Pathogenic bacteria

Pathogenic bacteria are bacteria that can cause disease.^[1] This article focuses on the bacteria that are pathogenic to humans. Most species of bacteria are harmless and are often beneficial but others can cause infectious diseases. The number of these pathogenic species in humans is estimated to be fewer than a hundred.^[2] By contrast, several thousand species are part of the gut flora present in the digestive tract.

Pathogenic bacteria
Neisseria gonorrhoeae (small red dots) in pus from a man with a urethral discharge (Gram stain)

The body is continually exposed to many species of bacteria, including beneficial commensals, which grow on the skin and mucous membranes, and saprophytes, which grow mainly in the soil and in decaying matter. The blood and tissue fluids contain nutrients sufficient to sustain the growth of many bacteria. The body has defence mechanisms that enable it to resist microbial invasion of its tissues and give it a natural immunity or innate resistance against many microorganisms.

Pathogenic bacteria are specially adapted and endowed with mechanisms for overcoming the normal body defences, and can invade parts of the body, such as the blood, where bacteria are not normally found. Some pathogens invade only the surface epithelium, skin or mucous membrane, but many travel more deeply, spreading through the tissues and disseminating by the lymphatic and blood streams. In some rare cases a pathogenic microbe can infect an entirely healthy person, but infection usually occurs only if the body's defence mechanisms are damaged by some local trauma or an underlying debilitating disease, such as wounding, intoxication, chilling, fatigue, and malnutrition. In many cases, it is important to differentiate infection and colonization, which is when the bacteria are causing little or no harm.

Caused by Mycobacterium tuberculosis bacteria, one of the diseases with the highest disease burden is tuberculosis, which killed 1.4 million people in 2019, mostly in sub-Saharan Africa.^[3] Pathogenic bacteria contribute to other globally important diseases, such as pneumonia, which can be caused by bacteria such as Staphylococcus, 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.^[4]

Most pathogenic bacteria can be grown in cultures and identified by Gram stain and other methods. Bacteria grown in this way are often tested to find which antibiotics will be an effective treatment for the infection. For hitherto unknown pathogens, Koch's postulates are the standard to establish a causative relationship between a microbe and a disease.

Diseases

 

Commensals vs pathogenic bacteria in COPD

Each species has specific effect and causes symptoms in people who are infected. Some people who are infected with a pathogenic bacteria do not have symptoms. Immunocompromised individuals are more susceptible to pathogenic bacteria.^[5]

Pathogenic susceptibility

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.^{[citation needed]}

 

An abscess caused by opportunistic S. aureus bacteria.

Some species of 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. Streptoccal infections include sepsis, pneumonia, and meningitis.^[6] These infections can become serious creating a systemic inflammatory response resulting in massive vasodilation, shock, and death.^[7]

Other bacteria are opportunistic pathogens and cause disease mainly in people with immunosuppression or cystic fibrosis. Examples of these opportunistic pathogens include Pseudomonas aeruginosa, Burkholderia cenocepacia, and Mycobacterium avium.^[8][9]

Intracellular

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.^{[citation needed]}

Chlamydia are intracellular parasites. These pathogens can cause pneumonia or urinary tract infection and may be involved in coronary heart disease.^[10]

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.^{[citation needed]}

Infections in specific tissue

Bacterial pathogens often cause infection in specific areas of the body. Others are generalists.

• Bacterial vaginosis is a condition of the vaginal microbiota in which an excessive growth of Gardnerella vaginalis and other mostly anaerobic bacteria displace the beneficial Lactobacilli species that maintain healthy vaginal microbial populations.^[11]
• Bacterial meningitis is a bacterial inflammation of the meninges, which are the protective membranes covering the brain and spinal cord.
• Bacterial pneumonia is a bacterial infection of the lungs.
• Urinary tract infection is predominantly caused by bacteria. Symptoms include the strong and frequent sensation or urge to urinate, pain during urination, and urine that is cloudy.^[12] The most frequent cause is Escherichia coli. Urine is typically sterile but contains a variety of salts, and waste products.^[13] Bacteria can ascend into the bladder or kidney and causing cystitis and nephritis.
• Bacterial gastroenteritis is caused by enteric, pathogenic bacteria. These pathogenic species are usually distinct from the usually harmless bacteria of the normal gut flora. But a different strain of the same species may be pathogenic. The distinction is sometimes difficult as in the case of Escherichia.
• Bacterial skin infections include:
  • Impetigo is a highly contagious bacterial skin infection commonly seen in children.^[14] It is caused by Staphylococcus aureus, and Streptococcus pyogenes.^[15]
  • Erysipelas is an acute streptococcus bacterial infection^[16] of the deeper skin layers that spreads via with lymphatic system.
  • Cellulitis is a diffuse inflammation^[17] of connective tissue with severe inflammation of dermal and subcutaneous layers of the skin. Cellulitis can be caused by normal skin flora or by contagious contact, and usually occurs through open skin, cuts, blisters, cracks in the skin, insect bites, animal bites, burns, surgical wounds, intravenous drug injection, or sites of intravenous catheter insertion. In most cases it is the skin on the face or lower legs that is affected, though cellulitis can occur in other tissues.

Mechanisms of damage

The symptoms of disease appear as pathogenic bacteria damage host tissues or interfere with their function. The bacteria can damage host cells directly or indirectly by provoking an immune response that inadvertently damages host cells,^[18] or by releasing toxins.^[19]

Direct

Once pathogens attach to host cells, they can cause direct damage as the pathogens use the host cell for nutrients and produce waste products.^[20] 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.^[21]

Toxin production

 

Protein structure of botulinum toxin.

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.^[22]

Indirect

An excessive or inappropriate immune response triggered by an infection may damage host cells.^[1]

Survival in host

Nutrients

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.^[22]

Bacterial pathogens also require access to carbon and energy sources for growth. To avoid competition with host cells for glucose which is the main energy source used by human cells, many pathogens including the respiratory pathogen Haemophilus influenzae specialise in using other carbon sources such as lactate that are abundant in the human body ^[23]

Identification

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.^[24]

Treatment

Main article: Antibiotics

See also: overview list below

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.^[25] 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.^[26] Phage therapy, using bacteriophages can also be used to treat certain bacterial infections.^[27]

Prevention

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).^{[citation needed]}

List of genera and microscopy features

Many genera contain pathogenic bacterial species. They often possess characteristics that help to classify and organize them into groups. The following is a partial listing.

Genus	Species	Gram staining	Shape	Oxygen requirement	Intra/Extracellular
Bacillus^[28]	Bacillus anthracis Bacillus cereus	Positive	Rods	Facultative anaerobic	Extracellular
Bartonella^[28]	Bartonella henselae Bartonella quintana	Negative	Rods	Aerobic	Facultative intracellular
Bordetella^[28]	Bordetella pertussis^[29]^[30]	Negative	Small coccobacilli	Aerobic	Extracellular
Borrelia^[28]	Borrelia burgdorferi Borrelia garinii Borrelia afzelii Borrelia recurrentis	Negative, stains poorly	Spirochete	Anaerobic	Extracellular
Brucella^[28]	Brucella abortus Brucella canis Brucella melitensis Brucella suis	Negative	Coccobacilli	Aerobic	Intracellular
Campylobacter^[28]	Campylobacter jejuni	Negative	Spiral rods^[31] coccoid in older cultures^[31]	Microaerophilic^[31]	Extracellular
Chlamydia and Chlamydophila^[28]	Chlamydia pneumoniae Chlamydia trachomatis Chlamydophila psittaci	(not Gram-stained)	Small, round, ovoid	Facultative or strictly aerobic	Obligate intracellular
Clostridium^[28]	Clostridium botulinum Clostridium difficile Clostridium perfringens Clostridium tetani	Positive	Large, blunt-ended rods	Obligate anaerobic	Extracellular
Corynebacterium^[28]	Corynebacterium diphtheriae^[30]^[32]^[33]	Positive (unevenly)	Rods	Mostly facultative anaerobic	Extracellular
Enterococcus^[30]^[34]	Enterococcus faecalis Enterococcus faecium	Positive	Cocci	Facultative Anaerobic	Extracellular
Escherichia^[4]^[30]^[35]	Escherichia coli	Negative	Rods	Facultative anaerobic	Extracellular or Intracellular
Francisella^[28]	Francisella tularensis	Negative	Coccobacillus	Strictly aerobic	Facultative intracellular
Haemophilus	Haemophilus influenzae^[30]^[36]	Negative	Coccobacilli to long and slender filaments	Facultative anaerobic 5 - 10% CO2	Extracellular
Helicobacter	Helicobacter pylori^[37]	Negative	Spiral rod	Microaerophile	Extracellular
Legionella^[28]	Legionella pneumophila	Negative, stains poorly	Cocobacilli	Aerobic	Facultative intracellular
Leptospira^[30]^[38]	Leptospira interrogans Leptospira santarosai Leptospira weilii Leptospira noguchii	Negative, stains poorly	Spirochete	Strictly aerobic	Extracellular
Listeria^[28]	Listeria monocytogenes	Positive, darkly	Slender, short rods	Facultative Anaerobic	Facultative intracellular
Mycobacterium^[28]	Mycobacterium leprae Mycobacterium tuberculosis Mycobacterium ulcerans	(none)	Long, slender rods	Aerobic	Intracellular
Mycoplasma^[28]	Mycoplasma pneumoniae	(none)	Indistinct 'fried egg' appearance, no cell wall	Mostly facultative anaerobic; M. pneumoniae strictly aerobic	Extracellular
Neisseria^[30]^[39]	Neisseria gonorrhoeae Neisseria meningitidis	Negative	Kidney bean-shaped	Aerobic	Gonococcus: facultative intracellular N. meningitidis: extracellular
Pseudomonas^[30]^[40]	Pseudomonas aeruginosa	Negative	Rods	Obligate aerobic	Extracellular
Rickettsia^[28]	Rickettsia rickettsii	Negative, stains poorly	Small, rod-like coccobacillary	Aerobic	Obligate intracellular
Salmonella^[28]	Salmonella typhi Salmonella typhimurium	Negative	Rods	Facultative anaerobica	Facultative intracellular
Shigella^[30]^[41]	Shigella sonnei	Negative	Rods	Facultative anaerobic	Extracellular
Staphylococcus^[4]	Staphylococcus aureus Staphylococcus epidermidis Staphylococcus saprophyticus	Positive, darkly	Round cocci	Facultative anaerobic	Extracellular, facultative intracellular
Streptococcus^[28]	Streptococcus agalactiae Streptococcus pneumoniae Streptococcus pyogenes	Positive	Ovoid to spherical	Facultative anaerobic	Extracellular
Treponema^[28]	Treponema pallidum	Negative, stains poorly	Spirochete	Aerobic	Extracellular
Ureaplasma^[4]	Ureaplasma urealyticum	Stains poorly^[42]	Indistinct, 'fried egg' appearance, no cell wall	Anaerobic	Extracellular
Vibrio^[30]^[43]	Vibrio cholerae	Negative	Spiral with single polar flagellum	Facultative anaerobic	Extracellular
Yersinia^[30]^[44]	Yersinia pestis Yersinia enterocolitica Yersinia pseudotuberculosis	Negative, bipolarly	Small rods	Facultative anaerobe	Intracellular

List of species and clinical characteristics

This is description of the more common genera and species presented with their clinical characteristics and treatments.

Species of human pathogenic bacteria

Species		Transmission	Diseases	Treatment	Prevention
Actinomyces israelii		Oral flora^[45]	Actinomycosis:^[45] painful abscesses and cysts MRSA in the mouth, lungs,^[46]^[47] or gastrointestinal tract.^[32]	Prolonged penicillin G and drainage^[45]
Bacillus anthracis		Contact with cattle, sheep, goats and horses^[48] Spores enter through inhalation or through abrasions^[30]	Anthrax: pulmonary, gastrointestinal and/or cutaneous symptoms.^[45]	In early infection:^[49] Penicillin Doxycycline Ciprofloxacin Raxibacumab^[50]	Anthrax vaccine^[30] Autoclaving of equipment^[30]
Bacteroides fragilis		Gut flora^[45]	Abscesses in gastrointestinal tract, pelvic cavity and lungs^[45]	metronidazole^[45]	Wound care^[51] Aspiration prevention^[51]
Bordetella pertussis		Contact with respiratory droplets expelled by infected human hosts.^[30]	Whooping cough^[30]^[45] Secondary bacterial pneumonia^[30]	Macrolides^[30] such as erythromycin,^[30]^[45] before paroxysmal stage^[45]	Pertussis vaccine,^[30]^[45] such as in DPT vaccine^[30]^[45]
Borrelia	B. burgdorferi^[30]^[45] B. garinii^[30] B. afzelii^[30]	Ixodes hard ticks Reservoir in mice, other small mammals, and birds^[52]	Lyme disease^[53]^[54] Early localized: erythema migrans Early disseminated: neuroborreliosis, Lyme carditis Late: Lyme arthritis, Achrodermatitis chronica (B. afzelii only)	Doxycycline for adults, amoxicillin for children, ceftriaxone for neurological involvement^[53]	Wearing clothing that limits skin exposure to ticks.^[30] Insect repellent.^[30] Avoid areas where ticks are found.^[30]
	B. recurrentis^[55] and others^[note 1]	Pediculus humanus corporis body louse (B. recurrentis only) and Ornithodoros soft ticks^[55]	Relapsing fever	Penicillin, tetracycline, doxycycline^[56]	Avoid areas where ticks are found^[55] Better access to washing facilities^[55] Reduce crowding^[55] Pesticides^[55]
Brucella	B. abortus B. canis B. melitensis B. suis	Direct contact with infected animal^[30] Oral, by ingestion of unpasteurized milk or milk products^[30]	Brucellosis: mainly fever, muscular pain and night sweats	doxycycline^[30] streptomycin or gentamicin^[30]
Campylobacter jejuni		Fecal-oral from animals (mammals and fowl)^[30]^[45] Uncooked meat (especially poultry)^[30]^[45] Contaminated water^[30]	Enteritis,^[30] bloody diarrhea^[45] Guillain–Barré syndrome^[45] (muscle weakness)	Treat symptoms^[30] Fluoroquinolone^[45] such as ciprofloxacin^[30] in severe cases^[30]	Good hygiene^[30] Avoiding contaminated water^[30] Pasteurizing milk and milk products^[30] Cooking meat (especially poultry)^[30]
Chlamydia	C. pneumoniae	Respiratory droplets^[30]^[45]	Atypical pneumonia^[45]	Doxycycline^[30]^[45] Erythromycin^[30]^[45]	None^[30]
	C. trachomatis	vaginal sex^[30] oral sex^[30] anal sex^[30] Vertical from mother to newborn(ICN)^[30] Direct or contaminated surfaces and flies (trachoma)^[30]	Trachoma^[30]^[45] Neonatal conjunctivitis^[30]^[45] Neonatal pneumonia^[30]^[45] Nongonococcal urethritis (NGU)^[30]^[45] Urethritis^[30]^[45] Pelvic inflammatory disease^[30]^[45] Epididymitis^[30]^[45] Prostatitis^[30]^[45] Lymphogranuloma venereum (LGV)^[30]^[45]	Erythromycin^[30]^[45] (adults)^[45]Doxycycline^[30]^[45] (infants and pregnant women)^[45]	Erythromycin or silver nitrate in newborn's eyes^[30] Safe sex^[30] Abstinence^[30]
Chlamydophila psittaci		Inhalation of dust with secretions or feces from birds (e.g. parrots)	Psittacosis, mainly atypical pneumonia	Tetracycline^[30] Doxycycline^[30] Erythromycin^[30]	-
Clostridium	C. botulinum	Spores from soil,^[30]^[45] persevere in canned food, smoked fish and honey^[45]	Botulism: Mainly muscle weakness and paralysis^[45]	Antitoxin^[30]^[45] Penicillin^[45] Hyperbaric oxygen^[45] Mechanical ventilation^[45]	Proper food preservation techniques
	C. difficile	Gut flora,^[30]^[45] overgrowing when other flora is depleted^[30]	Pseudomembranous colitis^[30]^[45]	Discontinuing responsible antibiotic^[30]^[45] Vancomycin or metronidazole if severe^[30]^[45]	Fecal bacteriotherapy
	C. perfringens	Spores in soil^[30]^[45] Vaginal flora and gut flora^[30]	Anaerobic cellulitis^[30]^[45] Gas gangrene^[30]^[45] Acute food poisoning^[30]^[45]	Gas gangrene: Debridement or amputation^[30]^[45] Hyperbaric medicine^[30]^[45] High doses of doxycycline^[30] or penicillin G^[30]^[45] and clindamycin^[45] Food poisoning: Supportive care is sufficient^[30]	Appropriate food handling^[30]
	C. tetani	Spores in soil, skin penetration through wounds^[30]^[45]	Tetanus: muscle spasms^[57]	Tetanus immune globulin^[30]^[45] Sedatives^[30] Muscle relaxants^[30] Mechanical ventilation^[30]^[45] Penicillin or metronidazole^[45]	Tetanus vaccine (such as in the DPT vaccine)^[30]
Corynebacterium diphtheriae		respiratory droplets part of human flora	Diphtheria: Fever, sore throat and neck swelling, potentially narrowing airways.^[58]	Horse serum antitoxin Erythromycin Penicillin	DPT vaccine
Ehrlichia	E. canis^[45] E. chaffeensis^[45]	Dog tick^[45]	Ehrlichiosis:^[45] headache, muscle aches, and fatigue	doxycycline^[45] rifampin^[45]
Enterococcus	E. faecalis E. faecium	Part of gut flora,^[45] opportunistic or entering through GI tract or urinary system wounds^[30]	Bacterial endocarditis,^[45] biliary tract infections,^[45] urinary tract infections^[45]	Ampicillin (combined with aminoglycoside in endocarditis)^[45]Vancomycin^[30]	No vaccine Hand washing and other nosocomial prevention
Escherichia	E. coli (generally)	Gut flora,^[30]^[45] and in urinary tract^[45] Spreading extraintestinally or proliferating in the GI tract^[30]	Diarrhea^[30]^[45] Urinary tract infections (UTI)^[30]^[45] Meningitis in infants^[30]^[45] Hospital-acquired pneumonia^[45] Hospital-acquired sepsis^[45]	UTI:^[30] (resistance-tests are required first) Co-trimoxazole Fluoroquinolone, e.g. ciprofloxacin Meningitis:^[30] Cephalosporin (e.g. cefotaxime) and gentamicin combination Diarrhea:^[30] Antibiotics above shorten duration Electrolyte and fluid replacement	(no vaccine or preventive drug)^[30] Cooking ground beef and pasteurizing milk against O157:H7^[30] Hand washing and disinfection^[30]
	Enterotoxigenic E. coli (ETEC)	Fecal-oral^[45] through food and water^[30] Direct physical contact^[30]	Traveller's diarrhea^[30]^[45]
	Enteropathogenic E. coli	Vertical, in utero or at birth^[30]	Diarrhea in infants^[30]
	Enteroinvasive E.coli (EIEC)	Fecal-oral^[59]	bloody diarrhea and fever^[45]
	Enterohemorrhagic (EHEC), including E. coli O157:H7	Reservoir in cattle^[30]	bloody diarrhea^[30]^[45] Hemolytic-uremic syndrome^[30]^[45]
Francisella tularensis		vector-borne by arthropods^[30] Infected wild or domestic animals, birds or house pets^[30]	Tularemia: Fever, ulceration at entry site and/or lymphadenopathy.^[60] Can cause severe pneumonia.^[60]	Streptomycin^[30] Gentamicin^[30]	Avoiding insect vectors^[30] Precautions when handling wild animals or animal products^[30]
Haemophilus influenzae		Droplet contact^[30] Human flora of e.g. upper respiratory tract^[30]	Bacterial meningitis^[30]^[45] Upper respiratory tract infections^[30]^[45] Pneumonia,^[30]^[45] bronchitis^[30] Septic arthritis in infants^[45]	Meningitis:^[30] (resistance-tests are required first) Third generation cephalosporin, e.g. cefotaxime or ceftriaxone^[30] Ampicillin and sulbactam combination^[30]	Hib vaccine to infants^[30]^[45] Rifampin prophylactically^[30]
Helicobacter pylori		Colonizing stomach^[30] Unclear person-to-person transmission^[30]	Peptic ulcer^[30]^[45] Chronic gastritis^[45] Risk factor for gastric carcinoma and gastric B-cell lymphoma^[30]	Tetracycline, metronidazole and bismuth salt combination^[30]	(No vaccine or preventive drug)^[30]
Klebsiella pneumoniae		Mouth, skin, and gut flora.^[61] Pneumonia upon aspiration	Klebsiella pneumonia, with significant lung necrosis and hemoptysis^[45] Hospital-acquired urinary tract infection and sepsis^[45]	3rd generation cephalosporin^[45] ciprofloxacin^[45]	hand hygiene.^[62]
Legionella pneumophila		Droplet contact, from e.g. cooling towers,^[30]^[45] humidifiers,^[30] air conditioners^[30]^[45] and water distribution systems^[30]	Legionnaire's Disease^[30]^[45] Pontiac fever^[30]^[45]	Macrolides, such as erythromycin^[30]^[45] Fluoroquinolones^[30] Rifampin^[45]	(no vaccine or preventive drug)^[30] Heating water^[30]
Leptospira species		Food and water contaminated by urine from infected wild or domestic animals. Leptospira survives for weeks in fresh water and moist soil.^[30]	Leptospirosis: Headaches, muscle pains, and fevers; possible jaundice, kidney failure, pulmonary hemorrhage, and meningitis.^[63]^[64]	Doxycycline for mild cases^[65] Intravenous penicillin for severe cases^[65]	Vaccine not widely used^[30] Doxycycline^[30] Prevention of exposure^[30] Rodent control^[30]
Listeria monocytogenes		Raw milk or cheese,^[30]^[45] ground meats,^[30] poultry^[30] Vertically to newborn or fetus^[30]^[45]	Listeriosis:^[30] Meningitis^[45] Sepsis^[45]	Ampicillin^[30]^[45] Co-trimoxazole^[30]^[45]	(no vaccine)^[30] Proper food preparation and handling^[30]
Mycobacterium	M. leprae	Prolonged human-human contact, e.g. through exudates from skin lesions to abrasion of other person^[30]	Leprosy (Hansen's disease):^[30] granulomas of the nerves, respiratory tract, skin, and eyes.^[66]	Tuberculoid form: Dapsone and rifampin^[30] Lepromatous form: Clofazimine^[30]	BCG vaccine shows some effects^[30]
	M. tuberculosis	Droplet contact^[30]	Tuberculosis: chronic cough with blood-containing sputum, fever, night sweats, and weight loss^[67]	(difficult, see Tuberculosis treatment for more details)^[30] Standard "short" course:^[30] First 2 months, combination: Isoniazid Rifampicin Pyrazinamide Ethambutol Further 4 months, combination: Isoniazid Rifampicin	BCG vaccine Isoniazid
Mycoplasma pneumoniae		Human flora^[30]^[45] Respiratory droplets^[30]^[45]	Mycoplasma pneumonia^[30]	Doxycycline and erythromycin^[30]^[45]
Neisseria	N. gonorrhoeae	Sexually transmitted^[30]^[45] vertical in birth^[30]	Gonorrhea^[30]^[45] Urethritis (men)^[45] Pelvic inflammatory disease (women)^[45] Ophthalmia neonatorum^[30]^[45] Septic arthritis^[30]^[45]	Uncomplicated gonorrhea:^[30] Ceftriaxone^[45] Tetracycline, e.g. doxycycline if also chlamydia is suspected^[45] Spectinomycin for resistance^[30]^[45] or patient allergy to cephalosporin^[30] Ophthalmia neonatorum: Erythromycin^[30]^[45] + ceftriaxone^[45]	(No vaccine)^[30] Safe sex^[30] Erythromycin into eyes of newborn at risk^[30]^[45]
	N. meningitidis	Droplet transmission^[30]	Meningococcal disease including meningitis^[30]^[45] Sepsis, including Waterhouse-Friderichsen syndrome^[30]^[45]	Penicillin G^[30]^[45] Ceftriaxone^[30]^[45]	NmVac4-A/C/Y/W-135 vaccine^[30]^[45] Rifampin^[30]^[45]
Pseudomonas aeruginosa		Opportunistic;^[45] Infects damaged tissues or people with immunodeficiency.^[30]	Pseudomonas infection:^[30] Pneumonia^[30]^[45] Urinary tract infection^[30]^[45] Corneal infection^[30]^[45] Endocarditis^[30]^[45] Osteomyelitis^[30]^[45] Burn wound infection^[45] Sepsis^[30]^[45] Malignant external otitis^[45]	Anti-pseudomonal penicillins^[30] such as ticarcillin^[45] Aminoglycoside^[30]	(no vaccine)^[30] Topical silver sulfadiazine for burn wounds^[30]
Nocardia asteroides		In soil^[45]	Nocardiosis:^[45] Pneumonia, endocarditis, keratitis, neurological or lymphocutaneous infection	TMP/SMX^[45]
Rickettsia rickettsii		Wood or dog tick^[30]^[45]	Rocky mountain spotted fever^[30]^[45]	Doxycycline^[30]^[45] Chloramphenicol^[30]^[45]	(no preventive drug or approved vaccine)^[30] Vector control, such as clothing^[30] Prompt removal of attached ticks^[30]
Salmonella	S typhi	Fecal-oral route, through food or water^[30]^[45]	Typhoid fever type salmonellosis^[30] (fever, abdominal pain, hepatosplenomegaly, rose spots)^[45] Chronic carrier state^[45]	Ceftriaxone^[30]^[45] Fluoroquinolones, e.g. ciprofloxacin^[30]^[45]	Ty21a and ViCPS vaccines^[30] Hygiene and food preparation^[30]
	Other Salmonella species e.g. S. typhimurium^[30]	Fecal-oral^[30] Food contaminated by fowl^[30] (e.g. uncooked eggs)^[45] or turtles^[45]	Salmonellosis^[30] with gastroenteritis^[30]^[45] Paratyphoid fever^[45] Osteomyelitis in people with sickle cells^[45] Sepsis^[45]	Fluid and electrolyte replacement for diarrhea^[30]^[45] Antibiotics (in neonates^[45] and immuno-compromised^[30]^[45]): Ciprofloxacin^[45] Ceftriaxone^[45] TMP/SMX^[45] Azithromycin^[45]	(No vaccine or preventive drug)^[30] Proper sewage disposal^[30] Food preparation^[30] Good personal hygiene^[30]
Shigella	S. sonnei^[30] S. dysenteriae^[45]	Fecal-oral^[30]^[45]	Shigellosis (bacillary dysentery)	Fluid and electrolyte replacement^[45] Fluoroquinolone^[45] such as ciprofloxacin^[30] if severe^[45]	Protection of water and food supplies^[30] Vaccines are in trial stage^[68]
Staphylococcus	aureus	Human flora on mucosae in e.g. anterior nares, skin and vagina,^[30]^[45] entering through wound	Coagulase-positive staphylococcal infections: Skin infections, including impetigo^[30]^[45] Acute infective endocarditis^[30]^[45] Septis^[30] Necrotizing pneumonia^[30] Meningitis^[45] Osteomyelitis^[45] Toxinoses Scalded skin syndrome^[30]^[45] Toxic shock syndrome^[30]^[45] Staphylococcal food poisoning^[30]^[45]	Incision and drainage of localized lesions^[30] Nafcillin,^[30]^[45] oxacillin,^[30] methicillin^[45] Vancomycin for Methicillin-resistant (MRSA)^[30]	(no vaccine or preventive drug) Barrier precautions, washing hands and fomite disinfection in hospitals
	epidermidis	Human flora in skin,^[30]^[45] anterior nares^[30] and mucous membranes^[45]	Infections of implanted prostheses (e.g. heart valves^[30] and joints^[45]) and catheters^[30]^[45]	Vancomycin^[30]^[45]	None^[30]
	saprophyticus	Part of normal vaginal flora^[30]	Cystitis in women^[30]^[45]	TMP/SMX or norfloxacin^[69]	None^[30]
Streptococcus	agalactiae	Human flora in vagina,^[30]^[45] urethral mucous membranes,^[30] rectum^[30] Vertically during childbirth^[30] Sexually^[30]	Neonatal meningitis^[30]^[45] Neonatal sepsis^[30]^[45] Neonatal pneumonia^[45] Endometritis in postpartum women^[30] Opportunistic infections with sepsis and pneumonia^[30]	Penicillin G^[30]^[45] Aminoglycoside in case of lethal infection^[30]	None^[30]
	pneumoniae	Respiratory droplets Human flora in nasopharynx^[45] (spreading in immunocompromised)^[30]	Acute bacterial pneumonia & meningitis in adults^[30]^[45] Otitis media and sinusitis in children^[30]^[45] Sepsis^[45]	Penicillin G^[30]^[45]	23-serotype vaccine for adults (PPV)^[30]^[45] Heptavalent conjugated vaccine for children (PCV)^[30]
	pyogenes	Respiratory droplets^[30] Direct physical contact with impetigo lesions^[30]	Streptococcal pharyngitis^[30]^[45] Sepsis^[45] Scarlet fever^[30]^[45] Rheumatic fever^[30]^[45] Impetigo and erysipelas^[30]^[45] Puerperal fever^[30] Necrotizing fasciitis^[30] Poststreptococcal glomerulonephritis^[45]	Penicillin G^[30]^[45] or V^[45] Macrolide, e.g. clarithromycin^[30] or erythromycin^[45] in penicillin allergy Drainage and debridement for necrotizing fasciitis^[30]	No vaccine^[30] Rapid antibiotic treatment helps prevent rheumatic fever^[30]
	viridans	Oral flora,^[45] penetration through abrasions	Subacute bacterial endocarditis^[45] Dental cavities^[45] Abscesses of brain and liver^[45]	Penicillin G^[45]
Treponema pallidum subspecies pallidum		Sexual^[30]^[45] Vertical (from mother to fetus)^[30]	Syphilis:^[30]^[45] First a chancre, (a painless skin ulceration), then diffuse rash.^[70] Later: gummas (soft growths), neurological, or heart symptoms.^[71] Congenital syphilis^[30]^[45]	Penicillin G^[30]^[45] Doxycycline if penicillin allergy^[30]^[45]	Penicillin offered to recent sexual partners^[72] Antibiotics to pregnant women if risk of transmitting to child^[30] No vaccine available^[30] Safe sex^[30]
Vibrio cholerae		Fecal-oral route^[45] Contaminated water and raw seafood^[30]	Cholera: Severe "rice water" diarrhea^[45]	Fluid^[45] and electrolyte replacement^[30] Doxycycline^[30]^[45]	Proper sanitation^[30] Adequate food preparation^[30]
Yersinia pestis		Fleas from animals^[30]^[73] Ingestion of animal tissues^[30] Respiratory droplets^[30]	Plague: Bubonic plague Pneumonic plague	Streptomycin primarily^[30]^[74]^[75] Tetracyclin^[30]^[76] Supportive therapy for shock^[30]	Plague vaccine^[77] Minimize exposure to rodents and fleas^[30]

Genetic transformation

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.^[78] 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.^[78] 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 meningitidis, Staphylococcus aureus, Streptococcus pneumoniae and Vibrio cholerae.^{[citation needed]}

See also

• Human microbiome project
• List of antibiotics
• Pathogenic viruses

Notes

1. Relapsing fever can also be caused by the following Borrelia species: B. crocidurae, B. duttonii, B. hermsii, B. hispanica, B. miyamotoi, B. persica, B. turicatae and B. venezuelensis.
   - Barbour, Alan G. (2017). "Relapsing Fever". In Kasper, Dennis L.; Fauci, Anthony S. (eds.). Harrison's Infectious Diseases (3rd ed.). New York: McGraw Hill Education. pp. 678–687. ISBN 978-1-259-83597-1.

References

1. Ryan, Kenneth J.; Ray, C. George; Ahmad, Nafees; Drew, W. Lawrence; Lagunoff, Michael; Pottinger, Paul; Reller, L. Barth; Sterling, Charles R. (2014). "Pathogenesis of Bacterial Infections". Sherris Medical Microbiology (6th ed.). New York: McGraw Hill Education. pp. 391–406. ISBN 978-0-07-181826-1.
2. McFall-Ngai, Margaret (2007-01-11). "Adaptive Immunity: Care for the community". Nature. 445 (7124): 153. Bibcode:2007Natur.445..153M. doi:10.1038/445153a. ISSN 0028-0836. PMID 17215830. S2CID 9273396.
3. "Tuberculosis (TB)". www.who.int.
4. Santosham, Mathuram; Chan, Grace J.; Lee, Anne CC; Baqui, Abdullah H.; Tan, Jingwen; Black, Robert E. (2013). "Risk of Early-Onset Neonatal Infection with Maternal Infection or Colonization: A Global Systematic Review and Meta-Analysis". PLOS Medicine. 10 (8): e1001502. doi:10.1371/journal.pmed.1001502. ISSN 1549-1676. PMC 3747995. PMID 23976885.
5. Azoulay E, Russell L, Van de Louw A, Metaxa V, Bauer P, Povoa P, Montero JG, Loeches IM, Mehta S, Puxty K, Schellongowski P, Rello J, Mokart D, Lemiale V, Mirouse A (February 2020). "Diagnosis of severe respiratory infections in immunocompromised patients". Intensive Care Medicine. 46 (2): 298–314. doi:10.1007/s00134-019-05906-5. PMC 7080052. PMID 32034433.
6. "Streptococcal Infections - Infectious Diseases". MSD Manual Professional Edition. Retrieved 2 May 2021.
7. Fish DN (February 2002). "Optimal antimicrobial therapy for sepsis". Am J Health Syst Pharm. 59 (Suppl 1): S13–9. doi:10.1093/ajhp/59.suppl_1.S13. PMID 11885408.
8. Heise E (1982). "Diseases associated with immunosuppression". Environ Health Perspect. 43: 9–19. doi:10.2307/3429162. JSTOR 3429162. PMC 1568899. PMID 7037390.
9. Saiman L (2004). "Microbiology of early CF lung disease". Paediatr Respir Rev. 5 (Suppl A): S367–9. doi:10.1016/S1526-0542(04)90065-6. PMID 14980298.
10. Belland R, Ouellette S, Gieffers J, Byrne G (2004). "Chlamydia pneumoniae and atherosclerosis". Cell Microbiol. 6 (2): 117–27. doi:10.1046/j.1462-5822.2003.00352.x. PMID 14706098. S2CID 45218449.
11. Muzny CA, Schwebke JR (August 2016). "Pathogenesis of Bacterial Vaginosis: Discussion of Current Hypotheses". The Journal of Infectious Diseases. 214 Suppl 1: S1–5. doi:10.1093/infdis/jiw121. PMC 4957507. PMID 27449868.
12. "Urinary Tract Infections". Retrieved 2010-02-04.
13. . Archived from the original on 2007-07-12. Retrieved 2007-08-25.
14. "Impetigo". National Health Service. 19 October 2017. Page last reviewed: 17/07/2014
15. Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N. (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 843 ISBN 978-1-4160-2973-1
16. "" at Dorland's Medical Dictionary
17. "" at Dorland's Medical Dictionary
18. Greenwood, David; Barer, Mike; Slack, Richard; Irving, Will (2012). "Bacterial Pathogenicity". Medical Microbiology, a Guide to Microbial Infections: Pathogenesis, Immunity, Laboratory Investigation, and Control (18th ed.). Edinburgh: Churchill Livingstone. pp. 156–167. ISBN 9780702040894.
19. Rudkin JK, McLoughlin RM, Preston A, Massey RC (September 2017). "Bacterial toxins: Offensive, defensive, or something else altogether?". PLOS Pathogens. 13 (9): e1006452. doi:10.1371/journal.ppat.1006452. PMC 5608399. PMID 28934339.
20. Tortora, Gerald J.; Funke, Berdell R.; Case, Christine L. (2016). "Microbial Mechanisms of Pathogenicity". Microbiology, an Introduction (12th ed.). Pearson Education. pp. 417–438. ISBN 978-0-321-92915-0.
21. Nash, Anthony A.; Dalziel, Robert G.; Fitzgerald, J. Ross (2015). "Mechanisms of Cell and Tissue Damage". Mims' Pathogenesis of Infectious Disease (6th ed.). London: Academic Press. pp. 171–231. ISBN 978-0-12-397188-3.
22. Tortota, Gerard (2013). Microbiology an Introduction. ISBN 978-0-321-73360-3.
23. Hosmer, Jennifer; Nasreen, Marufa; Dhouib, Rabeb; Essilfie, Ama-Tawiah; Schirra, Horst Joachim; Henningham, Anna; Fantino, Emmanuelle; Sly, Peter; McEwan, Alastair G.; Kappler, Ulrike (2022-01-27). "Access to highly specialized growth substrates and production of epithelial immunomodulatory metabolites determine survival of Haemophilus influenzae in human airway epithelial cells". PLOS Pathogens. 18 (1): e1010209. doi:10.1371/journal.ppat.1010209. ISSN 1553-7374. PMC 8794153. PMID 35085362.
24. Cassells AC (2012). "Pathogen and biological contamination management in plant tissue culture: phytopathogens, vitro pathogens, and vitro pests". Plant Cell Culture Protocols. Methods in Molecular Biology. Vol. 877. pp. 57–80. doi:10.1007/978-1-61779-818-4_6. ISBN 978-1-61779-817-7. PMID 22610620.
25. Yonath A, Bashan A (2004). "Ribosomal crystallography: initiation, peptide bond formation, and amino acid polymerization are hampered by antibiotics". Annu Rev Microbiol. 58: 233–51. doi:10.1146/annurev.micro.58.030603.123822. PMID 15487937.
26. Khachatourians GG (November 1998). "Agricultural use of antibiotics and the evolution and transfer of antibiotic-resistant bacteria". CMAJ. 159 (9): 1129–36. PMC 1229782. PMID 9835883.
27. Keen, E. C. (2012). "Phage Therapy: Concept to Cure". Frontiers in Microbiology. 3: 238. doi:10.3389/fmicb.2012.00238. PMC 3400130. PMID 22833738.
28. Unless else specified in boxes then ref is: Fisher, Bruce; Harvey, Richard P.; Champe, Pamela C. (2007). Lippincott's Illustrated Reviews: Microbiology (Lippincott's Illustrated Reviews Series). Hagerstown, MD: Lippincott Williams & Wilkins. pp. 332–353. ISBN 978-0-7817-8215-9.
29. Kurzynski TA, Boehm DM, Rott-Petri JA, Schell RF, Allison PE (1988). "Comparison of modified Bordet-Gengou and modified Regan-Lowe media for the isolation of Bordetella pertussis and Bordetella parapertussis". J. Clin. Microbiol. 26 (12): 2661–3. doi:10.1128/JCM.26.12.2661-2663.1988. PMC 266968. PMID 2906642.
30. Fisher, Bruce; Harvey, Richard P.; Champe, Pamela C. (2007). Lippincott's Illustrated Reviews: Microbiology (Lippincott's Illustrated Reviews Series). Hagerstown, MD: Lippincott Williams & Wilkins. pp. 332–353. ISBN 978-0-7817-8215-9.
31. Epps SV, Harvey RB, Hume ME, Phillips TD, Anderson RC, Nisbet DJ (2013). "Foodborne Campylobacter: infections, metabolism, pathogenesis and reservoirs". International Journal of Environmental Research and Public Health. 10 (12): 6292–304. doi:10.3390/ijerph10126292. PMC 3881114. PMID 24287853.
32. Bowden GHW (1996). Baron S; et al. (eds.). Actinomycosis in: Baron's Medical Microbiology (4th ed.). Univ of Texas Medical Branch. ISBN 978-0-9631172-1-2. (via NCBI Bookshelf).
33. Baron, Samuel (1996). Medical Microbiology (4th ed.). University of Texas Medical Branch at Galveston, Galveston, Texas. ISBN 978-0-9631172-1-2.
34. Rollins, David M. (2000). "BSCI424 Laboratory Media". University of Maryland. Retrieved 2008-11-18.
35. Cain, Donna (January 14, 2015). . Collin College. Archived from the original on April 26, 2015. Retrieved May 3, 2015.
36. Gunn BA (1984). "Chocolate agar, a differential medium for gram-positive cocci". Journal of Clinical Microbiology. 20 (4): 822–3. doi:10.1128/JCM.20.4.822-823.1984. PMC 271442. PMID 6490866.
37. Stevenson TH, Castillo A, Lucia LM, Acuff GR (2000). "Growth of Helicobacter pylori in various liquid and plating media". Lett. Appl. Microbiol. 30 (3): 192–6. doi:10.1046/j.1472-765x.2000.00699.x. PMID 10747249. S2CID 24668819.
38. Johnson RC, Harris VG (1967). "Differentiation of Pathogenic and Saprophytic Leptospires I. Growth at Low Temperatures". J. Bacteriol. 94 (1): 27–31. doi:10.1128/JB.94.1.27-31.1967. PMC 251866. PMID 6027998.
39. "Thayer Martin Agar (Modified) Procedure" (PDF). University of Nebraska-Medical Center, Clinical Laboratory Science Program. Retrieved 2015-05-03.
40. Allen, Mary E. (2005). . American Society for Microbiology. Archived from the original on 2015-05-07. Created: 30 September 2005. Last update: 01 April 2013
41. "Hektoen Enteric Agar". Austin Community College District. Retrieved 2015-05-03.
42. Cassell GH, Waites KB, Crouse DT, Rudd PT, Canupp KC, Stagno S, Cutter GR (1988). "Association of Ureaplasma urealyticum infection of the lower respiratory tract with chronic lung disease and death in very-low-birth-weight infants". Lancet. 2 (8605): 240–5. doi:10.1016/s0140-6736(88)92536-6. PMID 2899235. S2CID 6685738.
43. Pfeffer, C.; Oliver, J.D. (2003). "A comparison of thiosulphate-citrate-bile salts-sucrose (TCBS) agar and thiosulphate-chloride-iodide (TCI) agar for the isolation of Vibrio species from estuarine environments". Letters in Applied Microbiology. 36 (3): 150–151. doi:10.1046/j.1472-765X.2003.01280.x. PMID 12581373. S2CID 34004290.
44. "Yersinia pestis" (PDF). Wadsworth Center. 2006.
45. (PDF). Creighton University School of Medicine. Archived from the original (PDF) on 2015-05-01. Retrieved 2015-05-03.
46. Brook, I (Oct 2008). "Actinomycosis: diagnosis and management". Southern Medical Journal. 101 (10): 1019–23. doi:10.1097/SMJ.0b013e3181864c1f. PMID 18791528. S2CID 19554893.
47. Mabeza, GF; Macfarlane J (March 2003). "Pulmonary actinomycosis". European Respiratory Journal. 21 (3): 545–551. doi:10.1183/09031936.03.00089103. PMID 12662015.
48. "Anthrax in animals". Food and Agriculture Organization. 2001.
49. . Archived from the original on 5 May 2011. Retrieved 4 April 2011.
50. "FDA approves raxibacumab to treat inhalational anthrax". Food and Drug Administration. Retrieved 14 December 2012.
51. Itzhak Brook (Jan 28, 2014). "Bacteroides Infection Follow-up". Medscape. Retrieved 2015-09-25.
52. Shapiro ED (2014). "Clinical practice. Lyme disease". The New England Journal of Medicine. 370 (18): 1724–31. doi:10.1056/NEJMcp1314325. PMC 4487875. PMID 24785207.
53. Sanchez JL (2015). "Clinical Manifestations and Treatment of Lyme Disease". Clinics in Laboratory Medicine. 35 (4): 765–78. doi:10.1016/j.cll.2015.08.004. PMID 26593256.
54. Halperin JJ (2015). "Nervous System Lyme Disease". Clinics in Laboratory Medicine. 35 (4): 779–95. doi:10.1016/j.cll.2015.07.002. PMID 26593257.
55. Barbour, Alan G. (2017). "Relapsing Fever". In Kasper, Dennis L.; Fauci, Anthony S. (eds.). Harrison's Infectious Diseases (3rd ed.). New York: McGraw Hill Education. pp. 678–687. ISBN 978-1-259-83597-1.
56. Cutler SJ (2015). "Relapsing Fever Borreliae: A Global Review". Clinics in Laboratory Medicine. 35 (4): 847–65. doi:10.1016/j.cll.2015.07.001. PMID 26593261.
57. Atkinson, William (May 2012). Tetanus Epidemiology and Prevention of Vaccine-Preventable Diseases (12 ed.). Public Health Foundation. pp. 291–300. ISBN 9780983263135. from the original on 13 February 2015. Retrieved 12 February 2015.
58. "Diphtheria vaccine" (PDF). Wkly Epidemiol Rec. 81 (3): 24–32. 20 January 2006. PMID 16671240. (PDF) from the original on 6 June 2015.
59. "ESCHERICHIA COLI". Public Health Agency of Canada. 2012-04-30. Retrieved 2015-06-02.
60. "Signs & Symptoms". Centers for Disease Control and Prevention. 13 December 2018. Page last reviewed: October 26, 2015
61. Ryan, KJ; Ray, CG, eds. (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN 978-0-8385-8529-0.
62. "Klebsiella pneumoniae in Healthcare Settings". Centers for Disease Control and Prevention. 19 February 2021. Page last reviewed: November 24, 2010. Page last updated: August 27, 2012
63. Slack, A (Jul 2010). "Leptospirosis". Australian Family Physician. 39 (7): 495–8. PMID 20628664.
64. McBride, AJ; Athanazio, DA; Reis, MG; Ko, AI (Oct 2005). "Leptospirosis". Current Opinion in Infectious Diseases. 18 (5): 376–86. doi:10.1097/01.qco.0000178824.05715.2c. PMID 16148523. S2CID 220576544.
65. Hartskeerl, Rudy A.; Wagenaar, Jiri F.P. (2017). "Leptospirosis". In Kasper, Dennis L.; Fauci, Anthony S. (eds.). Harrison's Infectious Diseases. New York: McGraw Hill Education. pp. 672–678. ISBN 978-1-259-83597-1.
66. "Leprosy Fact sheet N°101". World Health Organization. January 2014. from the original on 2013-12-12.
67. "Tuberculosis Fact sheet N°104". WHO. October 2015. from the original on 23 August 2012. Retrieved 11 February 2016.
68. Institut Pasteur Press Office - Vaccine against shigellosis (bacillary dysentery):a promising clinical trial 2009-02-25 at the Wayback Machine 15 January 2009. Retrieved on 27 February 2009
69. Levinson, W. (2010). Review of Medical Microbiology and Immunology (11th ed.). pp. 94–9.
70. "Syphilis - CDC Fact Sheet (Detailed)". CDC. 2 November 2015. from the original on 6 February 2016. Retrieved 3 February 2016.
71. Kent ME, Romanelli F (February 2008). "Reexamining syphilis: an update on epidemiology, clinical manifestations, and management". Annals of Pharmacotherapy. 42 (2): 226–36. doi:10.1345/aph.1K086. PMID 18212261. S2CID 23899851.
72. Hook EW (2017). "Syphilis". Lancet. 389 (10078): 1550–1557. doi:10.1016/S0140-6736(16)32411-4. PMID 27993382. S2CID 208793678.
73. Zhou D, Han Y, Yang R (2006). "Molecular and physiological insights into plague transmission, virulence and etiology". Microbes Infect. 8 (1): 273–84. doi:10.1016/j.micinf.2005.06.006. PMID 16182593.
74. Wagle PM. (1948). "Recent advances in the treatment of bubonic plague". Indian J Med Sci. 2: 489–94.
75. Meyer KF. (1950). "Modern therapy of plague". JAMA. 144 (12): 982–5. doi:10.1001/jama.1950.02920120006003. PMID 14774219.
76. Kilonzo BS, Makundi RH, Mbise TJ (1992). "A decade of plague epidemiology and control in the Western Usambara mountains, north-east Tanzania". Acta Tropica. 50 (4): 323–9. doi:10.1016/0001-706X(92)90067-8. PMID 1356303.
77. Bubeck SS, Dube PH (September 2007). "Yersinia pestis CO92ΔyopH Is a Potent Live, Attenuated Plague Vaccine". Clin. Vaccine Immunol. 14 (9): 1235–8. doi:10.1128/CVI.00137-07. PMC 2043315. PMID 17652523.
78. Bernstein H, Bernstein C, Michod RE (2018). Sex in microbial pathogens. Infection, Genetics and Evolution volume 57, pages 8-25. https://doi.org/10.1016/j.meegid.2017.10.024

External links

• Bacterial Pathogen Pronunciation by Neal R. Chamberlain, Ph.D. at A.T. Still University
• Pathogenic bacteria genomes and related information at PATRIC, a Bioinformatics Resource Center funded by NIAID