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Sunday, October 5, 2025

TYPHOID FEVER

TYPHOID FEVER

TYPHOID FEVER

TYPHOID FEVER: TRANSMISSION AND PATHOLOGIC LESIONS
TYPHOID FEVER: TRANSMISSION AND PATHOLOGIC LESIONS


In popular culture, the potential devastation of typhoid fever has been best illustrated by the story of Typhoid Mary, also known as Mary Mallon, the personal chef to numerous affluent families in the greater New York City area in the early 20th century. She was an asymptomatic chronic carrier of the Salmonella enterica serotype typhi (previously, S. typhi) and caused approximately 50 deaths as she moved between families, rejecting the notion that she had a role in their demise. She spent the bulk of her last 30 years of life in and out of quarantine.

INFECTIOUS ENTERITIS

INFECTIOUS ENTERITIS

INFECTIOUS ENTERITIS

VIRAL ENTERITIS
VIRAL ENTERITIS


Infectious enteritis is a common worldwide illness with a multitude of underlying pathogens at play. The majority of infectious diarrheal diseases are acute in onset duration (< 2 weeks). Globally, acute enteritis is the fifth leading cause of death across all ages. Innumerable studies demonstrate that approximately 70% to 75% of acute diarrhea cases are viral in cause. Previously, culture techniques could not isolate most bacteria. With the advent of deep 16S ribosomal polymerase chain reaction sequencing techniques, genetic signatures can now identify bacteria, so it is not necessary to rely on tedious culture techniques. These technologies have isolated a bacterial source in approximately 15% of acute enteritis cases. Protozoal organisms are responsible for a lesser fraction of these cases.

HIV/AIDS Enteropathy

HIV/AIDS Enteropathy

HIV/AIDS Enteropathy

HIV/AIDS Enteropathy


Up to 50% of HIV patients in the United States report diarrhea, but a distinct cause is identified in only 60% to 70% of these cases. HIV enteropathy is characterized by chronic diarrhea lasting more than 4 weeks and accompanied by malabsorption and abdominal discomfort. As is characteristic of small bowel diarrhea, stools are typically voluminous and may occur postprandially. There may be marked electrolyte disturbances, severe dehydration, and unintentional weight loss.

ANOMALIES OF THE VENTRICULAR SEPTUM

ANOMALIES OF THE VENTRICULAR SEPTUM

ANOMALIES OF THE VENTRICULAR SEPTUM



Ventricular Septal Defects (“MEMBRANOUS”)

Of the anomalies involving ventricular septal defects, those located beneath the aortic valve, the membranous ventricular septal defects, are by far the most common. Not only are these defects frequently seen in association with other cardiac anomalies, but even when occurring as isolated lesions, the membranous VSDs constitute the most important and also the most common type of congenital heart disease. This is not surprising considering the complex embryologic history of the subaortic portion of the ventricular septum. This is the last part of the septum to close, a closure effected by the fusion of components from the embryonic muscular septum, endocardial cushions, and conal swellings. Anomalous development of any one or several of these contributors will lead to a defect of the ventricular septum. There fore, although located in the same general area, membranous VSDs may vary considerably in position and size. Some are found immediately beneath the right and posterior aortic valve cusps; these probably are caused mainly by deficiency of the conus septum and, because of a lack of support for the aortic valve cusps, may lead to prolapse of one or both cusps, causing aortic regurgitation. Other membranous VSDs mainly caused by deficiency of the right limb of the endocardial cushions, or failure of otherwise normally developed endocardial cushions to fuse with the ventricular septum and conus septum, are located a few millimeters away from the aortic valve, leaving a rim of muscular or fibrous tissue. All these defects are located in the general area where the membranous septum is found in the normal heart, and thus are usually rather loosely referred to as “membranous septal defects.”

ANOMALIES OF TRICUSPID VALVE

ANOMALIES OF TRICUSPID VALVE

ANOMALIES OF TRICUSPID VALVE

TRICUSPID ATRESIA
TRICUSPID ATRESIA


Of the congenital tricuspid valve anomalies, only two tricuspid valve atresia and Ebstein’s anomaly are clinically significant. Tricuspid regurgitation and stenosis occurring as isolated lesions are extremely rare. Some forms of septal defects, such as endocardial cushion defects or ventricular septal defects, may involve the tricuspid valve’s medial cusp, rendering this cusp insufficient or allowing for a direct shunt from the left ventricle to the right atrium. Tricuspid valve stenosis usually accompanies pulmonary atresia or severe stenosis when the ventricular septum is intact. Actually, the tricuspid valve in these patients, although small and often with thickened cusps, is normally formed, and the stenosis is a secondary hypoplasia.

HERPES ZOSTER (SHINGLES)

HERPES ZOSTER (SHINGLES)

HERPES ZOSTER (SHINGLES)

CLINICAL PRESENTATION OF HERPES ZOSTER
CLINICAL PRESENTATION OF HERPES ZOSTER

The varicella zoster virus (VZV) is responsible for causing varicella (chickenpox) as well as herpes zoster (shingles). Herpes zoster is caused by reactivation of dormant VZV. Only hosts who have previously been infected with VZV can develop herpes zoster. The incidence of herpes zoster is sure to decrease in the future, because the zoster vaccine has good efficacy in increasing immunity against the virus. The live attenuated vaccine is currently recommended for those individuals 60 years of age and older who fulfill the criteria for receiving a live vaccine. This age was chosen because the incidence of herpes zoster increases after age 60, possibly related to a waning immune response and anti-body titer remaining from the patient’s original VZV infection. Whether the VZV vaccine protects against herpes zoster will take years to determine. The United States introduced widespread childhood immunization against VZV in 1995, and none of these children have yet reached the age of 60. Whether future booster vaccinations or VZV revaccination will be required is yet to be determined.

Sunday, September 28, 2025

POST TRANSPLANT LYMPHOPROLIFERATIVE DISORDER

POST TRANSPLANT LYMPHOPROLIFERATIVE DISORDER

POST TRANSPLANT LYMPHOPROLIFERATIVE DISORDER

POST TRANSPLANT LYMPHOPROLIFERATIVE DISORDER


Solid-organ and allogeneic hematopoietic cell transplantation have revolutionized our ability to treat disease. Immunosuppression may have negative consequences, however, such as an earlier onset and an increased frequency of malignant tumors of the skin, cervix, and colon. A new entity, a group of disorders collectively known as post-transplant lymphoproliferative disorders (PTLDs), has emerged. The group contains primarily of B-cell–mediated lymphoid and/or plasmacytic cell proliferations that have the potential for malignant transformation to lymphoma. They are the most common causes of malignancy, following solid- organ transplantation. Conversely, PTLDs account for only a minority of cancers following hematopoietic cell transplantation. The risk is highest in the first year and then drops significantly. PTLDs remain a significant cause of early graft failure and death, however.

ABDOMINAL AND INTESTINAL TUBERCULOSIS

ABDOMINAL AND INTESTINAL TUBERCULOSIS

ABDOMINAL AND INTESTINAL TUBERCULOSIS

APPEARANCE OF MUCOSA
APPEARANCE OF MUCOSA


Worldwide, tuberculosis presents with an incidence of 7 to 10 million new cases per year, with a prevalence of approximately 2 billion people. Tuberculosis accounts for 6% of global deaths. Intestinal tuberculosis is the sixth most prevalent extrapulmonary manifestation (EPTB); it mimics primary disease of the entire digestive tract presenting as Crohn ileocolitis. Tuberculosis can also manifest as a disease affecting the peritoneum, presenting as peritonitis. Multiple factors additively contribute to propagating tuberculosis, including poverty, malnutrition, overcrowding, immigrant status, and the presence of HIV coinfection. Patients with HIV coinfection demonstrate a deficient cellular immune response, poor immune reconstitution, and a risk for latent tuberculosis reactivation. Hence, a higher incidence of EPTB, increased severity of disease, and more rapid progression of disease may be observed.

MYCOBACTERIUM AVIUM INTRACELLULARE INFECTION

MYCOBACTERIUM AVIUM INTRACELLULARE INFECTION

MYCOBACTERIUM AVIUM INTRACELLULARE INFECTION

MYCOBACTERIUM AVIUM INTRACELLULARE INFECTION


Historically, Mycobacterium tuberculosis infection was common throughout the world, particularly in underprivileged societies. Fortunately, the advent of antitubercular regimens dramatically eradicated the illness. A distinct cohort of nontuberculous mycobacterial pathogens was revealed to exist, however. Nontuberculous mycobacterial illness is predominantly caused by Mycobacterium avium-intracellulare (MAC) and Mycobacterium kansasii, with over 140 distinct species identified. Interestingly, before antiretroviral therapy was available for AIDS, MAC infection was more common in developed nations than underprivileged nations; this fact prompted the hypothesis that bacillus Calmette-Guérin vaccination or a history of tuberculosis may confer immunity. Intradermal reactivity rates were demonstrated to be equal in MAC patients in both developed and underdeveloped nations, however. The pathogenesis of the disease is poorly understood, but several mechanisms have been revealed.

DEFECTS OF THE ATRIAL SEPTUM

DEFECTS OF THE ATRIAL SEPTUM

DEFECTS OF THE ATRIAL SEPTUM

ATRIAL SEPTAL DEFECTS
ATRIAL SEPTAL DEFECTS


The atrial septum normally consists of two overlapping, closely adjacent components. Each forms an incomplete partition. The right-side component, corresponding to the embryonic septum secundum, is muscular and firm and has a posteroinferior oval-shaped opening, the foramen ovale. The left-side component, derived from the embryonic septum primum, is fibrous and thin and has a somewhat round opening anterosuperiorly, the ostium secundum. Together, the two components act as a one-way flap valve, allowing the flow of blood from right to left (normal before birth) but not from left to right. After birth, with the establishment of pulmonary circulation, the increased amount of blood entering the left atrium elevates the pressure in that chamber, thereby closing the flap valve. In most cases, this functional closure is eventually followed by anatomic closure; that is, the two components of the septum fuse. In the minority of cases where fusion fails, an increase in the right atrial pressure due to congenital cardiac anomalies, or any other condition that elevates right ventricular and right atrial pressure, causes the right atrial blood to flow again into the left atrium. Such a probe-patent foramen ovale, however, should not be considered a form of atrial septal defect; it causes no hemodynamic abnormalities by itself. In ASD there is an abnormal opening in the atrial septum allowing blood to flow either way; a predominantly left-to-right shunt usually exists. With associated anomalies or other conditions tending to increase right atrial pressure, the shunt is always from right to left, as in tricuspid valve atresia, or an initially left-to-right shunt reverses, as occurs after pulmonary vascular changes with pulmonary hypertension.

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