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==Overview==
==Test==


==Parenchymal lesions==
*Tuberculoma
:* Single or multiple lesions of > 0.5 cm
:* May occur in primary or secundary TB
:* Main finding on Chest X-ray in 5% cases of secondary TB<ref name="pmid3484866">{{cite journal| author=Woodring JH, Vandiviere HM, Fried AM, Dillon ML, Williams TD, Melvin IG| title=Update: the radiographic features of pulmonary tuberculosis. | journal=AJR Am J Roentgenol | year= 1986 | volume= 146 | issue= 3 | pages= 497-506 | pmid=3484866 | doi=10.2214/ajr.146.3.497 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3484866  }} </ref>
:* Results from the surrounding of M. tuberculosis with inflammatory or connective tissue.<ref name="pmid8456658">{{cite journal| author=Lee KS, Song KS, Lim TH, Kim PN, Kim IY, Lee BH| title=Adult-onset pulmonary tuberculosis: findings on chest radiographs and CT scans. | journal=AJR Am J Roentgenol | year= 1993 | volume= 160 | issue= 4 | pages= 753-8 | pmid=8456658 | doi=10.2214/ajr.160.4.8456658 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8456658  }} </ref><ref name="pmid472765">{{cite journal| author=Palmer PE| title=Pulmonary tuberculosis--usual and unusual radiographic presentations. | journal=Semin Roentgenol | year= 1979 | volume= 14 | issue= 3 | pages= 204-43 | pmid=472765 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=472765  }} </ref><ref name="pmid3484866">{{cite journal| author=Woodring JH, Vandiviere HM, Fried AM, Dillon ML, Williams TD, Melvin IG| title=Update: the radiographic features of pulmonary tuberculosis. | journal=AJR Am J Roentgenol | year= 1986 | volume= 146 | issue= 3 | pages= 497-506 | pmid=3484866 | doi=10.2214/ajr.146.3.497 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3484866  }} </ref>
:* The center of the tuberculoma is often necrotic
:* Satellite lesions (80%)
:* Nodular or diffused calcifications in 20-30% cases<ref name="pmid8456658">{{cite journal| author=Lee KS, Song KS, Lim TH, Kim PN, Kim IY, Lee BH| title=Adult-onset pulmonary tuberculosis: findings on chest radiographs and CT scans. | journal=AJR Am J Roentgenol | year= 1993 | volume= 160 | issue= 4 | pages= 753-8 | pmid=8456658 | doi=10.2214/ajr.160.4.8456658 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8456658  }} </ref>
*Thin-walled cavity
:* Present in active and inactive disease
:* May regress after treatment
:* Air-filled sect may persist<ref>{{cite book | last = Fraser | first = Richard | title = Synopsis of diseases of the chest | publisher = W.B. Saunders | location = Philadelphia | year = 1994 | isbn = 0721636691 }}</ref>
:* May be misidentified as an emphysematous bulla or pneumatocelle.
*Cicatrization:
:* Common in secondary TB
:* Marked fibrosis in ≤40% of secondary TB cases, which may present as:
::*Upper love atelectasis
::*Compensatory hyperinflation of the lower lobe
::*Hilar retraction
::*Mediastinal shift
*Unspecific X-Ray findings:<ref name="pmid11452057">{{cite journal| author=Kim HY, Song KS, Goo JM, Lee JS, Lee KS, Lim TH| title=Thoracic sequelae and complications of tuberculosis. | journal=Radiographics | year= 2001 | volume= 21 | issue= 4 | pages= 839-58; discussion 859-60 | pmid=11452057 | doi=10.1148/radiographics.21.4.g01jl06839 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11452057  }} </ref>
::*Parenchymal bands
::*Fibrotic cavities
::*Fibrotic nodules
::*Traction bronchiectasis
*Lung Destruction:<ref name="pmid11452057">{{cite journal| author=Kim HY, Song KS, Goo JM, Lee JS, Lee KS, Lim TH| title=Thoracic sequelae and complications of tuberculosis. | journal=Radiographics | year= 2001 | volume= 21 | issue= 4 | pages= 839-58; discussion 859-60 | pmid=11452057 | doi=10.1148/radiographics.21.4.g01jl06839 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11452057  }} </ref>
:*Common in end-stage of TB
:*Involvement of the airways and parenchyma
:*May follow primary TB or secondary TB
:*Spreads across the lung with cavitation and fibrosis<ref name="pmid8456658">{{cite journal| author=Lee KS, Song KS, Lim TH, Kim PN, Kim IY, Lee BH| title=Adult-onset pulmonary tuberculosis: findings on chest radiographs and CT scans. | journal=AJR Am J Roentgenol | year= 1993 | volume= 160 | issue= 4 | pages= 753-8 | pmid=8456658 | doi=10.2214/ajr.160.4.8456658 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8456658  }} </ref>
:*Concomitant infection with bacteria or bacteria may occur
:*Complicates assessment of TB activity in the lung with the X-ray.
*[[Aspergilloma]]
:*Mass of hyphae, cell debris and mucus, commonly located in a cavity or bronchus<ref name="pmid8744521">{{cite journal| author=Logan PM, Müller NL| title=CT manifestations of pulmonary aspergillosis. | journal=Crit Rev Diagn Imaging | year= 1996 | volume= 37 | issue= 1 | pages= 1-37 | pmid=8744521 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8744521  }} </ref><ref name="pmid8838945">{{cite journal| author=Miller WT| title=Aspergillosis: a disease with many faces. | journal=Semin Roentgenol | year= 1996 | volume= 31 | issue= 1 | pages= 52-66 | pmid=8838945 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8838945  }} </ref><ref name="pmid8577955">{{cite journal| author=Thompson BH, Stanford W, Galvin JR, Kurihara Y| title=Varied radiologic appearances of pulmonary aspergillosis. | journal=Radiographics | year= 1995 | volume= 15 | issue= 6 | pages= 1273-84 | pmid=8577955 | doi=10.1148/radiographics.15.6.8577955 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8577955  }} </ref>
:*Previous history of chronic cavitary TB in 25-55% of cases presenting with [[aspergilloma]]
:*Frequently courses with [[hemoptysis]] (50-90%)
:*X-ray shows a mobile mass ringed by an air shadow 
:*CT shows a mobile mass, generally interspaced with air shadows
:*May be calcified
*Bronchogenic carcinoma<ref name="pmid11452057">{{cite journal| author=Kim HY, Song KS, Goo JM, Lee JS, Lee KS, Lim TH| title=Thoracic sequelae and complications of tuberculosis. | journal=Radiographics | year= 2001 | volume= 21 | issue= 4 | pages= 839-58; discussion 859-60 | pmid=11452057 | doi=10.1148/radiographics.21.4.g01jl06839 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11452057  }} </ref>


:*May be misinterpreted as TB progression
:*Scar formation in TB may lead to carcinoma
:*May cause reactivation of TB<ref name="pmid4975011">{{cite journal| author=Snider GL, Placik B| title=The relationship between pulmonary tuberculosis and bronchogenic carcinoma. A topographic study. | journal=Am Rev Respir Dis | year= 1969 | volume= 99 | issue= 2 | pages= 229-36 | pmid=4975011 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4975011  }} </ref><ref name="pmid1265261">{{cite journal| author=Ting YM, Church WR, Ravikrishnan KP| title=Lung carcinoma superimposed on pulmonary tuberculosis. | journal=Radiology | year= 1976 | volume= 119 | issue= 2 | pages= 307-12 | pmid=1265261 | doi=10.1148/119.2.307 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1265261  }} </ref>


==Transmission==
==Airway Lesions==
<!--
-->


==Differential Diagnosis of Infectious Diarrhea==
Acute inflammatory diarrhea may be caused by different pathogens. Bellow is a table describing some of these pathogens in terms of transmission and symptoms:<ref name="pmid14702426">{{cite journal| author=Thielman NM, Guerrant RL| title=Clinical practice. Acute infectious diarrhea. | journal=N Engl J Med | year= 2004 | volume= 350 | issue= 1 | pages= 38-47 | pmid=14702426 | doi=10.1056/NEJMcp031534 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14702426  }} </ref><ref name="pmid15537721">{{cite journal| author=Khan AM, Faruque AS, Hossain MS, Sattar S, Fuchs GJ, Salam MA| title=Plesiomonas shigelloides-associated diarrhoea in Bangladeshi children: a hospital-based surveillance study. | journal=J Trop Pediatr | year= 2004 | volume= 50 | issue= 6 | pages= 354-6 | pmid=15537721 | doi=10.1093/tropej/50.6.354 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15537721  }} </ref>


{| style="border: 0px; font-size: 90%; margin: 3px;" align=center
! style="background: #4479BA; padding: 5px 5px;" rowspan=2 | {{fontcolor|#FFFFFF|Pathogen}}
! style="background: #4479BA; padding: 5px 5px;" rowspan=2  | {{fontcolor|#FFFFFF|Transmission}}
! style="background: #4479BA; padding: 5px 5px;" colspan=4 | {{fontcolor|#FFFFFF|Clinical Manifestations}}
|-
! style="background: #4479BA; padding: 5px 5px;" | {{fontcolor|#FFFFFF|Fever}}
! style="background: #4479BA; padding: 5px 5px;" | {{fontcolor|#FFFFFF|Nausea/Vomiting}}
! style="background: #4479BA; padding: 5px 5px;" | {{fontcolor|#FFFFFF|Abdominal Pain}}
! style="background: #4479BA; padding: 5px 5px;" | {{fontcolor|#FFFFFF|Bloody Stool}}
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" | ''[[Salmonella]]''
| style="padding: 5px 5px; background: #F5F5F5;" | Foodborne transmission, community-acquired
! style="padding: 5px 5px; background: #F5F5F5;" | ++
! style="padding: 5px 5px; background: #F5F5F5;" | +
! style="padding: 5px 5px; background: #F5F5F5;" | ++
! style="padding: 5px 5px; background: #F5F5F5;" | +
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" | ''[[Shigella]]''
| style="padding: 5px 5px; background: #F5F5F5;" | Community-acquired, person-to-person
! style="padding: 5px 5px; background: #F5F5F5;" | ++
! style="padding: 5px 5px; background: #F5F5F5;" | ++
! style="padding: 5px 5px; background: #F5F5F5;" | ++
! style="padding: 5px 5px; background: #F5F5F5;" | +
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" | ''[[Campylobacter]]''
| style="padding: 5px 5px; background: #F5F5F5;" | Community-acquired, ingestion of undercooked poultry
! style="padding: 5px 5px; background: #F5F5F5;" | ++
! style="padding: 5px 5px; background: #F5F5F5;" | +
! style="padding: 5px 5px; background: #F5F5F5;" | ++
! style="padding: 5px 5px; background: #F5F5F5;" | +
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" | [[Escherichia coli|''E. coli'' (EHEC or EIEC)]]
| style="padding: 5px 5px; background: #F5F5F5;" | Foodborne transmission, ingestion of undercooked hamburger meat
! style="padding: 5px 5px; background: #F5F5F5;" | ±
! style="padding: 5px 5px; background: #F5F5F5;" | +
! style="padding: 5px 5px; background: #F5F5F5;" | ++
! style="padding: 5px 5px; background: #F5F5F5;" | ++
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" | ''[[Clostridium difficile]]''
| style="padding: 5px 5px; background: #F5F5F5;" | Nosocomial spread, antibiotic use
! style="padding: 5px 5px; background: #F5F5F5;" | +
! style="padding: 5px 5px; background: #F5F5F5;" | ±
! style="padding: 5px 5px; background: #F5F5F5;" | +
! style="padding: 5px 5px; background: #F5F5F5;" | +
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" | ''[[Yersinia]]''
| style="padding: 5px 5px; background: #F5F5F5;" | Community-aquired, foodborne transmission
! style="padding: 5px 5px; background: #F5F5F5;" | ++
! style="padding: 5px 5px; background: #F5F5F5;" | +
! style="padding: 5px 5px; background: #F5F5F5;" | ++
! style="padding: 5px 5px; background: #F5F5F5;" | +
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" | ''[[Entamoeba histolytica]]''
| style="padding: 5px 5px; background: #F5F5F5;" | Travel to or emigration from tropical regions
! style="padding: 5px 5px; background: #F5F5F5;" | +
! style="padding: 5px 5px; background: #F5F5F5;" | ±
! style="padding: 5px 5px; background: #F5F5F5;" | +
! style="padding: 5px 5px; background: #F5F5F5;" | ±
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" | ''[[Aeromonas]]''
| style="padding: 5px 5px; background: #F5F5F5;" | Ingestion of contaminated water
! style="padding: 5px 5px; background: #F5F5F5;" | ++
! style="padding: 5px 5px; background: #F5F5F5;" | +
! style="padding: 5px 5px; background: #F5F5F5;" | ++
! style="padding: 5px 5px; background: #F5F5F5;" | +
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" | ''[[Plesiomonas]]''
| style="padding: 5px 5px; background: #F5F5F5;" | Ingestion of contaminated water or undercooked shellfish, travel to tropical regions
! style="padding: 5px 5px; background: #F5F5F5;" | ±
! style="padding: 5px 5px; background: #F5F5F5;" | ++
! style="padding: 5px 5px; background: #F5F5F5;" | +
! style="padding: 5px 5px; background: #F5F5F5;" | +
|}


==Genetics==
==References==
 
{{reflist|2}}
 
 
==Pathogenesis==
 
 
==Gross Pathology==
 
 
 
==Microscopic Pathology==
 
 
 
 
==Pathophysiology==
The bacterium normally remains in the [[endospore]] form in the soil, and can survive for decades in this state.
 
Once ingested by a ruminant or placed in an open cut, the bacterium begins multiplying inside the animal or human and if not treated, has a fatal outcome. Most anthrax bacteria inside the body are destroyed by anaerobic bacteria that can grow without oxygen. The greater danger lies in the bodily fluids and blood that spills from the body and spill into the soil where the anthrax bacteria turn into a dormant protective spore form. Once formed, the spores are very hard to eradicate.
 
The infection normally proceeds as follows:  once the spores are inhaled they are transported through the air passages into the lungs. The spores are then picked up by macrophages in the lungs and are transported through lymphatics to the lymph nodes in the mediastinum. Damage caused by the anthrax spores and bacilli to the central chest cavity  lungs can cause chest pain and difficulty breathing. Once in the lymph  nodes, the spores germinate into active  bacillus, that  multiply, and eventually bursts the macrophage cell, releasing many more bacilli into the bloodstream which are transferred to the entire body.  Once in the blood stream these bacilli release a tripartite toxin (composed of lethal factor, edema factor and protective antigen) which is known to be the primary agents of tissue destruction, bleeding, and death. If antibiotics are given too late, even if the antibiotics eradicate the bacteria, some people still will die because the toxins produced by the bacilli still remain in their system at lethal dose levels.
 
In order to enter the cells, the toxins use another protein produced by ''B. anthracis'', protective antigen. Edema factor inactivates [[neutrophil]]s (a type of phagocytic cell) so that they cannot phagocytose bacteria.  Historically, it was believed that lethal factor caused macrophages to make [[TNF-alpha]] and [[IL1B|interleukin 1, beta]] (IL1B), both normal components of the immune system used to induce an inflammatory reaction, ultimately leading to [[septic shock]] and death. However, recent evidence indicates that anthrax also targets endothelial cells (cells that lines serous cavities, lymph vessels, and blood vessels), causing vascular leakage (similar to hemorrhagic bleeding), and ultimately [[hypovolemic shock]] (low blood volume), and not only septic shock. In other words the patient bleeds to death internally.
 
The virulence of a strain of anthrax is dependent on multiple factors, primarily the poly-D-glutamic acid capsule that protects the bacterium from phagocytosis by host neutrophils and its [[anthrax toxin|toxins]], edema toxin and lethal toxin.
 
 
=== Exposure ===
Occupational exposure to infected animals or their products (such as skin wool and meat) is the usual pathway of exposure for humans. Workers who are exposed to dead animals and animal products are at the highest risk, especially in countries where anthrax is more common.  Anthrax in livestock  grazing on open range where they mix with wild animals still occasionally occurs in the [[United States]] and elsewhere.  Many workers who deal  with wool and animal hides are routinely exposed to low  levels of anthrax spores but most exposures are not sufficient  to develop anthrax infections. Presumably, the body’s natural defenses can destroy low levels of exposure. These people usually contract cutaneous anthrax if they catch anything. Historically, the most dangerous form of inhalation anthrax was called [[Anthrax#Pulmonary (pneumonic, respiratory, or inhalation) anthrax|Woolsorters' disease]] because it was an occupational hazard for people who sorted wool. Fortunately this is now a very rare form of infection because of the much reduced incidence of anthrax disease in animals.
The last fatal case of natural inhalation anthrax in the United States occurred in California in 1976, when a home weaver died after working with infected wool imported from Pakistan. The autopsy was done at UCLA hospital. To minimize the chance of spreading the disease, the deceased was transported to UCLA in a sealed plastic body bag within a sealed metal container. The details of this case have been described in a medical journal '''Human Pathology''' (Volume 9, pages 594-597, September, 1978).
 
In July 2006 an artist who worked with untreated animal skins became the first person in more than 30 years to die in the United Kingdom from anthrax.<ref>[http://news.independent.co.uk/uk/health_medical/article1219711.ece Artist dies from anthrax caught from animal skins] Independent News and Media Limited, [[17 August]] 2006. Retrieved [[6 October]] 2006. </ref>
 
=== Mode of infection ===
Anthrax can enter the human body through the intestines ('''ingestion'''), lungs ('''inhalation'''), or skin ('''cutaneous''') and causes distinct clinical symptoms based on its site of entry. An infected human will generally be quarantined. However, anthrax does not usually spread from an infected human to a noninfected human. But if the disease is fatal the person’s body and its mass of anthrax bacilli becomes a potential source of infection to others and special precautions should be used to prevent more contamination. Unfortunately inhalation anthrax, if left untreated until obvious symptoms occur, will usually result in death if treatment is started too late.
 
Anthrax is usually contracted by handling infected animals or their wool, germ warfare/terrorism or laboratory accidents.
 
<u>'''1) Pulmonary (pneumonic, respiratory, or inhalation) anthrax'''
</u>
Respiratory infection initially presents with cold or flu-like symptoms for several days, followed by severe (and often fatal) respiratory collapse. If not treated promptly soon after exposure, before symptoms appear, inhalational anthrax is highly fatal, with near 100% mortality.<ref name="bravata">Bravata DM, Holty JE, Liu H, McDonald KM, Olshen RA, Owens DK (2006), Systematic review: a century of inhalation anthrax cases from 1900 to 2005, Annals of Internal Medicine; 144(4): 270–80.</ref> A lethal dose of anthrax is reported to result from inhalation of about 10,000–20,000 spores. <ref name="urlwww.medicinenet.com">{{cite web |url=http://www.medicinenet.com/script/main/art.asp?articlekey=18812&page=2 |title=www.medicinenet.com |format= |work= |accessdate=2012-08-31}}</ref> Like all diseases there is probably a wide variation to susceptibility with evidence that some people may die from much lower exposures; there is little documented evidence to verify the exact or average number of spores need for infection. Inhalation anthrax is also known as Woolsorters' disease or as Ragpickers' disease since these people often caught it. Other practices associated with exposure include the slicing up of animal horns for the manufacture of buttons, the handling of hair bristles used for the manufacturing of brushes, and the handling of animal skins. Whether these animal skins came from animals that died of the disease or from animals that had simply laid on ground that had spores on it  is unknown. Anthrax is a very hard disease to eliminate since Anthrax spores are devilishly hard to kill and have been known to have reinfected animals over 70 years after burial sites of anthrax infected animals were disturbed. <ref>"Anthrax" by Jeanne Guillemin, University of California Press, 2001,ISBN 0-520-22917-7, pg. 3 </ref>
 
'''<u>2) Gastrointestinal (gastroenteric) anthrax</u>'''
Gastrointestinal infection is most often caused by eating  anthrax infected meat and is characterized by serious gastrointestinal difficulty, [[vomiting]] of blood, severe diarrhea, acute inflammation of the intestinal tract, and loss of appetite. Gastrointestinal infections can be treated but usually result in fatality rates of 25% to 60%, depending upon how soon treatment commences. <ref>{{cite web | title = Anthrax Q & A: Signs and Symptoms | work = Emergency Preparedness and Response | publisher = Centers for Disease Control and Prevention | date = 2003 | url = http://www.bt.cdc.gov/agent/anthrax/faq/signs.asp | accessdate = 2007-04-19 }}</ref>
 
<u>'''3) Cutaneous (skin) anthrax'''</u>
[[Image:Milzbrand.jpg|thumb|left|250px|Anthrax skin lesion.]]
Cutaneous (on the skin) anthrax  infection shows up as a boil-like skin lesion that eventually forms an ulcer with a black center (i.e., eschar). The black eschar often shows up as a large, painless necrotic ulcers (beginning as an irritating and itchy skin lesion or blister that is dark and usually concentrated as a black dot, somewhat resembling bread mold) at the site of infection. Cutaneous infections generally form within the site of spore penetration within 2 to 5 days after exposure. Unlike bruises or most other lesions, cutaneous anthrax infections normally  do not cause pain. Cutaneous infection is the least fatal form of anthrax infection if treated. But without treatment, approximately 20% of all cutaneous skin infection cases may progress to [[toxemia]] and death. <ref>{{cite web | title = Anthrax Q & A: Signs and Symptoms | work = Emergency Preparedness and Response | publisher = Centers for Disease Control and Prevention | date = 2003 | url = http://www.bt.cdc.gov/agent/anthrax/faq/signs.asp | accessdate = 2007-04-19 }}</ref> Treated cutaneous anthrax is rarely fatal.<ref name="bravata"/>

Latest revision as of 18:19, 16 September 2014

Test

Parenchymal lesions

  • Tuberculoma
  • Single or multiple lesions of > 0.5 cm
  • May occur in primary or secundary TB
  • Main finding on Chest X-ray in 5% cases of secondary TB[1]
  • Results from the surrounding of M. tuberculosis with inflammatory or connective tissue.[2][3][1]
  • The center of the tuberculoma is often necrotic
  • Satellite lesions (80%)
  • Nodular or diffused calcifications in 20-30% cases[2]
  • Thin-walled cavity
  • Present in active and inactive disease
  • May regress after treatment
  • Air-filled sect may persist[4]
  • May be misidentified as an emphysematous bulla or pneumatocelle.
  • Cicatrization:
  • Common in secondary TB
  • Marked fibrosis in ≤40% of secondary TB cases, which may present as:
  • Upper love atelectasis
  • Compensatory hyperinflation of the lower lobe
  • Hilar retraction
  • Mediastinal shift
  • Unspecific X-Ray findings:[5]
  • Parenchymal bands
  • Fibrotic cavities
  • Fibrotic nodules
  • Traction bronchiectasis
  • Lung Destruction:[5]
  • Common in end-stage of TB
  • Involvement of the airways and parenchyma
  • May follow primary TB or secondary TB
  • Spreads across the lung with cavitation and fibrosis[2]
  • Concomitant infection with bacteria or bacteria may occur
  • Complicates assessment of TB activity in the lung with the X-ray.
  • Mass of hyphae, cell debris and mucus, commonly located in a cavity or bronchus[6][7][8]
  • Previous history of chronic cavitary TB in 25-55% of cases presenting with aspergilloma
  • Frequently courses with hemoptysis (50-90%)
  • X-ray shows a mobile mass ringed by an air shadow
  • CT shows a mobile mass, generally interspaced with air shadows
  • May be calcified
  • Bronchogenic carcinoma[5]
  • May be misinterpreted as TB progression
  • Scar formation in TB may lead to carcinoma
  • May cause reactivation of TB[9][10]

Airway Lesions

Differential Diagnosis of Infectious Diarrhea

Acute inflammatory diarrhea may be caused by different pathogens. Bellow is a table describing some of these pathogens in terms of transmission and symptoms:[11][12]

Pathogen Transmission Clinical Manifestations
Fever Nausea/Vomiting Abdominal Pain Bloody Stool
Salmonella Foodborne transmission, community-acquired ++ + ++ +
Shigella Community-acquired, person-to-person ++ ++ ++ +
Campylobacter Community-acquired, ingestion of undercooked poultry ++ + ++ +
E. coli (EHEC or EIEC) Foodborne transmission, ingestion of undercooked hamburger meat ± + ++ ++
Clostridium difficile Nosocomial spread, antibiotic use + ± + +
Yersinia Community-aquired, foodborne transmission ++ + ++ +
Entamoeba histolytica Travel to or emigration from tropical regions + ± + ±
Aeromonas Ingestion of contaminated water ++ + ++ +
Plesiomonas Ingestion of contaminated water or undercooked shellfish, travel to tropical regions ± ++ + +

References

  1. ↑ 1.0 1.1 Woodring JH, Vandiviere HM, Fried AM, Dillon ML, Williams TD, Melvin IG (1986). "Update: the radiographic features of pulmonary tuberculosis". AJR Am J Roentgenol. 146 (3): 497–506. doi:10.2214/ajr.146.3.497. PMID 3484866.
  2. ↑ 2.0 2.1 2.2 Lee KS, Song KS, Lim TH, Kim PN, Kim IY, Lee BH (1993). "Adult-onset pulmonary tuberculosis: findings on chest radiographs and CT scans". AJR Am J Roentgenol. 160 (4): 753–8. doi:10.2214/ajr.160.4.8456658. PMID 8456658.
  3. ↑ Palmer PE (1979). "Pulmonary tuberculosis--usual and unusual radiographic presentations". Semin Roentgenol. 14 (3): 204–43. PMID 472765.
  4. ↑ Fraser, Richard (1994). Synopsis of diseases of the chest. Philadelphia: W.B. Saunders. ISBN 0721636691.
  5. ↑ 5.0 5.1 5.2 Kim HY, Song KS, Goo JM, Lee JS, Lee KS, Lim TH (2001). "Thoracic sequelae and complications of tuberculosis". Radiographics. 21 (4): 839–58, discussion 859-60. doi:10.1148/radiographics.21.4.g01jl06839. PMID 11452057.
  6. ↑ Logan PM, Müller NL (1996). "CT manifestations of pulmonary aspergillosis". Crit Rev Diagn Imaging. 37 (1): 1–37. PMID 8744521.
  7. ↑ Miller WT (1996). "Aspergillosis: a disease with many faces". Semin Roentgenol. 31 (1): 52–66. PMID 8838945.
  8. ↑ Thompson BH, Stanford W, Galvin JR, Kurihara Y (1995). "Varied radiologic appearances of pulmonary aspergillosis". Radiographics. 15 (6): 1273–84. doi:10.1148/radiographics.15.6.8577955. PMID 8577955.
  9. ↑ Snider GL, Placik B (1969). "The relationship between pulmonary tuberculosis and bronchogenic carcinoma. A topographic study". Am Rev Respir Dis. 99 (2): 229–36. PMID 4975011.
  10. ↑ Ting YM, Church WR, Ravikrishnan KP (1976). "Lung carcinoma superimposed on pulmonary tuberculosis". Radiology. 119 (2): 307–12. doi:10.1148/119.2.307. PMID 1265261.
  11. ↑ Thielman NM, Guerrant RL (2004). "Clinical practice. Acute infectious diarrhea". N Engl J Med. 350 (1): 38–47. doi:10.1056/NEJMcp031534. PMID 14702426.
  12. ↑ Khan AM, Faruque AS, Hossain MS, Sattar S, Fuchs GJ, Salam MA (2004). "Plesiomonas shigelloides-associated diarrhoea in Bangladeshi children: a hospital-based surveillance study". J Trop Pediatr. 50 (6): 354–6. doi:10.1093/tropej/50.6.354. PMID 15537721.
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