Bacteriology, Mycology and Parasitology
Introduction
Bacteria are the smallest organisms capable of a free-living existence. That is, with the exception of a few highly evolved examples, they are able to take up nutrients from the environment, grow and self-replicate independently of other living cells. Their basic biochemical pathways are similar to those of other organisms, and while they are morphologically less complex than the cells of higher organisms, they are orders of magnitude more metabolically diverse. The niches in which they are found are also hugely diverse, ranging from kilometres below the sea floor to extremes of both temperature and pH, and have even been to the moon and back, as unforeseen passengers in the Apollo space program. Their ubiquity stems from their fast rates of growth, high levels of exchange of genetic information and their high rates of evolution. When these traits are combined it leads to the wide range of adaptations that bacteria show to allow them to colonise these niches. The adjective ‘prokaryotic’ distinguishes the absence of membrane-bound organelles characteristic of bacteria from the ‘eukaryotic’ cell characterised by the presence of a nuclear membrane.
Morphology and Structure
Most bacteria are 1 μm in diameter or larger, which means that they are readily visible by light microscopy and conventional bright-field illumination. However, to visualise the internal structures of the cell, the resolving power of an electron microscope is required. Fig. 7.1 is a diagrammatic representation of the internal structures of the prokaryotic cell.
Many bacteria have a capsule or loose slime around the cell wall. This capsule is an important protective mechanism. The ability of organisms such as Staphylococcus epidermidis to produce slime (biofilm) on the surfaces of cannulae results in the protection of the organism from the action of antimicrobial agents, and difficulty in eradicating the organism in catheter-associated sepsis.
The cell wall of bacteria is unique in its composition and plays a structural role. This macromolecule consists of a backbone of N -acetyl-glucosamine and N -acetyl-muramic acid residues linked to polypeptides, polysaccharides and lipids, and is collectively called ‘peptidoglycan’. Peptidoglycan is responsible for the rigidity of the cell wall and maintenance of the characteristic shape of an organism. Gram stain differentiates bacteria into those that take up and retain a complex of crystal violet and iodine, and those that do not. This ability is a function of the cell wall. Gram-positive organisms (stained blue/black) have a cell wall consisting largely of peptidoglycan linked to teichoic acids. In contrast, the cell wall of Gram-negative organisms (usually counterstained pink) is far more complex with an outer membrane of lipoprotein and lipopolysaccharide (LPS; also unique to bacteria), separated from the peptidoglycan layer by the periplasmic space. This arrangement has important consequences for the ability of Gram-negative bacteria to neutralise the activity of certain antimicrobial agents such as the cell wall active β-lactams (e.g. penicillins and cephalosporins) and prevents glycopeptides (vancomycin) from entering the cell and stopping peptidoglycans from being fully synthesised. Peptidoglycan is synthesised with the assistance of transpeptidases, also known as penicillin-binding proteins (PBPs), which are a target for β-lactams. This group of antibacterial agents is therefore acting against a metabolic pathway unique to bacteria, with consequent low toxicity to eukaryotic cells. The presence of β-lactamases in the periplasmic space may result in the bacteria being resistant to these agents. Mycoplasmas are unique among bacteria in not having a rigid cell wall, while the chlamydiae lack peptidoglycan. Not surprisingly, these bacteria are essentially resistant to β-lactams-based antibiotics.
The cell wall of acid-fast bacteria such as the mycobacteria and Nocardia spp. contains a high lipid content. They are difficult to stain by most stains, but a solution of hot phenolic carbol fuchsin, or the fluorochrome auramine, which binds to the lipid, will resist decolouration with sulphuric acid, and stain the organism.
The nucleus is a tightly coiled circular double strand of DNA, which replicates by fission. Other units of straight or circular DNA termed ‘plasmids’ may occur loosely in the cytoplasm. These may code for non-essential features such as antibiotic resistance or ability to ferment certain sugars such as lactose. The ability of bacteria to transfer plasmid DNA between bacteria of the same or different species may result in the spread of antimicrobial resistance (plasmid mediated). Bacteria may also transfer genetic material from the nucleus (the so-called ‘jumping gene’), leading to stable, chromosomally mediated resistance.
Projecting through the cell wall may be flagellae, fimbriae or pili. Flagellae are long whip-like structures associated with motility. Fimbriae form a fringe around bacteria allowing gliding movement. Pili are longer than fimbriae, and more numerous than flagellae. They are associated with conjugation between bacteria of the same or different species, during which the exchange of genetic material, and hence transferable antibiotic resistance, can occur.
Bacteria are morphologically constrained, they are either rod-shaped (bacilli), spherical (cocci), spirillum (actually helical and not a spiral) or vibrios (curved or comma shaped), budding and filamentous (actinomycetes). Cocci may be in chains (e.g. streptococci) or in clusters (e.g. staphylococci). However, in smears, lactobacilli which are morphologically similar may appear to branch, leading to confusion in the evaluation of cervical specimens for actinomycosis. Some members of the Actinobacteria (i.e. the genus Bifidobacteria form ‘Y’-shaped cells). Many members of the Gram-positive bacteria are also able to produce endospores, a highly resistant resting and survival phase, and can be seen in genera such as Bacillus and Clostridium .
Classification and Typing
The classification of bacteria was complicated by the lack of clear-cut morphological relationships between different members, however in the late 1970s Carl Woese and George E. Fox (Woese and Fox, 1977) proposed a new topology for the tree of life based on DNA. For the first time a rationale framework for classifying bacteria had been devised which did not require biochemical tests or morphological phenotypes. It also maintained the Linnean hierarchy of species, genus, family, order, etc. and preserved grouping of organisms with shared characteristics. However, fine characteristics were not discernible, for example, Escherichia coli strains are indistinguishable in phylogenetic trees which are created from the DNA sequences of the small subunit ribosomal RNA (rRNA) gene, also known as the 16 S rRNA gene. This lack of resolution means that it is not possible to determine if you have isolated a pathogen (e.g. E. coli O157) or have a probiotic (e.g. E. coli Nissle (1917)). Such information has obvious clinical implications. Despite this, knowledge of an organism’s classification/taxonomy is, however, important for a number of reasons. It enables communication between scientists, gives a broad picture of how the organism may behave in vitro and in vivo, and may give some indication of the likely efficacy of proposed antimicrobial chemotherapy. With the cost of DNA sequencing plummeting and currently heading towards 0.1 pence or cent per base, whole genome sequencing (WGS) has become the main tool to characterise and classify bacteria. With a WGS project costing around £30 to 40 for the raw sequence (2021), it is possible to obtain a draft genome which shows the main properties and functions of the organism of interest. The use of WGS is also making its way into public health systems for tracking pathogen outbreaks, including viral pathogens and for fast classification of pathogen virulence factors and antibiotic resistance profiles.
The naming of newly discovered bacterial isolates follows the conventional Latin binomial system, which is overseen by an international body that applies strict rules. The genus is always written with a capitalised first letter and followed by the specific epithet commencing with a lower-case letter. Both components are written in italics – thus, Staphylococcus spp. and Staphylococcus aureus . The generic name may be abbreviated after first use, thus S. aureus , or if confusion is likely to arise, Staph. aureus . All other references to the specific bacterial taxonomic lineage (e.g. family names such as ‘Staphylococcaceae’ and order ‘Bacillales’) should also be italicised, however, this practice is not enforced by many journals. Trivial names such as ‘coliform’, or adjectives such as ‘staphylococcal’ or ‘staphylococci’ are not written in italics and are not proper nouns. Table 7.1 is a simple classification of medically important bacteria based on these characteristics.
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In addition to a need to classify bacteria, it is often necessary to distinguish between infecting organisms of the same species, for example when trying to trace the source of a staphylococcal outbreak or confirming the chain of infection in a case of alleged sexual abuse. A variety of methods are available, some more applicable to some species than others. With the advent of WGS and DNA-based approaches the majority of strain typing is based on molecular approaches. Where an organism can be isolated to purity, WGS offers a cheap and relatively quick approach for source tracking in nosocomial outbreaks (Quainoo et al., 2017). For organisms which are harder to grow nucleic-acid based approaches are the most feasible assay, and the Center for Disease Control recommends the use of DNA-based approaches to identify and type Chlamydia .
Pathogenesis
The distinction between commensal and pathogenic organisms is far from clear-cut. Indeed, many of the organisms associated with common infections are part of the normal or transient microbiota of the body. Mere isolation of the organism from a specimen does not necessarily equate with disease. Rather isolation of an organism from a site normally considered sterile is more indicative of infection and disease. For example, the presence of E. coli in the small intestine reflects its normal habitat, but its presence in bladder urine indicates a urinary tract infection. Haemophilus influenzae , Streptococcus pneumoniae and Moraxella catarrhalis are all normal inhabitants of the upper respiratory tract, but each are capable of causing lower respiratory tract infection.
All bacterial species complexes have a Dr Jekyll and Mr Hyde persona, with examples of non-pathogenic strains and highly virulent strains. Examples include the plague bacillus, Brucella spp. and Treponema spp., however in general these genera are considered to be predominantly pathogenic. At the other extreme are organisms that are usually referred to as ‘Generally regarded as safe’ or ‘GRAS’ and are considered quite innocuous unless the host’s defences are markedly impaired. These include ‘opportunistic’ organisms, such as Pseudomonas aeruginosa , which are often associated with sepsis in the immunosuppressed. There are also case reports of probiotic species causing pathologies when an opportunity arises (Boumis et al., 2018). Since it is not possible to continuously maintain a biological surface as sterile in an open system, the surface (e.g. an initially sterile burn) will soon become colonised with whatever organisms are in close proximity. In addition, if the biological surface has become selective because of antibiotic administration, the colonising organism is likely to be resistant to that antibiotic. The concept of creating the selective medium is important; it is, after all, what the laboratory does to select a single organism from a mixture – merely an in-vitro version of what the clinician may unwittingly be doing in vivo.
While a breakdown in the host immune system may lead to commensal organisms causing disease, bacteria have evolved a number of mechanisms to enhance their disease-causing potential and allow them to evade the immune system. Resistance to lysis by serum is a feature of the Enterobacteriaceae , associated with the presence of LPS at the cell surface. Initial contact with the host may be facilitated by a variety of adhesions. Once attached, the presence of a capsule, with or without antigenic similarity to the host, or the production of a protective biofilm may protect the organism against the host’s immune system. More sophisticated evasive mechanisms include the production of proteases that cleave IgA, a feature of pathogens invading via mucosal surfaces such as Neisseria spp., or coating with host proteins, such as fibronectin as found in T. pallidum . Chlamydia trachomatis is able to prevent the fusion of lysosomes to the intracellular phagosome containing the infectious elementary body (EB); thus the host protects the invading organism from destruction. To initiate an infection of a clean wound with Staph. aureus , some 10 5 organisms are required. However, the presence of a foreign body, be it traumatic or a medically inserted cannula, reduces the required inoculum by 99% to 10 3 . Such numbers are small by microbiological standards.
Iron is an important growth factor for many bacteria, which enables them to fix iron-binding proteins either through specific receptors for lactoferrin or transferrin (e.g. Staph. aureus ), or by producing extracellular chelators such as siderophore (e.g. enterobactin from E. coli ). Other extracellular products such as hyaluronidase and the ureases of Proteus spp. and Helicobacter pylori may also contribute to pathogenesis.
Toxin production is important for the ability of many pathogens to cause disease (virulence). These toxins may be found extracellularly as exotoxins or released upon cell death as endotoxins. Exotoxins are a feature of Gram-positive and Gram-negative organisms. Examples of the action of exotoxins include the neuromuscular effects of Clostridium botulinum and Cl. tetani toxins, gastrointestinal symptoms of cholera, E. coli , Shigella spp. and Staph. aureus , and skin necrosis from Staph. aureus . Some toxins require the infection of the bacteria with a phage for expression, such as diphtheria toxin, which affects the heart and lungs, and the erythrogenic toxin of Str. pyogenes (Group A streptococcus). Staphylococcal toxic shock syndrome toxin is a potent pyrogen. Some exotoxins can be formalin fixed to produce toxoids, which are used as vaccines (e.g. tetanus toxoid).
Endotoxin, otherwise known as LPS, is a feature of the Gram-negative cell wall. An important component of LPS is lipid A, which links it to the outer membrane. Lipid A seems to be responsible for the inflammatory responses associated with the endotoxic shock found in severe Gram-negative septicaemia. While the LPS of the Enterobacteriaceae are among some of the most potent triggers of inflammatory responses there are many other endotoxins that are often overlooked including flagellin, peptidoglycan and lipoteichoic acid (Gram-positive cell wall component). Some of these antigens are also triggers of the innate immune system and need to also be considered as they can influence a host’s response to some of the more canonical antigens such as LPS from E. coli .
Laboratory Identification
Specimen Collection
The quality of the specimen is particularly important in microbiology. A poor specimen transported to a laboratory under less-than-ideal conditions could lead to a result that is at best, unhelpful, and, at worst, highly misleading. In general, specimens from sites thought to be infected will be collected for microscopy, culture and antigen or genome sequencing. In addition, serum samples may be sent for antibody determination. While the pressures on a clinician are appreciated, it is important that full clinical details including any current or intended antimicrobial therapy are also provided. Such information informs how clinical microbiology laboratories will undertake tests and interpret results.
Specimens should almost always be taken before treatment is commenced. Sensitive bacteria will not survive in the presence of antibiotics (unless the agent is bacteriostatic rather than bactericidal), and even if clinically resistant may not be recoverable on artificial media. The correct transport medium should always be used for swabs, to maintain the balance of organisms as similar to that observed at the site and time of sampling, and to ensure survival of pathogens. Because organisms will continue to divide at ambient temperature, specimens should be kept at +4°C and transported to the laboratory as soon as possible. Some organisms are highly sensitive to storage conditions. For example, while conventional deep freeze at −20°C is satisfactory for preserving many species, it is lethal to chlamydiae and many viruses, which survive better when stored below −70°C. Some fastidious organisms such as the gonococcus, which do not survive well out of their in vivo niche, should be either direct plated at the bedside or rapidly transported to the laboratory. To increase the likelihood of a positive result, liquid pus should always be preferred to a swab dipped in the pus. Different antigen or genome tests require different collection media, even where the same organism is being detected. It is therefore necessary to check with the laboratory before sending these specimens. If the possibility of sexual abuse arises, it is vital to set up a formal chain of evidence with the laboratory, or the evidence may not be admissible in court.
Culture
The majority of bacteria are still identified by culture on solid agar media in public health and clinical microbiology laboratories, however, there is a slow adoption of culture-independent assays which expedite identification. Using culture means that a minimum of 18 hours will elapse before even presumptive results are available. Microscopy will assist in some cases, but where there is a high abundance of normal microbiota, such as in the respiratory tract, identification of potential pathogens will be challenging and will thus facilitate some form of DNA or biomarker approach. It is never possible to speciate organisms by microscopy. Thus, intracellular Gram-negative cocci are not necessarily synonymous with Neisseria gonorrhoeae and should never be reported as such until confirmatory results are available. Culture of organisms is necessary in most circumstances to define a full picture of the organisms colonising or infecting a particular site. Sites that are considered to contain very low levels of microbial biomass, such as blood and cerebrospinal fluid, should present little problem to the laboratory as any organism cultured ought to be significant. However, the possibility of contamination of the specimen during collection, even under optimal conditions, may make interpretation of the results difficult. The problem is much greater with specimens from a site with a normal microbiota, because, as previously stated, many potentially pathogenic organisms may also be part of the normal microbiota. Further, it is not yet routinely possible to predict sensitivity to antibiotics without exposing actively divided organisms to them. However, developments in shotgun metagenomics offer a promising approach to meet the challenge of providing clinicians with timely and germane information, without the need to culture. Extraction of bacterial DNA for sequencing on third-generation sequencing platforms such as the Nanopore MinION and bioinformatic analyses may facilitate identification of the predominate strain present and its predicted antibiotic susceptibilities, within 5 hours of the sample being delivered to the laboratory.
Antigen Detection
While no microbiological test is 100% sensitive, the specificity of culture approaches 100%. The same may not be true of antigen-detection systems, although even here the tendency is to concentrate on good specificity over sensitivity. This aim is because a false-positive diagnosis is more likely to mislead than a false-negative one. In the latter situation clinical impression will override the negative report from the laboratory. Non-culture detection tests provide two useful functions. First, they may be used in situations where rapid diagnosis has important therapeutic and public health consequences (e.g. meningitis). Second, the tests are useful to diagnose pathogens that are difficult or slow to isolate in the laboratory. A good example of this is in the diagnosis of chlamydial infection. Because of the need for cell culture to isolate the organism, the development of non-culture detection tests has served to highlight the prevalence and importance of the organism, and also to make diagnostic facilities more widely available. The disadvantage is that the tests are of variable sensitivity, and in some hands, specificity is less than optimal. Direct immunofluorescence tests are of good sensitivity but are subjective; in contrast enzyme-immunoassay systems are of high specificity, but generally of lower sensitivity. The importance of this discussion is that, in low prevalence populations, a low sensitivity (around 90%) may lead to a positive predictive value of under 50%. That is, one in two positive results may be a false positive.
Nucleic Acid Detection
Molecular technology has revolutionised diagnostic microbiology. Tests based on the amplification of DNA such as the polymerase chain reaction (PCR) and the closely related ligase chain reaction (LCR) are now established in the routine diagnosis of certain pathogens (e.g. Neisseria meningitidis and C. trachomatis ). However, because of their extreme sensitivity, these techniques are subject to contamination problems. Only validated tests should ever be used for routine diagnostic purposes. Biological inhibitors may reduce the sensitivity of these tests in practice. The use of WGS is becoming much more routine as a tool to classify and characterise both viral and bacterial pathogens. In part this adoption has been accelerated by the ever-decreasing cost of DNA sequencing and the ease of access to second-generation sequencing platforms such as the Illumina HiSeq, Nextseq500 and MiSeq. In the future it will be much more commonplace for public health microbiology laboratories to rely on WGS and bioinformatic tools to classify a bacterial sample rather than culture-based approaches.
Antibody Detection
Antibody detection tests have the theoretical advantage that all that is required is a sample of clotted blood. Unfortunately, in practice, it is unusual for a definitive diagnosis to be made on a single sample of serum. The antibody rise takes a minimum of 10 to 14 days, and in some infections (e.g. chlamydial infections) more than 3 weeks may elapse. The safest criterion for the diagnosis of infection using serology is a greater than fourfold rise in specific antibody titre in at least a pair of sera. The exceptions are diseases where antibodies to the organism in question are rare in the normal population, or the organism cannot be cultured. An example of the former is plague, and of the latter syphilis. In the case of syphilis, several different tests are carried out on a single specimen in an attempt to confirm the treponemal infection, and also to define the stage of the disease.
Bacteria and Disease
Normal Microbiota
The relationship between humans and their microbes is complex, and it represents a shared co-evolutionary history. Products synthesised by one organism may assist the growth of another organism, which may in turn produce factors which will protect the host from invasion by extraneous organisms. Constant stimulation of the host immune system by resident bacteria will lead to early recognition and elimination of related, but potentially pathogenic, organisms, as well as contributing to the control of potentially neoplastic host cells by virtue of antigens similar to aberrant host ones. Intestinal microorganisms are capable of synthesising vitamins. The interactions of the various species of organism found on the skin are important for maintaining a healthy integument by production of fatty acids and other substances that inhibit the growth of potential pathogens. Disruption of this delicate balance will result in symptoms; for example, antibiotics that affect the normal gut microbiota will result in a change in the proportion of different bacterial species, with overgrowth of some at the expense of others. This imbalance is manifest by diarrhoea. A more sinister consequence may be the proliferation of Clostridioides difficile , an anaerobic spore-former present in 2% to 3% of the population, leading to toxin-mediated pseudomembranous colitis. However, it was recently discovered that the opportunity for C. difficile to propagate and to cause infection is most probably due to the use of antibiotics that remove the ability of other bacteria in the community to create colonisation resistance. If the functions of these bacteria are re-introduced, for example, through the use of faecal microbiota transplantation, C. difficile can no longer thrive.
The interaction of aerobic organisms with anaerobic organisms is particularly intriguing. The aerobes serve to consume oxygen, thus lowering the oxygen tension (eH) to very low levels and allowing the proliferation of strictly anaerobic organisms. The anaerobes outnumber the aerobes by 10:1 to 100:1 on the skin, rising to over 1000-fold excess in the large intestine. One gram of faeces contains some 10 8 aerobic organisms and 10 11 anaerobic organisms. Maintenance of the anaerobic gut microbiota is essential for health, and the use of anaerobe-sparing antibiotics (e.g. ciprofloxacin) where indicated is less likely to lead to diarrhoea as a side-effect.
The predominantly Gram-positive resident microbiota of the skin is supplemented by transient organisms, usually from the environment, and often Gram-negative. They are unable to establish themselves but may survive for several hours. This period is long enough for transfer to occur to susceptible individuals via the examining fingers.
Normal Genital Tract Microbiota of Women
Lactobacillus species have long been recognised as being predominant members of the genital tract microbiota. More recently, metataxonomic approaches have indicated that there exists 5 major vaginal bacterial profile types or community state types (CST), 4 of which were dominated by species from the genus Lactobacillus and a fourth CST which is dominated by strictly anaerobic and low levels of lactic acid bacteria. Specifically, CST I, II, II and V are dominated by L. crispatus , L. gasseri , L. iners and L. jensenii respectively, and are considered to be low diversity communities. CST IV is a relatively high diversity community colonised by species from the Prevotella , Megasphaera , Atopobium and Sneathia genera, for example. Several groups have now independently replicated these findings in different patient cohorts and identified interesting correlations between these CSTs and pre-term birth and cervical cancer, thus identifying the potential for interventions that modulate the vaginal microbiota and abrogate these issues.
The normal microbiota of the vagina changes under the influence of circulating oestrogens. The presence of oestrogen leads to an environment rich in glycogen, and the release of glucose via vaginal α-amylase activity favours the growth of lactobacilli and other acid-tolerant organisms. The metabolism of glycogen breakdown products to lactic acid, results in a pH less than 4.5. Other bacteria commonly present include anaerobic cocci, diphtheroids, coagulase-negative staphylococci and α-haemolytic streptococci. In addition, a number of organisms that are also potential pathogens may colonise. These include β-haemolytic streptococci including Str. agalactiae and Actinomyces spp. The balance between health and disease in the vagina is delicate. Factors leading to alteration of this balance will lead to overgrowth of organisms at the expense of the lactobacilli leading to bacterial vaginosis. Specific disease can be caused by yeast-like fungi (e.g. Candida spp.) or infection with the protozoon Trichomonas vaginalis . Gonococcal and chlamydial infections affect the cervix, causing genital discharge. Bacterial vaginosis, gonococcal and chlamydial infections all predispose to ascending infection resulting in endometritis and salpingitis, with the attendant sequelae of ectopic pregnancy or infertility. Bacterial vaginosis also appears to be a factor in the pathogenesis of pre-term labour.
Gram-Positive and Gram-Negative Bacteria
Table 7.2 lists some of the more medically important bacteria. Staph. aureus is distinguished from other staphylococci by production of coagulase. Increasingly, these organisms are proving to be resistant to the anti-staphylococcal β-lactam antibiotics (penicillins and cephalosporins). Such strains are designated methicillin-resistant Staph. aureus (MRSA) after the now obsolete antibiotic used as a laboratory test to detect them. Strains are frequently also multi-resistant, and some are able to spread easily through clinical areas (epidemic MRSA – EMRSA). MRSA are usually no more virulent than other coagulase-positive staphylococci, and frequently colonise wounds and carrier sites. However, when they do cause infection the antibiotic choice is considerably limited compared with methicillin-sensitive strains.
| Group or Genus | Important Species | Diseases Caused, Comments |
|---|---|---|
| Gram-Positive Cocci | ||
| Staphylococci | Staphylococcus aureus | Wound infections, abscess, bacteraemia/septicaemia, osteomyelitis, tampon-associated toxic shock syndrome, food poisoning |
| S. epidermidis | Vascular cannula-associated infection | |
| Staph. saprophyticus | Urinary tract infections | |
| Streptococci (α-haemolytic) | Streptococcus milleri | Normal mouth microbiota, deep-seated abscesses, endocarditis |
| S. pneumoniae | Lobar pneumonia | |
| Enterococcus ( Streptococcus ) faecalis | Normal bowel microbiota, urinary tract infection, opportunistic wound infection | |
| Streptococci (β-haemolytic) | S. pyogenes (Group A) | Bacterial upper respiratory tract infection, wound infection, abscesses, bacteraemia/septicaemia, puerperal sepsis, necrotising fasciitis, scarlet fever, septic arthritis |
| S. agalactiae (Group B) | Normal vaginal microbiota, neonatal bacteraemia/septicaemia and meningitis | |
| Peptostreptococcus | P. anaerobius | Anaerobic abscesses |
| Gram-Positive Bacilli | ||
| Bacillus spp. | B. anthracis | Anthrax |
| B. cereus | Normal microbiota of air, food poisoning with diarrhoea and vomiting | |
| Lactobacilli | Lactobacillus casei | Normal vaginal microbiota |
| Corynebacteria | Corynebacterium diphtheriae | Diphtheria |
| C. jeikeium | Skin microbiota, line- (cannula/vascular) associated bacteraemia/septicaemia | |
| Listeria | L. monocytogenes | Maternal and neonatal listeriosis |
| Clostridium spp. | C. perfringens | Gas gangrene |
| C. tetani | Tetanus | |
| Actinomycetes | Actinomyces israelii | Pelvic actinomycosis |
| Nocardia | N. asteroides | Chronic infection in transplant patients |
| Gram-Negative Cocci | ||
| Neisseriae | Neisseria gonorrhoeae | Gonorrhoea, pelvic inflammatory disease, arthritis, bacteraemia/septicaemia, infertility, neonatal ocular infection |
| N. meningitidis | Meningitis | |
| Moraxellae | Moraxella (Branhamella) catarrhalis | Respiratory microbiota, exacerbations of chronic bronchitis |
| Veillonella | Veillonella spp. | Normal oropharyngeal microbiota |
| Gram-Negative Bacilli | ||
| Haemophilus spp. | H. influenzae | Respiratory microbiota, exacerbations of chronic bronchitis |
| Legionella spp. | L. pneumophila | Atypical pneumonia |
| Pasteurella spp. | P. multocida | Animal bites |
| Yersinia | Y. pestis | Plague |
| Y. enterocolitica | Mesenteric adenitis | |
| Comma-shaped | Vibrio cholerae | Cholera |
| Helically curved | Campylobacter fetus | Normal microbiota of chickens, food poisoning with diarrhoea |
| Helicobacter spp. | Gastritis and peptic ulcers | |
| Bartonellae | Bartonella henselae | Cat-scratch disease, bacillary peliosis, bacillary angiomatosis |
| Enterobacteriaceae | Escherichia coli, Klebsiella pneumoniae, Enterobacter cloacae | Urinary tract infection, abdominal sepsis, wound infection, bacteraemia/septicaemia, nosocomial respiratory infection |
| Proteus mirabilis | Enteric fever | |
| Salmonella typhi, Salmonella enteritidis | Food poisoning with diarrhoea | |
| Shigella dysenteriae | Dysentery | |
| Pseudomonads | Pseudomonas aeruginosa | Nosocomial urinary tract infection and respiratory infection, opportunistic wound infection, bacteraemia/septicaemia |
| Stenotrophomonas maltophilia | ||
| Anaerobic Gram-negative bacteria | Bacteroides fragilis | Normal gut microbiota, abdominal sepsis, pelvic inflammatory disease |
| Prevotella melaninogenica | Respiratory tract infection | |
| P. bivia | Normal vaginal microbiota, abdominal sepsis, pelvic inflammatory disease | |
| Fusobacterium nucleatum | Severe oral sepsis | |
| Others | ||
| Gram-variable coccobacilli | Mobiluncus curtisii | Normal vaginal microbiota, but predominant in bacterial vaginosis |
| Gardnerella vaginalis | Associated with clue cells | |
| Mycobacteria | Mycobacterium tuberculosis | Tuberculosis |
| M. avium-intracellulare | Chronic respiratory infection and bacteraemia in severely immunosuppressed patients | |
| Spirochaetes | Treponema pallidum | Syphilis |
| T. pertenue | Yaws | |
| Leptospira interrogans | Leptospirosis | |
| Borrelia recurrentis | Relapsing fever | |
| Mycoplasmas | Mycoplasma pneumoniae | Atypical pneumonia |
| M. hominis | Normal vaginal microbiota, pyelonephritis, pelvic inflammatory disease | |
| Ureaplasma urealyticum | Normal vaginal microbiota, non-gonococcal non-chlamydial urethritis, neonatal respiratory infection | |
| Chlamydiae | Chlamydia trachomatis | Non-gonococcal urethritis, cervicitis, endometritis, pelvic inflammatory disease, infertility, neonatal ocular and respiratory infection |
| C. pneumoniae | Atypical pneumonia, possible association with coronary heart disease | |
| C. psittaci | Animal pathogen, atypical pneumonia in humans | |
| Rickettsiae and Coxiella spp. | Rickettsia prowazekii | Typhus |
| Coxiella burnetii | Q fever | |
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