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|Clostridium tetani is a pathogenic bacterium that causes tetanus|
|Classification and external resources|
Pathogenic bacteria are bacteria that can cause disease. This article deals with human pathogenic bacteria. Although most bacteria are harmless or often beneficial, some are pathogenic, with the number of species estimated as fewer than 100 that are seen to cause infectious diseases in humans. By contrast, several thousand species exist in the human digestive system.
One of the bacterial diseases with the highest disease burden is tuberculosis, caused by the bacterium Mycobacterium tuberculosis, which kills about 2 million people a year, mostly in sub-Saharan Africa. Pathogenic bacteria contribute to other globally important diseases, such as pneumonia, which can be caused by bacteria such as Streptococcus and Pseudomonas, and foodborne illnesses, which can be caused by bacteria such as Shigella, Campylobacter, and Salmonella. Pathogenic bacteria also cause infections such as tetanus, typhoid fever, diphtheria, syphilis, and leprosy. Pathogenic bacteria are also the cause of high infant mortality rates in developing countries.
Each species has specific effect and causes symptoms in people who are infected. Some, if not most people who are infected with a pathogenic bacteria do not have symptoms. Immuno-compromised individuals are more susceptible to pathogenic bacteria.
Some pathogenic bacteria cause disease under certain conditions, such as entry through the skin via a cut, through sexual activity or through a compromised immune function.
Streptococcus and Staphylococcus are part of the normal skin microbiota and typically reside on healthy skin or in the nasopharangeal region. Yet these species can potentially initiate skin infections. They are also able to cause sepsis, pneumonia or meningitis. These infections can become quite serious creating a systemic inflammatory response resulting in massive vasodilation, shock, and death.
Other bacteria are opportunistic pathogens and cause disease mainly in people suffering from immunosuppression or cystic fibrosis. Examples of these opportunistic pathogens include Pseudomonas aeruginosa, Burkholderia cenocepacia, and Mycobacterium avium.
Obligate intracellular parasites (e.g. Chlamydophila, Ehrlichia, Rickettsia) have the ability to only grow and replicate inside other cells. Even these intracellular infections may be asymptomatic, requiring an incubation period. An example of this is Rickettsia which causes typhus. Another causes Rocky Mountain spotted fever.
Other groups of intracellular bacterial pathogens include Salmonella, Neisseria, Brucella, Mycobacterium, Nocardia, Listeria, Francisella, Legionella, and Yersinia pestis. These can exist intracellularly, but can exist outside of host cells.
Bacterial pathogens often cause infection in specific areas of the body. Others are generalists.
The symptoms of disease appear as pathogenic bacteria damage host tissues or interfere with their function. The bacteria can damage host cells directly. They can also cause damage indirectly by provoking an immune response that inadvertently damages host cells.
Once pathogens attach to host cells, they can cause direct damage as the pathogens use the host cell for nutrients and produce waste products. For example, Streptococcus mutans, a component of dental plaque, metabolizes dietary sugar and produces acid as a waste product. The acid decalcifies the tooth surface to cause dental caries. However, toxins produced by bacteria cause most of the direct damage to host cells.
Endotoxins are the lipid portions of lipopolysaccharides that are part of the outer membrane of the cell wall of gram negative bacteria. Endotoxins are released when the bacteria lyses, which is why after antibiotic treatment, symptoms can worsen at first as the bacteria are killed and they release their endotoxins. Exotoxins are secreted into the surrounding medium or released when the bacteria die and the cell wall breaks apart.
An excessive or inappropriate immune response triggered by an infection may damage host cells.
Iron is required for humans, as well as the growth of most bacteria. To obtain free iron, some pathogens secrete proteins called siderophores, which take the iron away from iron-transport proteins by binding to the iron even more tightly. Once the iron-siderophore complex is formed, it is taken up by siderophore receptors on the bacterial surface and then that iron is brought into the bacterium.
Typically identification is done by growing the organism in a wide range of cultures which can take up to 48 hours. The growth is then visually or genomically identified. The cultured organism is then subjected to various assays to observe reactions to help further identify species and strain.
Bacterial infections may be treated with antibiotics, which are classified as bacteriocidal if they kill bacteria or bacteriostatic if they just prevent bacterial growth. There are many types of antibiotics and each class inhibits a process that is different in the pathogen from that found in the host. For example, the antibiotics chloramphenicol and tetracyclin inhibit the bacterial ribosome but not the structurally different eukaryotic ribosome, so they exhibit selective toxicity. Antibiotics are used both in treating human disease and in intensive farming to promote animal growth. Both uses may be contributing to the rapid development of antibiotic resistance in bacterial populations. Phage therapy can also be used to treat certain bacterial infections.
Infections can be prevented by antiseptic measures such as sterilizing the skin prior to piercing it with the needle of a syringe and by proper care of indwelling catheters. Surgical and dental instruments are also sterilized to prevent infection by bacteria. Disinfectants such as bleach are used to kill bacteria or other pathogens on surfaces to prevent contamination and further reduce the risk of infection. Bacteria in food are killed by cooking to temperatures above 73 °C (163 °F).
|Genus||Species||Gram staining||Shape||Oxygen requirement||Intra/Extracellular|
|Borrelia||Negative, stains poorly||spirochete||Anaerobic||Extracellular|
coccoid in older cultures
|Chlamydia and Chlamydophila||(not Gram-stained)||Small, round, ovoid||Facultative or strictly aerobic||Obligate intracellular|
|Clostridium||Positive||Large, blunt-ended rods||Obligate anaerobic||extracellular|
|Corynebacterium||Positive (unevenly)||bacilli||Mostly facultative anaerobic||extracellular|
|Escherichia||Negative||Bacillus||Facultative anaerobic||extracellular or intracellular|
|Francisella||Negative||coccobacillus||strictly aerobic||Facultative intracellular|
|Haemophilus||Negative||coccobacilli to long and slender filaments||extracellular|
|Legionella||Negative, stains poorly||cocobacilli||aerobic||facultative intracellular|
|Leptospira||Negative, stains poorly||Spirochete||Strictly aerobic||extracellular|
|Listeria||Positive, darkly||Slender, short rods||Facultative Anaerobic||intracellular|
|Mycobacterium||(none)||Long, slender rods||aerobic||extracellular|
|Mycoplasma||(none)||'fried egg' appearance, no cell wall||Mostly facultative anaerobic; M. pneumoniae strictly aerobic||extracellular|
|Neisseria||Negative||Kidney bean-shaped||aerobic||Gonococcus: facultative intracellular|
N. meningitidis: extracellular
|Rickettsia||Negative, stains poorly||Small, rod-like coccobacillary||Aerobic||Obligate intracellular|
|Salmonella||Negative||Bacillus shape||Facultative anaerobica||Facultative intracellular|
|Staphylococcus||Positive, darkly||Round cocci||Facultative anaerobic||extracellular, facultative intracellular|
|Streptococcus||Positive||ovoid to spherical||Facultative anaerobic||extracellular|
|Treponema||Negative, stains poorly||Spirochete||Aerobic||extracellular|
|Ureaplasma||Stains poorly||indistinct, 'fried egg' appearance, no cell wall||anaerobic||extracellular|
|Vibrio||Negative||Spiral with single polar flagellum||Facultative anaerobic||extracellular|
|Yersinia||Negative, bipolarly||Small rods||Facultative Anaerobe||Intracellular|
This is description of the more common genera and species presented with their clinical characteristics and treatments.
|Actinomyces israelii||Oral flora||Actinomycosis: painful abscesses in the mouth, lungs, or gastrointestinal tract.||Prolonged penicillin G and drainage|
|Bacillus anthracis||In early infection:
|Bacteroides fragilis||Gut flora||Abscesses in gastrointestinal tract, pelvic cavity and lungs||metronidazole||Wound care|
Contact with respiratory droplets expelled by infected human hosts.
|Macrolides such as erythromycin, before paroxysmal stage|
and others[note 1]
|Pediculus humanus corporis body louse (B. recurrentis only) and Ornithodoros soft ticks||Relapsing fever||Penicillin, tetracycline, doxycycline||Avoid areas where ticks are found|
|Chlamydia||C. pneumoniae||Atypical pneumonia||None|
|Chlamydophila psittaci||Inhalation of dust with secretions or feces from birds (e.g. parrots)||Psittacosis, mainly atypical pneumonia||-|
|Clostridium||C. botulinum||Spores from soil, persevere in canned food, smoked fish and honey||
Proper food preservation techniques
|C. difficile||Fecal bacteriotherapy|
|C. perfringens||Gas gangrene:||Appropriate food handling|
||Dog tick||Ehrlichiosis: headache, muscle aches, and fatigue|
No vaccine Hand washing and other nosocomial prevention
|Escherichia||E. coli (generally)||UTI:
(resistance-tests are required first)
|(no vaccine or preventive drug)|
|Enterotoxigenic E. coli (ETEC)|
|Enteropathogenic E. coli||
|Enteroinvasive E.coli (EIEC)|
|Enterohemorrhagic (EHEC), including E. coli O157:H7||
|Francisella tularensis||Tularemia: Fever, ulceration at entry site and/or lymphadenopathy. Can cause severe pneumonia.|
(resistance-tests are required first)
|Helicobacter pylori||(No vaccine or preventive drug)|
|Legionella pneumophila||(no vaccine or preventive drug)
||Vaccine not widely used
Prevention of exposure
|Listeria monocytogenes||(no vaccine)
Standard "short" course:
|Neisseria||N. gonorrhoeae||Uncomplicated gonorrhea:
|Pseudomonas aeruginosa||Opportunistic; Infects damaged tissues or people with immunodeficiency.||Pseudomonas infection:||(no vaccine)|
|Nocardia asteroides||In soil||Nocardiosis: Pneumonia, endocarditis, keratitis, neurological or lymphocutaneous infection||TMP/SMX|
|Rickettsia rickettsii||(no preventive drug or approved vaccine)|
|Other Salmonella species||
||(No vaccine or preventive drug)|
|Staphylococcus||aureus||Coagulase-positive staphylococcal infections:||(no vaccine or preventive drug)
|epidermidis||Human flora in skin, anterior nares and mucous membranes||None|
|saprophyticus||Part of normal vaginal flora||None|
|Streptococcus||agalactiae||Human flora in vagina, urethral mucous membranes, rectum||None|
|viridans||Oral flora, penetration through abrasions||Penicillin G|
|Treponema pallidum subspecies pallidum|
Of the 59 species listed in the table with their clinical characteristics, 11 species (or 19%) are known to be capable of natural genetic transformation. Natural transformation is a bacterial adaptation for transferring DNA from one cell to another. This process includes the uptake of exogenous DNA from a donor cell by a recipient cell and its incorporation into the recipient cell’s genome by recombination. Transformation appears to be an adaptation for repairing damage in the recipient cell’s DNA. Among pathogenic bacteria, transformation capability likely serves as an adaptation that facilitates survival and infectivity. The pathogenic bacteria able to carry out natural genetic transformation (of those listed in the table) are Campylobacter jejuni, Enterococcus faecalis, Haemophilus influenzae, Helicobacter pylori, Klebsiella pneumoniae, Legionella pneumophila, Neisseria gonorrhoeae, Neisseria meningitides, Staphylococcus aureus, Streptococcus pneumoniae and Vibrio cholerae.