Q fever pathophysiology: Difference between revisions

	Q fever Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Q fever from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications, and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Chest X Ray
CT
MRI
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary prevention
Secondary prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Q fever pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Q fever pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Q fever pathophysiology
CDC on Q fever pathophysiology
Q fever pathophysiology in the news
Blogs on Q fever pathophysiology
Directions to Hospitals Treating Q fever
Risk calculators and risk factors for Q fever pathophysiology

← Older edit Newer edit →

VisualWikitext

Revision as of 15:54, 6 June 2017

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Pathophysiology

Transmission:

The organism is transmitted through:

Aerosoloes: Inhalation of contaminated aerosoles is the main mode of transmission.
Ingestion of raw dairy products
Vertical (mother to fetus) transmission has been reported
Parentral
(Through tick bites

Pathogenesis:

C. Brutenii has the ability to exist in 2 forms:

Small cell form: Often described as the spore form of C. Brutenii Resists the external environmental factors as heat, pressure and dissinfectants for long periods

Large cell form: The active form of the organism Large cell form persists in the macrophages inside acidic vacuoles.

Small and large cell forms are antigenically different and this plays a role in the virulence of the organism. The genome of C. Brutenii has been analysed in 1995. Multiple genes encoding for Na/ ion proton exchanger have been discovered and this explains the ability of the organism to survive in low PH.

The infection has 2 phases that correlate with changes in the lipopolysaccharide of C. Brutenii.

Phase I: characterized by smooth lipopolysacharide capsule. Despite being less efficient in invasion of host cells, antibodies against phase I is always isolated from acute Q fever patients.

Phase II: characterized by rough lipopolysacharide capsule and antibodies against phase II have been isolated from chronic Q fever patients.

Q fever as a biological weapon:

C. Brutenii is an extremely virulent organism. According to WHO estimates, an amount of 50 kg of C. Brutenii if spread in an area of 2 square kilometers is capable of:

Infecting 500,000 humans
Killing 150 individuals
Causing acute illness in 125,000 individuals
Causing chronic illness in 9,000 individuals

Microscopic pathology:

C. Brutenii is a gram negative polymorphic intracellular organism.
It was previously classified as a ricketsia, but now is considered a proteobacterium.

References

Template:WikiDoc Sources

@@ Line 6: / Line 6: @@
 ==Pathophysiology==
+===Transmission:===
+The organism is transmitted through:
+*Aerosoloes: Inhalation of contaminated aerosoles is the main mode of transmission.
+*Ingestion of raw dairy products
+*Vertical (mother to fetus) transmission has been reported
+*Parentral
+*(Through tick bites
+===Pathogenesis:===
+C. Brutenii has the ability to exist in 2 forms:
+Small cell form:
+Often described as the spore form of C. Brutenii
+Resists the external environmental factors as heat, pressure and dissinfectants for long periods
+Large cell form:
+The active form of the organism
+Large cell form persists in the macrophages inside acidic vacuoles.
+Small and large cell forms are antigenically different and this plays a role in the virulence of the organism.
+The genome of C. Brutenii has been analysed in 1995. Multiple genes encoding for Na/ ion proton exchanger have been discovered and this explains the ability of the organism to survive in low PH.
+The infection has 2 phases that correlate with changes in the lipopolysaccharide of C. Brutenii.
+Phase I: characterized by smooth lipopolysacharide capsule. Despite being less efficient in invasion of host cells, antibodies against phase I is always isolated  from acute Q fever patients.
+Phase II: characterized by rough lipopolysacharide capsule and antibodies against phase II have been isolated from chronic Q fever patients.
+Q fever as a biological weapon:
+C. Brutenii is an extremely virulent organism.
+According to WHO estimates, an amount of 50 kg of  C. Brutenii if spread in an area of 2 square kilometers is capable of:
+*Infecting 500,000 humans
+*Killing 150 individuals
+*Causing acute illness in 125,000 individuals
+*Causing chronic illness in 9,000 individuals
+Microscopic pathology:
+*C. Brutenii is a gram negative polymorphic intracellular organism.
+*It was previously classified as a ricketsia, but now is considered a proteobacterium.
-{| style="float: right; width: 350px;"
-| [[Image:Coxiella burnetii.JPG|right|300px|C. burnetii, the Q fever causing agent]]
-|}
-* Cattle, sheep, and goats are the primary reservoirs of [[Coxiella burnetii|C. burnetii]].  The infection has been noted in a wide variety of other animals, including other species of livestock and in domesticated pets.
-* [[Coxiella burnetii]] does not usually cause clinical disease in these animals, although abortion in goats and sheep has been linked to C. burnetii infection.
-* [[Organisms]] are excreted in milk, urine, and feces of infected animals. Most importantly, during birthing, the organisms are shed in high numbers within the [[Amniotic fluid|amniotic fluids]] and the placenta.
-* The [[organisms]] are resistant to heat, drying, and many common disinfectants.  These features enable the [[bacteria]] to survive for long periods in the environment.
-* Infection of humans usually occurs by inhalation of these [[organisms]] from the air that contains airborne barnyard dust contaminated by dried placental material, birth fluids, and excreta of infected herd animals.
-* Humans are often very susceptible to the disease, and very few [[organisms]] may be required to cause infection.  Ingestion of contaminated milk, followed by regurgitation and inspiration of the contaminated food, is a less common mode of transmission.
-* Other modes of transmission to humans, including [[tick bites]] and human to human transmission, are rare.
 ==References==