Saturday Cimema: How mushrooms can save the world

Good Germs, Bad Germs: Health and Survival in a Bacterial World

Both friendly and destructive bacteria live in our mouths, eyes, skin and elsewhere. Over millions of years, the body has come to an accommodation with those creatures, generally striking a balance ensuring survival. This balance has been severely offset in recent years, due to a “cleanliness” obsession that arose when it became clear that some germs were responsible for diseases. This idea was effectively demonstrated by UK researcher David Strachan, whose research led to what is now called the “hygiene hypothesis” - respiratory illnesses result from lack of cross-microbe activity to build immunities. In short, rich, small families were more prone to allergies than large, poorer ones. As Sachs points out, humans in our society overreacted to the new knowledge about disease-causing germs and sought to eliminate them all. The imbalance has led to many tragic situations, and initiated a guarantee that more, perhaps worse, situations are in the offing. What are we to do about it?

Jessica Sachs guides us through the findings of scores of scientists’ work that has revised the approach we were taught about “germs” in our childhood. Eating mud, something many of us were at least verbally chastised for, turns out to be a good thing, even a necessity. From birth, the introduction of certain microbes initiate processes the body needs to keep going. For most people today, it’s well known that microbes in our tummies are part of the process of digestion. Escherichia coli is known to be a true friend - in controlled numbers and certain strains. What’s less known is how many other bacteria the body relies on to get certain jobs done. One of those jobs is keeping the immune system properly tuned. A lazy immune system is unresponsive or unable to react to invasion. An overly ambitious one can turn on its own body and destroy it.

Publisher Hill & Wang, Oct 2007, ISBN-10: 0809050633

Related:

• The Hygiene Hypothesis

Salmonella

Salmonella are Gram-negative bacteria which cause intestinal infections. The taxonomy of Salmonella species is complicated. Formally, there are only two species within this genus: S. bongori and S. enterica (formerly called S. choleraesuis), which are divided into six subspecies:

I - enterica
II - salamae
IIIa - arizonae
IIIb - diarizonae
IV - houtenae
V - bongori
VI - indica

However, there are numerous (over 2,500) serovars within both of these species. For the sake of simplicity, the CDC recommends that Salmonella species be referred to only by their genus and serovar, e.g. Salmonella Typhi instead of: Salmonella enterica subspecies enterica serovar Typhi. The Kauffman-White classification divides Salmonella isolates according to their somatic O antigens and flagellar H antigens. H antigens are further divided into phase 1 and phase 2, but in practice, most labs leave this level of detail to specialized reference laboratories.

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Prevention of Salmonella as a cause of food poisoning mostly involves effective sanitary precautions. Salmonellosis can also be caught from pet animals. All the disease-causing Salmonella species are now classified as a single species, Salmonella enterica, with numerous serovars. Most Salmonella isolates cause gastroenteritis which is usually self-limiting and does not require treatment with antibiotics. However, these infections can be life-threatening in the very young, very old and the seriously ill. Salmonella Typhi causes typhoid fever, a more serious systemic infection which does require medical intervention.

Investigation of the mechanisms that underlie the interactions of Salmonellae with their hosts has advanced greatly over the past decade, mainly through the study of Salmonella enterica serovar Typhimurium in tissue culture and animal models of infection. Knowledge of the bacterial processes and host responses has painted a dynamic and complex picture of the interactions between salmonellae and animal cells (Salmonellae interplay with host cells. Nature Reviews Microbiology 2008 6: 53-66).

Most Salmonella infections are acquired by ingestion of contaminated food or water. Salmonellae have an adaptive acid-tolerance response that promotes their survival in the low pH of the stomach. After entering the small intestine, they enter the intestinal mucous layer in order to gain access to the underlying epithelium and so evade being killed by digestive enzymes, bile salts, secretory IgA, antimicrobial peptides and other innate immune defences. The presence of Salmonella in the gut results also in production of pro-inflammatory cytokines such as IL-8, which stimulate inflammatory response leading to diarrhoea.

Salmonellae invade non-phagocytic enterocytes of the intestinal epithelium by bacterial-mediated endocytosis. After adherence to the apical surface of the cell, the bacteria disrupt the epithelial brush border and induce membrane ruffles that engulf the organism. Alternatively, they can translocate through the intestinal epithelia after uptake by CD18-expressing phagocytes. In vitro, Salmonellae are able to disrupt tight junctions, which seal the epithelial cell layer and restrict the passage of ions, water and immune cells. This, in addition to intestinal inflammatory responses, probably contributes to the induction of diarrhoea. The fact that there are multiple mechanisms for crossing the intestinal barrier indicates the importance of this strategy to the lifestyle of these bacteria. At least five different virulence proteins are required for efficient invasion of cultured epithelial cells, and optimal invasion of animal tissues might be even more complex and diverse.

Emerging technologies such as whole-genome sequencing will allow us to investigate the diversity of effectors that are used by the many pathogenic Salmonella isolates. The study of Salmonella pathogenesis should yield a rich treasure trove of information for those who are interested in microbial pathogenesis, innate immunity, cell biology and genomics, and will remain an important model system of host pathogen interactions for many years to come.

Tuberculosis - is the white plague winning?

Tuberculosis has had many names, including consumption, scrofula and the great white plague, but whatever you call it, this disease still claims one life every 10 seconds and global mortality rates are increasing despite the use of chemotherapy (Drugs versus bugs: in pursuit of the persistent predator Mycobacterium tuberculosis. 2008 Nature Reviews Microbiology 6: 41-52). Why have we not progressed further towards the eradication of this disease? There are many answers, including politics and poverty, and some less shameful excuses such as HIV and drug resistance. Whatever the reason, without new weapons in the armory against TB, the disease will continue to make ground.

Two factors, persistence and resistance, make the treatment of Mycobacterium tuberculosis infections particularly difficult. The term persistence describes the survival of the causative organism despite the use of antibiotics. The local concentration of antibiotics in lesions such as granulomas might not be adequate to kill the cells, or some bacteria might adopt a physiological state that renders them less susceptible to antibiotics. For these reasons, drug treatments must be extended. Currently, even the most effective regimes require a combination of at least 3 drugs and last for six months. Because patients feel better within 1 2 weeks, they have little motivation to continue with therapy, so the current World Health Organization guidelines call for treatment to be directly observed (DOTS). This can be difficult to provide in much of the world, including the areas where tuberculosis rates are highest.

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There is an excellent chance that patients who have tuberculosis can be cured using currently available drugs if they complete the required course of therapy. But what characteristics should new drugs have to improve on current treatments?

• Oral bioavailability: to avoid the need for injections.
• Good tolerance: to avoid unwanted side-effects might cause treatment to be abandoned.
• Widespread usability: including AIDS patients, young children and pregnant women.
• Compatibility with anti-retroviral drugs: because co-infection with HIV and TB is common.
• Infrequent dosing: once a day drugs improve treatment compliance.
• Activity against drug-resistant TB strains: possibly the most important factor with the rise of MDR and XDR-TB.
• Rapid clearance of chronic infection: so that treatment times can be shortened.
• Affordability: so they can be used in the areas of the world where TB is most prevalent.

Mycobacterium tuberculosis has no significant animal or environmental reservoirs and shows limited genetic diversity. In spite of this, TB continues to be a widespread and devastating disease. The need for new faster-acting drugs is clear. Recent work by my colleague Dr Mark Carr from the School of Biological Sciences at the University of Leicester might help in future drug development. The M. tuberculosis ESAT-6/CFP-10 complex consists of two proteins which, together, allow the bacteria to survive inside white blood cells. Removal of the genes for these proteins from the TB genome renders the bacteria unable to cause disease. Similarly, studies of the structure of the protein complex have shown that removal of a “long arm” from the molecule prevents the complex s ability to bind to the outer surface of human white blood cells. In the structure of the ESAT-6/CFP-10 complex above, the “long arm” is in red on the right side of CFP-10. When this is intact, it allows the complex to attach to the outside of host white blood cells. When the long arm is cleaved off, the complex shows greatly reduced attachment. This data provides an insight into the important components of this complex. Mark Carr says: “Current work is attempting to identify the exact components of the human white blood cells that this complex is targeting. Once found, this should give us a greater knowledge of the action of these molecular weapons of TB and give us the edge in the war against an ancient, reawakened foe.”

Related:

• Resuscitating Mycobacterium tuberculosis
• Gamma interferon - key, but not sufficient for protection against TB?
• Tuberculosis virulence gene inhibits apoptosis of infected host cells
• Extreme drug resistant tuberculosis (XDR-TB) update

New Drugs for Nasty Nematodes

The nematodes, or roundworms, comprise a large number of pathogens of man and domestic animals. Gastrointestinal nematodes, such as the blood-sucking Haemonchus contortus, are major parasites of ruminants that cause substantial economic losses to livestock production worldwide. In the absence of vaccines for gastrointestinal nematodes, control of infections relies mainly on chemotherapy. Drug resistance in human and animal pathogenic helminths has been spreading in prevalence and severity to a point where multidrug resistance against the three major classes of anthelmintics - the benzimidazoles, imidazothiazoles and macrocyclic lactones - has become a global phenomenon in gastrointestinal nematodes of farm animals. Hence, there is an urgent need for an anthelmintic with a new mode of action. This paper report the discovery of the amino-acetonitrile derivatives (AADs) as a new chemical class of synthetic anthelmintics and describes the development of drug candidates that are effective against various species of livestock-pathogenic nematodes. These drug candidates seem to have a novel mode of action involving a unique, nematode-specific clade of acetylcholine receptor subunits. The AADs are well tolerated and of low toxicity to mammals, and overcome existing resistances to the currently available anthelmintics.
These optimized AAD compounds meet the following requirements for an urgently needed new anthelmintic for livestock: low toxicity, favourable pharmacokinetic properties and broad-spectrum efficacy against sheep and cattle nematodes. Moreover, this efficacy includes multidrug-resistant parasites owing to a presumed activation of signalling. However, nematodes will ultimately develop resistance to any new drug, including the AADs. To secure the maximum lifespan of the AADs as well as the current anthelmintic drugs, monitoring of drug resistance and rational exploration of combinations with current or future drugs will be necessary. If the excellent tolerability of the AADs in ruminants can be proven for humans, the class may offer an alternative anthelmintic for human medical practice.

A new class of anthelmintics effective against drug-resistant nematodes
Nature 2008 452: 176-180

Microbes on the skin: disease or defence?

Most reviews of skin microbes concentrate on understanding the population of bacteria inhabiting the skin, or on how a subset of these microbes can become pathogens. In the past decade, interdisciplinary collaborations at the interface between microbiology and immunology have greatly advanced our understanding of the host-pathogen relationship (Skin microbiota: a source of disease or defence? British Journal of Dermatology 2008 158: 442-455).
Does the hygiene hypothesis apply to the skin? Several studies have shown that the surface microflora can influence the host innate immune system. These findings complement studies that suggest disruption in microbial exposure early in development may lead to allergies. The beneficial effect of microbes in the gut has been used to support the use of probiotics. But unlike the intestine, the role of microbes on the skin surface has not been well studied.

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The relationship between the skin flora and the host can fall into three categories: parasitism, commensalism or mutualism. Symbiotic relationships can exist in which only one organism benefits while the other is harmed (parasitism, predation and competition), one organism benefits and no harm occurs to the other (commensalism) or both organisms benefit (mutualism and co-operation). Microbes found on the surface of the skin that are only infrequently associated with disease are typically referred to as commensal. This term implies that the microbe lives in peaceful coexistence with the host while benefiting from a sheltered ecological niche. An example of such a microbe is the Gram-positive bacterium Staphylococcus epidermidis. Emerging evidence indicates that this species and other so-called skin commensals may play an active role in host defence, such that they may represent a mutualistic association.

It is important to recognize that the distinction between what we consider to be harmless flora or a pathogenic agent often lies in the skin’s capacity to resist infection, and not the inherent properties of the microbe. Host cutaneous defence occurs through the combined action of a large variety of complementary systems. These include the physical barrier, a hostile surface pH, and the active synthesis of gene-encoded host defence molecules such as antimicrobial peptides, proteases, lysozymes and cytokines and chemokines that serve as activators of the cellular and adaptive immune responses. Virulence factors expressed by a microbe may enable it to avoid host defences, but it is ultimately the effectiveness of the host response that determines if a microbe is a commensal (or mutual) organism, or a dangerous pathogen for the host.

Staphylococcus epidermidis:
Staphylococcus epidermidis comprises more than 90% of the resident aerobic skin flora. Despite its generally innocuous nature, S. epidermidis is a frequent cause of infections. This species primarily infects compromised patients including drug abusers, those on immunosuppressive therapy, AIDS patients, premature babies and patients with an indwelling medical device such as a catheter. After entry, virulent strains of S. epidermidis form biofilms that partially shield the dividing bacteria from the host’s immune system and from exogenous antibiotics. In addition to catheter infections, patients with necrotic tumour masses also have a high tendency towards infection by S. epidermidis. In other conditions, S. epidermidis normally resides benignly on the skin surface, with infections arising only in conjunction with specific host predispositions.

Corynebacterium diphtheriae:
Coryneforms are Gram-positive, nonmotile, facultative anaerobic actinobacteria. The common members of the skin flora are divided into two species: Corynebacterium diphtheriae and nondiphtheriae corynebacteria (called diphtheroids). Toxinogenic C. diphtheriae produce the highly lethal diphtheria toxin, which can induce fatal toxaemia. Nontoxinogenic (nontoxin-producing) C. diphtheriae are capable of producing septicaemia, septic arthritis, endocarditis and osteomyelitis. Both non-toxigenic and toxigenic C. diphtheriae can be isolated from cutaneous ulcers of alcoholics, intravenous drug users and from hosts with poor hygiene standards, such as in endemic outbreaks in areas of low socioeconomic status.
The nondiphtheriae corynebacteria (diphtheroids) are a diverse group, containing 17 different species, not all of which are present on human skin. Several species commonly colonize cattle, while others, such as Corynebacterium jeikeium are normal inhabitants of human epithelium. C. jeikeium causes infections in immunocompromised patients, in conjunction with underlying malignancies, on implanted medical devices. Once the bacterium has penetrated the skin barrier, this bacterium can cause sepsis or endocarditis.

Propionibacterium acnes:
Propionibacterium acnes is an aerotolerant anaerobic, Gram-positive bacillus that produces propionic acid as a metabolic byproduct. This bacterium resides in the sebaceous glands, derives energy from the fatty acids of sebum, and is susceptible to ultraviolet radiation due to the presence of endogenous porphyrins (so step away from the computer and spend some time in the sun). The most well-known ailment associated with P. acnes is the skin condition known as acne vulgaris, affecting up to 80% of adolescents in the USA. Several factors are thought to contribute to an individual’s susceptibility. Hormones, medications (including steroids and oral contraceptives), the keratinization pattern of the hair follicle, stress and genetic factors all contribute to acne. In the sebaceous gland, P. acnes produces free fatty acids as a result of triglyceride metabolism. These byproducts can irritate the follicular wall and induce inflammation through neutrophil chemotaxis to the site of residence. Inflammation due to host tissue damage or production of immunogenic factors by P. acnes subsequently leads to cutaneous infections. Like S. epidermidis, P. acnes causes many postoperative infections. Prosthetic joints, catheters and heart valves transport the cutaneous microflora into the body. Sepsis and endocarditis result from systemic infections. Another common port of entry for P. acnes is through eye injuries or operations. Propionibacterium acnes can cause endophthalmitis (inflammation of the interior of the eye causing blindness) weeks or months after trauma or eye surgery. The infection delay probably results from low-virulence phenotypes of P. acnes.

Group A Streptococcus (Streptococcus pyogenes):
Known for causing superficial infections as well as invasive diseases, GAS (such as S. pyogenes) form chains of Gram-positive cocci. GAS strains are further subclassified by their M-protein and T-antigen serotypes, which indicate the strain’s potential to cause superficial or invasive disease. GAS infections are diverse in their symptoms, with strep throat, mucosal infections and impetigo being most common. GAS is also associated with deeper-seated skin infections such as cellulitis, infections of connective tissue and underlying adipose tissue. These types of disease occur frequently in the elderly and in people in densely populated accommodation. The invasive necrotizing fasciitis, or flesh-eating disease, carries a high degree of morbidity and mortality and is frequently complicated by streptococcal toxic shock syndrome. GAS can also cause infections in many other organs including lung, bone and joint, muscle and heart valve, essentially mimicking the disease spectrum of S. aureus.

Pseudomonas aeruginosa:
Pseudomonas aeruginosa is commonly found in nonsterile areas on healthy individuals and, much like S. epidermidis, is considered a normal constituent of a person’s natural microflora. The bacteria normally live innocuously on human skin and in the mouth, but are able to infect practically any tissue with which they come into contact. Flexible, nonstringent metabolic requirements allow P. aeruginosa to occupy a variety of niches, making it the epitome of an opportunistic pathogen. Due to the general harmlessness of the bacteria, infections occur primarily in compromised patients and in hospital-acquired infections. Immunocompromised individuals with AIDS, cystic fibrosis and haematological and malignant diseases develop systemic or localized P. aeruginosa infections. Transmission often occurs through contamination of inanimate objects and can result in ventilator-associated pneumonia and other medical device-related infections. The main route of entry is through compromised skin, with burn victims commonly suffering from P. aeruginosa infections. On the skin, P. aeruginosa occasionally causes dermatitis or deeper soft-tissue infections. Dermatitis occurs when skin comes into contact with infected water, for example in hot tubs. The infection is very mild and is treated easily with topical antibiotics.

Much current research related to infectious diseases of the skin targets microbial virulence factors and aims to eliminate harmful organisms. Some of these same microbes potentially also play an opposite role by protecting the host. The complex host-microbe and microbe-microbe interactions that exist on the surface of human skin illustrate that the microbiota have a beneficial role, much like that of the gut microflora.

Related:

• Staphylococcus aureus: superbug
• Microbes and puberty: a teenager’s guide
• Bad Hair Day

E. coli O157:H7 - getting to the bottom of the burger bug

The Zoonotic and Animal Pathogens Research Laboratory at the University of Edinburgh has worked with a UK-based animation company to produce a full-length animation representing the key stages of E. coli O157:H7 interaction within the gastrointestinal tract. This movie was featured in the August 2004 issue of Microbiology Today, published by the Society for General Microbiology.

Drugs for treatment of prion infections

Prion diseases are fatal and at present there are neither cures nor therapies available to delay disease onset or progression in humans. Inspired in part by therapeutic approaches in the fields of Alzheimer’s disease and amyotrophic lateral sclerosis, researchers tested five different drugs which are known to efficiently pass through the blood-brain barrier in a mouse prion system. Groups of intracerebrally prion-challenged mice were treated with the drugs curcumin, dapsone, ibuprofen, memantine and minocycline. Treatment with antibiotics dapsone and minocycline had no therapeutic benefit. Ibuprofen-treated mice showed severe adverse effects, which prevented assessment of therapeutic efficacy. Mice treated with low- but not high-dose curcumin and mice treated with memantine survived infections significantly longer than untreated controls. These results encourage further research efforts to improve the therapeutic effect of these drugs.

Evaluation of drugs for treatment of prion infections of the central nervous system. 2008 J Gen Virol. 89: 594-597

Related:

• Fears over new wave of vCJD deaths
• A General Model of Prion Strains and Their Pathogenicity
• Prions, Proteasomes, and Mad Cows

Peptidoglycan - the strength and weakness of bacteria

The peptidoglycan layer is a unique and essential structural element in the cell wall of most bacteria (Peptidoglycan structure and architecture. FEMS Microbiology Reviews, 08 Jan 2008). Made of glycan strands cross-linked by short peptides, the so-called peptidoglycan sacculus forms a closed, bag-shaped structure surrounding the cytoplasmic membrane. Peptidoglycan sacculi have the strength to withstand the cell’s turgor pressure of up to 25 atmospheres. On the other hand, the sacculi are not rigid walls but are flexible structures, allowing reversible expansion under pressure, and they have relatively wide pores, enabling diffusion of large molecules such as proteins. Because the peptidoglycan completely surrounds the cytoplasmic membrane, the sacculus has a similar size and shape as the bacterial cells from which it was isolated.

The main function of peptidoglycan is to preserve cell integrity by withstanding the turgor pressure inside the cell. Inhibition of peptidoglycan biosynthesis (e.g. by mutations or antibiotics such as penicillin) or degradation (e.g. by lysozyme) in growing cells results in cell lysis. Peptidoglycan contributes to the maintenance of a defined cell shape (e.g. rod or sphere) and serves as a scaffold for anchoring other cell envelope components such as proteins and teichoic acids. It is intimately involved in the processes of cell growth and cell division. However, peptidoglycan is absent in some bacteria such as Mycoplasma species, Planctomyces, Rickettsia and Chlamidiae.

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Peptidoglycan is composed of an overlapping lattice of two sugars, N-acetyl glucosamine (NAG) and N-acetyl muramic acid (NAM) cross-linked by amino acid bridges. The exact molecular makeup of these cross-bridges is species-specific. NAM is only found in the cell walls of bacteria and nowhere else. Attached to NAM is a side chain generally composed of four amino acids. In the best-studied bacterial cell wall (that of Esccherichia coli) the cross-bridge is most commonly composed of L-alanine, D-alanine, D-glutamic acid and diaminopimelic acid. In Staphylococcus aureus, the pentapeptide coming off the NAM is composed of the amino acids L-alanine, D-glutamine, L-lysine, and two D-alanines.

There is a two-layered organization of the bacterial cell wall, with a zone of low density next to the plasma membrane. This “inner wall zone” or “periplasmic space” has a thickness between 16 nm (in Staphylococcus aureus) and 22 nm (in Bacillus subtilis). The “outer wall zone” of higher density is the polymeric peptidoglycan–teichoic acid complex with its attached surface proteins. The thickness of the outer zone varies with the species, growth phase of the cells and growth conditions, but is in the range of 15–30 nm. Unravelling the molecular architecture of the bacterial cell wall has been a constant aspiration for microbiologists, but is proving to be a frustrating topic. In particular, the architecture of the cell wall of Gram-positive bacteria is far from being understood. Gram-positive species not only have a thick, multi-layered peptidoglycan but other major surface polymers linked to it.

The essential functions of peptidoglycan and its confinement to bacteria make it a perfect target for attacking these organisms. β-lactams and glycopeptides, powerful bactericidal antibiotics, interfere with the last steps of peptidoglycan synthesis. Glycopeptides such as vancomycin bind the C-terminal end of the peptidoglycan disaccharide-pentapeptide precursor, preventing its incorporation into peptidoglycan. The targets of β-lactams were identified as penicillin-binding proteins (PBPs), and multiple PBPs with different affinities for β-lactams are generally present in the cell envelope. Resistance to β-lactams and glycopeptides is of major concern in the treatment of bacterial infections. Frequently, bacteria produce enzymes (β-lactamases) that inactivate these antibiotics. Gram-negative cells can reduce the permeability of their outer membrane and many bacteria lower the antibiotic concentration near the targets using efflux proteins. However, bacteria are also able to modify one or more important PBPs such that their affinity for the antibiotic is reduced, as is the case in peumococci. Methicillin resistant Staphylococcus aureus (MRSA) and Enterococci possess low affinity PBPs that replace the other PBPs in the presence of antibiotics. Resistance to glycopeptides was reported for the first time in enterococci in the 1980s. It results from the acquisition of genetic elements that allow the synthesis of modified peptidoglycan precursors showing a reduced binding capacity for the antibiotics. More recently, it was demonstrated that peptidoglycan has a role in innate immunity in mammals and insects and could contribute to bacterial pathogenesis.

In the last two decades, the improvement of analytical methods has shown that within a particular species, variations in peptidoglycan structure occur as a function of aging, growth medium, pathogenesis, or in the presence of antibiotics. This type of research has implications not only in the field of bacterial physiology, but also in those of innate immunity, pathogenicity, and antibacterial therapy.

Related:

• Getting bacteria into shape
• Cytoskeletal structure of Mycoplasma mobile
• Resuscitating Mycobacterium tuberculosis

Incidence of bacteriophage lysogeny in temperate and extreme soil environments

A previous study indicated that approximately 30% of cultivable soil bacteria may contain inducible prophage; however, the degree to which this cultivation-based estimate applies to indigenous soil bacteria is unknown. To estimate the prevalence of lysogeny within soil bacterial communities, induction assays were carried out by extracting bacteria from soil and subsequently exposing extracts to mitomycin C, or by exposing bacteria to mitomycin C through direct addition to soil slurries. Induction was assessed as an increase in viral direct counts relative to those obtained in controls, as detected by epifluorescence microscopy. Extracting bacteria from soils followed by 18 hours mitomycin C exposure generated significantly higher prophage induction than all other treatments. For three Antarctic soil samples, estimates of inducible fraction were statistically indistinguishable across two independent assays, indicating that this approach is highly reproducible. Although the inducible fraction was lower in Antarctic soils and higher in temperate Delaware soils (22-68%), no clear correlations were found between lysogeny and soil physical properties. For Delaware soils, inducible fraction estimates were similar between whole soil assays (44%) and cultivation-based approaches (30%). While these data suggest that lysogeny is common among soil bacteria, the specific factors which promote temperate interactions remain unclear.

Incidence of lysogeny within temperate and extreme soil environments.
Environ Microbiol. 2007 9: 2563-2574

Related:

• Bacteriophage lysogeny
• Humans in the crossfire
• Bacteriophages for plant disease control