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Related Concept Videos

Pulmonary Tuberculosis I01:29

Pulmonary Tuberculosis I

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Tuberculosis, often called TB, is a contagious illness primarily caused by Mycobacterium tuberculosis. It mainly affects the lung parenchyma but can also impact other body parts.
Causative Organism
The primary infectious agent causing tuberculosis is Mycobacterium tuberculosis, a slow-growing, acid-fast, aerobic rod that exhibits sensitivity to heat and ultraviolet light. Instances of Mycobacterium bovis and Mycobacterium avium contributing to the development of TB infection are rare.
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Infection01:20

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When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
The chain begins with pathogens: bacteria, viruses, fungi, prions, or parasites such as protozoa helminths. These can be present on the skin as transient or resident flora, or they can be acquired from the environment. Identifying and treating the type of infection and...
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Pulmonary Tuberculosis II01:28

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Tuberculosis, or TB, is a bacterial infectious disease caused by Mycobacterium tuberculosis. While its primary impact is on the lungs, leading to pulmonary tuberculosis, it can also affect various other organs, a condition referred to as extrapulmonary tuberculosis.
Here is a detailed explanation of its pathophysiology:
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Reservoir of Infection01:30

Reservoir of Infection

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Infectious diseases arise from intricate interactions between pathogens and their reservoirs. A reservoir of infection refers to the natural habitat where a pathogen lives, grows, and multiplies, serving as a continual source of infection. Reservoirs are broadly classified as either living or nonliving, and each plays a unique role in disease transmission, significantly influencing public health interventions and control strategies.Humans act as reservoirs for a wide array of pathogens,...
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Bacterial Transformation01:33

Bacterial Transformation

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In 1928, bacteriologist Frederick Griffith worked on a vaccine for pneumonia, which is caused by Streptococcus pneumoniae bacteria. Griffith studied two pneumonia strains in mice: one pathogenic and one non-pathogenic. Only the pathogenic strain killed host mice.
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Intracellular Movement of Viruses and Bacteria01:10

Intracellular Movement of Viruses and Bacteria

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Intracellular bacteria and viruses often comprise a group of highly infectious pathogens that can cause several diseases. Bacterial pathogens include those belonging to the genus Rickettsia responsible for conditions such as rocky mountain spotted fever and the Mediterranean spotted fever; Chlamydia, a genus responsible for a sexually transmitted disease; Coxiella burnetii, an agent responsible for Q fever. Viral pathogens include vaccinia—a poxvirus, and herpes simplex virus—a...
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A Deadly Path: Bacterial Spread During Bubonic Plague.

Rodrigo J Gonzalez1, Virginia L Miller2

  • 1Department of Microbiology and Immunology, University of North Carolina, 125 Mason Farm Road, CB# 7290, University of North Carolina, Chapel Hill, NC 27599, USA.

Trends in Microbiology
|February 16, 2016
PubMed
Summary
This summary is machine-generated.

Yersinia pestis causes deadly bubonic plague by suppressing immune responses. New models reveal how the bacteria spread, which is crucial for understanding infection and host immunity.

Keywords:
Yersinia pestisbubonic plaguedissemination

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Area of Science:

  • Microbiology and Immunology
  • Infectious Diseases
  • Pathogenesis Research

Background:

  • Yersinia pestis is the causative agent of bubonic plague, a severe and often fatal illness.
  • The disease is characterized by the abrogation of host immune responses, facilitating bacterial proliferation.
  • Understanding bacterial dissemination is critical for comprehending plague's pathology.

Purpose of the Study:

  • To investigate the mechanisms of Yersinia pestis spread within the host.
  • To elucidate the interplay between Y. pestis and the host immune system during infection.
  • To leverage recent advancements in in vivo plague models for novel insights.

Main Methods:

  • Utilized recently developed in vivo models of Yersinia pestis infection.
  • Employed techniques to track and analyze bacterial dissemination patterns.
  • Observed host immune responses in the context of bacterial spread.

Main Results:

  • New insights into the dynamics of Y. pestis spread within the host organism.
  • Characterization of bacterial dissemination pathways.
  • Data contributing to the understanding of immune evasion strategies employed by Y. pestis.

Conclusions:

  • Deciphering bacterial spread is fundamental to understanding Yersinia pestis pathogenesis.
  • In vivo models provide valuable tools for studying plague and host-pathogen interactions.
  • Further research into bacterial spread will enhance strategies for combating bubonic plague.