroadenoma]]
* [[Fibrocystic Change]]
* [[Phyllodes Tumor]]
* [[Myofibroblastoma]]
* [[MALIGNANT]]
* [[lobular Carcinoma]]
* [[Paget Disease and DCIS]]
* [[Invasive Ductal Carcinoma]]

== Virtual Microscopy ==
== Benign ==
=== Infiltrating Ductal Carcinoma ===
<peir-vm>IPLab7IDC</peir-vm>

== Teaching Cases ==
This is a compilation of cases with examples of normal cytology findings, benign entities, and malignant entities. These cases are designed to help teach residents, students, and fellows; what findings can be seen in different specimens.

{{Cytologically Yours}}

Cytologically Yours

2025-04-09T19:03:35Z

Peter Anderson: /* Breast */

Welcome to '''Cytologically Yours''', an online library of teaching materials from the University of Alabama at Birmingham, Department of Pathology. It is maintained and curated under the direction of [https://scholars.uab.edu/2122-peter-anderson] Dr. Peter Anderson.

== Cases of the Week ==
The following are a collection of interesting cytology cases seen at our institution.

* [[Cytologically Yours: CoW: 20131125|Current Case of the Week]]
* [[Cytologically Yours: CoW|Cases of the Week Index]]

== Unknowns ==
The following cases are compiled by the Cytopathology Fellows for conference discussion every month.

* [[Cytologically Yours: Unknowns: 2014#May|Current Unknowns]]
* [[Cytologically Yours: Unknowns|Unknowns Index]]

== HSOM Systemic Pathology Virtual Microscopy Slides ==
Virtual Microscopy slides for HCOM Systemic Pathology Modules. Slides curated by Dr. Peter Anderson and by Dr. Jennifer Gordetsky (currently at the Department of Pathology, Vanderbilt University).

* Current Resident Writeup
* Resident Writeups Index

=== Breast ===
<gallery heights="250px" widths="250px">
File:IPLab7IDC1b.jpg|</gallery>

* Normal Breast
<peir-vm>IPLab7IDC_Normal_Breast</peir-vm>

== Normal Breast ==
<peir-vm>IPLab7IDC_Normal_Breast</peir-vm>

* [[BENIGN]]
* [[Fibroadenoma]]
* [[Fibrocystic Change]]
* [[Phyllodes Tumor]]
* [[Myofibroblastoma]]
* [[MALIGNANT]]
* [[lobular Carcinoma]]
* [[Paget Disease and DCIS]]
* [[Invasive Ductal Carcinoma]]

== Virtual Microscopy ==
== Benign ==
=== Infiltrating Ductal Carcinoma ===
<peir-vm>IPLab7IDC</peir-vm>

== Teaching Cases ==
This is a compilation of cases with examples of normal cytology findings, benign entities, and malignant entities. These cases are designed to help teach residents, students, and fellows; what findings can be seen in different specimens.

{{Cytologically Yours}}

Cytologically Yours

2025-04-09T18:59:05Z

Peter Anderson: /* Breast */

Welcome to '''Cytologically Yours''', an online library of teaching materials from the University of Alabama at Birmingham, Department of Pathology. It is maintained and curated under the direction of [https://scholars.uab.edu/2122-peter-anderson] Dr. Peter Anderson.

== Cases of the Week ==
The following are a collection of interesting cytology cases seen at our institution.

* [[Cytologically Yours: CoW: 20131125|Current Case of the Week]]
* [[Cytologically Yours: CoW|Cases of the Week Index]]

== Unknowns ==
The following cases are compiled by the Cytopathology Fellows for conference discussion every month.

* [[Cytologically Yours: Unknowns: 2014#May|Current Unknowns]]
* [[Cytologically Yours: Unknowns|Unknowns Index]]

== HSOM Systemic Pathology Virtual Microscopy Slides ==
Virtual Microscopy slides for HCOM Systemic Pathology Modules. Slides curated by Dr. Peter Anderson and by Dr. Jennifer Gordetsky (currently at the Department of Pathology, Vanderbilt University).

* Current Resident Writeup
* Resident Writeups Index

=== Breast ===
<gallery heights="250px" widths="250px">
File:IPLab7IDC1b.jpg|</gallery>

== Normal Breast ==
<peir-vm>IPLab7IDC_Normal_Breast</peir-vm>

* [[BENIGN]]
* [[Fibroadenoma]]
* [[Fibrocystic Change]]
* [[Phyllodes Tumor]]
* [[Myofibroblastoma]]
* [[MALIGNANT]]
* [[lobular Carcinoma]]
* [[Paget Disease and DCIS]]
* [[Invasive Ductal Carcinoma]]

== Virtual Microscopy ==
== Benign ==
=== Infiltrating Ductal Carcinoma ===
<peir-vm>IPLab7IDC</peir-vm>

== Teaching Cases ==
This is a compilation of cases with examples of normal cytology findings, benign entities, and malignant entities. These cases are designed to help teach residents, students, and fellows; what findings can be seen in different specimens.

{{Cytologically Yours}}

Cytologically Yours

2025-04-09T18:51:55Z

Peter Anderson: /* Breast */

Welcome to '''Cytologically Yours''', an online library of teaching materials from the University of Alabama at Birmingham, Department of Pathology. It is maintained and curated under the direction of [https://scholars.uab.edu/2122-peter-anderson] Dr. Peter Anderson.

== Cases of the Week ==
The following are a collection of interesting cytology cases seen at our institution.

* [[Cytologically Yours: CoW: 20131125|Current Case of the Week]]
* [[Cytologically Yours: CoW|Cases of the Week Index]]

== Unknowns ==
The following cases are compiled by the Cytopathology Fellows for conference discussion every month.

* [[Cytologically Yours: Unknowns: 2014#May|Current Unknowns]]
* [[Cytologically Yours: Unknowns|Unknowns Index]]

== HSOM Systemic Pathology Virtual Microscopy Slides ==
Virtual Microscopy slides for HCOM Systemic Pathology Modules. Slides curated by Dr. Peter Anderson and by Dr. Jennifer Gordetsky (currently at the Department of Pathology, Vanderbilt University).

* Current Resident Writeup
* Resident Writeups Index

== Breast ==
<gallery heights="250px" widths="250px">
File:IPLab7IDC1b.jpg|</gallery>
* [[NORMAL]]
* [[BENIGN]]
* [[Fibroadenoma]]
* [[Fibrocystic Change]]
* [[Phyllodes Tumor]]
* [[Myofibroblastoma]]
* [[MALIGNANT]]
* [[lobular Carcinoma]]
* [[Paget Disease and DCIS]]
* [[Invasive Ductal Carcinoma]]

== Virtual Microscopy ==
== Benign ==
=== Infiltrating Ductal Carcinoma ===
<peir-vm>IPLab7IDC</peir-vm>

== Teaching Cases ==
This is a compilation of cases with examples of normal cytology findings, benign entities, and malignant entities. These cases are designed to help teach residents, students, and fellows; what findings can be seen in different specimens.

{{Cytologically Yours}}

Cytologically Yours

2025-04-09T17:52:47Z

Peter Anderson: /* Virtual Microscopy */

Welcome to '''Cytologically Yours''', an online library of teaching materials from the University of Alabama at Birmingham, Department of Pathology. It is maintained and curated under the direction of [https://scholars.uab.edu/2122-peter-anderson] Dr. Peter Anderson.

== Cases of the Week ==
The following are a collection of interesting cytology cases seen at our institution.

* [[Cytologically Yours: CoW: 20131125|Current Case of the Week]]
* [[Cytologically Yours: CoW|Cases of the Week Index]]

== Unknowns ==
The following cases are compiled by the Cytopathology Fellows for conference discussion every month.

* [[Cytologically Yours: Unknowns: 2014#May|Current Unknowns]]
* [[Cytologically Yours: Unknowns|Unknowns Index]]

== HSOM Systemic Pathology Virtual Microscopy Slides ==
Virtual Microscopy slides for HCOM Systemic Pathology Modules. Slides curated by Dr. Peter Anderson and by Dr. Jennifer Gordetsky (currently at the Department of Pathology, Vanderbilt University).

* Current Resident Writeup
* Resident Writeups Index

== Breast ==
<gallery heights="250px" widths="250px">
File:IPLab7IDC1b.jpg|</gallery>

== Virtual Microscopy ==
== Benign ==
=== Infiltrating Ductal Carcinoma ===
<peir-vm>IPLab7IDC</peir-vm>

== Teaching Cases ==
This is a compilation of cases with examples of normal cytology findings, benign entities, and malignant entities. These cases are designed to help teach residents, students, and fellows; what findings can be seen in different specimens.

{{Cytologically Yours}}

Cytologically Yours

2025-04-09T17:49:01Z

Peter Anderson: /* Breast */

Welcome to '''Cytologically Yours''', an online library of teaching materials from the University of Alabama at Birmingham, Department of Pathology. It is maintained and curated under the direction of [https://scholars.uab.edu/2122-peter-anderson] Dr. Peter Anderson.

== Cases of the Week ==
The following are a collection of interesting cytology cases seen at our institution.

* [[Cytologically Yours: CoW: 20131125|Current Case of the Week]]
* [[Cytologically Yours: CoW|Cases of the Week Index]]

== Unknowns ==
The following cases are compiled by the Cytopathology Fellows for conference discussion every month.

* [[Cytologically Yours: Unknowns: 2014#May|Current Unknowns]]
* [[Cytologically Yours: Unknowns|Unknowns Index]]

== HSOM Systemic Pathology Virtual Microscopy Slides ==
Virtual Microscopy slides for HCOM Systemic Pathology Modules. Slides curated by Dr. Peter Anderson and by Dr. Jennifer Gordetsky (currently at the Department of Pathology, Vanderbilt University).

* Current Resident Writeup
* Resident Writeups Index

== Breast ==
<gallery heights="250px" widths="250px">
File:IPLab7IDC1b.jpg|</gallery>

== Virtual Microscopy ==
=== Infiltrating Ductal Carcinoma ===
<peir-vm>IPLab7IDC</peir-vm>

== Teaching Cases ==
This is a compilation of cases with examples of normal cytology findings, benign entities, and malignant entities. These cases are designed to help teach residents, students, and fellows; what findings can be seen in different specimens.

{{Cytologically Yours}}

Cytologically Yours

2025-04-09T17:47:13Z

Peter Anderson: /* Breast */

Welcome to '''Cytologically Yours''', an online library of teaching materials from the University of Alabama at Birmingham, Department of Pathology. It is maintained and curated under the direction of [https://scholars.uab.edu/2122-peter-anderson] Dr. Peter Anderson.

== Cases of the Week ==
The following are a collection of interesting cytology cases seen at our institution.

* [[Cytologically Yours: CoW: 20131125|Current Case of the Week]]
* [[Cytologically Yours: CoW|Cases of the Week Index]]

== Unknowns ==
The following cases are compiled by the Cytopathology Fellows for conference discussion every month.

* [[Cytologically Yours: Unknowns: 2014#May|Current Unknowns]]
* [[Cytologically Yours: Unknowns|Unknowns Index]]

== HSOM Systemic Pathology Virtual Microscopy Slides ==
Virtual Microscopy slides for HCOM Systemic Pathology Modules. Slides curated by Dr. Peter Anderson and by Dr. Jennifer Gordetsky (currently at the Department of Pathology, Vanderbilt University).

* Current Resident Writeup
* Resident Writeups Index

== Breast ==
<gallery heights="250px" widths="250px">
File:IPLab7IDC1b.jpg|</gallery>

== Teaching Cases ==
This is a compilation of cases with examples of normal cytology findings, benign entities, and malignant entities. These cases are designed to help teach residents, students, and fellows; what findings can be seen in different specimens.

{{Cytologically Yours}}

Cytologically Yours

2025-04-09T17:43:21Z

Peter Anderson: /* HSOM Systemic Pathology Virtual Microscopy Slides */

Welcome to '''Cytologically Yours''', an online library of teaching materials from the University of Alabama at Birmingham, Department of Pathology. It is maintained and curated under the direction of [https://scholars.uab.edu/2122-peter-anderson] Dr. Peter Anderson.

== Cases of the Week ==
The following are a collection of interesting cytology cases seen at our institution.

* [[Cytologically Yours: CoW: 20131125|Current Case of the Week]]
* [[Cytologically Yours: CoW|Cases of the Week Index]]

== Unknowns ==
The following cases are compiled by the Cytopathology Fellows for conference discussion every month.

* [[Cytologically Yours: Unknowns: 2014#May|Current Unknowns]]
* [[Cytologically Yours: Unknowns|Unknowns Index]]

== HSOM Systemic Pathology Virtual Microscopy Slides ==
Virtual Microscopy slides for HCOM Systemic Pathology Modules. Slides curated by Dr. Peter Anderson and by Dr. Jennifer Gordetsky (currently at the Department of Pathology, Vanderbilt University).

* Current Resident Writeup
* Resident Writeups Index

== Breast ==
<gallery heights="250px" widths="250px">
File:IPLab1MyocardialInfarction1.jpg|In this gross photograph of the heart from this case, note the area of fresh myocardial infarction (arrows) in the anterior portion of the left ventricle and extending into the anterior portion of the interventricular septum. Note that the walls of the left and right ventricle are slightly thicker than normal. </gallery>

== Teaching Cases ==
This is a compilation of cases with examples of normal cytology findings, benign entities, and malignant entities. These cases are designed to help teach residents, students, and fellows; what findings can be seen in different specimens.

{{Cytologically Yours}}

Cytologically Yours

2025-04-09T17:41:58Z

Peter Anderson: /* HSOM Systemic Pathology Virtual Microscopy Slides */

Welcome to '''Cytologically Yours''', an online library of teaching materials from the University of Alabama at Birmingham, Department of Pathology. It is maintained and curated under the direction of [https://scholars.uab.edu/2122-peter-anderson] Dr. Peter Anderson.

== Cases of the Week ==
The following are a collection of interesting cytology cases seen at our institution.

* [[Cytologically Yours: CoW: 20131125|Current Case of the Week]]
* [[Cytologically Yours: CoW|Cases of the Week Index]]

== Unknowns ==
The following cases are compiled by the Cytopathology Fellows for conference discussion every month.

* [[Cytologically Yours: Unknowns: 2014#May|Current Unknowns]]
* [[Cytologically Yours: Unknowns|Unknowns Index]]

== HSOM Systemic Pathology Virtual Microscopy Slides ==
Virtual Microscopy slides for HCOM Systemic Pathology Modules. Slides curated by Jennifer B. Gordetsky M.D. (currently at the Department of Pathology, Vanderbilt University) and Dr. Peter Anderson.

* Current Resident Writeup
* Resident Writeups Index

== Breast ==
<gallery heights="250px" widths="250px">
File:IPLab1MyocardialInfarction1.jpg|In this gross photograph of the heart from this case, note the area of fresh myocardial infarction (arrows) in the anterior portion of the left ventricle and extending into the anterior portion of the interventricular septum. Note that the walls of the left and right ventricle are slightly thicker than normal. </gallery>

== Teaching Cases ==
This is a compilation of cases with examples of normal cytology findings, benign entities, and malignant entities. These cases are designed to help teach residents, students, and fellows; what findings can be seen in different specimens.

{{Cytologically Yours}}

Cytologically Yours

2025-04-09T17:28:18Z

Peter Anderson: /* Resident Writeups */

Welcome to '''Cytologically Yours''', an online library of teaching materials from the University of Alabama at Birmingham, Department of Pathology. It is maintained and curated under the direction of [https://scholars.uab.edu/2122-peter-anderson] Dr. Peter Anderson.

== Cases of the Week ==
The following are a collection of interesting cytology cases seen at our institution.

* [[Cytologically Yours: CoW: 20131125|Current Case of the Week]]
* [[Cytologically Yours: CoW|Cases of the Week Index]]

== Unknowns ==
The following cases are compiled by the Cytopathology Fellows for conference discussion every month.

* [[Cytologically Yours: Unknowns: 2014#May|Current Unknowns]]
* [[Cytologically Yours: Unknowns|Unknowns Index]]

== HSOM Systemic Pathology Virtual Microscopy Slides ==
Virtual Microscopy slides for HCOM Systemic Pathology Modules. Slides curated by Jennifer B. Gordetsky M.D. (currently at the Department of Pathology, Vanderbilt University) and Dr. Peter Anderson.

* Current Resident Writeup
* Resident Writeups Index

== Teaching Cases ==
This is a compilation of cases with examples of normal cytology findings, benign entities, and malignant entities. These cases are designed to help teach residents, students, and fellows; what findings can be seen in different specimens.

{{Cytologically Yours}}

Cytologically Yours

2025-04-09T17:18:35Z

Peter Anderson:

IPLab:Lab 6:PAN

2024-05-13T18:37:23Z

Peter Anderson: /* Additional Resources */

== Clinical Summary ==
This was a 27-year-old white female who presented to the emergency room with fever, diarrhea, and abdominal pain that had increased in intensity over a 3-day period. Her blood pressure on admission was 165/108 mm Hg. She had been diagnosed with polyarteritis nodosa two years prior to this admission and had been treated with corticosteroids and cyclophosphamide. She had discontinued her corticosteroids because they made her gain weight; in addition, she was not taking the medications prescribed for her hypertension. At this admission it was suspected that the patient had bowel ischemia due to mesenteric artery occlusion. Angiographic evaluation revealed significant vascular damage to the mesenteric arteries with aneurysmal dilatations and thromboses. Significant vascular changes were also observed in the renal and hepatic circulation. On the second hospital day, the patient developed acute severe abdominal pain and an emergency laparotomy was performed to resect an 18-cm section of infarcted and ruptured ileum. After surgery she continued to run a fever, her white blood cell count was 13,500 cells/mm³, and she developed renal failure. Two days after surgery the patient died due to sepsis and multisystem failure.

At autopsy there were several 0.5 to 1.0-cm firm nodules in the dermis. There were numerous aneurysmal dilatations grossly visible in the mesenteric arteries. There were multiple shrunken infarcts on the surface of the kidneys and the surface also had a fine granular appearance indicative of hypertensive renal disease. On cut section both the kidney and the liver had multiple firm white nodules.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab6PAN1.jpg|This angiogram of the abdominal viscera demonstrates numerous aneurysms throughout the mesenteric circulation (arrows).
File:IPLab6PAN2.jpg|This angiogram of the liver also demonstrates numerous aneurysms throughout the hepatic circulation (arrows).
File:IPLab6PAN3.jpg|This angiogram of the kidneys demonstrates numerous aneurysmal dilatations in the renal circulation (arrows).
File:IPLab6PAN4.jpg|This is a low-power photomicrograph of a mesenteric vessel from this case of polyarteritis nodosa (arrow). The vessel is completely occluded by thrombotic material and the vessel wall is infiltrated with inflammatory cells.
File:IPLab6PAN5.jpg|This is a higher-power photomicrograph of this mesenteric vessel. Note the thrombotic material occluding the vessel (arrows) and the inflammatory cell infiltrate in the wall of the vessel and in the surrounding adventitia.
File:IPLab6PAN7.jpg|This is a high-power photomicrograph of the vessel wall. There is hemorrhage and infiltration with inflammatory cells--primarily neutrophils (arrows).
File:IPLab6PAN8.jpg|This is a high-power photomicrograph of a small vessel with a rim of fibrinoid necrosis (arrow).
File:IPLab6PAN11.jpg|This is a low-power photomicrograph of the heart. There are areas of fibrosis in the myocardium (arrows). Note that the large epicardial coronary artery is normal.
File:IPLab6PAN12.jpg|This is a higher-power photomicrograph of the affected vessels in the heart (arrows). There are areas of fibrosis (old infarcts) in the myocardium adjacent to these affected vessels.
File:IPLab6PAN13.jpg|This is a high-power photomicrograph of the affected vessel in the heart. The vessel lumen is completely occluded.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab6PAN</peir-vm>

== Study Questions ==
* <spoiler text="What vessels are usually affected in PAN?">PAN affects small and medium-sized muscular arteries. The renal and visceral arteries are typically affected while the pulmonary arteries are often spared.</spoiler>
* <spoiler text="What is the etiology of PAN?">The etiology is unknown but the disease is believed to be a type III hypersensitivity reaction Some studies have shown that approximately 30% of patients with PAN have hepatitis B antigenemia. In addition, some patients with PAN have been shown to have circulating antineutrophil cytoplasmic autoantibodies. In some cases the level of these autoantibodies is associated with the severity of the disease.</spoiler>
* <spoiler text="What is the prognosis for patients with PAN?">The clinical course of PAN may be acute, subacute, or chronic and is frequently remittent, with long symptom-free intervals. Acute episodes of the disease are treated with corticosteroids and cyclophosphamide. Aggressive immunosuppressive treatment leads to remission or cure in approximately 90% of patients with PAN.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/330717-overview eMedicine Medical Library: Polyarteritis Nodosa]
* [http://emedicine.medscape.com/article/332622-overview eMedicine Medical Library: Wegener Granolomatosis]
* [http://www.merckmanuals.com/professional/musculoskeletal_and_connective_tissue_disorders/vasculitis/polyarteritis_nodosa_pan.html Merck Manual: Polyarteritis Nodosa]

=== Journal Articles ===
* Kaito Aoki, M.D., and Marenori Kojima, Ph.D. [https://www.nejm.org/doi/full/10.1056/NEJMicm2309365?query=TOC&cid=NEJM%20eToc,%20May%209,%202024%20DM2339743_NEJM_Non_Subscriber&bid=-2018601491 Polyarteritis Nodosa]. ''NEJM'' 2024 390 (18)
* Morgan AJ, Schwartz RA. [http://www.ncbi.nlm.nih.gov/pubmed/20618492 Cutaneous polyarteritis nodosa: a comprehensive review]. ''Int J Dermatol'' 2010 Jul;49(7):750-6.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/244-polyarteritis_nodosa PEIR Digital Library: Polyarteritis Nodosa Images]

{{IPLab 6}}

[[Category: IPLab:Lab 6]]

IPLab:Lab 3:Sarcoidosis

2021-09-13T18:16:35Z

Peter Anderson: /* Journal Articles */

== Clinical Summary ==
This 33-year-old white female was admitted for evaluation of abnormal findings on a chest x-ray. She was asymptomatic and a physical examination revealed no significant abnormalities. Laboratory results indicated hypercalcemia and elevated gamma globulin. Radiographic examination showed enlarged subcarinal, hilar, and right paratracheal lymph nodes. A right paratracheal lymph node was biopsied. Special stains for acid-fast bacilli and fungi were negative and a diagnosis of sarcoidosis was made.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab3Sarcoidosis1.jpg|This is a low-power photomicrograph of a lymph node. Note the rather pale-pink color of the tissue with dark-staining cells found in only a few scattered areas. These darker cells represent the original lymphocytes of this lymphoid organ.
File:IPLab3Sarcoidosis2b.jpg|This photomicrograph of lymph node tissue illustrates a paucity of lymphocytes as well as numerous small, pale-staining nodules (arrows) throughout the tissue.
File:IPLab3Sarcoidosis3b.jpg|This is a photomicrograph of the small nodules (arrows) seen in the previous image. Close examination reveals that they are composed of large macrophages (epithelioid macrophages). These small granulomas form multiple series of reaction centers throughout the lymph node. Note the remaining lymphocytes surrounding the granulomas.
File:IPLab3Sarcoidosis4.jpg|This photomicrograph of a single granuloma illustrates the individual macrophages (arrows) which make up the bulk of this tissue. There is an absence of necrosis in the center of the lesions in this case.
File:IPLab3Sarcoidosis5b.jpg|This is a photomicrograph of a multinucleated giant cell (1). In the center of this foreign body-containing giant cell there is a small asteroid body (2). There is no functional significance to this asteroid body.
</gallery>

== Virtual Microscopy ==
=== Lymph Node: Sarcoidosis ===
<peir-vm>IPLab3Sarcoidosis</peir-vm>

=== Lymph Node ===
<peir-vm>UAB-Histology-00035</peir-vm>

== Study Questions ==
* <spoiler text="What is sarcoidosis?">The exact cause of sarcoidosis is unknown. Sarcoidosis is characterized by non-caseating granulomas in many tissues and organs.</spoiler>
* <spoiler text="What is the characteristic phenotype of sarcoid granulomas?">The typical characteristic of a sarcoid granuloma is a non-caseating granuloma which consists of an aggregate of tightly-clustered epitheliod cells, often with Langhans’ or multinucleated giant cells. Occasionally, asteroid bodies may be seen.</spoiler>
* <spoiler text="What are asteroid bodies and are they pathognomonic for sarcoid or are they seen in other diseases?">Asteroid bodies are stellate inclusions within giant cells. They are not pathognomonic for sarcoid; they can be seen in other granulomatous disease processes (e.g., berylliosis).</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/809047-overview eMedicine Medical Library: Acute Complications of Sarcoidosis]
* [http://emedicine.medscape.com/article/301914-overview eMedicine Medical Library: Sarcoidosis]
* [http://emedicine.medscape.com/article/1123970-overview eMedicine Medical Library: Dermatologic Manifestations of Sarcoidosis]
* [http://emedicine.medscape.com/article/1147324-overview eMedicine Medical Library: Neurosarcoidosis]
* [http://www.merckmanuals.com/professional/pulmonary_disorders/sarcoidosis/sarcoidosis.html Merck Manual: Sarcoidosis]

=== Journal Articles ===
* Drent M, Crouser ED, Grunewald J. [https://www.nejm.org/doi/full/10.1056/NEJMra2101555 Challenges of Sarcoidosis and Its Management]. ''N Engl J Med'' 2021; 385:1018-1032
* English JC, Patel PJ, Greer KE. [http://www.mdconsult.com/das/article/body/421068364-2/jorg=journal&source=MI&sp=11817316&sid=119276088/N/217466/1.html?issn= Sarcoidosis]. ''J Am Acad Dermatol'' 2001;44:725-43
* Johns CJ, Michele TM. [http://www.ncbi.nlm.nih.gov/pubmed/10195091 The clinical management of sarcoidosis. A 50-year experience at the Johns Hopkins Hospital]. ''Medicine (Baltimore)'' 1999 Mar;78(2):65-111.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/531-sarcoidosis PEIR Digital Library: Sarcoidosis Images]
* [http://library.med.utah.edu/WebPath/LUNGHTML/LUNGIDX.html#2 WebPath: Granulomatous Disease]

== Related IPLab Cases ==
* [[IPLab:Lab 2:Metastatic Calcification|Lab 2: Lung: Metastatic Calcification]]

{{IPLab 3}}
[[Category: IPLab:Lab 3]]

IPLab:Lab 12:Thoracic Mesothelioma

2020-07-13T20:53:18Z

Peter Anderson: /* Autopsy Findings */

== Clinical Summary ==
This 61-year-old white male had a known history of asbestos exposure as well as a 40 pack-year history of smoking and coronary artery disease. Two years ago an open lung biopsy showed a thoracic mesothelioma. At this admission the patient complained of shortness of breath, orthopnea, and pedal edema. Physical examination revealed mild respiratory distress on nasal oxygen and a dull left hemothorax. Chest x-ray demonstrated a left hemothorax opacity, small right pleural effusions, and pleural plaques. The patient subsequently developed atrial fibrillation and immediately prior to his death he suffered a stroke.

At autopsy tumor plaque covered 100% of the left lung, 50% of the right lung, and extended into the thoracic wall, the diaphragm, and the heart.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab12Mesothelioma1.jpg|This is a gross photograph of the lungs removed at autopsy. There is thickening of the pleural surface due to the tumor (arrows). The apical portion of the left lobe of the lung was ripped while trying to sever the adhesions between the lung and the chest wall.
File:IPLab12Mesothelioma2.jpg|This is a gross photograph of cut sections of the lungs. The right lung is congested. The left lung is shrunken and filled with tumor. There is a thick layer of tumor along the inferior portion of the lung (arrow).
File:IPLab12Mesothelioma3.jpg|This is a gross photograph of the thoracic surface of the diaphragm demonstrating the distinctive fibrocalcific plaque (arrows) produced by mesothelioma and multiple smaller plaques over the pleural surface of the diaphragm.
File:IPLab12Mesothelioma4.jpg|This is a low-power photomicrograph of a section of the left lung. At this magnification you can see areas of consolidation (arrows), especially around blood vessels.
File:IPLab12Mesothelioma5.jpg|This higher-power photomicrograph of left lung shows areas of consolidation and fibrosis (arrows). Also note that in many of these areas there are clusters of blue cells.
File:IPLab12Mesothelioma6.jpg|In this higher-power photomicrograph the clusters of tumor cells (arrows) can be appreciated.
File:IPLab12Mesothelioma7.jpg|In this higher-power photomicrograph there is a blood vessel (1) and adjacent lymphatics that contain tumor cells (2). There are also accumulations of brown material adjacent to these vessels.
File:IPLab12Mesothelioma8.jpg|This high-power photomicrograph shows brown asbestos bodies (1), accumulations of anthracotic pigment (2), and tumor cells (3) all adjacent to a blood vessel (4).
File:IPLab12Mesothelioma9.jpg|This is a high-power photomicrograph of the brown asbestos bodies showing the characteristic beaded appearance (arrows).
File:IPLab12Mesothelioma10.jpg|Another high-power photomicrograph of the brown asbestos bodies showing the characteristic beaded appearance (arrows). Tumor cells are evident adjacent to the asbestos bodies.
File:IPLab12Mesothelioma11.jpg|Scanning electron micrograph of asbestos bodies. Note the rough surface and the beaded appearance caused by the material adhering to the surface of the asbestos fiber.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab12Mesothelioma</peir-vm>

== Study Questions ==
* <spoiler text="What is the significance of the patient's history of asbestos exposure in this case?">Asbestos has been identified as a risk factor for developing:
# localized fibrous plaques or, rarely, diffuse pleural fibrosis;
# pleural effusions;
# parenchymal interstitial fibrosis (asbestosis);
# bronchogenic carcinoma;
# mesotheliomas; and
# laryngeal and perhaps other extrapulmonary neoplasms, including colon carcinomas.</spoiler>
* <spoiler text="What is the most common tumor produced by asbestos and what is the significance of both asbestos expose and smoking?">Bronchiogenic carcinoma is the most common tumor associated with asbestos (five times increased risk after asbestos exposure). However, the risk for developing mesothelioma (which is normally an extremely rare tumor) increases by 1,000-fold after asbestos exposure.Concentration, size, shape, and solubility of the different forms of asbestos dictate whether disease will occur.</spoiler>
* <spoiler text="What type of asbestos fiber is most harmful?">There are two distinct geometric forms of asbestos:
* serpentine (curly and flexible fibers), and
* amphibole (straight, stiff, and brittle fibers).
The serpentine chrysotile chemical form accounts for most of the asbestos used in industry.

Amphiboles, though less prevalent, are more pathogenic than chrysotiles, particularly with respect to induction of malignant pleural tumors (mesotheliomas). Indeed, some studies of mesotheliomas have shown the link is almost always to amphibole exposure.</spoiler>
* <spoiler text="What are asbestos bodies?">Asbestos bodies appear as golden-brown, fusiform or beaded rods with a translucent center. They are composed of an asbestos fiber coated with an iron-containing proteinaceous material. They arise when macrophages attempt to phagocytose asbestos fibers; the iron (ferritin) binds to the fiber within the phagocyte. Other inorganic particles may also be incorporated onto the asbestos fiber along with the ferritin.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/359470-overview eMedicine Medical Library: Malignant Mesothelioma Imaging]
* [http://emedicine.medscape.com/article/352900-overview eMedicine Medical Library: Asbestosis Imaging]
* [http://www.merckmanuals.com/professional/pulmonary_disorders/environmental_pulmonary_diseases/asbestos-related_disorders.html Merck Manual: Asbestos-Related Disorders]

=== Journal Articles ===
* Whitaker D. [http://www.ncbi.nlm.nih.gov/pubmed/10877273 The cytology of malignant mesothelioma]. ''Cytopathology'' 2000 Jun;11(3):139-51.
* Johnson JS, Edwards JM. [http://www.ncbi.nlm.nih.gov/pubmed/11256938 Malignant mesothelioma mimicking squamous carcinoma in a pleural fluid aspirate]. ''Cytopathology'' 2001 Feb;12(1):54-6.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/180-mesothelioma PEIR Digital Library: Mesothelioma Images]
* [http://library.med.utah.edu/WebPath/LUNGHTML/LUNGIDX.html#8 WebPath: Pulmonary Neoplasms]

{{IPLab 12}}

[[Category: IPLab:Lab 12]]

IPLab:Lab 11:Cysticercosis

2020-07-09T22:03:19Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==
This 29-year-old woman was admitted to the hospital because of repeated tonic-clonic seizures. The patient was a tour guide leading groups of tourist to Tibet for two-month walking/camping tours in the Himalayas. Her seizures were easily controlled by intravenous administration of phenytoin. The WBC count was 13,000, with 5% eosinophils and the erythrocyte sedimentation rate was slightly elevated. A cranial CT performed with and without contrast revealed two ring-enhancing lesions. The patient underwent a craniotomy and excisional biopsy.

Histopathologic exam of the surgical specimen revealed a capsule of dense connective tissue surrounding a cavity that contained a partially degenerated scolex of Taenia solium.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab11Cysticercosis1.jpg|This is a head CT showing the two cysts (arrows).
File:IPLab11Cysticercosis2.jpg|This is a photograph of the cyst that was surgically removed. The cyst is filled with a clear fluid and contains a scolex.
File:IPLab11Cysticercosis3.jpg|This photograph of an autopsy specimen from another patient shows an adult tapeworm in the intestine. Note that the worm attaches to the luminal surface of the intestine via the scolex.
File:IPLab11Cysticercosis4.jpg|This is a photograph of the body of an adult tapeworm. Note the body segments.
</gallery>

== Study Questions ==
* <spoiler text="How did this patient get this parasite?">Cysticercosis is caused by the cestode parasite, Taenia solium (pig tapeworm). Cysticercosis is contracted by ingesting eggs from the feces of a person infected with an adult Taenia solium. The eggs can survive for several weeks in soil but are also infectious as soon as passed. The larvae migrate through the intestinal wall and are disseminated via the blood stream and can encyst in the brain, heart, skeletal muscle, or skin.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/215589-overview eMedicine Medical Library: Cysticercosis]
* [http://emedicine.medscape.com/article/781845-overview eMedicine Medical Library: Cysticercosis in Emergency Medicine]
* [http://www.merckmanuals.com/professional/infectious_diseases/cestodes_tapeworms/taeniasis_solium_and_cysticercosis.html Merck Manual: Taeniasis Solium and Cysticercosis]

=== Journal Articles ===
* Garcia HH, Del Brutto OH. [http://www.ncbi.nlm.nih.gov/pubmed/10738675 Taenia solium cysticercosis]. ''Infect Dis Clin North Am'' 2000 Mar;14(1):97-119, ix.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/1622-cysticercosis PEIR Digital Library: Cysticercosis Images]

{{IPLab 11}}

[[Category: IPLab:Lab 11]]

IPLab:Lab 11:Cysticercosis

2020-07-09T22:02:31Z

Peter Anderson: /* Surgical Specimen */

== Clinical Summary ==
This 29-year-old woman was admitted to the hospital because of repeated tonic-clonic seizures. The patient was a tour guide leading groups of tourist to Tibet for two-month walking/camping tours in the Himalayas. Her seizures were easily controlled by intravenous administration of phenytoin. The WBC count was 13,000, with 5% eosinophils and the erythrocyte sedimentation rate was slightly elevated. A cranial CT performed with and without contrast revealed two ring-enhancing lesions. The patient underwent a craniotomy and excisional biopsy.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab11Cysticercosis1.jpg|This is a head CT showing the two cysts (arrows).
File:IPLab11Cysticercosis2.jpg|This is a photograph of the cyst that was surgically removed. The cyst is filled with a clear fluid and contains a scolex.
File:IPLab11Cysticercosis3.jpg|This photograph of an autopsy specimen from another patient shows an adult tapeworm in the intestine. Note that the worm attaches to the luminal surface of the intestine via the scolex.
File:IPLab11Cysticercosis4.jpg|This is a photograph of the body of an adult tapeworm. Note the body segments.
</gallery>

== Study Questions ==
* <spoiler text="How did this patient get this parasite?">Cysticercosis is caused by the cestode parasite, Taenia solium (pig tapeworm). Cysticercosis is contracted by ingesting eggs from the feces of a person infected with an adult Taenia solium. The eggs can survive for several weeks in soil but are also infectious as soon as passed. The larvae migrate through the intestinal wall and are disseminated via the blood stream and can encyst in the brain, heart, skeletal muscle, or skin.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/215589-overview eMedicine Medical Library: Cysticercosis]
* [http://emedicine.medscape.com/article/781845-overview eMedicine Medical Library: Cysticercosis in Emergency Medicine]
* [http://www.merckmanuals.com/professional/infectious_diseases/cestodes_tapeworms/taeniasis_solium_and_cysticercosis.html Merck Manual: Taeniasis Solium and Cysticercosis]

=== Journal Articles ===
* Garcia HH, Del Brutto OH. [http://www.ncbi.nlm.nih.gov/pubmed/10738675 Taenia solium cysticercosis]. ''Infect Dis Clin North Am'' 2000 Mar;14(1):97-119, ix.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/1622-cysticercosis PEIR Digital Library: Cysticercosis Images]

{{IPLab 11}}

[[Category: IPLab:Lab 11]]

IPLab:Lab 10:Mucormycosis

2020-07-09T21:59:19Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==

This 63-year-old white male was in his usual state of good health until eight weeks before his death when he developed sudden onset of shortness of breath. A thoracotomy was performed for plication of ruptured emphysematous blebs. Following improvement and discharge from the hospital he developed weakness, lethargy, and a left lower lobe lung infiltrate. The patient's condition soon deteriorated further, with almost every organ system having failed. The patient developed DIC and peripheral embolic phenomena, including gangrene of his extremities and face. A single antemortem blood culture grew Staphylococcus aureus.

Autopsy revealed severe emphysema, severe widespread abscessiform and necrotizing pneumonia, and bacterial (Staphylococcus aureus) endocarditis of the pulmonic valve. The right internal carotid artery was occluded by a thrombus and there were areas of necrosis due to CVAs (strokes) in the brain.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Mucor1.jpg|This is a low-power photomicrograph of a section of carotid artery containing a mural thrombus.
File:IPLab10Mucor2.jpg|This is a higher-power photomicrograph of the wall of the carotid artery (1) and the thrombus (2).
File:IPLab10Mucor3.jpg|This is an even higher-power photomicrograph of the wall of the carotid artery (1) and the thrombus (2). Within the wall of the artery and in the thrombus there are multiple variably shaped clear areas (3). At this magnification and with this stain, it is impossible to determine what these clear spaces represent.
File:IPLab10Mucor4.jpg|This is a higher-power photomicrograph of just the wall of the carotid artery. Note the ribbon-like clear structure with roughly parallel walls (non-septate hyphae) and right-angle branching (arrow). This is the Mucor organism.
File:IPLab10Mucor5.jpg|This is another high-power photomicrograph of the wall of the artery and the thrombus. Within the thrombus there are multiple variably-shaped clear areas that represent longitudinal sections and cross sections of the Mucor organisms (arrows).
File:IPLab10Mucor6.jpg|This medium-power photomicrograph shows the thrombus stained to outline the Mucor organisms (arrows). Note again the ribbon-like morphology and the wide-angle branching.
File:IPLab10Mucor7.jpg|This is an even higher-power photomicrograph of the thrombus stained to outline the Mucor organisms (arrows).
File:IPLab10Mucor8.jpg|This is another high-power photomicrograph of the thrombus stained to outline the Mucor organisms (arrows).
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab10Mucor</peir-vm>

== Study Questions ==
* <spoiler text="How is Mucor spread?">The spores are widespread in dust and air and can be inhaled or ingested. They are ubiquitous contaminants colonizing the normal human skin or gut without causing illness in immunocompetent people.</spoiler>
* <spoiler text="What are the common sites of infection with Mucor?">Mucor commonly causes vasculitis and thrombosis.

The three primary sites of Mucor invasion are the nasal sinuses, lungs, and gastrointestinal tract.</spoiler>
* <spoiler text="What special risks of Mucor infection are associated with diabetes?">In diabetics, the fungus may spread from nasal sinuses to the orbit, and subsequently the brain, giving rise to rhinocerebral mucormycosis.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/222551-overview eMedicine Medical Library: Mucormycosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/mucormycosis.html Merck Manual: Mucormycosis]

=== Journal Articles ===
* Marcó del Pont J, De Cicco L, Gallo G, Llera J, De Santibanez E, D'agostino D. [http://www.ncbi.nlm.nih.gov/pubmed/11429008 Hepatic arterial thrombosis due to Mucor species in a child following orthotopic liver transplantation]. ''Transpl Infect Dis'' 2000 Mar;2(1):33-5.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2158-mucormycosis PEIR Digital Library: Mucormycosis Images]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html WebPath: Infection]

== Related IPLab Cases ==

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

IPLab:Lab 10:Mucormycosis

2020-07-09T21:58:37Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==

This 63-year-old white male was in his usual state of good health until eight weeks before his death when he developed sudden onset of shortness of breath. A thoracotomy was performed for plication of ruptured emphysematous blebs. Following improvement and discharge from the hospital he developed weakness, lethargy, and a left lower lobe lung infiltrate. The patient's condition soon deteriorated further, with almost every organ system having failed. The patient developed DIC and peripheral embolic phenomena, including gangrene of his extremities and face. A single antemortem blood culture grew Staphylococcus aureus.

Autopsy revealed severe emphysema, severe widespread abscessiform and necrotizing pneumonia, and bacterial (Staphylococcus aureus) endocarditis of the pulmonic valve. The right internal carotid artery was occluded by a thrombus and there were areas of necrosis (due to CVAs) in the brain.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Mucor1.jpg|This is a low-power photomicrograph of a section of carotid artery containing a mural thrombus.
File:IPLab10Mucor2.jpg|This is a higher-power photomicrograph of the wall of the carotid artery (1) and the thrombus (2).
File:IPLab10Mucor3.jpg|This is an even higher-power photomicrograph of the wall of the carotid artery (1) and the thrombus (2). Within the wall of the artery and in the thrombus there are multiple variably shaped clear areas (3). At this magnification and with this stain, it is impossible to determine what these clear spaces represent.
File:IPLab10Mucor4.jpg|This is a higher-power photomicrograph of just the wall of the carotid artery. Note the ribbon-like clear structure with roughly parallel walls (non-septate hyphae) and right-angle branching (arrow). This is the Mucor organism.
File:IPLab10Mucor5.jpg|This is another high-power photomicrograph of the wall of the artery and the thrombus. Within the thrombus there are multiple variably-shaped clear areas that represent longitudinal sections and cross sections of the Mucor organisms (arrows).
File:IPLab10Mucor6.jpg|This medium-power photomicrograph shows the thrombus stained to outline the Mucor organisms (arrows). Note again the ribbon-like morphology and the wide-angle branching.
File:IPLab10Mucor7.jpg|This is an even higher-power photomicrograph of the thrombus stained to outline the Mucor organisms (arrows).
File:IPLab10Mucor8.jpg|This is another high-power photomicrograph of the thrombus stained to outline the Mucor organisms (arrows).
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab10Mucor</peir-vm>

== Study Questions ==
* <spoiler text="How is Mucor spread?">The spores are widespread in dust and air and can be inhaled or ingested. They are ubiquitous contaminants colonizing the normal human skin or gut without causing illness in immunocompetent people.</spoiler>
* <spoiler text="What are the common sites of infection with Mucor?">Mucor commonly causes vasculitis and thrombosis.

The three primary sites of Mucor invasion are the nasal sinuses, lungs, and gastrointestinal tract.</spoiler>
* <spoiler text="What special risks of Mucor infection are associated with diabetes?">In diabetics, the fungus may spread from nasal sinuses to the orbit, and subsequently the brain, giving rise to rhinocerebral mucormycosis.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/222551-overview eMedicine Medical Library: Mucormycosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/mucormycosis.html Merck Manual: Mucormycosis]

=== Journal Articles ===
* Marcó del Pont J, De Cicco L, Gallo G, Llera J, De Santibanez E, D'agostino D. [http://www.ncbi.nlm.nih.gov/pubmed/11429008 Hepatic arterial thrombosis due to Mucor species in a child following orthotopic liver transplantation]. ''Transpl Infect Dis'' 2000 Mar;2(1):33-5.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2158-mucormycosis PEIR Digital Library: Mucormycosis Images]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html WebPath: Infection]

== Related IPLab Cases ==

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

IPLab:Lab 10:Mucormycosis

2020-07-09T21:57:46Z

Peter Anderson: /* Autopsy Findings */

== Clinical Summary ==

This 63-year-old white male was in his usual state of good health until eight weeks before his death when he developed sudden onset of shortness of breath. A thoracotomy was performed for plication of ruptured emphysematous blebs. Following improvement and discharge from the hospital he developed weakness, lethargy, and a left lower lobe lung infiltrate. The patient's condition soon deteriorated further, with almost every organ system having failed. The patient developed DIC and peripheral embolic phenomena, including gangrene of his extremities and face. A single antemortem blood culture grew Staphylococcus aureus.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Mucor1.jpg|This is a low-power photomicrograph of a section of carotid artery containing a mural thrombus.
File:IPLab10Mucor2.jpg|This is a higher-power photomicrograph of the wall of the carotid artery (1) and the thrombus (2).
File:IPLab10Mucor3.jpg|This is an even higher-power photomicrograph of the wall of the carotid artery (1) and the thrombus (2). Within the wall of the artery and in the thrombus there are multiple variably shaped clear areas (3). At this magnification and with this stain, it is impossible to determine what these clear spaces represent.
File:IPLab10Mucor4.jpg|This is a higher-power photomicrograph of just the wall of the carotid artery. Note the ribbon-like clear structure with roughly parallel walls (non-septate hyphae) and right-angle branching (arrow). This is the Mucor organism.
File:IPLab10Mucor5.jpg|This is another high-power photomicrograph of the wall of the artery and the thrombus. Within the thrombus there are multiple variably-shaped clear areas that represent longitudinal sections and cross sections of the Mucor organisms (arrows).
File:IPLab10Mucor6.jpg|This medium-power photomicrograph shows the thrombus stained to outline the Mucor organisms (arrows). Note again the ribbon-like morphology and the wide-angle branching.
File:IPLab10Mucor7.jpg|This is an even higher-power photomicrograph of the thrombus stained to outline the Mucor organisms (arrows).
File:IPLab10Mucor8.jpg|This is another high-power photomicrograph of the thrombus stained to outline the Mucor organisms (arrows).
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab10Mucor</peir-vm>

== Study Questions ==
* <spoiler text="How is Mucor spread?">The spores are widespread in dust and air and can be inhaled or ingested. They are ubiquitous contaminants colonizing the normal human skin or gut without causing illness in immunocompetent people.</spoiler>
* <spoiler text="What are the common sites of infection with Mucor?">Mucor commonly causes vasculitis and thrombosis.

The three primary sites of Mucor invasion are the nasal sinuses, lungs, and gastrointestinal tract.</spoiler>
* <spoiler text="What special risks of Mucor infection are associated with diabetes?">In diabetics, the fungus may spread from nasal sinuses to the orbit, and subsequently the brain, giving rise to rhinocerebral mucormycosis.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/222551-overview eMedicine Medical Library: Mucormycosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/mucormycosis.html Merck Manual: Mucormycosis]

=== Journal Articles ===
* Marcó del Pont J, De Cicco L, Gallo G, Llera J, De Santibanez E, D'agostino D. [http://www.ncbi.nlm.nih.gov/pubmed/11429008 Hepatic arterial thrombosis due to Mucor species in a child following orthotopic liver transplantation]. ''Transpl Infect Dis'' 2000 Mar;2(1):33-5.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2158-mucormycosis PEIR Digital Library: Mucormycosis Images]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html WebPath: Infection]

== Related IPLab Cases ==

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

IPLab:Lab 10:Blastomycosis

2020-07-09T21:57:27Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==
About three weeks before his death, this 17-year-old white male developed a "chest cold" which gradually worsened. The patient was eventually admitted three days before his death. At that time, the patient was very dyspneic. Chest x-ray showed consolidation of the entire left lung. The initial impression by his care team was staphylococcal pneumonia. However, Blastomyces dermatitides was identified in stained smears of sputum the next day. In spite of appropriate antifungal therapy, the patient deteriorated rapidly and died.

At autopsy the both lungs had areas of consolidation and necrosis.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Blasto1.jpg|This gross photograph of the lungs shows areas of necrosis and consolidation.
File:IPLab10Blasto2.jpg|This higher-power view of the lung shows more clearly the areas of necrosis (1) and consolidation (2). Satellite lesions are also present (3).
File:IPLab10Blasto3.jpg|This is a low-power photomicrograph of lung showing many areas of consolidation (arrows).
File:IPLab10Blasto4.jpg|This is a high-power photomicrograph of lung section with pleura. The pleura (1) is thickened and contains inflammatory cells and fibrin. The areas of consolidation (2) are dense and filled with inflammatory cells.
File:IPLab10Blasto5.jpg|This is a higher-power photomicrograph of lung section with pleura. The pleura (arrows) is thickened and contains inflammatory cells and fibrin. The alveoli are filled with inflammatory cells. Some of the alveolar septa are congested with red blood cells.
File:IPLab10Blasto6.jpg|This high-power photomicrograph shows what appear to be inflammatory cells filling the alveoli. At this magnification, numerous round bodies (arrows) that look like inflammatory cell nuclei can be seen. However, on closer examination, some of these round bodies are surrounded by clear halos.
File:IPLab10Blasto7.jpg|This high-power photomicrograph shows an alveolus filled with numerous round bodies up to 25 mm in diameter. Some of these double-contour bodies (1) have a dense center and a clear halo. These are the Blastomyces organisms. The typical B. dermatitides organism is smoothly-outlined with a central, densely basophilic cytoplasm surrounded by a clear halo. When stained with hematoxylin and eosin, the organism is outlined by a relatively thick cell wall. There are also numerous inflammatory cells (2) in the alveolus--neutrophils, lymphocytes and macrophages--which produce a pyogranulomatous inflammatory reaction.
File:IPLab10Blasto8.jpg|This is a high-power photomicrograph showing an alveolus filled with Blastomyces organisms. This section is stained with Periodic Acid-Schiff (PAS) to stain the Blastomyces organisms.
File:IPLab10Blasto9.jpg|This high-power photomicrograph shows Blastomyces organisms stained with PAS. Note the budding organism (arrow). Blastomyces has a characteristic presentation of budding which aids in diagnosis of the fungus.
File:IPLab10Blasto10.jpg|This is a very high-power photomicrograph showing Blastomyces organisms stained with PAS. Note the budding organism (arrow) and the underlying pyogranulomatous inflammatory reaction in the background.
</gallery>

== Virtual Microscopy ==
=== H&E ===
<peir-vm>IPLab10Blasto_HE</peir-vm>

=== PAS ===
<peir-vm>IPLab10Blasto_PAS</peir-vm>

== Study Questions ==
* <spoiler text="What is the route of infection of Blastomyces?">Blastomyces is acquired by inhalation of infectious spores from the soil.</spoiler>
* <spoiler text="Blastomyces has a restricted geographical distribution in the US. What regions are endemic?">In the United States, infection is usually limited to areas along the Mississippi, Ohio, and St. Lawrence Rivers, and along the Great Lakes.</spoiler>
* <spoiler text="What groups of people are at increased risk for Blastomyces?">Those exposed to dust--construction workers exposed to dust from construction sites, hunters and outdoors people who walk in dusty areas, and farm workers.</spoiler>
* <spoiler text="What is the usual clinical manifestation of Blastomyces infection?">Most patients get a pyogranulomatous pneumonia. However, Blastomyces can spread outside the lungs to the skin, bones, and prostate.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/354067-overview eMedicine Medical Library: Imaging in Thoracic Blastomycosis]
* [http://emedicine.medscape.com/article/296870-overview eMedicine Medical Library: Blastomycosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/blastomycosis.html Merck Manual: Blastomycosis]

=== Journal Articles ===
* Rooney PJ, Klein BS. [http://www.ncbi.nlm.nih.gov/pubmed/11906450 Linking fungal morphogenesis with virulence]. ''Cell Microbiol'' 2002 Mar;4(3):127-37.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/542-blastomycosis PEIR Digital Library: Blastomycosis Images]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html Webpath: Infection]

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

IPLab:Lab 10:Blastomycosis

2020-07-09T21:56:38Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==
About three weeks before his death, this 17-year-old white male developed a "chest cold" which gradually worsened. The patient was eventually admitted three days before his death. At that time, the patient was very dyspneic. Chest x-ray showed consolidation of the entire left lung. The initial impression by his care team was staphylococcal pneumonia. However, Blastomyces dermatitides was identified in stained smears of sputum the next day. In spite of appropriate antifungal therapy, the patient deteriorated rapidly and died.

At autopsy the both lungs had areas of consolidation and had multiple hemorrhagic areas.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Blasto1.jpg|This gross photograph of the lungs shows areas of necrosis and consolidation.
File:IPLab10Blasto2.jpg|This higher-power view of the lung shows more clearly the areas of necrosis (1) and consolidation (2). Satellite lesions are also present (3).
File:IPLab10Blasto3.jpg|This is a low-power photomicrograph of lung showing many areas of consolidation (arrows).
File:IPLab10Blasto4.jpg|This is a high-power photomicrograph of lung section with pleura. The pleura (1) is thickened and contains inflammatory cells and fibrin. The areas of consolidation (2) are dense and filled with inflammatory cells.
File:IPLab10Blasto5.jpg|This is a higher-power photomicrograph of lung section with pleura. The pleura (arrows) is thickened and contains inflammatory cells and fibrin. The alveoli are filled with inflammatory cells. Some of the alveolar septa are congested with red blood cells.
File:IPLab10Blasto6.jpg|This high-power photomicrograph shows what appear to be inflammatory cells filling the alveoli. At this magnification, numerous round bodies (arrows) that look like inflammatory cell nuclei can be seen. However, on closer examination, some of these round bodies are surrounded by clear halos.
File:IPLab10Blasto7.jpg|This high-power photomicrograph shows an alveolus filled with numerous round bodies up to 25 mm in diameter. Some of these double-contour bodies (1) have a dense center and a clear halo. These are the Blastomyces organisms. The typical B. dermatitides organism is smoothly-outlined with a central, densely basophilic cytoplasm surrounded by a clear halo. When stained with hematoxylin and eosin, the organism is outlined by a relatively thick cell wall. There are also numerous inflammatory cells (2) in the alveolus--neutrophils, lymphocytes and macrophages--which produce a pyogranulomatous inflammatory reaction.
File:IPLab10Blasto8.jpg|This is a high-power photomicrograph showing an alveolus filled with Blastomyces organisms. This section is stained with Periodic Acid-Schiff (PAS) to stain the Blastomyces organisms.
File:IPLab10Blasto9.jpg|This high-power photomicrograph shows Blastomyces organisms stained with PAS. Note the budding organism (arrow). Blastomyces has a characteristic presentation of budding which aids in diagnosis of the fungus.
File:IPLab10Blasto10.jpg|This is a very high-power photomicrograph showing Blastomyces organisms stained with PAS. Note the budding organism (arrow) and the underlying pyogranulomatous inflammatory reaction in the background.
</gallery>

== Virtual Microscopy ==
=== H&E ===
<peir-vm>IPLab10Blasto_HE</peir-vm>

=== PAS ===
<peir-vm>IPLab10Blasto_PAS</peir-vm>

== Study Questions ==
* <spoiler text="What is the route of infection of Blastomyces?">Blastomyces is acquired by inhalation of infectious spores from the soil.</spoiler>
* <spoiler text="Blastomyces has a restricted geographical distribution in the US. What regions are endemic?">In the United States, infection is usually limited to areas along the Mississippi, Ohio, and St. Lawrence Rivers, and along the Great Lakes.</spoiler>
* <spoiler text="What groups of people are at increased risk for Blastomyces?">Those exposed to dust--construction workers exposed to dust from construction sites, hunters and outdoors people who walk in dusty areas, and farm workers.</spoiler>
* <spoiler text="What is the usual clinical manifestation of Blastomyces infection?">Most patients get a pyogranulomatous pneumonia. However, Blastomyces can spread outside the lungs to the skin, bones, and prostate.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/354067-overview eMedicine Medical Library: Imaging in Thoracic Blastomycosis]
* [http://emedicine.medscape.com/article/296870-overview eMedicine Medical Library: Blastomycosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/blastomycosis.html Merck Manual: Blastomycosis]

=== Journal Articles ===
* Rooney PJ, Klein BS. [http://www.ncbi.nlm.nih.gov/pubmed/11906450 Linking fungal morphogenesis with virulence]. ''Cell Microbiol'' 2002 Mar;4(3):127-37.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/542-blastomycosis PEIR Digital Library: Blastomycosis Images]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html Webpath: Infection]

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

IPLab:Lab 10:Blastomycosis

2020-07-09T21:55:45Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==
About three weeks before his death, this 17-year-old white male developed a "chest cold" which gradually worsened. The patient was eventually admitted three days before his death. At that time, the patient was very dyspneic. Chest x-ray showed consolidation of the entire left lung. The initial impression by his care team was staphylococcal pneumonia. However, Blastomyces dermatitides was identified in stained smears of sputum the next day. In spite of appropriate antifungal therapy, the patient deteriorated rapidly and died.

At autopsy the entire left lung was consolidated and had multiple hemorrhagic areas.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Blasto1.jpg|This gross photograph of the lungs shows areas of necrosis and consolidation.
File:IPLab10Blasto2.jpg|This higher-power view of the lung shows more clearly the areas of necrosis (1) and consolidation (2). Satellite lesions are also present (3).
File:IPLab10Blasto3.jpg|This is a low-power photomicrograph of lung showing many areas of consolidation (arrows).
File:IPLab10Blasto4.jpg|This is a high-power photomicrograph of lung section with pleura. The pleura (1) is thickened and contains inflammatory cells and fibrin. The areas of consolidation (2) are dense and filled with inflammatory cells.
File:IPLab10Blasto5.jpg|This is a higher-power photomicrograph of lung section with pleura. The pleura (arrows) is thickened and contains inflammatory cells and fibrin. The alveoli are filled with inflammatory cells. Some of the alveolar septa are congested with red blood cells.
File:IPLab10Blasto6.jpg|This high-power photomicrograph shows what appear to be inflammatory cells filling the alveoli. At this magnification, numerous round bodies (arrows) that look like inflammatory cell nuclei can be seen. However, on closer examination, some of these round bodies are surrounded by clear halos.
File:IPLab10Blasto7.jpg|This high-power photomicrograph shows an alveolus filled with numerous round bodies up to 25 mm in diameter. Some of these double-contour bodies (1) have a dense center and a clear halo. These are the Blastomyces organisms. The typical B. dermatitides organism is smoothly-outlined with a central, densely basophilic cytoplasm surrounded by a clear halo. When stained with hematoxylin and eosin, the organism is outlined by a relatively thick cell wall. There are also numerous inflammatory cells (2) in the alveolus--neutrophils, lymphocytes and macrophages--which produce a pyogranulomatous inflammatory reaction.
File:IPLab10Blasto8.jpg|This is a high-power photomicrograph showing an alveolus filled with Blastomyces organisms. This section is stained with Periodic Acid-Schiff (PAS) to stain the Blastomyces organisms.
File:IPLab10Blasto9.jpg|This high-power photomicrograph shows Blastomyces organisms stained with PAS. Note the budding organism (arrow). Blastomyces has a characteristic presentation of budding which aids in diagnosis of the fungus.
File:IPLab10Blasto10.jpg|This is a very high-power photomicrograph showing Blastomyces organisms stained with PAS. Note the budding organism (arrow) and the underlying pyogranulomatous inflammatory reaction in the background.
</gallery>

== Virtual Microscopy ==
=== H&E ===
<peir-vm>IPLab10Blasto_HE</peir-vm>

=== PAS ===
<peir-vm>IPLab10Blasto_PAS</peir-vm>

== Study Questions ==
* <spoiler text="What is the route of infection of Blastomyces?">Blastomyces is acquired by inhalation of infectious spores from the soil.</spoiler>
* <spoiler text="Blastomyces has a restricted geographical distribution in the US. What regions are endemic?">In the United States, infection is usually limited to areas along the Mississippi, Ohio, and St. Lawrence Rivers, and along the Great Lakes.</spoiler>
* <spoiler text="What groups of people are at increased risk for Blastomyces?">Those exposed to dust--construction workers exposed to dust from construction sites, hunters and outdoors people who walk in dusty areas, and farm workers.</spoiler>
* <spoiler text="What is the usual clinical manifestation of Blastomyces infection?">Most patients get a pyogranulomatous pneumonia. However, Blastomyces can spread outside the lungs to the skin, bones, and prostate.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/354067-overview eMedicine Medical Library: Imaging in Thoracic Blastomycosis]
* [http://emedicine.medscape.com/article/296870-overview eMedicine Medical Library: Blastomycosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/blastomycosis.html Merck Manual: Blastomycosis]

=== Journal Articles ===
* Rooney PJ, Klein BS. [http://www.ncbi.nlm.nih.gov/pubmed/11906450 Linking fungal morphogenesis with virulence]. ''Cell Microbiol'' 2002 Mar;4(3):127-37.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/542-blastomycosis PEIR Digital Library: Blastomycosis Images]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html Webpath: Infection]

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

IPLab:Lab 10:Blastomycosis

2020-07-09T21:54:26Z

Peter Anderson: /* Autopsy Findings */

== Clinical Summary ==

About three weeks before his death, this 17-year-old white male developed a "chest cold" which gradually worsened. The patient was eventually admitted three days before his death. At that time, the patient was very dyspneic. Chest x-ray showed consolidation of the entire left lung. The initial impression by his care team was staphylococcal pneumonia. However, Blastomyces dermatitides was identified in stained smears of sputum the next day. In spite of appropriate antifungal therapy, the patient deteriorated rapidly and died.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Blasto1.jpg|This gross photograph of the lungs shows areas of necrosis and consolidation.
File:IPLab10Blasto2.jpg|This higher-power view of the lung shows more clearly the areas of necrosis (1) and consolidation (2). Satellite lesions are also present (3).
File:IPLab10Blasto3.jpg|This is a low-power photomicrograph of lung showing many areas of consolidation (arrows).
File:IPLab10Blasto4.jpg|This is a high-power photomicrograph of lung section with pleura. The pleura (1) is thickened and contains inflammatory cells and fibrin. The areas of consolidation (2) are dense and filled with inflammatory cells.
File:IPLab10Blasto5.jpg|This is a higher-power photomicrograph of lung section with pleura. The pleura (arrows) is thickened and contains inflammatory cells and fibrin. The alveoli are filled with inflammatory cells. Some of the alveolar septa are congested with red blood cells.
File:IPLab10Blasto6.jpg|This high-power photomicrograph shows what appear to be inflammatory cells filling the alveoli. At this magnification, numerous round bodies (arrows) that look like inflammatory cell nuclei can be seen. However, on closer examination, some of these round bodies are surrounded by clear halos.
File:IPLab10Blasto7.jpg|This high-power photomicrograph shows an alveolus filled with numerous round bodies up to 25 mm in diameter. Some of these double-contour bodies (1) have a dense center and a clear halo. These are the Blastomyces organisms. The typical B. dermatitides organism is smoothly-outlined with a central, densely basophilic cytoplasm surrounded by a clear halo. When stained with hematoxylin and eosin, the organism is outlined by a relatively thick cell wall. There are also numerous inflammatory cells (2) in the alveolus--neutrophils, lymphocytes and macrophages--which produce a pyogranulomatous inflammatory reaction.
File:IPLab10Blasto8.jpg|This is a high-power photomicrograph showing an alveolus filled with Blastomyces organisms. This section is stained with Periodic Acid-Schiff (PAS) to stain the Blastomyces organisms.
File:IPLab10Blasto9.jpg|This high-power photomicrograph shows Blastomyces organisms stained with PAS. Note the budding organism (arrow). Blastomyces has a characteristic presentation of budding which aids in diagnosis of the fungus.
File:IPLab10Blasto10.jpg|This is a very high-power photomicrograph showing Blastomyces organisms stained with PAS. Note the budding organism (arrow) and the underlying pyogranulomatous inflammatory reaction in the background.
</gallery>

== Virtual Microscopy ==
=== H&E ===
<peir-vm>IPLab10Blasto_HE</peir-vm>

=== PAS ===
<peir-vm>IPLab10Blasto_PAS</peir-vm>

== Study Questions ==
* <spoiler text="What is the route of infection of Blastomyces?">Blastomyces is acquired by inhalation of infectious spores from the soil.</spoiler>
* <spoiler text="Blastomyces has a restricted geographical distribution in the US. What regions are endemic?">In the United States, infection is usually limited to areas along the Mississippi, Ohio, and St. Lawrence Rivers, and along the Great Lakes.</spoiler>
* <spoiler text="What groups of people are at increased risk for Blastomyces?">Those exposed to dust--construction workers exposed to dust from construction sites, hunters and outdoors people who walk in dusty areas, and farm workers.</spoiler>
* <spoiler text="What is the usual clinical manifestation of Blastomyces infection?">Most patients get a pyogranulomatous pneumonia. However, Blastomyces can spread outside the lungs to the skin, bones, and prostate.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/354067-overview eMedicine Medical Library: Imaging in Thoracic Blastomycosis]
* [http://emedicine.medscape.com/article/296870-overview eMedicine Medical Library: Blastomycosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/blastomycosis.html Merck Manual: Blastomycosis]

=== Journal Articles ===
* Rooney PJ, Klein BS. [http://www.ncbi.nlm.nih.gov/pubmed/11906450 Linking fungal morphogenesis with virulence]. ''Cell Microbiol'' 2002 Mar;4(3):127-37.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/542-blastomycosis PEIR Digital Library: Blastomycosis Images]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html Webpath: Infection]

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

IPLab:Lab 10:Cryptococcosis

2020-07-09T21:54:05Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==

This 46-year-old male presented with a complaint of right-sided chest pain of six months duration. Chest x-ray showed a nodular mass in the lower lobe of the right lung. The mass was resected surgically.

The 3.5 x 2.5-cm mass was firm, gray, and gelatinous. The mass proved to be a cryptococcal lesion.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Crypto1.jpg|This is the chest x-ray showing the mass (arrow) in the right lower lobe.
File:IPLab10Crypto2.jpg|This is a gross photomicrograph of this lung taken at autopsy. Note the areas of emphysema (1) and consolidation (2).
File:IPLab10Crypto3.jpg|This is another section of this lung showing consolidation (arrows).
File:IPLab10Crypto4.jpg|This is a low-power photomicrograph of the lung from the lesion seen on x-ray. Note that there is little, if any, inflammatory reaction.
File:IPLab10Crypto5.jpg|This is a higher-power photomicrograph of the cryptococcal lesion. The air spaces are filled with organisms (arrows).
File:IPLab10Crypto6.jpg|This is a high-power photomicrograph of the cryptococcal lesion. Some of the organisms have been expelled during processing, but some cryptococcal organisms can be seen (arrows).
File:IPLab10Crypto7.jpg|This is another high-power photomicrograph of the cryptococcal lesion. In this section, numerous cryptococcal organisms (5-10 mm in diameter) can be seen (arrows). Note that there is very little inflammatory reaction.
File:IPLab10Crypto8.jpg|Cryptococcal organisms can also be seen in this high-power photomicrograph of the cryptococcal lesion. Some of the organisms have a well-defined halo (arrows) due to the mucopolysaccharide coat which surrounds them.
File:IPLab10Crypto9.jpg|This higher-power photomicrograph of a cryptococcal organism shows more clearly the nucleus surrounded by the large extracellular capsule (arrows).
File:IPLab10Crypto10.jpg|This is a low-power photomicrograph of lung section stained with Alcian blue, which stains the acidic glycosaminoglycans making up the coat of the cryptococcal organism.
File:IPLab10Crypto11.jpg|This is a higher-power photomicrograph of lung section stained with Alcian blue. The mucopolysaccharide capsule shrinks during processing with this stain, thereby producing a shrunken central appearance with the formation of spikes around each organism.
File:IPLab10Crypto12.jpg|This is a touch prep of fresh lung tissue that was allowed to air dry and then stained to show the mucopolysaccharide capsule around the cryptococcal organisms (arrows).
</gallery>

== Virtual Microscopy ==
=== H&E ===
<peir-vm>IPLab10Crypto_HE</peir-vm>

=== Mucicarmine ===
<peir-vm>IPLab10Crypto_Muci</peir-vm>

== Study Questions ==
* <spoiler text="How is Cryptococcus neoformans usually transmitted to man?">Cryptococcus neoformans is present in the soil and in bird (particularly pigeon) droppings.

The organism infects humans when it is inhaled.</spoiler>
* <spoiler text="Who is susceptible to infection with C. neoformans?">Normal healthy people can get cryptococcal meningoencephalitis but cryptococcal infections are more common in individuals

(1) who receive high-dose corticosteroids and/or

(2) who have AIDS, leukemia, lymphoma, systemic lupus erythematosus,
Hodgkin’s disease, sarcoidosis, or transplant patients.</spoiler>
* <spoiler text="What virulence factors facilitate infection by C. neoformans?">Three properties of Cryptococcus neoformans are associated with virulence:

(1) the capsular polysaccharide;
(2) resistance to killing by alveolar macrophages; and
(3) production of phenoloxidase an enzyme that consumes host epinephrine in the synthesis of fungal melanin and thus protects the fungi from the epinephrine oxidative system present in the host nervous system.

It is thought that one reason why Cryptococcus neoformans preferentially infects the brain may be because the CSF lacks alternative pathway complement components (present in serum) that bind to the carbohydrate capsule and facilitate phagocytosis and killing by polymorphonuclear cells.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/215354-overview eMedicine Medical Library: Cryptococcosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/cryptococcosis.html Merck Manual: Cryptococcosis]

=== Journal Articles ===
* Rooney PJ, Klein BS. [http://www.ncbi.nlm.nih.gov/pubmed/11906450 Linking fungal morphogenesis with virulence]. ''Cell Microbiol'' 2002 Mar;4(3):127-37.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2157-cryptococcosis PEIR Digital Library: Cryptococcosis]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html WebPath: Infection]

== Related IPLab Cases ==
* [[IPLab:Lab 5:α1 Antitrypsin Deficiency|Lab 5: Lung: α1-Antitrypsin Deficiency]]
* [[IPLab:Lab 12:COPD|Lab 12: Lung: Chronic Obstructive Pulmonary Disease]]

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

IPLab:Lab 10:Cryptococcosis

2020-07-09T21:53:37Z

Peter Anderson: /* Autopsy Findings */

== Clinical Summary ==

This 46-year-old male presented with a complaint of right-sided chest pain of six months duration. Chest x-ray showed a nodular mass in the lower lobe of the right lung. The mass was resected surgically.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Crypto1.jpg|This is the chest x-ray showing the mass (arrow) in the right lower lobe.
File:IPLab10Crypto2.jpg|This is a gross photomicrograph of this lung taken at autopsy. Note the areas of emphysema (1) and consolidation (2).
File:IPLab10Crypto3.jpg|This is another section of this lung showing consolidation (arrows).
File:IPLab10Crypto4.jpg|This is a low-power photomicrograph of the lung from the lesion seen on x-ray. Note that there is little, if any, inflammatory reaction.
File:IPLab10Crypto5.jpg|This is a higher-power photomicrograph of the cryptococcal lesion. The air spaces are filled with organisms (arrows).
File:IPLab10Crypto6.jpg|This is a high-power photomicrograph of the cryptococcal lesion. Some of the organisms have been expelled during processing, but some cryptococcal organisms can be seen (arrows).
File:IPLab10Crypto7.jpg|This is another high-power photomicrograph of the cryptococcal lesion. In this section, numerous cryptococcal organisms (5-10 mm in diameter) can be seen (arrows). Note that there is very little inflammatory reaction.
File:IPLab10Crypto8.jpg|Cryptococcal organisms can also be seen in this high-power photomicrograph of the cryptococcal lesion. Some of the organisms have a well-defined halo (arrows) due to the mucopolysaccharide coat which surrounds them.
File:IPLab10Crypto9.jpg|This higher-power photomicrograph of a cryptococcal organism shows more clearly the nucleus surrounded by the large extracellular capsule (arrows).
File:IPLab10Crypto10.jpg|This is a low-power photomicrograph of lung section stained with Alcian blue, which stains the acidic glycosaminoglycans making up the coat of the cryptococcal organism.
File:IPLab10Crypto11.jpg|This is a higher-power photomicrograph of lung section stained with Alcian blue. The mucopolysaccharide capsule shrinks during processing with this stain, thereby producing a shrunken central appearance with the formation of spikes around each organism.
File:IPLab10Crypto12.jpg|This is a touch prep of fresh lung tissue that was allowed to air dry and then stained to show the mucopolysaccharide capsule around the cryptococcal organisms (arrows).
</gallery>

== Virtual Microscopy ==
=== H&E ===
<peir-vm>IPLab10Crypto_HE</peir-vm>

=== Mucicarmine ===
<peir-vm>IPLab10Crypto_Muci</peir-vm>

== Study Questions ==
* <spoiler text="How is Cryptococcus neoformans usually transmitted to man?">Cryptococcus neoformans is present in the soil and in bird (particularly pigeon) droppings.

The organism infects humans when it is inhaled.</spoiler>
* <spoiler text="Who is susceptible to infection with C. neoformans?">Normal healthy people can get cryptococcal meningoencephalitis but cryptococcal infections are more common in individuals

(1) who receive high-dose corticosteroids and/or

(2) who have AIDS, leukemia, lymphoma, systemic lupus erythematosus,
Hodgkin’s disease, sarcoidosis, or transplant patients.</spoiler>
* <spoiler text="What virulence factors facilitate infection by C. neoformans?">Three properties of Cryptococcus neoformans are associated with virulence:

(1) the capsular polysaccharide;
(2) resistance to killing by alveolar macrophages; and
(3) production of phenoloxidase an enzyme that consumes host epinephrine in the synthesis of fungal melanin and thus protects the fungi from the epinephrine oxidative system present in the host nervous system.

It is thought that one reason why Cryptococcus neoformans preferentially infects the brain may be because the CSF lacks alternative pathway complement components (present in serum) that bind to the carbohydrate capsule and facilitate phagocytosis and killing by polymorphonuclear cells.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/215354-overview eMedicine Medical Library: Cryptococcosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/cryptococcosis.html Merck Manual: Cryptococcosis]

=== Journal Articles ===
* Rooney PJ, Klein BS. [http://www.ncbi.nlm.nih.gov/pubmed/11906450 Linking fungal morphogenesis with virulence]. ''Cell Microbiol'' 2002 Mar;4(3):127-37.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2157-cryptococcosis PEIR Digital Library: Cryptococcosis]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html WebPath: Infection]

== Related IPLab Cases ==
* [[IPLab:Lab 5:α1 Antitrypsin Deficiency|Lab 5: Lung: α1-Antitrypsin Deficiency]]
* [[IPLab:Lab 12:COPD|Lab 12: Lung: Chronic Obstructive Pulmonary Disease]]

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

IPLab:Lab 10:Histoplasmosis

2020-07-09T21:53:17Z

Peter Anderson: /* Images */

== Clinical Summary ==

For four months before death, this two-year-old black female infant ate poorly and lost weight. When hospitalized, she appeared chronically ill with signs of infection. An exploratory laparotomy showed the patient had enormously enlarged abdominal lymph nodes, the biopsy of which disclosed active histoplasmosis. Despite intensive therapy, the patient died three weeks after admission.

Autopsy showed widespread enlargement of lymph nodes, ulcers of the intestines, and enlarged adrenal glands exhibiting multifocal granulomas.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Histo1b.jpg|This low-power photomicrograph shows a section of adrenal gland with several irregularly-outlined areas of necrosis.
File:IPLab10Histo2.jpg|This higher-power photomicrograph of the previous adrenal gland shows more clearly the irregularly-shaped area of necrosis (arrows).
File:IPLab10Histo3.jpg|This is an even higher-power photomicrograph of an area of necrosis (arrows). There is loss of cellular detail within this area. There are inflammatory cells present; however, it is difficult to differentiate the inflammatory cells from the native lymphocytes of the adrenal gland--which is a lymph node.
File:IPLab10Histo4.jpg|This high-power photomicrograph was taken at the edge of the area of necrosis. There is a mild inflammatory infiltrate along the edge of the necrosis.
File:IPLab10Histo5.jpg|This high-power photomicrograph shows small (2-5 mm) dark-staining organisms in the cytoplasm of many of these cells (arrows).
File:IPLab10Histo6.jpg|This is a high-power photomicrograph of the same section of tissue as the previous slide. This section, however, has been stained with methenamine silver which causes the Histoplasma organisms to stain black (arrows).
File:IPLab10Histo7.jpg|This photomicrograph was taken under oil immersion to show the silver-stained Histoplasma organisms. Some of the organisms appear to be budding (arrows).
</gallery>

== Virtual Microscopy ==
=== H&E ===
<peir-vm>IPLab10Histo_HE</peir-vm>

=== GMS ===
<peir-vm>IPLab10Histo_GMS</peir-vm>

== Study Questions ==
* <spoiler text="What is the usual route of infection with Histoplasma?">Histoplasma capsulatum infection is usually acquired by inhalation of dust particles from soil contaminated with bird or bat droppings. The droppings contain small spores (microconidia).</spoiler>
* <spoiler text="What types of infections does Histoplasma produce?">1) A self-limited primary pulmonary involvement which may result in coin lesions on chest x-ray;

2) chronic, progressive, lung disease, which often localizes to the lung apices and causes cough, fever, and night sweats;

3) localized lesions in extrapulmonary sites, including mediastinum, adrenals, liver, or meninges; and

4) a widely disseminated involvement, particularly in immunosuppressed patients.</spoiler>
* <spoiler text="How do Histoplasma organisms infect cells?">Histoplasma conidia and yeasts bind to the beta-chain of the integrins receptors LFA-1 (CD11a/CD18) and MAC-1 (CD11b/CD18).

Histoplasma yeasts are phagocytosed by the unstimulated macrophages, multiply within the phagolysosome, and lyse the host cells.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/299054-overview eMedicine Medical Library: Histoplasmosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/histoplasmosis.html Merck Manual: Histoplasmosis]

=== Journal Articles ===
* de Pauw BE. [http://www.ncbi.nlm.nih.gov/pubmed/11429012 Advances in the management of invasive fungal infections in organ transplant recipients: step by step]. ''Transpl Infect Dis'' 2000 Jun;2(2):48-50.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/263-histoplasmosis PEIR Digital Library: Histoplasmosis]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html WebPath: Infection]

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

File:IPLab10Histo1b.jpg

2020-07-09T21:51:13Z

Peter Anderson:

IPLab:Lab 10:Histoplasmosis

2020-07-09T21:46:16Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==

For four months before death, this two-year-old black female infant ate poorly and lost weight. When hospitalized, she appeared chronically ill with signs of infection. An exploratory laparotomy showed the patient had enormously enlarged abdominal lymph nodes, the biopsy of which disclosed active histoplasmosis. Despite intensive therapy, the patient died three weeks after admission.

Autopsy showed widespread enlargement of lymph nodes, ulcers of the intestines, and enlarged adrenal glands exhibiting multifocal granulomas.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Histo1.jpg|This low-power photomicrograph shows a section of adrenal gland with several irregularly-outlined areas of necrosis.
File:IPLab10Histo2.jpg|This higher-power photomicrograph of the previous adrenal gland shows more clearly the irregularly-shaped area of necrosis (arrows).
File:IPLab10Histo3.jpg|This is an even higher-power photomicrograph of an area of necrosis (arrows). There is loss of cellular detail within this area. There are inflammatory cells present; however, it is difficult to differentiate the inflammatory cells from the native lymphocytes of the adrenal gland--which is a lymph node.
File:IPLab10Histo4.jpg|This high-power photomicrograph was taken at the edge of the area of necrosis. There is a mild inflammatory infiltrate along the edge of the necrosis.
File:IPLab10Histo5.jpg|This high-power photomicrograph shows small (2-5 mm) dark-staining organisms in the cytoplasm of many of these cells (arrows).
File:IPLab10Histo6.jpg|This is a high-power photomicrograph of the same section of tissue as the previous slide. This section, however, has been stained with methenamine silver which causes the Histoplasma organisms to stain black (arrows).
File:IPLab10Histo7.jpg|This photomicrograph was taken under oil immersion to show the silver-stained Histoplasma organisms. Some of the organisms appear to be budding (arrows).
</gallery>

== Virtual Microscopy ==
=== H&E ===
<peir-vm>IPLab10Histo_HE</peir-vm>

=== GMS ===
<peir-vm>IPLab10Histo_GMS</peir-vm>

== Study Questions ==
* <spoiler text="What is the usual route of infection with Histoplasma?">Histoplasma capsulatum infection is usually acquired by inhalation of dust particles from soil contaminated with bird or bat droppings. The droppings contain small spores (microconidia).</spoiler>
* <spoiler text="What types of infections does Histoplasma produce?">1) A self-limited primary pulmonary involvement which may result in coin lesions on chest x-ray;

2) chronic, progressive, lung disease, which often localizes to the lung apices and causes cough, fever, and night sweats;

3) localized lesions in extrapulmonary sites, including mediastinum, adrenals, liver, or meninges; and

4) a widely disseminated involvement, particularly in immunosuppressed patients.</spoiler>
* <spoiler text="How do Histoplasma organisms infect cells?">Histoplasma conidia and yeasts bind to the beta-chain of the integrins receptors LFA-1 (CD11a/CD18) and MAC-1 (CD11b/CD18).

Histoplasma yeasts are phagocytosed by the unstimulated macrophages, multiply within the phagolysosome, and lyse the host cells.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/299054-overview eMedicine Medical Library: Histoplasmosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/histoplasmosis.html Merck Manual: Histoplasmosis]

=== Journal Articles ===
* de Pauw BE. [http://www.ncbi.nlm.nih.gov/pubmed/11429012 Advances in the management of invasive fungal infections in organ transplant recipients: step by step]. ''Transpl Infect Dis'' 2000 Jun;2(2):48-50.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/263-histoplasmosis PEIR Digital Library: Histoplasmosis]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html WebPath: Infection]

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

IPLab:Lab 10:Histoplasmosis

2020-07-09T21:46:03Z

Peter Anderson: /* Autopsy Findings */

== Clinical Summary ==

For four months before death, this two-year-old black female infant ate poorly and lost weight. When hospitalized, she appeared chronically ill with signs of infection. An exploratory laparotomy showed the patient had enormously enlarged abdominal lymph nodes, the biopsy of which disclosed active histoplasmosis. Despite intensive therapy, the patient died three weeks after admission.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Histo1.jpg|This low-power photomicrograph shows a section of adrenal gland with several irregularly-outlined areas of necrosis.
File:IPLab10Histo2.jpg|This higher-power photomicrograph of the previous adrenal gland shows more clearly the irregularly-shaped area of necrosis (arrows).
File:IPLab10Histo3.jpg|This is an even higher-power photomicrograph of an area of necrosis (arrows). There is loss of cellular detail within this area. There are inflammatory cells present; however, it is difficult to differentiate the inflammatory cells from the native lymphocytes of the adrenal gland--which is a lymph node.
File:IPLab10Histo4.jpg|This high-power photomicrograph was taken at the edge of the area of necrosis. There is a mild inflammatory infiltrate along the edge of the necrosis.
File:IPLab10Histo5.jpg|This high-power photomicrograph shows small (2-5 mm) dark-staining organisms in the cytoplasm of many of these cells (arrows).
File:IPLab10Histo6.jpg|This is a high-power photomicrograph of the same section of tissue as the previous slide. This section, however, has been stained with methenamine silver which causes the Histoplasma organisms to stain black (arrows).
File:IPLab10Histo7.jpg|This photomicrograph was taken under oil immersion to show the silver-stained Histoplasma organisms. Some of the organisms appear to be budding (arrows).
</gallery>

== Virtual Microscopy ==
=== H&E ===
<peir-vm>IPLab10Histo_HE</peir-vm>

=== GMS ===
<peir-vm>IPLab10Histo_GMS</peir-vm>

== Study Questions ==
* <spoiler text="What is the usual route of infection with Histoplasma?">Histoplasma capsulatum infection is usually acquired by inhalation of dust particles from soil contaminated with bird or bat droppings. The droppings contain small spores (microconidia).</spoiler>
* <spoiler text="What types of infections does Histoplasma produce?">1) A self-limited primary pulmonary involvement which may result in coin lesions on chest x-ray;

2) chronic, progressive, lung disease, which often localizes to the lung apices and causes cough, fever, and night sweats;

3) localized lesions in extrapulmonary sites, including mediastinum, adrenals, liver, or meninges; and

4) a widely disseminated involvement, particularly in immunosuppressed patients.</spoiler>
* <spoiler text="How do Histoplasma organisms infect cells?">Histoplasma conidia and yeasts bind to the beta-chain of the integrins receptors LFA-1 (CD11a/CD18) and MAC-1 (CD11b/CD18).

Histoplasma yeasts are phagocytosed by the unstimulated macrophages, multiply within the phagolysosome, and lyse the host cells.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/299054-overview eMedicine Medical Library: Histoplasmosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/histoplasmosis.html Merck Manual: Histoplasmosis]

=== Journal Articles ===
* de Pauw BE. [http://www.ncbi.nlm.nih.gov/pubmed/11429012 Advances in the management of invasive fungal infections in organ transplant recipients: step by step]. ''Transpl Infect Dis'' 2000 Jun;2(2):48-50.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/263-histoplasmosis PEIR Digital Library: Histoplasmosis]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html WebPath: Infection]

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

IPLab:Lab 10:Candidiasis

2020-07-09T21:45:43Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==
This 73-year-old black male was in good health until about three months before his death when he noticed enlarged lymph nodes first in both inguinal regions and later elsewhere. Antileukemic therapy was begun. About two weeks prior to his death the patient presented to the emergency room with uncontrollable epistaxis. On physical examination, the liver was palpable but the spleen was not. The white blood count was below normal and consisted mainly of lymphocytes with many atypical cells. The patient's bone marrow was also found to be heavily loaded with lymphocytes. Platelets were extremely low and remained so despite platelet transfusions. Subsequently, the patient developed pneumonia which progressed until death. Antemortem cultures yielded Candida tropicalis and Pseudomonas aeruginosa.

At autopsy, there was evidence of disseminated candidiasis.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Candidiasis1.jpg|This autopsy photograph of the kidneys demonstrates the multifocal punctate lesions visible on the serosal surface (arrows). Don't confuse these small yellow punctate lesions with the fat that is adherent to the renal capsule.
File:IPLab10Candidiasis2.jpg|This photograph of the cut surface of these kidneys shows that these multifocal punctate lesions are primarily in the cortex (arrows).
File:IPLab10Candidiasis3.jpg|This is a low-power photomicrograph of lymph node with three prominent areas of Candida colonies (arrows). Even at this low magnification, the purple-staining yeast and pseudohyphae can be easily seen. This section was stained with Periodic Acid-Schiff Hematoxylin (PASH ), which stains the cell wall of fungi to make them more easily visible.
File:IPLab10Candidiasis4.jpg|This is a low-power photomicrograph of one of the Candida colonies from this lymph node. The chains of yeast which are termed "pseudohyphae" are apparent at this magnification.
File:IPLab10Candidiasis5.jpg|This higher-power photomicrograph shows the yeasts and pseudohyphae in this focus of Candida organisms.
File:IPLab10Candidiasis6.jpg|This high-power photomicrograph shows the yeasts (1) and pseudohyphae (2).
File:IPLab10Candidiasis7.jpg|This is a low-power photomicrograph of the kidney from this same case. Note the Candida colonies (arrows). The pseudohyphae are evident around the periphery of these colonies even at this low magnification.
File:IPLab10Candidiasis8.jpg|This is a higher-power photomicrograph of a Candida colony in the kidney. Note the pseudohyphae of the Candida organisms.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab10Candidiasis</peir-vm>

== Study Questions ==
* <spoiler text="What is the significance of seeing yeast and hyphae in these histologic tissue sections?">Candida is the only fungus which grows as:
# a yeast form,
# pseudohyphae, and
# true hyphae with septa.

All three of these forms may be present in the same section of tissue.</spoiler>
* <spoiler text="Who is at risk for developing systemic candidiasis?">Neutropenic patients.

Candida species--especially C. albicans--are part of the normal flora of the skin, mouth, and GI tract, and are the most frequent cause of human fungal infections. These infections vary from superficial lesions in healthy persons to disseminated infections in neutropenic patients.

Severe disseminated candidiasis is associated with neutropenia secondary to chronic granulomatous disease, leukemia, anticancer therapy, or immunosuppression after transplantation.

Candida can be introduced into the bloodstream by intravenous lines, catheters, peritoneal dialysis, cardiac surgery, or intravenous drug abuse.</spoiler>
* <spoiler text="What types of infections does Candida cause in humans?">Candida infections can occur in the oral cavity (thrush), vagina, and in the skin--especially in warm moist areas (i.e., between the fingers and toes and in inguinal creases, inframammary folds, and the anogenital region).

Candida esophagitis can occur with nasogastric tube placement.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/781215-overview eMedicine Medical Library: Candidiasis in Emergency Medicine]
* [http://emedicine.medscape.com/article/213853-overview eMedicine Medical Library: Candidiasis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/candidiasis_invasive.html Merck Manual: Candidiasis (Invasive)]

=== Journal Articles ===
* Marr KA, Bowden RA. [http://www.ncbi.nlm.nih.gov/pubmed/11428995 Fungal infections in patients undergoing blood and marrow transplantation]. ''Transpl Infect Dis'' 1999 Dec;1(4):237-46.
* Marr KA, Bowden RA. [http://www.nejm.org/doi/full/10.1056/NEJMra1315399 Invasive Candidiasis]. ''NEJM'' 2015 Oct 8;373:1445-1456.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2156-candidiasis PEIR Digital Library: Candidiasis]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html Webpath: Infection]

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

IPLab:Lab 10:Candidiasis

2020-07-09T21:45:32Z

Peter Anderson: /* Autopsy Findings */

== Clinical Summary ==
This 73-year-old black male was in good health until about three months before his death when he noticed enlarged lymph nodes first in both inguinal regions and later elsewhere. Antileukemic therapy was begun. About two weeks prior to his death the patient presented to the emergency room with uncontrollable epistaxis. On physical examination, the liver was palpable but the spleen was not. The white blood count was below normal and consisted mainly of lymphocytes with many atypical cells. The patient's bone marrow was also found to be heavily loaded with lymphocytes. Platelets were extremely low and remained so despite platelet transfusions. Subsequently, the patient developed pneumonia which progressed until death. Antemortem cultures yielded Candida tropicalis and Pseudomonas aeruginosa.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab10Candidiasis1.jpg|This autopsy photograph of the kidneys demonstrates the multifocal punctate lesions visible on the serosal surface (arrows). Don't confuse these small yellow punctate lesions with the fat that is adherent to the renal capsule.
File:IPLab10Candidiasis2.jpg|This photograph of the cut surface of these kidneys shows that these multifocal punctate lesions are primarily in the cortex (arrows).
File:IPLab10Candidiasis3.jpg|This is a low-power photomicrograph of lymph node with three prominent areas of Candida colonies (arrows). Even at this low magnification, the purple-staining yeast and pseudohyphae can be easily seen. This section was stained with Periodic Acid-Schiff Hematoxylin (PASH ), which stains the cell wall of fungi to make them more easily visible.
File:IPLab10Candidiasis4.jpg|This is a low-power photomicrograph of one of the Candida colonies from this lymph node. The chains of yeast which are termed "pseudohyphae" are apparent at this magnification.
File:IPLab10Candidiasis5.jpg|This higher-power photomicrograph shows the yeasts and pseudohyphae in this focus of Candida organisms.
File:IPLab10Candidiasis6.jpg|This high-power photomicrograph shows the yeasts (1) and pseudohyphae (2).
File:IPLab10Candidiasis7.jpg|This is a low-power photomicrograph of the kidney from this same case. Note the Candida colonies (arrows). The pseudohyphae are evident around the periphery of these colonies even at this low magnification.
File:IPLab10Candidiasis8.jpg|This is a higher-power photomicrograph of a Candida colony in the kidney. Note the pseudohyphae of the Candida organisms.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab10Candidiasis</peir-vm>

== Study Questions ==
* <spoiler text="What is the significance of seeing yeast and hyphae in these histologic tissue sections?">Candida is the only fungus which grows as:
# a yeast form,
# pseudohyphae, and
# true hyphae with septa.

All three of these forms may be present in the same section of tissue.</spoiler>
* <spoiler text="Who is at risk for developing systemic candidiasis?">Neutropenic patients.

Candida species--especially C. albicans--are part of the normal flora of the skin, mouth, and GI tract, and are the most frequent cause of human fungal infections. These infections vary from superficial lesions in healthy persons to disseminated infections in neutropenic patients.

Severe disseminated candidiasis is associated with neutropenia secondary to chronic granulomatous disease, leukemia, anticancer therapy, or immunosuppression after transplantation.

Candida can be introduced into the bloodstream by intravenous lines, catheters, peritoneal dialysis, cardiac surgery, or intravenous drug abuse.</spoiler>
* <spoiler text="What types of infections does Candida cause in humans?">Candida infections can occur in the oral cavity (thrush), vagina, and in the skin--especially in warm moist areas (i.e., between the fingers and toes and in inguinal creases, inframammary folds, and the anogenital region).

Candida esophagitis can occur with nasogastric tube placement.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/781215-overview eMedicine Medical Library: Candidiasis in Emergency Medicine]
* [http://emedicine.medscape.com/article/213853-overview eMedicine Medical Library: Candidiasis]
* [http://www.merckmanuals.com/professional/infectious_diseases/fungi/candidiasis_invasive.html Merck Manual: Candidiasis (Invasive)]

=== Journal Articles ===
* Marr KA, Bowden RA. [http://www.ncbi.nlm.nih.gov/pubmed/11428995 Fungal infections in patients undergoing blood and marrow transplantation]. ''Transpl Infect Dis'' 1999 Dec;1(4):237-46.
* Marr KA, Bowden RA. [http://www.nejm.org/doi/full/10.1056/NEJMra1315399 Invasive Candidiasis]. ''NEJM'' 2015 Oct 8;373:1445-1456.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2156-candidiasis PEIR Digital Library: Candidiasis]
* [http://library.med.utah.edu/WebPath/INFEHTML/INFECIDX.html Webpath: Infection]

{{IPLab 10}}

[[Category: IPLab:Lab 10]]

IPLab:Lab 9:Actinomycosis

2020-07-09T21:45:03Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==
This 18-year-old black female felt well until one year before death, when she developed a persistent, progressive skin rash and weight loss. One month before death, draining abscesses appeared in the perirectal region. Biopsy showed actinomycosis. Despite treatment, the patient died.

Autopsy revealed a large abscess around the cecum which had ruptured. The perirectal abscesses had originated from extensions of this pericecal abscess.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab9Actinomycosis1.jpg|This is a low-power photomicrograph of the retroperitoneal abscess. At this magnification, multiple dark-staining foci can be appreciated. These foci are Actinomyces colonies (arrows). These colonies are known as "sulfur granules" because in gross specimens they are visible to the naked eye as yellow grains, thus resembling grains of sulfur.
File:IPLab9Actinomycosis2.jpg|This is a higher-power photomicrograph of an abscess demonstrating a pocket of purulent exudate that contains numerous actinomycotic colonies (arrows).
File:IPLab9Actinomycosis3.jpg|This is a higher-power photomicrograph of actinomycotic colonies in the abscess.
File:IPLab9Actinomycosis4.jpg|This is an even higher-power photomicrograph of actinomycotic colonies in the abscess. The filamentous nature (arrows) of the actinomyces organisms in these colonies can be appreciated.
File:IPLab9Actinomycosis5.jpg|This is a high-power photomicrograph of an actinomycotic colony. The filamentous nature (arrows) of the actinomyces organisms is more easily appreciated at this power.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab9Actinomycosis</peir-vm>

== Study Questions ==
* <spoiler text="These organisms are ubiquitous in the environment but they seldom cause disease. Why?">Actinomyces requires an anaerobic environment deep within tissue to flourish. As a non-invasive bacterium, the Actinomyces organisms must be introduced into these deep tissues before causing harm.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/211587-overview eMedicine Medical Library: Actinomycosis]
* [http://emedicine.medscape.com/article/960759-overview eMedicine Medical Library: Pediatric Actinomycosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/anaerobic_bacteria/actinomycosis.html Merck Manual: Actinomycosis]

=== Journal Articles ===
* Yildiz O, Doganay M. [http://www.ncbi.nlm.nih.gov/pubmed/16582679 Actinomycoses and Nocardia pulmonary infections]. ''Curr Opin Pulm Med'' 2006 May;12(3):228-34.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2154-actinomycosis PEIR Digital Library: Actinomycosis Images]

{{IPLab 9}}

[[Category: IPLab:Lab 9]]

IPLab:Lab 9:Actinomycosis

2020-07-09T21:44:52Z

Peter Anderson: /* Autopsy Findings */

== Clinical Summary ==
This 18-year-old black female felt well until one year before death, when she developed a persistent, progressive skin rash and weight loss. One month before death, draining abscesses appeared in the perirectal region. Biopsy showed actinomycosis. Despite treatment, the patient died.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab9Actinomycosis1.jpg|This is a low-power photomicrograph of the retroperitoneal abscess. At this magnification, multiple dark-staining foci can be appreciated. These foci are Actinomyces colonies (arrows). These colonies are known as "sulfur granules" because in gross specimens they are visible to the naked eye as yellow grains, thus resembling grains of sulfur.
File:IPLab9Actinomycosis2.jpg|This is a higher-power photomicrograph of an abscess demonstrating a pocket of purulent exudate that contains numerous actinomycotic colonies (arrows).
File:IPLab9Actinomycosis3.jpg|This is a higher-power photomicrograph of actinomycotic colonies in the abscess.
File:IPLab9Actinomycosis4.jpg|This is an even higher-power photomicrograph of actinomycotic colonies in the abscess. The filamentous nature (arrows) of the actinomyces organisms in these colonies can be appreciated.
File:IPLab9Actinomycosis5.jpg|This is a high-power photomicrograph of an actinomycotic colony. The filamentous nature (arrows) of the actinomyces organisms is more easily appreciated at this power.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab9Actinomycosis</peir-vm>

== Study Questions ==
* <spoiler text="These organisms are ubiquitous in the environment but they seldom cause disease. Why?">Actinomyces requires an anaerobic environment deep within tissue to flourish. As a non-invasive bacterium, the Actinomyces organisms must be introduced into these deep tissues before causing harm.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/211587-overview eMedicine Medical Library: Actinomycosis]
* [http://emedicine.medscape.com/article/960759-overview eMedicine Medical Library: Pediatric Actinomycosis]
* [http://www.merckmanuals.com/professional/infectious_diseases/anaerobic_bacteria/actinomycosis.html Merck Manual: Actinomycosis]

=== Journal Articles ===
* Yildiz O, Doganay M. [http://www.ncbi.nlm.nih.gov/pubmed/16582679 Actinomycoses and Nocardia pulmonary infections]. ''Curr Opin Pulm Med'' 2006 May;12(3):228-34.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2154-actinomycosis PEIR Digital Library: Actinomycosis Images]

{{IPLab 9}}

[[Category: IPLab:Lab 9]]

IPLab:Lab 9:ARF

2020-07-09T21:44:25Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==
This 21-year-old black male with sickle cell anemia had recurrent attacks of acute rheumatic fever beginning at age 14. Mitral insufficiency and stenosis were present by age 16. On prophylactic antibiotics, the patient had no evidence of recurrence until three weeks before his final admission, when an upper respiratory infection developed. A few weeks later he developed acute migratory polyarthritis. This was associated with rapid deterioration of cardiac function and death.

At autopsy, the heart was enlarged--weighing 675 grams--especially the left atrium. Both the aortic and mitral valves showed fibrosis as well as the fresh, tiny verrucae characteristic of acute rheumatic fever.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab9ARF1.jpg|This is a gross photograph of mitral valve demonstrating marked thickening and fibrosis of the valve leaflet. There are also numerous foci of fibrinoid necrosis within the cusps and friable vegetations (verrucae) along the lines of closure (arrows). These irregular, warty projections are found at sites of erosion on the inflamed endocardial surface. The verrucae probably result from the precipitation of fibrin where the leaflets impinge on each other.
File:IPLab9ARF2.jpg|This is a low-power photomicrograph of heart tissue. Little can be seen at this magnification, except that the tissue looks relatively normal.
File:IPLab9ARF3.jpg|This is a higher-power photomicrograph of myocardium showing cellular accumulations--Aschoff bodies (arrows)--within the interstitium of the myocardium. These are found especially around blood vessels.
File:IPLab9ARF4.jpg|This is a higher-power photomicrograph of myocardium containing Aschoff bodies (arrows) within the interstitium.
File:IPLab9ARF5.jpg|This high-power photomicrograph of myocardium shows the cellular detail of an Aschoff body. Aschoff bodies are foci of fibrinoid necrosis surrounded by lymphocytes, macrophages, an occasional plasma cell, and plump “activated” histiocytes called Anitschkow cells or Aschoff cells (arrows). These distinctive cells have abundant amphophilic cytoplasm and central round-to-ovoid nuclei in which the chromatin is disposed in a central, slender, wavy ribbon resembling a caterpillar (hence the designation “caterpillar cells”).
File:IPLab9ARF6.jpg|This high-power photomicrograph of myocardium shows the cellular detail of another Aschoff body. In this case there appears to be a multinucleated Aschoff giant cell (arrow).
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab9ARF</peir-vm>

== Study Questions ==
* <spoiler text="What is the etiology of rheumatic myocarditis?">Rheumatic fever is an acute, often recurrent, inflammatory disease that principally affects children following a pharyngeal (but not skin) infection with group A beta-hemolytic streptococci. Evidence strongly suggests that rheumatic fever is the result of an immune response to streptococcal antigens inciting either a cross-reaction to tissue antigens or a streptococcal-induced autoimmune reaction to normal tissue antigens.</spoiler>
* <spoiler text="Would it be possible to culture the causative agent from these lesions on the heart valves?">No. Rheumatic fever is an immune-mediated disease. No organisms can be cultured from the heart valves or from the Aschoff bodies.</spoiler>
* <spoiler text="Is this case an example of acute rheumatic fever?">Yes and no!

This patient has acute ramifications of rheumatic fever (acute valve lesions and Aschoff bodies) but there are also a number of old lesions in the heart suggesting that this patient has had numerous bouts of rheumatic fever over the course of many years.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/236582-overview eMedicine Medical Library: Rheumatic Fever]
* [http://emedicine.medscape.com/article/808945-overview eMedicine Medical Library: Rheumatic Fever in Emergency Medicine]
* [http://emedicine.medscape.com/article/333103-overview eMedicine Medical Library: Acute Rheumatic Fever]
* [http://www.merckmanuals.com/professional/pediatrics/rheumatic_fever/rheumatic_fever.html Merck Manual: Rheumatic Fever]

=== Journal Articles ===
* American Heart Association Committee on Rheumatic Fever. [http://dx.doi.org/10.1161/CIR.0000000000000205 Revision of the Jones Criteria for the Diagnosis of Acute Rheumatic Fever in the Era of Doppler Echocardiography]. ''Circulation'' 2015 April 23; 131:1806-1818.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2153-streptococcus PEIR Digital Library: Streptococcus Images]
* [http://library.med.utah.edu/WebPath/CVHTML/CVIDX.html#8 Webpath: Myocarditis]

{{IPLab 9}}

[[Category: IPLab:Lab 9]]

IPLab:Lab 9:ARF

2020-07-09T21:44:11Z

Peter Anderson: /* Autopsy Findings */

== Clinical Summary ==
This 21-year-old black male with sickle cell anemia had recurrent attacks of acute rheumatic fever beginning at age 14. Mitral insufficiency and stenosis were present by age 16. On prophylactic antibiotics, the patient had no evidence of recurrence until three weeks before his final admission, when an upper respiratory infection developed. A few weeks later he developed acute migratory polyarthritis. This was associated with rapid deterioration of cardiac function and death.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab9ARF1.jpg|This is a gross photograph of mitral valve demonstrating marked thickening and fibrosis of the valve leaflet. There are also numerous foci of fibrinoid necrosis within the cusps and friable vegetations (verrucae) along the lines of closure (arrows). These irregular, warty projections are found at sites of erosion on the inflamed endocardial surface. The verrucae probably result from the precipitation of fibrin where the leaflets impinge on each other.
File:IPLab9ARF2.jpg|This is a low-power photomicrograph of heart tissue. Little can be seen at this magnification, except that the tissue looks relatively normal.
File:IPLab9ARF3.jpg|This is a higher-power photomicrograph of myocardium showing cellular accumulations--Aschoff bodies (arrows)--within the interstitium of the myocardium. These are found especially around blood vessels.
File:IPLab9ARF4.jpg|This is a higher-power photomicrograph of myocardium containing Aschoff bodies (arrows) within the interstitium.
File:IPLab9ARF5.jpg|This high-power photomicrograph of myocardium shows the cellular detail of an Aschoff body. Aschoff bodies are foci of fibrinoid necrosis surrounded by lymphocytes, macrophages, an occasional plasma cell, and plump “activated” histiocytes called Anitschkow cells or Aschoff cells (arrows). These distinctive cells have abundant amphophilic cytoplasm and central round-to-ovoid nuclei in which the chromatin is disposed in a central, slender, wavy ribbon resembling a caterpillar (hence the designation “caterpillar cells”).
File:IPLab9ARF6.jpg|This high-power photomicrograph of myocardium shows the cellular detail of another Aschoff body. In this case there appears to be a multinucleated Aschoff giant cell (arrow).
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab9ARF</peir-vm>

== Study Questions ==
* <spoiler text="What is the etiology of rheumatic myocarditis?">Rheumatic fever is an acute, often recurrent, inflammatory disease that principally affects children following a pharyngeal (but not skin) infection with group A beta-hemolytic streptococci. Evidence strongly suggests that rheumatic fever is the result of an immune response to streptococcal antigens inciting either a cross-reaction to tissue antigens or a streptococcal-induced autoimmune reaction to normal tissue antigens.</spoiler>
* <spoiler text="Would it be possible to culture the causative agent from these lesions on the heart valves?">No. Rheumatic fever is an immune-mediated disease. No organisms can be cultured from the heart valves or from the Aschoff bodies.</spoiler>
* <spoiler text="Is this case an example of acute rheumatic fever?">Yes and no!

This patient has acute ramifications of rheumatic fever (acute valve lesions and Aschoff bodies) but there are also a number of old lesions in the heart suggesting that this patient has had numerous bouts of rheumatic fever over the course of many years.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/236582-overview eMedicine Medical Library: Rheumatic Fever]
* [http://emedicine.medscape.com/article/808945-overview eMedicine Medical Library: Rheumatic Fever in Emergency Medicine]
* [http://emedicine.medscape.com/article/333103-overview eMedicine Medical Library: Acute Rheumatic Fever]
* [http://www.merckmanuals.com/professional/pediatrics/rheumatic_fever/rheumatic_fever.html Merck Manual: Rheumatic Fever]

=== Journal Articles ===
* American Heart Association Committee on Rheumatic Fever. [http://dx.doi.org/10.1161/CIR.0000000000000205 Revision of the Jones Criteria for the Diagnosis of Acute Rheumatic Fever in the Era of Doppler Echocardiography]. ''Circulation'' 2015 April 23; 131:1806-1818.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2153-streptococcus PEIR Digital Library: Streptococcus Images]
* [http://library.med.utah.edu/WebPath/CVHTML/CVIDX.html#8 Webpath: Myocarditis]

{{IPLab 9}}

[[Category: IPLab:Lab 9]]

IPLab:Lab 9:Diphtheria

2020-07-09T21:43:55Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==
This 4-year-old black female had an upper respiratory infection and a sore throat with increasing difficulty in breathing. Membranous exudate over one tonsil led to a working diagnosis of diphtheria, and the child was admitted. On the day of her admission, the child developed signs of respiratory tract obstruction and a tracheotomy was performed. However, the procedure was unable to establish a patent airway and the child died.

At autopsy, a dense grayish pink membrane extended from both tonsils to the mid-trachea. The lungs were edematous and showed signs of pneumonia.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab9Diphtheria1.jpg|This is a low-power photomicrograph of the trachea with the diphtheritic membrane (1), which has pulled away from the tracheal lining during histological processing. Note the tracheal cartilage (2) present in this section.
File:IPLab9Diphtheria2.jpg|This is a higher-power photomicrograph of trachea with the diphtheritic membrane (1). Even though, the main part of the membrane has pulled away from the tracheal lining during histological processing, in this section part of the membrane is still loosely attached. Once again, note the tracheal cartilage (2).
File:IPLab9Diphtheria3.jpg|This is an even higher-power photomicrograph of the tracheal mucosa and the diphtheritic membrane. The mucosal surface of the trachea is ulcerated (total loss of epithelial cells) and the only remaining epithelial cells are found in the glands (arrows). The diphtheritic membrane consists of fibrin and inflammatory cells, most of which are dead.
File:IPLab9Diphtheria4.jpg|In this higher-power photomicrograph of the tissue from the previous image, the ulcerated tracheal mucosa and the diphtheritic membrane are more clearly seen. Although difficult to make out at this magnification, most of the cells in this inflammatory exudate are neutrophils.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab9Diphtheria</peir-vm>

== Study Questions ==
* <spoiler text="What organism causes diphtheria?">Diphtheria is caused by Corynebacterium diphtheriae. This organism is passed from person to person by aerosols or by skin shedding.</spoiler>
* <spoiler text="What toxins are involved in the pathogenesis of diphtheria?">C. diphtheriae has only one toxin, which is encoded by a lysogenic phage. Thus, C. diphtheriae cannot cause diphtheria unless the phage first infects the bacteria and provides it with the DNA necessary for production of the toxin.</spoiler>
* <spoiler text="How does diphtheria toxin cause cell killing?">The toxin is composed of fragment B that attaches to host cells and fragment A which is linked to fragment B by a disulfide bridge. Bound diphtheria toxin enters the acidic endosome of cells, fuses with the endosomal membrane, and then enters the cell cytoplasm. There the disulfide bond of the toxin is broken, releasing the enzymatically active fragment A which then catalyzes the covalent transfer of adenosine diphosphate ribose (ADPR) from nicotinamide-adenine dinucleotide (NAD) to EF-2. EF-2, a ribosomal elongation factor necessary for protein synthesis, is thus inactivated. One molecule of diphtheria toxin can kill a cell by ADP-ribosylating more than a million EF-2 molecules.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/782051-overview eMedicine Medical Library: Diphtheria]
* [http://emedicine.medscape.com/article/963334-overview eMedicine Medical Library: Pediatric Pneumonia]
* [http://emedicine.medscape.com/article/215100-overview eMedicine Medical Library: Corynebacterium Infections]
* [http://www.merckmanuals.com/professional/infectious_diseases/gram-positive_bacilli/diphtheria.html Merck Manual: Diphtheria]

=== Journal Articles ===
* Zakikhany K, Efstratiou A. [http://www.ncbi.nlm.nih.gov/pubmed/22568715 Diphtheria in Europe: current problems and new challenges]. ''Future Microbiol'' 2012 May;7(5):595-607.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2152-diphtheria PEIR Digital Library: Diphtheria Images]
* [http://library.med.utah.edu/WebPath/LUNGHTML/LUNGIDX.html#1 WebPath: Pneumonias]

{{IPLab 9}}

[[Category: IPLab:Lab 9]]

IPLab:Lab 9:Diphtheria

2020-07-09T21:43:41Z

Peter Anderson: /* Autopsy Findings */

== Clinical Summary ==
This 4-year-old black female had an upper respiratory infection and a sore throat with increasing difficulty in breathing. Membranous exudate over one tonsil led to a working diagnosis of diphtheria, and the child was admitted. On the day of her admission, the child developed signs of respiratory tract obstruction and a tracheotomy was performed. However, the procedure was unable to establish a patent airway and the child died.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab9Diphtheria1.jpg|This is a low-power photomicrograph of the trachea with the diphtheritic membrane (1), which has pulled away from the tracheal lining during histological processing. Note the tracheal cartilage (2) present in this section.
File:IPLab9Diphtheria2.jpg|This is a higher-power photomicrograph of trachea with the diphtheritic membrane (1). Even though, the main part of the membrane has pulled away from the tracheal lining during histological processing, in this section part of the membrane is still loosely attached. Once again, note the tracheal cartilage (2).
File:IPLab9Diphtheria3.jpg|This is an even higher-power photomicrograph of the tracheal mucosa and the diphtheritic membrane. The mucosal surface of the trachea is ulcerated (total loss of epithelial cells) and the only remaining epithelial cells are found in the glands (arrows). The diphtheritic membrane consists of fibrin and inflammatory cells, most of which are dead.
File:IPLab9Diphtheria4.jpg|In this higher-power photomicrograph of the tissue from the previous image, the ulcerated tracheal mucosa and the diphtheritic membrane are more clearly seen. Although difficult to make out at this magnification, most of the cells in this inflammatory exudate are neutrophils.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab9Diphtheria</peir-vm>

== Study Questions ==
* <spoiler text="What organism causes diphtheria?">Diphtheria is caused by Corynebacterium diphtheriae. This organism is passed from person to person by aerosols or by skin shedding.</spoiler>
* <spoiler text="What toxins are involved in the pathogenesis of diphtheria?">C. diphtheriae has only one toxin, which is encoded by a lysogenic phage. Thus, C. diphtheriae cannot cause diphtheria unless the phage first infects the bacteria and provides it with the DNA necessary for production of the toxin.</spoiler>
* <spoiler text="How does diphtheria toxin cause cell killing?">The toxin is composed of fragment B that attaches to host cells and fragment A which is linked to fragment B by a disulfide bridge. Bound diphtheria toxin enters the acidic endosome of cells, fuses with the endosomal membrane, and then enters the cell cytoplasm. There the disulfide bond of the toxin is broken, releasing the enzymatically active fragment A which then catalyzes the covalent transfer of adenosine diphosphate ribose (ADPR) from nicotinamide-adenine dinucleotide (NAD) to EF-2. EF-2, a ribosomal elongation factor necessary for protein synthesis, is thus inactivated. One molecule of diphtheria toxin can kill a cell by ADP-ribosylating more than a million EF-2 molecules.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/782051-overview eMedicine Medical Library: Diphtheria]
* [http://emedicine.medscape.com/article/963334-overview eMedicine Medical Library: Pediatric Pneumonia]
* [http://emedicine.medscape.com/article/215100-overview eMedicine Medical Library: Corynebacterium Infections]
* [http://www.merckmanuals.com/professional/infectious_diseases/gram-positive_bacilli/diphtheria.html Merck Manual: Diphtheria]

=== Journal Articles ===
* Zakikhany K, Efstratiou A. [http://www.ncbi.nlm.nih.gov/pubmed/22568715 Diphtheria in Europe: current problems and new challenges]. ''Future Microbiol'' 2012 May;7(5):595-607.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2152-diphtheria PEIR Digital Library: Diphtheria Images]
* [http://library.med.utah.edu/WebPath/LUNGHTML/LUNGIDX.html#1 WebPath: Pneumonias]

{{IPLab 9}}

[[Category: IPLab:Lab 9]]

IPLab:Lab 9:Bacterial Meningitis

2020-07-09T21:42:50Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==
This 45-year-old white female with a history of psychiatric illness sustained self-inflicted third degree burns over 49% of her body surface. After initially doing well under treatment, she developed severe respiratory distress and became comatose. Antemortem blood cultures were positive for Pseudomonas aeruginosa.

At autopsy the principal findings were in the lungs and brain. Bronchopneumonia was present in all lobes of both lungs. The brain weighed 1450 grams and the leptomeninges contained a thick yellow purulent exudate most prominent over the frontoparietal areas and at the base of the brain.

== Images ==
<gallery heights="250px" widths="250px">
IPLab9BacterialMeningitis1.jpg|This gross photograph of the autopsy specimen from this case demonstrates the purulent exudate (arrows) in the leptomeninges.
IPLab9BacterialMeningitis2.jpg|This is a low-power photomicrograph of brain section. Note the exudate (1) in the meninges and congestion of the vessels (2) in the leptomeninges.
IPLab9BacterialMeningitis3.jpg|This is a higher-power view of a congested blood vessel. Inflammatory exudate is present within the vessel and throughout the leptomeninges.
IPLab9BacterialMeningitis4.jpg|This higher-power photomicrograph of a sulcus shows the congested vessels and the inflammatory exudate in the leptomeninges.
IPLab9BacterialMeningitis5.jpg|This is a higher-power photomicrograph of inflammatory exudate in a sulcus. The majority of cells in this exudate are neutrophils. There is also abundant fibrin (arrows) and red blood cells are present in the congested vessels.
IPLab9BacterialMeningitis6.jpg|This is a high-power photomicrograph of a blood vessel from the previous image. The vessel is surrounded by neutrophils (arrows).
IPLab9BacterialMeningitis7.jpg|This is a high-power photomicrograph of exudate from the leptomeninges which has been Gram-stained. Note the Gram-negative bacteria (arrows) throughout this section.
IPLab9BacterialMeningitis8.jpg|This photomicrograph of brain tissue demonstrates diffuse edema.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab9BacterialMeningitis</peir-vm>

== Study Questions ==
* <spoiler text="What is the most common etiologic agent that causes bacterial meningitis?">The specific etiologic agent varies with the age of the patient:
* in neonates: the organisms include Escherichia coli and the group B streptococci;
* in infants and children: S. pneumoniae and N. meningitidis pervade in immunized children (H. influenzae type b (Hib) vaccine is routine in the U.S.), while Haemophilus influenzae is more prominent in non-immunized children;
* in adolescents and in young adults: Neisseria meningitidis;
* in the elderly: Streptococcus pneumoniae and Listeria.</spoiler>
* <spoiler text="What organism caused meningitis in this case and why?">Burn patients are at high risk for developing Pseudomonas infections. In this case, the patient was debilitated due to the extensive severe burn and developed a Pseudomonas septicemia which then led to the Pseudomonas meningitis.</spoiler>
* <spoiler text="Why is there fibrin in these lesions?">Because of the acute inflammatory reaction, there is extravasation of fibrin as well as the recruitment of neutrophils.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/961497-overview eMedicine Medical Library: Pediatric Bacterial Meningitis]
* [http://emedicine.medscape.com/article/232915-overview eMedicine Medical Library: Meningitis]
* [http://emedicine.medscape.com/article/1278244-overview eMedicine Medical Library: Thermal Burns]
* [http://emedicine.medscape.com/article/226748-overview eMedicine Medical Library: Pseudomonas aeruginosa Infections]
* [http://www.merckmanuals.com/professional/neurologic_disorders/meningitis/acute_bacterial_meningitis.html Merck Manual: Acute Bacterial Meningitis]
* [http://www.merckmanuals.com/professional/injuries_poisoning/burns/burns.html Merck Manual: Burns]

=== Journal Articles ===
* Grände PO, Myhre EB, Nordström CH, Schliamser S. [http://www.ncbi.nlm.nih.gov/pubmed/11939916 Treatment of intracranial hypertension and aspects on lumbar dural puncture in severe bacterial meningitis]. ''Acta Anaesthesiol Scand'' 2002 Mar;46(3):264-70.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/403-meningitis PEIR Digital Library: Meningitis Images]
* [http://library.med.utah.edu/WebPath/CNSHTML/CNSIDX.html#6 WebPath: CNS Infections]

{{IPLab 9}}

[[Category: IPLab:Lab 9]]

IPLab:Lab 9:Bacterial Meningitis

2020-07-09T21:42:35Z

Peter Anderson: /* Autopsy Findings */

== Clinical Summary ==
This 45-year-old white female with a history of psychiatric illness sustained self-inflicted third degree burns over 49% of her body surface. After initially doing well under treatment, she developed severe respiratory distress and became comatose. Antemortem blood cultures were positive for Pseudomonas aeruginosa.

== Images ==
<gallery heights="250px" widths="250px">
IPLab9BacterialMeningitis1.jpg|This gross photograph of the autopsy specimen from this case demonstrates the purulent exudate (arrows) in the leptomeninges.
IPLab9BacterialMeningitis2.jpg|This is a low-power photomicrograph of brain section. Note the exudate (1) in the meninges and congestion of the vessels (2) in the leptomeninges.
IPLab9BacterialMeningitis3.jpg|This is a higher-power view of a congested blood vessel. Inflammatory exudate is present within the vessel and throughout the leptomeninges.
IPLab9BacterialMeningitis4.jpg|This higher-power photomicrograph of a sulcus shows the congested vessels and the inflammatory exudate in the leptomeninges.
IPLab9BacterialMeningitis5.jpg|This is a higher-power photomicrograph of inflammatory exudate in a sulcus. The majority of cells in this exudate are neutrophils. There is also abundant fibrin (arrows) and red blood cells are present in the congested vessels.
IPLab9BacterialMeningitis6.jpg|This is a high-power photomicrograph of a blood vessel from the previous image. The vessel is surrounded by neutrophils (arrows).
IPLab9BacterialMeningitis7.jpg|This is a high-power photomicrograph of exudate from the leptomeninges which has been Gram-stained. Note the Gram-negative bacteria (arrows) throughout this section.
IPLab9BacterialMeningitis8.jpg|This photomicrograph of brain tissue demonstrates diffuse edema.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab9BacterialMeningitis</peir-vm>

== Study Questions ==
* <spoiler text="What is the most common etiologic agent that causes bacterial meningitis?">The specific etiologic agent varies with the age of the patient:
* in neonates: the organisms include Escherichia coli and the group B streptococci;
* in infants and children: S. pneumoniae and N. meningitidis pervade in immunized children (H. influenzae type b (Hib) vaccine is routine in the U.S.), while Haemophilus influenzae is more prominent in non-immunized children;
* in adolescents and in young adults: Neisseria meningitidis;
* in the elderly: Streptococcus pneumoniae and Listeria.</spoiler>
* <spoiler text="What organism caused meningitis in this case and why?">Burn patients are at high risk for developing Pseudomonas infections. In this case, the patient was debilitated due to the extensive severe burn and developed a Pseudomonas septicemia which then led to the Pseudomonas meningitis.</spoiler>
* <spoiler text="Why is there fibrin in these lesions?">Because of the acute inflammatory reaction, there is extravasation of fibrin as well as the recruitment of neutrophils.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/961497-overview eMedicine Medical Library: Pediatric Bacterial Meningitis]
* [http://emedicine.medscape.com/article/232915-overview eMedicine Medical Library: Meningitis]
* [http://emedicine.medscape.com/article/1278244-overview eMedicine Medical Library: Thermal Burns]
* [http://emedicine.medscape.com/article/226748-overview eMedicine Medical Library: Pseudomonas aeruginosa Infections]
* [http://www.merckmanuals.com/professional/neurologic_disorders/meningitis/acute_bacterial_meningitis.html Merck Manual: Acute Bacterial Meningitis]
* [http://www.merckmanuals.com/professional/injuries_poisoning/burns/burns.html Merck Manual: Burns]

=== Journal Articles ===
* Grände PO, Myhre EB, Nordström CH, Schliamser S. [http://www.ncbi.nlm.nih.gov/pubmed/11939916 Treatment of intracranial hypertension and aspects on lumbar dural puncture in severe bacterial meningitis]. ''Acta Anaesthesiol Scand'' 2002 Mar;46(3):264-70.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/403-meningitis PEIR Digital Library: Meningitis Images]
* [http://library.med.utah.edu/WebPath/CNSHTML/CNSIDX.html#6 WebPath: CNS Infections]

{{IPLab 9}}

[[Category: IPLab:Lab 9]]

IPLab:Lab 9:RMSF

2020-07-09T21:42:12Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==
This 9-year-old child was admitted with headache, fever, and a morbilliform rash on the arms and legs. There was a history of a tick being removed from her back. By the time a biopsy was performed, the rash had become petechial. Antibiotics were given and the child recovered within one week.

Examination of a skin biopsy of this patient's lesion was stained with hematoxylin and eosin. A different section was also stained with an immunoperoxidase technique using antibody against Rickettsia rickettsii. Organisms were demonstrated in the endothelial cells.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab9RMSF1.jpg|This is a low-power photomicrograph of the skin biopsy. Note areas of hemorrhage (arrow) in the dermis.
File:IPLab9RMSF2.jpg|This is a higher-power photomicrograph demonstrating areas of hemorrhage immediately underneath the epidermis. Also note the cellularity and thrombosis of the small vessels in the dermis (arrow).
File:IPLab9RMSF3.jpg|This is a photomicrograph of a small vessel in the dermis which is demonstrating mild vasculitis.
File:IPLab9RMSF4.jpg|This is a higher-power photomicrograph of a dermal vessel with mild vasculitis.
File:IPLab9RMSF5.jpg|This is a photomicrograph of dermis with an area of more severe vasculitis (arrow).
File:IPLab9RMSF6.jpg|This is a high-power photomicrograph of severe vasculitis in the dermis.
File:IPLab9RMSF7.jpg|This is a high-power photomicrograph of a dermal vessel (arrow) which is exhibiting vasculitis and thrombosis.
File:IPLab9RMSF8.jpg|This is a high-power photomicrograph of a thrombosed vessel in the dermis. Note that the endothelial cells are missing along part of the circumference of the vessel (arrows)--this is where the main part of the thrombus has attached. Also note the inflammation surrounding the vessel.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab9RMSF</peir-vm>

== Study Questions ==
* <spoiler text="What organism causes Rocky Mountain Spotted Fever and how is it transmitted?">Rickettsia rickettsii. Rodent and dog ticks transmit R. rickettsii to man. Rickettsiae enter the skin with the bite or with scratching of skin covered with insect feces.</spoiler>
* <spoiler text="What is the usual clinical course of Rocky Mountain Spotted Fever?">An eschar develops at the site of the tick bite followed by a hemorrhagic rash that extends over the entire body, including the palms of the hands and soles of the feet. The vascular lesions that underlie the rash often lead to acute necrosis, fibrin extravasation, and thrombosis of the small blood vessels, including arterioles. In severe RMSF, foci of necrotic skin can form on the fingers, toes, elbows, ears, and scrotum.</spoiler>
* <spoiler text="How does Rickettsia rickettsii produce the vasculitis?">Rickettsiae predominantly infect host endothelial and vascular smooth muscle cells causing a widespread vasculitis that may be complicated by thrombi and hemorrhages. Rickettsiae bind to cholesterol-containing receptors, are endocytosed into phagolysosomes, escape into the cytosol, and multiply until they burst the cells. Rickettsiae have an endotoxin but lack secreted toxins. In addition, R. rickettsii activate host kallikrein and kinins and cause local clotting.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/228042-overview eMedicine Medical Library: Rocky Mountain Spotted Fever]
* [http://www.merckmanuals.com/professional/infectious_diseases/rickettsiae_and_related_organisms/rocky_mountain_spotted_fever_rmsf.html Merck Manual: Rocky Mountain Spotted Fever]
* [http://www.merckmanuals.com/professional/infectious_diseases/rickettsiae_and_related_organisms/overview_of_rickettsial_infections.html Merck Manual: Overview of Rickettsial Infections]

=== Journal Articles ===
* Pantanowitz L, Telford SR, Cannon ME. [http://www.ncbi.nlm.nih.gov/pubmed/11982962 Tick-borne diseases in transfusion medicine]. ''Transfus Med'' 2002 Apr;12(2):85-106.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2151-rmsf PEIR Digital Library: RMSF Images]

{{IPLab 9}}

[[Category: IPLab:Lab 9]]

IPLab:Lab 9:RMSF

2020-07-09T21:41:00Z

Peter Anderson: /* Biopsy Findings */

== Clinical Summary ==
This 9-year-old child was admitted with headache, fever, and a morbilliform rash on the arms and legs. There was a history of a tick being removed from her back. By the time a biopsy was performed, the rash had become petechial. Antibiotics were given and the child recovered within one week.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab9RMSF1.jpg|This is a low-power photomicrograph of the skin biopsy. Note areas of hemorrhage (arrow) in the dermis.
File:IPLab9RMSF2.jpg|This is a higher-power photomicrograph demonstrating areas of hemorrhage immediately underneath the epidermis. Also note the cellularity and thrombosis of the small vessels in the dermis (arrow).
File:IPLab9RMSF3.jpg|This is a photomicrograph of a small vessel in the dermis which is demonstrating mild vasculitis.
File:IPLab9RMSF4.jpg|This is a higher-power photomicrograph of a dermal vessel with mild vasculitis.
File:IPLab9RMSF5.jpg|This is a photomicrograph of dermis with an area of more severe vasculitis (arrow).
File:IPLab9RMSF6.jpg|This is a high-power photomicrograph of severe vasculitis in the dermis.
File:IPLab9RMSF7.jpg|This is a high-power photomicrograph of a dermal vessel (arrow) which is exhibiting vasculitis and thrombosis.
File:IPLab9RMSF8.jpg|This is a high-power photomicrograph of a thrombosed vessel in the dermis. Note that the endothelial cells are missing along part of the circumference of the vessel (arrows)--this is where the main part of the thrombus has attached. Also note the inflammation surrounding the vessel.
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab9RMSF</peir-vm>

== Study Questions ==
* <spoiler text="What organism causes Rocky Mountain Spotted Fever and how is it transmitted?">Rickettsia rickettsii. Rodent and dog ticks transmit R. rickettsii to man. Rickettsiae enter the skin with the bite or with scratching of skin covered with insect feces.</spoiler>
* <spoiler text="What is the usual clinical course of Rocky Mountain Spotted Fever?">An eschar develops at the site of the tick bite followed by a hemorrhagic rash that extends over the entire body, including the palms of the hands and soles of the feet. The vascular lesions that underlie the rash often lead to acute necrosis, fibrin extravasation, and thrombosis of the small blood vessels, including arterioles. In severe RMSF, foci of necrotic skin can form on the fingers, toes, elbows, ears, and scrotum.</spoiler>
* <spoiler text="How does Rickettsia rickettsii produce the vasculitis?">Rickettsiae predominantly infect host endothelial and vascular smooth muscle cells causing a widespread vasculitis that may be complicated by thrombi and hemorrhages. Rickettsiae bind to cholesterol-containing receptors, are endocytosed into phagolysosomes, escape into the cytosol, and multiply until they burst the cells. Rickettsiae have an endotoxin but lack secreted toxins. In addition, R. rickettsii activate host kallikrein and kinins and cause local clotting.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/228042-overview eMedicine Medical Library: Rocky Mountain Spotted Fever]
* [http://www.merckmanuals.com/professional/infectious_diseases/rickettsiae_and_related_organisms/rocky_mountain_spotted_fever_rmsf.html Merck Manual: Rocky Mountain Spotted Fever]
* [http://www.merckmanuals.com/professional/infectious_diseases/rickettsiae_and_related_organisms/overview_of_rickettsial_infections.html Merck Manual: Overview of Rickettsial Infections]

=== Journal Articles ===
* Pantanowitz L, Telford SR, Cannon ME. [http://www.ncbi.nlm.nih.gov/pubmed/11982962 Tick-borne diseases in transfusion medicine]. ''Transfus Med'' 2002 Apr;12(2):85-106.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2151-rmsf PEIR Digital Library: RMSF Images]

{{IPLab 9}}

[[Category: IPLab:Lab 9]]

IPLab:Lab 8:Hepatitis B

2020-07-09T21:39:56Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==

This was a 55-year-old white male with chronic renal failure who acquired hepatitis B virus (HBV) in a renal dialysis unit. Death was the result of multiple disease processes, which included active pulmonary tuberculosis and heart failure due to ischemic heart disease. There were few or no symptoms or signs of hepatitis during life other than seroconversion from negative to HBsAg positive.

At autopsy, the liver was enlarged due primarily to severe passive congestion.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab8HBV1.jpg|This is a low-power photomicrograph of liver from this case. This section was stained with a modified aldehyde fuchsin and counterstained with hematoxylin and eosin. Modified aldehyde fuchsin colors cystine-rich proteins--such as HBsAg and elastic fibers--deep purple. The cytoplasm of most liver cells (and RBCs) stain red due to the eosin and have dark blue nuclei.
File:IPLab8HBV2.jpg|This is a higher-power photomicrograph of liver from this case. Note the severe congestion (RBCs in sinusoids) and the presence of occasional hepatocytes with dark red/magenta-stained cytoplasm (arrows).
File:IPLab8HBV3.jpg|This is a higher-power photomicrograph of the periportal region exhibiting some inflammation and bile duct hyperplasia. There is also congestion and some loss of hepatocytes with disruption of the hepatic cords.
File:IPLab8HBV4.jpg|This is a high-power photomicrograph of liver with numerous hepatocytes containing accumulations of magenta-staining material in the cytoplasm (arrows).
File:IPLab8HBV5.jpg|This high-power photomicrograph showing hepatocytes, the cytoplasm of which contain intracytoplasmic accumulations (arrows) of hepatitis B surface antigen.
File:IPLab8HBV6.jpg|This is a photomicrograph of a liver section from another case of hepatitis B. In this H&E-stained section, the typical "ground glass" appearance of the hepatocytes can be appreciated (arrows).
File:IPLab8HBV7.jpg|This is a low-power photomicrograph of liver from the previous image which has been reacted with antibody specific for HBsAg. The hepatocytes that contain HBsAg stain brown.
File:IPLab8HBV8.jpg|This higher-power photomicrograph of the previous section shows more clearly the HBsAg positive cells (arrows). Upon staining with H&E, these same cells exhibit a "ground glass" appearance, which is due to the accumulation of HBsAg in the hepatocyte cytoplasm.
File:IPLab8HBV9.jpg|This is a low-power photomicrograph of the same liver reacted with antibody specific for hepatitis B core antigen (HBcAg). The hepatocytes that contain HBcAg stain brown. Note that even at this low magnification, many brown-staining nuclei can be seen.
File:IPLab8HBV10.jpg|This high-power photomicrograph of the previous section shows the HBcAg positive nuclei (arrows).
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab8HBV</peir-vm>

== Study Questions ==
* <spoiler text="What sorts of clinical/pathologic syndromes can occur after infection with HBV?">HBV can produce:
# acute hepatitis,
# chronic nonprogressive hepatitis,
# progressive chronic disease ending in cirrhosis,
# fulminant hepatitis with massive liver necrosis, and
# an asymptomatic carrier state with or without progressive disease.</spoiler>
* <spoiler text="What is the association between HBV and hepatocellular carcinoma?">There is a strong association between HBV infection and the occurrence of liver cancer (hepatocellular carcinoma). In Taiwan, HBV infected people have a greater than 200-fold increased risk of developing liver cancer as compared with uninfected individuals. However, the precise role of HBV in the causation of human liver cancer is not clear.</spoiler>
* <spoiler text="What are the characteristics of the hepatitis B 'carrier state'?">With hepatotropic viruses, there are those who:
# harbor one of the viruses but suffer little or no adverse effects (a "healthy" carrier) and those who
# have chronic disease but are essentially free of symptoms or disability.
Both constitute reservoirs of infection. HBV infection early in life, particularly via vertical transmission during childbirth, produces a carrier state 90 to 95% of the time. In contrast, only 1 to 10% of adult infections yield a carrier state. Individuals with impaired immunity are more likely to become carriers.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/177632-overview eMedicine Medical Library: Hepatitis B]
* [http://www.merckmanuals.com/professional/hepatic_and_biliary_disorders/hepatitis/acute_viral_hepatitis.html Merck Manual: Acute Viral Hepatitis]
* [http://www.merckmanuals.com/professional/pediatrics/infections_in_neonates/neonatal_hepatitis_b_virus_infection.html Merck Manual: Neonatal Hepatitis B Virus Infection]

=== Journal Articles ===
* Merle P, Trepo C. [http://www.ncbi.nlm.nih.gov/pubmed/11703569 Therapeutic management of hepatitis B-related cirrhosis]. ''J Viral Hepat'' 2001 Nov;8(6):391-9.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/115-hepatitis PEIR Digital Library: Hepatitis Images]
* [http://library.med.utah.edu/WebPath/LIVEHTML/LIVERIDX.html#5 WebPath: Viral Hepatitis]

== Related IPLab Cases ==
* [[IPLab:Lab 4:Chronic Passive Congestion|Lab 4: Liver: Chronic Passive Congestion]]

{{IPLab 8}}

[[Category: IPLab:Lab 8]]

IPLab:Lab 8:Hepatitis B

2020-07-09T21:39:42Z

Peter Anderson: /* Autopsy Findings */

== Clinical Summary ==

This was a 55-year-old white male with chronic renal failure who acquired hepatitis B virus (HBV) in a renal dialysis unit. Death was the result of multiple disease processes, which included active pulmonary tuberculosis and heart failure due to ischemic heart disease. There were few or no symptoms or signs of hepatitis during life other than seroconversion from negative to HBsAg positive.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab8HBV1.jpg|This is a low-power photomicrograph of liver from this case. This section was stained with a modified aldehyde fuchsin and counterstained with hematoxylin and eosin. Modified aldehyde fuchsin colors cystine-rich proteins--such as HBsAg and elastic fibers--deep purple. The cytoplasm of most liver cells (and RBCs) stain red due to the eosin and have dark blue nuclei.
File:IPLab8HBV2.jpg|This is a higher-power photomicrograph of liver from this case. Note the severe congestion (RBCs in sinusoids) and the presence of occasional hepatocytes with dark red/magenta-stained cytoplasm (arrows).
File:IPLab8HBV3.jpg|This is a higher-power photomicrograph of the periportal region exhibiting some inflammation and bile duct hyperplasia. There is also congestion and some loss of hepatocytes with disruption of the hepatic cords.
File:IPLab8HBV4.jpg|This is a high-power photomicrograph of liver with numerous hepatocytes containing accumulations of magenta-staining material in the cytoplasm (arrows).
File:IPLab8HBV5.jpg|This high-power photomicrograph showing hepatocytes, the cytoplasm of which contain intracytoplasmic accumulations (arrows) of hepatitis B surface antigen.
File:IPLab8HBV6.jpg|This is a photomicrograph of a liver section from another case of hepatitis B. In this H&E-stained section, the typical "ground glass" appearance of the hepatocytes can be appreciated (arrows).
File:IPLab8HBV7.jpg|This is a low-power photomicrograph of liver from the previous image which has been reacted with antibody specific for HBsAg. The hepatocytes that contain HBsAg stain brown.
File:IPLab8HBV8.jpg|This higher-power photomicrograph of the previous section shows more clearly the HBsAg positive cells (arrows). Upon staining with H&E, these same cells exhibit a "ground glass" appearance, which is due to the accumulation of HBsAg in the hepatocyte cytoplasm.
File:IPLab8HBV9.jpg|This is a low-power photomicrograph of the same liver reacted with antibody specific for hepatitis B core antigen (HBcAg). The hepatocytes that contain HBcAg stain brown. Note that even at this low magnification, many brown-staining nuclei can be seen.
File:IPLab8HBV10.jpg|This high-power photomicrograph of the previous section shows the HBcAg positive nuclei (arrows).
</gallery>

== Virtual Microscopy ==
<peir-vm>IPLab8HBV</peir-vm>

== Study Questions ==
* <spoiler text="What sorts of clinical/pathologic syndromes can occur after infection with HBV?">HBV can produce:
# acute hepatitis,
# chronic nonprogressive hepatitis,
# progressive chronic disease ending in cirrhosis,
# fulminant hepatitis with massive liver necrosis, and
# an asymptomatic carrier state with or without progressive disease.</spoiler>
* <spoiler text="What is the association between HBV and hepatocellular carcinoma?">There is a strong association between HBV infection and the occurrence of liver cancer (hepatocellular carcinoma). In Taiwan, HBV infected people have a greater than 200-fold increased risk of developing liver cancer as compared with uninfected individuals. However, the precise role of HBV in the causation of human liver cancer is not clear.</spoiler>
* <spoiler text="What are the characteristics of the hepatitis B 'carrier state'?">With hepatotropic viruses, there are those who:
# harbor one of the viruses but suffer little or no adverse effects (a "healthy" carrier) and those who
# have chronic disease but are essentially free of symptoms or disability.
Both constitute reservoirs of infection. HBV infection early in life, particularly via vertical transmission during childbirth, produces a carrier state 90 to 95% of the time. In contrast, only 1 to 10% of adult infections yield a carrier state. Individuals with impaired immunity are more likely to become carriers.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/177632-overview eMedicine Medical Library: Hepatitis B]
* [http://www.merckmanuals.com/professional/hepatic_and_biliary_disorders/hepatitis/acute_viral_hepatitis.html Merck Manual: Acute Viral Hepatitis]
* [http://www.merckmanuals.com/professional/pediatrics/infections_in_neonates/neonatal_hepatitis_b_virus_infection.html Merck Manual: Neonatal Hepatitis B Virus Infection]

=== Journal Articles ===
* Merle P, Trepo C. [http://www.ncbi.nlm.nih.gov/pubmed/11703569 Therapeutic management of hepatitis B-related cirrhosis]. ''J Viral Hepat'' 2001 Nov;8(6):391-9.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/115-hepatitis PEIR Digital Library: Hepatitis Images]
* [http://library.med.utah.edu/WebPath/LIVEHTML/LIVERIDX.html#5 WebPath: Viral Hepatitis]

== Related IPLab Cases ==
* [[IPLab:Lab 4:Chronic Passive Congestion|Lab 4: Liver: Chronic Passive Congestion]]

{{IPLab 8}}

[[Category: IPLab:Lab 8]]

IPLab:Lab 13:Meningococcemia

2020-07-09T21:37:40Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==
This 20-month-old black female was active and without complaint until 4 p.m. on the evening prior to her death, when according to her mother she acted as if she did not feel well. The mother reported that the child had felt warm at bedtime (8 p.m.) so she had given her some acetaminophen. At midnight, the child was given another dose of acetaminophen. The child slept with her mother that night who reported last hearing her daughter make a sound at approximately 7:30 a.m. The mother checked in on her daughter at 8:45 a.m. and found her to be unresponsive. The girl was dead when paramedics arrived. Her past medical history was unremarkable and there had been no recent illness among other family members.

At autopsy external examination revealed multiple purpuric and ecchymotic cutaneous lesions, most notable in the inguinal areas. Microscopic examination of these skin lesions revealed thrombosis and rupture of small dermal vessels. There were scattered visceral petechial hemorrhages and both adrenal glands were grossly hemorrhagic. There was no gross or microscopic evidence of meningitis. However, a Gram stain of cerebrospinal fluid showed Gram-negative diplococci. Cultures were positive for Neisseria meningitides.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab13Meningococcemia1.jpg|In this gross photograph from the autopsy, note the areas of hemorrhage in the inguinal region.
File:IPLab13Meningococcemia2.jpg|This is a closer view of the inguinal region taken at autopsy. The areas of hemorrhage include purpura and petechiae (arrows).
File:IPLab13Meningococcemia3.jpg|In this gross photograph of the abdomen taken at the autopsy, there are petechial hemorrhages on the viscera (arrows).
File:IPLab13Meningococcemia4.jpg|This photomicrograph of the skin shows thrombi and fibrin clots in small vessels in the dermis. This is indicative of the endothelial damage caused by the Neisseria meningitidis endotoxin. This endotoxin-induced damage to the endothelium of small blood vessels throughout the body results in widespread petechiae and purpura.
File:IPLab13Meningococcemia5.jpg|This is a gross photograph of cross sections through the adrenal glands from this case. Both adrenal glands are markedly hemorrhagic.
File:IPLab13Meningococcemia6.jpg|This is a low-power photomicrograph of the adrenal gland from this case. Note that the entire gland is hemorrhagic.
File:IPLab13Meningococcemia7.jpg|This higher-power photomicrograph of the adrenal gland from this case provides an example of hemorrhagic necrosis.
File:IPLab13Meningococcemia8.jpg|This is a higher-power photomicrograph of a smear of cerebrospinal fluid taken at autopsy. Note the Gram-negative cocci in this smear, indicative of N. meningitidis.
</gallery>

== Study Questions ==
* <spoiler text="What is the Waterhouse-Friderichsen syndrome?">This is a syndrome consisting of the sudden onset of rapidly progressing illness with shock, cyanosis, hemorrhagic skin lesions, bilateral adrenal cortical hemorrhage, and usually death within 24 hours. It is the result of fulminant bacterial sepsis, often due to Neisseria meningitides, although many other organisms can be involved. N. meningitides releases a toxin that damages endothelial cells in small vessels all over the body. In the adrenal, this vascular damage and subsequent thrombosis leads to hemorrhagic necrosis.</spoiler>
* <spoiler text="What is the source of Neisseria meningitides?">Man is the only host. The organism lives in the nasopharynges of apparently unaffected individuals.</spoiler>
* <spoiler text="What is the favorite site of growth of Neisseria meningitides during clinical illness?">Cerebrospinal fluid is the favorite site of growth for the bacteria and meningitis is the most common illness. Other sites include heart valves, pericardium, joints, and the lungs.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/221473-overview eMedicine Medical Library: Meningococcemia]
* [http://www.merckmanuals.com/professional/neurologic_disorders/meningitis/acute_bacterial_meningitis.html Merck Manual: Acute Bacterial Meningitis]

=== Journal Articles ===
* Leclerc F, Leteurtre S, Cremer R, Fourier C, Sadik A. [http://www.ncbi.nlm.nih.gov/pubmed/11007200 Do new strategies in meningococcemia produce better outcomes?] ''Crit Care Med'' 2000 Sep;28(9 Suppl):S60-3.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2175-meningococcus PEIR Digital Library: Meningococcemia Images]
* [{{SERVER}}/library/index.php?/tags/2176-adrenal_hemorrhage PEIR Digital Library: Adrenal Hemorrhage Images]

{{IPLab 13}}

[[Category: IPLab:Lab 13]]

IPLab:Lab 13:Meningococcemia

2020-07-09T21:37:06Z

Peter Anderson: /* Autopsy Findings */

== Clinical Summary ==
This 20-month-old black female was active and without complaint until 4 p.m. on the evening prior to her death, when according to her mother she acted as if she did not feel well. The mother reported that the child had felt warm at bedtime (8 p.m.) so she had given her some acetaminophen. At midnight, the child was given another dose of acetaminophen. The child slept with her mother that night who reported last hearing her daughter make a sound at approximately 7:30 a.m. The mother checked in on her daughter at 8:45 a.m. and found her to be unresponsive. The girl was dead when paramedics arrived. Her past medical history was unremarkable and there had been no recent illness among other family members.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab13Meningococcemia1.jpg|In this gross photograph from the autopsy, note the areas of hemorrhage in the inguinal region.
File:IPLab13Meningococcemia2.jpg|This is a closer view of the inguinal region taken at autopsy. The areas of hemorrhage include purpura and petechiae (arrows).
File:IPLab13Meningococcemia3.jpg|In this gross photograph of the abdomen taken at the autopsy, there are petechial hemorrhages on the viscera (arrows).
File:IPLab13Meningococcemia4.jpg|This photomicrograph of the skin shows thrombi and fibrin clots in small vessels in the dermis. This is indicative of the endothelial damage caused by the Neisseria meningitidis endotoxin. This endotoxin-induced damage to the endothelium of small blood vessels throughout the body results in widespread petechiae and purpura.
File:IPLab13Meningococcemia5.jpg|This is a gross photograph of cross sections through the adrenal glands from this case. Both adrenal glands are markedly hemorrhagic.
File:IPLab13Meningococcemia6.jpg|This is a low-power photomicrograph of the adrenal gland from this case. Note that the entire gland is hemorrhagic.
File:IPLab13Meningococcemia7.jpg|This higher-power photomicrograph of the adrenal gland from this case provides an example of hemorrhagic necrosis.
File:IPLab13Meningococcemia8.jpg|This is a higher-power photomicrograph of a smear of cerebrospinal fluid taken at autopsy. Note the Gram-negative cocci in this smear, indicative of N. meningitidis.
</gallery>

== Study Questions ==
* <spoiler text="What is the Waterhouse-Friderichsen syndrome?">This is a syndrome consisting of the sudden onset of rapidly progressing illness with shock, cyanosis, hemorrhagic skin lesions, bilateral adrenal cortical hemorrhage, and usually death within 24 hours. It is the result of fulminant bacterial sepsis, often due to Neisseria meningitides, although many other organisms can be involved. N. meningitides releases a toxin that damages endothelial cells in small vessels all over the body. In the adrenal, this vascular damage and subsequent thrombosis leads to hemorrhagic necrosis.</spoiler>
* <spoiler text="What is the source of Neisseria meningitides?">Man is the only host. The organism lives in the nasopharynges of apparently unaffected individuals.</spoiler>
* <spoiler text="What is the favorite site of growth of Neisseria meningitides during clinical illness?">Cerebrospinal fluid is the favorite site of growth for the bacteria and meningitis is the most common illness. Other sites include heart valves, pericardium, joints, and the lungs.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/221473-overview eMedicine Medical Library: Meningococcemia]
* [http://www.merckmanuals.com/professional/neurologic_disorders/meningitis/acute_bacterial_meningitis.html Merck Manual: Acute Bacterial Meningitis]

=== Journal Articles ===
* Leclerc F, Leteurtre S, Cremer R, Fourier C, Sadik A. [http://www.ncbi.nlm.nih.gov/pubmed/11007200 Do new strategies in meningococcemia produce better outcomes?] ''Crit Care Med'' 2000 Sep;28(9 Suppl):S60-3.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2175-meningococcus PEIR Digital Library: Meningococcemia Images]
* [{{SERVER}}/library/index.php?/tags/2176-adrenal_hemorrhage PEIR Digital Library: Adrenal Hemorrhage Images]

{{IPLab 13}}

[[Category: IPLab:Lab 13]]

IPLab:Lab 13:Cystic Fibrosis

2020-07-09T21:36:14Z

Peter Anderson: /* Clinical Summary */

== Clinical Summary ==
This white female infant was the product of an uncomplicated term delivery, though meconium staining was noted at birth. During the first day post-partum, the infant's abdomen became progressively distended and a meconium ileus was suspected. Surgery confirmed the presence of a meconium ileus and a section of perforated atretic jejunum proximal to the ileus was resected. Eight days later, the patient's condition had deteriorated. A second operation revealed a segment of necrotic bowel, which was removed. Subsequently the infant's pulmonary function deteriorated and she required frequent suctioning. She developed repeated episodes of pneumonia (E. coli and Pseudomonas grew out on cultures) complicated by atelectasis secondary to pneumothorax. The patient died at 25-days-of-age in respiratory failure.

At autopsy extensive bilateral organizing bronchopneumonia was present with evidence of a pneumothorax and atelectasis. There were significant changes in the pancreas consistent with cystic fibrosis as well as involvement of the small intestine and changes related to the surgical procedures.

== Images ==
<gallery heights="250px" widths="250px">
File:IPLab13CF1.jpg|This is a gross photograph of liver and pancreas from the autopsy. The pancreas is slightly smaller than normal and it has a mucous consistency.
File:IPLab13CF2.jpg|This section of duodenum demonstrates dilation, loss of rugae, and areas of ulceration (arrows).
File:IPLab13CF3.jpg|This low-power photomicrograph of pancreas shows increased interstitial connective tissue resulting in accentuation of the lobular pattern.
File:IPLab13CF4.jpg|This higher-power photomicrograph of the pancreas shows interstitial tissue and the presence of small cystic spaces (1) within the acinar lobules. These spaces are filled with an eosinophilic proteinaceous material. The islets of Langerhans (2) are unaffected.
File:IPLab13CF5.jpg|This higher-power photomicrograph shows a cystic space (1) within an acinar lobule. Islets of Langerhans (2) are also visible.
File:IPLab13CF6.jpg|This high-power photomicrograph shows more clearly these variably-sized cystic spaces within the acinar pancreas.
File:IPLab13CF7.jpg|This is another high-power photomicrograph showing cystic spaces (1) within the acinar pancreas and a normal islet of Langerhans (2).
File:IPLab13CF8.jpg|This low-power photomicrograph of intestine shows the normal layers of the intestine, including the serosa (1), the muscularis (2), the submucosa (3), and the mucosal layer (4) with its deep mucosal crypts. There is yet another cystic space within the mucosa (5).
File:IPLab13CF9.jpg|A higher-power photomicrograph shows the bottom of the intestinal crypts and the other normal layers of the intestine. Even at this magnification, accumulations of eosinophilic debris can be seen in many of the intestinal crypts (arrows).
File:IPLab13CF10.jpg|This is a higher-power photomicrograph showing the eosinophilic debris in many of the intestinal crypts (arrows).
File:IPLab13CF11.jpg|This higher-power photomicrograph shows more clearly the eosinophilic debris (arrows) in the intestinal crypts.
File:IPLab13CF12.jpg|This is a low-power photomicrograph from another section of the intestine. Saggital sections of the intestinal crypts show the crypts along their full length, extending to the mucosal surface.
File:IPLab13CF13.jpg|A higher-power photomicrograph of intestine shows the vacuolated intestinal epithelial cells lining the crypts and necrotic debris and inspissated secretions within the crypts (arrows).
File:IPLab13CF14.jpg|Another high-power photomicrograph of intestine shows the vacuolated intestinal epithelial cells lining the crypts and necrotic debris and inspissated secretions within the crypts (arrows).
</gallery>

== Virtual Microscopy ==
=== Pancreas ===
<peir-vm>IPLab13CF_Pancreas</peir-vm>

=== Duodenum ===
<peir-vm>IPLab13CF_Duodenum</peir-vm>

== Study Questions ==
* <spoiler text="What is the mode of inheritance of cystic fibrosis (CF)?">CF is autosomal recessive.

The frequency of CF in whites is 1/200. Thus, one out of every 20 whites must be heterozygous (heterozygotes have no recognizable symptoms).

Other racial groups have a very low incidence of CF.</spoiler>
* <spoiler text="What is the sweat chloride test?">CF causes altered cellular chloride transport leading to increased chloride levels in the sweat.

A sweat chloride level greater than 60 mEq/L is diagnostic for CF if other clinical signs are also present.</spoiler>
* <spoiler text="What are the most common presenting signs in patients with CF and when do they occur?">When children are 2-12 months of age they develop malodorous steatorrhea and recurrent chronic pulmonary infections. Lower than normal weight gain is also common.</spoiler>
* <spoiler text="What organs are affected by CF?">Lung - chronic pneumonia, viscous mucous secretions, distended bronchioles, hypertrophy and hyperplasia of mucus-secreting glands, chronic bronchitis and bronchiolitis.

Pancreas - atrophy of exocrine pancreas, plugging of ducts, progressive fibrosis and fatty replacement. Insufficiency of exocrine pancreas leads to steatorrhea and fat soluble vitamin deficiencies (e.g., low vitamin K leads to bleeding disorders).

Liver - plugging of bile canaliculi, biliary cirrhosis.

Salivary glands - dilation of ducts, plugging, squamous metaplasia of lining epithelium, fibrosis.

Wolffian duct obstruction - infertility in males who live to puberty.</spoiler>

== Additional Resources ==
=== Reference ===
* [http://emedicine.medscape.com/article/1001602-overview eMedicine Medical Library: Cystic Fibrosis]
* [http://emedicine.medscape.com/article/1001602-treatment eMedicine Medical Library: Cystic Fibrosis Treatment and Management]
* [http://emedicine.medscape.com/article/862538-overview eMedicine Medical Library: Sinonasal Manifestations of Cystic Fibrosis]
* [http://www.merckmanuals.com/professional/pediatrics/cystic_fibrosis_cf/cystic_fibrosis.html Merck Manual: Cystic Fibrosis (CF)]

=== Journal Articles ===
* De Boeck K, Alifier M, Vandeputte S. [http://www.ncbi.nlm.nih.gov/pubmed/10933091 Sputum induction in young cystic fibrosis patients]. ''Eur Respir J'' 2000 Jul;16(1):91-4.
* Aurora P, Wade A, Whitmore P, Whitehead B. [http://www.ncbi.nlm.nih.gov/pubmed/11292105 A model for predicting life expectancy of children with cystic fibrosis]. ''Eur Respir J'' 2000 Dec;16(6):1056-60.

=== Images ===
* [{{SERVER}}/library/index.php?/tags/2174-cystic_fibrosis PEIR Digital Library: Cystic Fibrosis Images]

{{IPLab 13}}

[[Category: IPLab:Lab 13]]