Q fever pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
m (Bot: Removing from Primary care)
 
(27 intermediate revisions by 6 users not shown)
Line 1: Line 1:
__NOTOC__
__NOTOC__
{{CMG}}
 
{{CMG}};{{AE}}{{AY}}  
{{Q fever}}
{{Q fever}}
==Overview==
==Overview==
Q fever is a disease caused by C. brutenii, an intracellular gram negative bacterium. The disease can have a wide range of clinical presentations and affect many organ systems due to the unique virulence factors of the organism.
Q fever is a disease caused by [[Coxiella burnetii|''C. burnetii'']], an [[intracellular]], [[gram-negative]]  [[proteobacteria|proteobacterium]]. The disease can have a wide range of clinical presentations and affect many organ systems due to the unique [[virulence factors]] of the [[organism]].


==Pathophysiology==
==Pathophysiology==
===Transmission:===
===Transmission===
The organism is transmitted through:<ref name="pmid17423643">{{cite journal |vauthors=Marrie TJ |title=Q fever - a review |journal=Can. Vet. J. |volume=31 |issue=8 |pages=555–63 |year=1990 |pmid=17423643 |pmc=1480833 |doi= |url=}}</ref>
The organism is transmitted through:<ref name="pmid17423643">{{cite journal |vauthors=Marrie TJ |title=Q fever - a review |journal=Can. Vet. J. |volume=31 |issue=8 |pages=555–63 |year=1990 |pmid=17423643 |pmc=1480833 |doi= |url=}}</ref>
*Aerosoloes: Inhalation of contaminated aerosoles is the main mode of transmission.
*Aerosols: Inhalation of contaminated aerosols is the main mode of transmission
*Ingestion of raw dairy products
*Ingestion of raw dairy products
*Vertical (mother to fetus) transmission has been reported
*[[vertical transmission|Vertical (mother to fetus) transmission]] has been reported
*Parentral
*[[Parenteral]]
*Through tick bites
*[[Tick bites]]
   
   
===Pathogenesis:===
===Pathogenesis===
   
   
C. Brutenii has the ability to exist in 2 forms:
The infection has two phases, which correlate to changes in the [[lipopolysaccharide]] of ''[[Coxiella burnetii|C.]] [[Coxiella burnetii|burnetii]]'':<ref name="pmid1489455">{{cite journal |vauthors=Choyce DP |title=Anterior chamber lens exchange |journal=J Cataract Refract Surg |volume=18 |issue=5 |pages=537 |year=1992 |pmid=1489455 |doi= |url=}}</ref>
:*Phase I: Characterized by a smooth [[lipopolysaccharide]] capsule. Despite being less efficient in the invasion of host cells, [[antibodies]] against phase I are always isolated from acute Q fever patients.
:*Phase II: Characterized by a rough [[lipopolysaccharide]] capsule. [[Antibodies]] against phase II have been isolated from chronic Q fever patients.
[[Coxiella burnetii|''C. burnetii'']] can exist in two forms: the small cell form and the large cell form. The small and large cell forms are [[Antigen|antigenically different]], which plays a role in the [[virulence]] of the [[organism]].
   
   
====Small cell form:====<ref name="urlDiagnosis of Q Fever">{{cite web |url=http://jcm.asm.org/content/36/7/1823.short |title=Diagnosis of Q Fever |format= |work= |accessdate=}}</ref>
====Small cell form<ref name="urlDiagnosis of Q Fever">{{cite web |url=http://jcm.asm.org/content/36/7/1823.short |title=Diagnosis of Q Fever |format= |work= |accessdate=}}</ref>====
Often described as the spore form of C. Brutenii
The small cell form is often described as the spore form of [[Coxiella burnetii|''C. burnetii'']]. It can resist external environmental factors such as heat, pressure, and disinfectants for long periods of time.
Resists the external environmental factors as heat, pressure and dissinfectants for long periods
   
   
====Large cell form:====
====Large cell form====
The active form of the organism
The large cell form is the active form of the [[organism]]. It persists in [[macrophages]] inside acidic [[vacuoles]].
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 ''[[Coxiella burnetii|C.]] [[Coxiella burnetii|burnetii]]'' was analyzed in 1995. Multiple [[genes]] encoding for [[sodium|Na+ ion]] proton exchange have been discovered, explaining the ability of the organism to survive in a [[PH|low pH]] environment.
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.
 
* There is a delay between the entry of the [[organism]] into the host cell and the fusion with [[lysosomes]]. This delay is thought to be due to the transformation from the small cell variant into the large cell variant.
The infection has 2 phases that correlate with changes in the lipopolysaccharide of C. Brutenii:<ref name="pmid1489455">{{cite journal |vauthors=Choyce DP |title=Anterior chamber lens exchange |journal=J Cataract Refract Surg |volume=18 |issue=5 |pages=537 |year=1992 |pmid=1489455 |doi= |url=}}</ref>
* The [[acidic]] environment inside the [[lysosome]] has little effect on the large cell form of the organism.
*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.
====Virulence factors====
 
Phase II: characterized by rough lipopolysacharide capsule and antibodies against phase II have been isolated from chronic Q fever patients.
*The [[lipopolysaccharide]] capsule is one of the most important [[virulence factors]] of the organism.
 
*The different phases of infection are associated with changes in the [[lipopolysaccharide]] capsule.
:*[[Lipopolysaccharide|Lipopolysaccharide phase I]] (smooth polysaccharide) is associated with protection against the host's [[immune response]].
:*[[Lipopolysaccharide|Lipopolysaccharide phase II]] (rough polysaccharide) is isolated from avirulent, non-infectious host cells and is not associated with protection of the virus from the host cell.
 
*Both [[Humoral immunity|humoral]] and [[cell mediated immunity]] are involved in the immune response against ''[[Coxiella burnetii|C. burnetii]]''. However, [[cell mediated immunity]] is more important in defending against the organism and people with [[Immunosuppression|deficient cell mediated immunity]] are more susceptible to developing [[chronic]] [[infection]].
 
===Q fever as a biological weapon===


===Q fever as a biological weapon:===
*Because of its route of infection, ''[[Coxiella burnetii|C. burnetii]]'' can be used as a [[biological warfare]] agent.
*Q-fever is a category "B" agent. It is highly contagious and very stable in aerosols at a wide range of temperatures.
C. Brutenii is an extremely virulent organism.
*Just 1-2 particles are enough to infect an individual.
*Q-fever [[microorganisms]] can survive on surfaces up to 60 days (like sporulating bacteria).
*According to [[WHO]] estimates,  50 kg of [[Coxiella burnetii|''C. burnetii'']], if spread in an area of 2 square kilometers, is capable of:<ref name="urlapps.who.int">{{cite web |url=http://apps.who.int/iris/bitstream/10665/39444/1/24039.pdf |title=apps.who.int |format= |work= |accessdate=}}</ref>
:*Infecting 500,000 humans
:*Killing 150 individuals
:*Causing acute illness in 125,000 individuals
:*Causing chronic illness in 9,000 individuals


According to WHO estimates<ref name="urlapps.who.int">{{cite web |url=http://apps.who.int/iris/bitstream/10665/39444/1/24039.pdf |title=apps.who.int |format= |work= |accessdate=}}</ref>, an amount of 50 kg of  C. Brutenii if spread in an area of 2 square kilometers is capable of:
==Microscopic pathology==
*Infecting 500,000 humans
*Killing 150 individuals
*Causing acute illness in 125,000 individuals
*Causing chronic illness in 9,000 individuals
   
   
==Microscopic pathology:==
*''[[Coxiella burnetii|C.]] [[Coxiella burnetii|burnetii]]'' is a [[gram negative]], polymorphic, [[Intracellular|intracellular organism]].<ref name="urlQ Fever on JSTOR">{{cite web |url=http://www.jstor.org/stable/4458369?seq=1#page_scan_tab_contents |title=Q Fever on JSTOR |format= |work= |accessdate=}}</ref>
*It was previously classified as a ''Rickettsia'', but now is considered a [[Proteobacteria|proteobacterium]].
*C. Brutenii is a gram negative polymorphic intracellular organism.<ref name="urlQ Fever on JSTOR">{{cite web |url=http://www.jstor.org/stable/4458369?seq=1#page_scan_tab_contents |title=Q Fever on JSTOR |format= |work= |accessdate=}}</ref>
*It was previously classified as a ricketsia, but now is considered a proteobacterium.
{| class="wikitable"
{| class="wikitable"
![[Image:Q_fever.jpg|center|300px|thumb|Coxiella brutenii ]]
![[Image:Q_fever.jpg|center|300px|thumb|''Coxiella brutenii'']]
![[Image:Immunohistochemical detection of Coxiella burnetii in resected cardiac valve of a 60-year-old man with Q fever endocarditis - By Mahamat A, Edouard S, Demar M, Abboud P, Patrice J-Y, La Scola B, et al. -Public domain-, via Wikime.jpg|center|300px|thumb|Immunohistochemical detection of Coxiella burnetii in resected cardiac valve of a 60-year-old man with Q fever - By Mahamat A, Edouard S, Demar M, Abboud P, Patrice J-Y, La Scola B, et al. -Public domain-, via Wikime ]]
![[Image:Immunohistochemical detection of Coxiella burnetii in resected cardiac valve of a 60-year-old man with Q fever endocarditis - By Mahamat A, Edouard S, Demar M, Abboud P, Patrice J-Y, La Scola B, et al. -Public domain-, via Wikime.jpg|center|300px|thumb|Immunohistochemical detection of ''Coxiella burnetii'' in resected cardiac valve of a 60-year-old man with Q fever - By Mahamat A, Edouard S, Demar M, Abboud P, Patrice J-Y, La Scola B, et al. -Public domain-, via Wikime ]]
|}
|}


Line 56: Line 66:
{{Reflist|2}}
{{Reflist|2}}


[[Category:Needs overview]]
[[Category:Emergency mdicine]]
[[Category:Disease]]
[[Category:Up-To-Date]]
[[Category:Infectious disease]]
[[Category:Infectious disease]]
[[Category:Bacterial diseases]]
[[Category:Gastroenterology]]
 
[[Category:Hepatology]]
{{WikiDoc Help Menu}}
[[Category:Pulmonology]]
{{WikiDoc Sources}}

Latest revision as of 23:56, 29 July 2020


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]

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

Overview

Q fever is a disease caused by C. burnetii, an intracellular, gram-negative proteobacterium. The disease can have a wide range of clinical presentations and affect many organ systems due to the unique virulence factors of the organism.

Pathophysiology

Transmission

The organism is transmitted through:[1]

Pathogenesis

The infection has two phases, which correlate to changes in the lipopolysaccharide of C. burnetii:[2]

  • Phase I: Characterized by a smooth lipopolysaccharide capsule. Despite being less efficient in the invasion of host cells, antibodies against phase I are always isolated from acute Q fever patients.
  • Phase II: Characterized by a rough lipopolysaccharide capsule. Antibodies against phase II have been isolated from chronic Q fever patients.

C. burnetii can exist in two forms: the small cell form and the large cell form. The small and large cell forms are antigenically different, which plays a role in the virulence of the organism.

Small cell form[3]

The small cell form is often described as the spore form of C. burnetii. It can resist external environmental factors such as heat, pressure, and disinfectants for long periods of time.

Large cell form

The large cell form is the active form of the organism. It persists in macrophages inside acidic vacuoles.

  • The genome of C. burnetii was analyzed in 1995. Multiple genes encoding for Na+ ion proton exchange have been discovered, explaining the ability of the organism to survive in a low pH environment.
  • There is a delay between the entry of the organism into the host cell and the fusion with lysosomes. This delay is thought to be due to the transformation from the small cell variant into the large cell variant.
  • The acidic environment inside the lysosome has little effect on the large cell form of the organism.

Virulence factors

  • The different phases of infection are associated with changes in the lipopolysaccharide capsule.

Q fever as a biological weapon

  • Because of its route of infection, C. burnetii can be used as a biological warfare agent.
  • Q-fever is a category "B" agent. It is highly contagious and very stable in aerosols at a wide range of temperatures.
  • Just 1-2 particles are enough to infect an individual.
  • Q-fever microorganisms can survive on surfaces up to 60 days (like sporulating bacteria).
  • According to WHO estimates, 50 kg of C. burnetii, if spread in an area of 2 square kilometers, is capable of:[4]
  • Infecting 500,000 humans
  • Killing 150 individuals
  • Causing acute illness in 125,000 individuals
  • Causing chronic illness in 9,000 individuals

Microscopic pathology

Coxiella brutenii
Immunohistochemical detection of Coxiella burnetii in resected cardiac valve of a 60-year-old man with Q fever - By Mahamat A, Edouard S, Demar M, Abboud P, Patrice J-Y, La Scola B, et al. -Public domain-, via Wikime

References

  1. ↑ Marrie TJ (1990). "Q fever - a review". Can. Vet. J. 31 (8): 555–63. PMC 1480833. PMID 17423643.
  2. ↑ Choyce DP (1992). "Anterior chamber lens exchange". J Cataract Refract Surg. 18 (5): 537. PMID 1489455.
  3. ↑ "Diagnosis of Q Fever".
  4. ↑ "apps.who.int" (PDF).
  5. ↑ "Q Fever on JSTOR".
Retrieved from "https://www.wikidoc.org/index.php?title=Q_fever_pathophysiology&oldid=1642719"