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Brogden KA, Guthmiller JM, editors. Polymicrobial Diseases. Washington (DC): ASM Press; 2002.

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Polymicrobial Diseases.

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Chapter 1Polymicrobial Diseases of Animals and Humans


Respiratory Diseases of Livestock Research Unit, National Animal Disease Center, USDA Agricultural Research Service, Ames, IA 50010.

Polymicrobial diseases represent the clinical and pathologic manifestations induced by the presence of multiple microorganisms. These are serious diseases whose etiologic agents are sometimes difficult to diagnose and treat. They are often called complex infections (136), complicated infections (26), dual infections (15, 76, 82, 186), mixed infections (40), secondary infections (179), coinfections (1, 51, 106, 123), synergistic infections (87), concurrent infections (186), or polymicrobial infections (65, 75). The multiple etiologies often induce a characteristic set of clinical signs and lesions referred to as "complexes" or syndromes. Examples include bovine respiratory disease complex (4, 126), porcine respiratory disease complex (24, 174, 176), and acquired immunodeficiency syndrome (70). Polymicrobial etiologies of multiple sclerosis in humans (39, 77, 125), poult enteritis mortality syndrome in turkeys (76, 139, 188), papillomatous digital dermatitis in dairy cattle (33, 59, 177), and postweaning multisystemic wasting syndrome in pigs (2, 3, 97) are strong suspects but yet to be proven.

Polymicrobial disease is a rapidly emerging and highly researched area, yet it represents a neglected concept. For example, in recent reviews of host-pathogen interactions, the basic concepts of virulence and pathogenicity were redefined (36, 37), and new definitions were based on a pathogen's ability to cause damage as a function of the host's immune response (37). Virulence was defined as a property of the pathogen, which is modulated by host susceptibility and resistance, and disease was defined as a complex outcome, which can arise because of pathogen-mediated damage, hostmediated damage, or both (37). Unfortunately, these were "single etiologic agent" concepts not seriously addressing polymicrobial infections and diseases.

In this book, we focus on the common theme of polymicrobial infections and, in part I, present an integrated view of polymicrobial diseases in animals and humans including a representative list of these diseases, the etiologic agents, and the underlying mechanisms of pathogenesis (chapter 1). Also included is a chapter describing the difficulties in establishing methods for their study (chapter 2). Part II discusses polyviral infections in animals (chapter 3), infections with multiple hepatotropic viruses (chapter 4), multiple retroviral infections (chapter 5), and viruses associated with multiple sclerosis (chapter 6). Part III discusses polybacterial infections and includes bacterial vaginosis (chapter 7), periodontal disease (chapter 8), abscesses (chapter 9), and atrophic rhinitis in swine (chapter 10). Part IV discusses polymicrobial diseases involving viruses and bacteria. These are the infections seen in respiratory disease in humans (chapter 11) and animals (chapters 12 and 13), otitis media (chapter 14), and intestinal disorders (chapter 15). An emerging role of viruses in periodontal disease is also discussed (chapter 16). Part V includes chapters on polymicrobial mycotic infections (chapter 17) and Candida interactions with bacterial biofilms (chapter 18). Part VI discusses polymicrobial diseases that result from microbe-induced immunosuppression (chapter 19), often allowing other microbes to become established (chapter 20). Part VII summarizes the state of polymicrobial infections in animals and humans (chapter 21).

Historical Perspective

Polymicrobial diseases are not new, and infections involving numerous pathogens were recognized early in the 20th century (87, 161). In animals, foot rot (160) and chronic nonprogressive pneumonia (40, 91, 92) in sheep were among the first diseases found to have multiple etiologies. Respiratory disease in cattle was also shown early to have multiple etiologies (66, 161), which are still being characterized (67, 164, 165). More recently, atrophic rhinitis in swine (128) and porcine respiratory disease complex (25, 68, 163, 168) have been included, the latter because of the emergence of porcine reproductive and respiratory syndrome virus (57, 180).

In humans, acute necrotizing ulcerative gingivitis (87) and respiratory disease were recognized very early as having polymicrobial etiology. In the 1920s, the polymicrobial etiology of respiratory disease was firmly established, and Haemophilus influenzae or Streptococcus pneumoniae were routinely found in individuals with viral respiratory disease (79). A similar relationship was seen during the influenza pandemics in 1918, 1957, and 1968–1969. Detailed accounts were reported earlier (12, 38, 79). In the 1968–1969 pandemic alone, a threefold increase in Staphylococcus aureus pneumonia occurred (153). Later studies confirmed the polymicrobial etiology of respiratory disease (64, 79, 81, 121, 130) and otitis media (79). In otitis media with middle ear effusion, coinfections with bacteria were detected in 65% of cases (81).

Etiologic Agents

Polymicrobial diseases in animals and humans are more common than generally realized, and many perceived "single etiologic agent diseases," when examined closely, contain polymicrobial etiologies (Table 1). These include respiratory diseases, gastroenteritis, conjunctivitis, keratitis, hepatitis, Lyme disease, multiple sclerosis, genital infections, intra-abdominal infections, and pertussis.

Table 1. Reports of polymicrobial infection and disease.

Table 1

Reports of polymicrobial infection and disease.

Polymicrobial diseases can be categorized as those originating from polyviral infections, polybacterial infections, viral and bacterial infections, polymicrobial mycotic infections, and those that result in immunosuppression (Table 2). In respiratory diseases (chapters 11 to 13), abscesses (chapter 9), and periodontal disease (chapters 8, 16, and 18), the list of potential etiologic agents is very extensive. For example, in bovine respiratory disease complex, up to 13 viruses and 12 bacteria have been described. These include infectious bovine rhinotracheitis virus, bovine viral diarrhea virus, bovine respiratory syncytial virus, parainfluenza virus, bovine herpesvirus 4, malignant catarrhal fever virus, bovine adenovirus, bovine rhinovirus, bovine reovirus, bovine calicivirus, bovine coronavirus, bovine parvovirus, or bovine enterovirus; and Mannheimia haemolytica, Pasteurella multocida, Haemophilus somnus, Arcanobacterium pyogenes, Mycoplasma bovis, Mycoplasma dispar, Mycoplasma hyorhinis, Ureaplasma diversum, Chlamydia spp., Mycobacterium bovis, S. pneumoniae, or S. aureus (4, 10, 34, 67, 94, 109, 126, 137, 165). Once the upper respiratory tract is colonized, large numbers of bacteria can enter the lung and induce severe fibrinonecrotic pneumonia (126, 182). Similarly, in porcine respiratory disease complex, up to five viruses and eight bacteria have been described and include porcine reproductive and respiratory syndrome virus, swine influenza virus, pseudorabies virus, porcine respiratory coronavirus, or porcine circovirus as well as Mycoplasma hyopneumoniae, Bordetella bronchiseptica, Actinobacillus pleuropneumoniae, P. multocida, Haemophilus parasuis, Streptococcus suis, Actinobacillus suis, or A. pyogenes (24, 25, 68, 162, 163, 168). In abscesses, aerobic, anaerobic, gram-positive, and gram-negative bacteria are present (2732). The predominant aerobic and facultative bacteria are Escherichia coli and Streptococcus spp., and the predominant anaerobes are Bacteroides spp., Peptostreptococcus spp., Clostridium spp., and Fusobacterium spp. In periodontal disease, a vast combination of bacteria, viruses, and possibly fungi are present (99, 113, 131, 132, 134, 159). Although periodontal disease is a major cause of tooth loss in adults (45, 86), periodontal infections are now thought to play a significant role in systemic health. Numerous systemic infections are thought to originate in the oral cavity (156), which may lead to an increased risk of systemic disease including coronary heart disease (13, 55, 118, 124).

Table 2. Reported examples of polymicrobial diseases.

Table 2

Reported examples of polymicrobial diseases.


Reproducing polymicrobial disease is often difficult. In some cases, polymicrobial disease can be induced by simply administering comixtures of microorganisms. This approach was successful in inducing experimental chronic nonprogressive pneumonia (40, 91, 92). In other cases, disease can only be induced by sequential administration of causative agents. This approach was successful in inducing respiratory disease in sheep (26, 51, 52, 105) and swine (25). In swine, P. multocida could not be isolated from pigs challenged with P. multocida alone or after inoculation with porcine reproductive and respiratory syndrome virus. However, P. multocida could be isolated from pigs challenged sequentially with porcine reproductive and respiratory syndrome virus, B. bronchiseptica, and P. multocida. Finally, physical stress may be required. In cattle, abrupt changes in temperature (56, 90) and exercise (6) increase the numbers of M. haemolytica in the nasopharynx, thus increasing the susceptibility of cattle to respiratory infection.

A number of models have been described to study in vivo and in vitro polymicrobial interactions in periodontal disease. In vivo models allow the study of host response to infection. Ligature-induced models of periodontitis in nonhuman primates (58), dogs (115), and rodents have helped identify the profiles of gingival crevicular fluid mediators and their relationship to gingival inflammation. In vitro models allow for the study of the oral bacterial interactions in suspension in continuous culture chemostat systems (20), constant depth film fermenters (183), and flow cells (100). These techniques have identified the parameters involved in the formation of plaque, the interactions among members of the resident flora, factors involved in the transition of the biofilm from a commensal to a pathogenic relationship with the host, and the mode of action of antimicrobials and antiplaque agents (21). More detailed information is available in chapter 2.

Common Underlying Mechanisms of Pathogenesis

Despite the spectrum of etiologic agents in Tables 1 and 2, five common underlying mechanisms exist that can lead to disease. First, physical, physiologic, or metabolic abnormalities including stress can predispose the host to polymicrobial disease (17, 41, 65). Second, alterations induced in the mucosa by one organism favor the colonization of others (79). Third, synergistic triggering of proinflammatory cytokines increases severity of disease, reactivates latent infections, or favors the colonization of other microorganisms. Fourth, sharing of determinants among organisms allows activities that neither organism possesses individually (161). Finally, obliteration of the immune system by one organism allows the colonization of others.

Stress, Physiologic Abnormalities, and Metabolic Disease Favor the Colonization of Multiple Organisms

Stress is a strong predisposing factor increasing the susceptibility of animals and humans to polymicrobial diseases. In animals, common stresses include heat, crowding, limited space, exposure to inclement weather, poor ventilation with high levels of moisture and barnyard gases, handling and transport, castration and docking, weaning and change in feed, exhaustion and hunger during transportation, excessive dust in feedlots, high loads of parasites, and mixing of animals from different sources (43, 69, 98, 114). Stressed animals usually have increased body temperature; increased heart rate; increased plasma cortisol, glucose, free fatty acids, β-hydroxybutyrate, and urea; decreased body weight; and decreased hydration (93, 98, 133, 167).

In humans, stress is also a strong predisposing factor increasing the susceptibility of individuals to polymicrobial diseases. Respiratory tract infections (17, 41, 72, 73), necrotizing ulcerative gingivitis (147), and oral infections are often used as examples. Physiologic and psychological stress increases an individual's susceptibility to upper respiratory tract infections (17, 41, 72). The stress and hassles of life events, the moderating effects of psychological coping style, social support, and family environment all influence susceptibility (41). High-stress groups experience significantly more episodes and symptom days of respiratory illness than low-stress groups (72). However, sex (female) and age also seem to be important correlates of respiratory illness (72).

Physiologic abnormalities can favor polymicrobial diseases, but only a few examples exist. In pastured and feedlot cattle, acute interstitial pneumonia is precipitated by a predisposing metabolic event that often develops into a polymicrobial disease (83, 107, 108). During anaerobic ruminal fermentation of tryptophan, 3-methylindole is produced and is absorbed across the ruminal and intestinal wall and disseminated throughout the body. Metabolism of 3-methylindole produces free radicals that contribute to cellular injury in Clara and type I alveolar epithelia in the lung. A metabolite of 3-methylindole, 3-methyleneindolenine also induces damage by covalently binding to cellular macromolecules. In some cases, cellular injury is insufficient to induce acute interstitial pneumonia without the presence of other factors, but it is thought to predispose cattle to concurrent bronchopneumonia in a mechanism involving tumor necrosis factor alpha (TNF-α) and interleukin-1β(IL-1β).

Finally, polymicrobial diseases occur in individuals with coexisting metabolic diseases. Individuals with diabetes are at risk for advanced periodontal disease (122).

Alterations in the Mucosa by One Organism Favor the Colonization of Another

Bacterial infections of mucosal surfaces may, in some instances, contribute to increased adherence and replication of other microbes. C. albicans adheres more readily to epithelial cells preincubated with staphylococcal serine protease perhaps by enzymatically altering receptors on mucosal epithelium (120). These same proteases are also thought to increase the severity of viral influenza by cleaving the viral hemagglutinin (38).

Similarly, viral infections of mucosal surfaces contribute to increased incidence of secondary bacterial infections (79). First, viruses physically damage respiratory epithelium and impair ciliary clearance of bacteria. This is seen in respiratory syncytial virus (170) and influenza virus infections (178). Second, viruses alter epithelial cell surfaces thus creating receptors for bacterial adherence (38, 79, 121). For example, during replication of influenza virus, neuraminidase and hemagglutinin are inserted into the host cell membranes serving as receptors for S. pneumoniae. Pneumococcal adherence can be blocked by treating influenza A virus-infected cells with antiviral antibodies (150) or neuraminidase (54). Similarly, during replication of respiratory syncytial virus (RSV), glycoproteins F and G are inserted into the host cell membranes serving as receptors for Neisseria meningitidis (142). Increased amounts of CD14, CD15, and CD18 are also produced which enhance the adherence of nonpiliated N. meningitidis (143). H. influenzae and S. pneumoniae adhere more readily to RSV-infected cells via P5 fimbriae-binding and platelet-activating factor, respectively. In the latter, RSV infection induces the production of TNF-αand IL-1α (48, 49), which activates production of platelet-activating factor on endothelial surfaces.

During infectious bovine rhinotracheitis virus infection in vivo, neutrophil elastase cleavage of epithelial cell surface fibronectin and exposure of receptors was thought to increase colonization of M. haemolytica (23). Elastase activity in nasal mucus of sick calves increased about 15-fold within 3 days and peaked about 60-fold over baseline by 7 days after virus exposure. Increased elastase activity preceded colonization by M. haemolytica and decreasing elastase activity preceded decreasing M. haemolytica concentration in the nasal secretions (23).

Synergistic Triggering of Proinflammatory Cytokines Increases Severity of Disease, Reactivates Latent Infections, or Favors the Colonization of Another Organism

Synergistic induction and release of proinflammatory cytokines can lead to extensive clinical and pathologic polymicrobial disease in situations where neither individual organism induces high and sustained cytokine levels alone. An excellent example of this mechanism is the lipopolysaccharide (LPS)-induced release of TNF-α and IL-1 from virus-infected cells. In vitro, mouse-adapted influenza virus, which induces minimal TNF-α in leukocyte cultures, primes cells for massive TNF-α secretion after exposure to H. influenzae LPS (127). Similarly, influenza virus alone induces a massive TNF-α accumulation in leukocytes, but efficient translation into bioactive protein occurs on further stimulation by LPS (14). In vivo, an enhanced serum TNF-α response was observed when influenza-infected mice were given an intravenous dose of LPS (116). Similarly, pigs exposed to both porcine respiratory coronavirus and LPS from E. coli O111:B4 developed severe respiratory disease (174) with significantly enhanced TNF-α and IL-1 levels. The effects of separate virus or LPS inoculations were subclinical and failed to induce high and sustained cytokine levels.

Polymicrobial infections are associated with transient bursts of human immunodeficiency virus (HIV) viremia in patients (123) involving LPS from systemic gram-negative bacterial infections (123), gut-associated bacterial translocation (123), or periodontal pathogens (11). Systemic up-regulation of monocyte proinflammatory cytokine secretion by LPS is thought to induce activation of HIV-1 from latently infected resting CD4+ T cells (123). To demonstrate this, supernatants from macrophages exposed to LPS induced the in vitro activation of HIV-1 from latently infected, resting CD4+ T cells obtained from HIV-infected individuals. Depletion of proinflammatory cytokines from the supernatant markedly reduced the ability of the supernatant to induce replication of HIV-1. Similarly, Lore et al. (110) demonstrated that infection of cultured dendritic cells, in vitro, with macrophage-tropic HIV-1 did not induce detectable cytokine or chemokine protein expression in these cells. However, LPS stimulation of HIV-1-infected dendritic cells resulted in significantly increased levels of cells producing TNF-α and IL-1β but reduced IL-1 receptor antagonist (IL-1ra). This suggests that gram-negative bacterial infection in HIV-1- infected individuals may result in endotoxin-mediated reactivation of HIV-1 in bystander CD4 CD45RO T cells caused by the increased production of proinflammatory cytokines in dendritic cells.

In patients with advanced HIV infections, systemic up-regulation of monocyte proinflammatory cytokine secretion might also occur by LPS from periodontal pathogens (11). Indeed, cultured monocytes from HIV-infected patients, incubated with Porphyromonas gingivalis or Fusobacterium nucleatum LPS, produced greater amounts of TNF-α, IL-1β, and IL-6 than monocytes from uninfected controls.

TNF-α and IL-1 also alter the expression of epithelial and endothelial cell receptors thus facilitating bacterial adherence (50). TNF-α and IL-1 increase the expression of E selectin and globotriosylceramide on vascular endothelial cells (148, 173). Similarly, these cytokines also increase glycoconjugate receptors on type II alveolar epithelium and vascular endothelium, facilitating the 30% and 70% increased attachment of S. pneumoniae, respectively (50). Enhanced S. pneumoniae adherence was associated with the appearance of new receptor specificity for GlcNAc within the Ga1NAcβ1-3Gal receptor family (50). Reciprocal changes in pneumococcal adhesive ligands matched the changes in the eucaryotic cell surface in those strains that achieved successful colonization.

Sharing of Determinants among Organisms Allows Activities that Neither Organism Possesses Individually

In 1982, Smith proposed a concept to explain how nonpathogenic or weakly pathogenic microorganisms can interact synergistically to cause harmful, even fatal, infections (161). Ovine foot rot, bovine shipping fever, periodontal disease, and abdominal abscesses were assigned to this group (161). The underlying mechanism for pathogenic synergy was thought to be the sharing of determinants among determinant-deficient organisms. Although little progress has been made in this area since then, many recent observations strongly support this concept. This may occur in multistrain infections of Mycoplasma ovipneumoniae (40, 91, 92). Sheep with severe lesions had three to four distinct M. ovipneumoniae genotypes, whereas sheep with lesser lesions had only two distinct genotypes (40). Other multistrain infections include Hemobartonella felis (181), bovine virus diarrhea virus (19), Trichophyton rubrum (60), and Dichelobacter nodosus (89). In the latter study, the proportions of protease-type D. nodosus S1, U1, and T strains in samples of foot rot lesion material were 58, 22, and 18%, respectively, at a ratio that remained constant during two apparent peaks in foot rot transmission. Although strain S1 was the dominant protease type in new clinical lesions, the occurrence of S1 strains did not increase relative to U1 and T strains. Strains S1, U1, and T remained in equilibrium despite changes in environment, genetic types in the population of S1 strains, and host resistance to foot rot. All these studies suggest that a single member of the multistrain population cannot alone produce the full complement of factors needed for disease production. Together, the full complement of factors can be attained. To what extent this concept occurs in other polymicrobial diseases such as periodontal disease and abscesses is still to be determined.

Tuomanen proposed a specific mechanism for the sharing (or piracy) of determinants (171), and this concept also helps explain the synergy between nonpathogenic or weakly pathogenic microorganisms to cause harmful, even fatal, infections (161). Bordetella pertussis produces a 220-kDa filamentous hemagglutinin capable of binding with ciliary glycoconjugates by its lectin domain, glycoconjugates in respiratory mucus by its heparin-binding domain, erythrocytes by its heparin-binding domain and N-terminal lectin domains, and leukocyte integrins by its RGD and factor X-like domains (50). B. pertussis also produces a 105-kDa pertussis toxin with the A–B architecture (50). B. pertussis infection is frequently associated with secondary infections caused by H. influenzae, S. pneumoniae, and S. aureus. Adherence of these other pathogens to cilia is usually low. In contrast, these bacteria adhere remarkably well to human cilia pretreated with B. pertussis or pertussis toxin (171). B. pertussis apparently secretes its adhesins into the environment and then recaptures them. Likewise, heterologous species of bacteria can bind to B. pertussis adhesins; this piracy may contribute to superinfection in mucosal diseases such as whooping cough. Recently, P. multocida was found to have open reading frames that encode large proteins with homology to the virulenceassociated filamentous hemagglutinin of B. pertussis (119). Whether P. multocida and B. bronchiseptica (44) share filamentous hemagglutinin leading to cocolonization (25) will have to be determined.

Obliteration of the Immune System by One Organism Allows the Colonization of Others

In poultry, infectious bursal disease virus (149, 157, 158) and hemorrhagic enteritis virus (140, 141, 149) induce an acute infection followed by immunosuppression, resulting in lowered resistance to a variety of infectious agents by destroying immunoglobulin-producing cells and altering antigen-presenting and helper T-cell functions. Chicken anemia virus (146), avian leukosis virus, reticuloendotheliosis virus (62, 111), Salmonella enterica serovar Typhimurium (80), and Bordetella avium (145) also induce immunosuppression resulting in secondary coinfections.

In pigs, porcine reproductive and respiratory syndrome virus infection destroys circulating lymphocytes, reduces numerous alveolar macrophages, and reduces mucociliary clearance of commensals (57). This leads to secondary infections with M. hyopneumoniae, P. multocida, H. parasuis, or S. suis (25, 57, 163, 168).

In ruminants, bovine respiratory syncytial virus depresses the proliferative responses of normal ovine peripheral blood lymphocytes to mitogens (95, 96). Persistent infections with bovine viral diarrhea virus also increase the vulnerability of cattle to secondary infections (138). The virus replicates in all the major lymphocyte subpopulations and in accessory cells, resulting in leukopenia that is often a sequel of infection (85). The envelope glycoprotein Erns, an RNase, totally inhibits mitogen-induced proliferation of porcine, bovine, and ovine lymphocytes and strongly inhibits protein synthesis of lymphocytes without cell membrane damage and apoptosis of lymphocytes (35).

In humans, human T-cell leukemia virus type 1 (HTLV-1) results in extensive immunosuppression leading to infections by polymicrobial diseases involving other viruses (74, 106, 152, 172), bacteria, fungi (22, 78, 184), protozoans, and parasites (71). Similarly, HIV infection induces extensive immunosuppression (42, 46, 63, 187) resulting in infections with other viruses (5, 8, 74, 77, 106, 152, 172); bacteria, especially Mycobacterium avium complex and Mycobacterium tuberculosis (46, 154); fungi (22, 70, 78, 175, 184); protozoans (104); and parasites (104). After primary infection, acute viremia occurs and is characterized by major expansions of certain subsets of CD8+ T cells (63). The virus binds to and infects a range of CD4+ leukocytes, depending on the coreceptor specificity. In addition, inappropriate immune activation and elevated secretion of certain proinflammatory cytokines occur during HIV infection; these cytokines play a role in the regulation of HIV expression in the tissues. T-cell-tropic HIV strains tend to bind to the CXCR-4 chemokine receptor (46), whereas macrophage-tropic strains tend to bind to the CCR-5 chemokine receptor (42, 187). Immunosuppression is induced in many ways. Besides depletion of virus-infected T cells, antigen-specific T-cell clones can be selectively deleted by mechanisms such as defective antigen presentation by HIV-infected macrophages (46). HIV infection of CD4+ T cells also results in inducing the secretion of proinflammatory cytokines that the virus uses to its own replicative advantage (42). All this leads to falling T-cell counts, B-cell dysregulation, and macrophage dysfunction (46). Opportunistic infections exploit this immunosuppressed environment.


Polymicrobial diseases in animals and humans are induced by polyviral infections (chapters 3 to 6), polybacterial infections (chapters 7 to 10), polymicrobial infections involving viruses and bacteria (chapters 11 to 16), polymicrobial infections involving fungi and parasites (chapters 17 and 18), and polymicrobial infections as a result of microbe-induced immunosuppression (chapters 19 and 20). They are serious diseases whose etiologic agents are sometimes difficult to diagnose and treat. Five common mechanisms of disease pathogenesis exist. First, physical, physiologic, or metabolic abnormalities and stress predispose the host to polymicrobial disease. Second, one organism induces changes in the mucosa that may favor the colonization of others. Third, microorganisms or their products trigger proinflammatory cytokines to increase the severity of disease, reactivate latent infections, or favor the colonization of other microorganisms. Fourth, organisms may share determinants among each other, which gives them the ability to damage tissue. Finally, one organism can alter the immune system, which allows the colonization of the host by other microorganisms. Many areas of study in polymicrobial diseases are in their infancy, and we hope that this text will stimulate interest and work in this evolving field.


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