chop pneumonia pathway

A Pathway for Community-Acquired Pneumonia With Rapid Conversion to Oral Therapy Improves Health Care Value Open Forum Infect Dis. Large-scale identification of virulence genes from, Lau GW, et al. Mubarak A, et al. Gutierrez-Fernandez J, et al. A Pathway for Community-Acquired Pneumonia With Rapid - PubMed Identification of an active dissaccharide unit of a glycoconjugate receptor for pneumococci attaching to human pharyngeal epithelial cells. Such signalling involves the two- On the other hand, they can cause severe disease when bacterial and host factors allow them to invade essentially sterile sites, such as the middle ear spaces, lungs, bloodstream and meninges. Many of the factors contributing to the eventual clearance of S. pneumoniae have been delineated. Host-to-host transmission of, Matthias KA, Roche AM, Standish AJ, Shchepetov M, Weiser JN. Gratz N, et al. Progression to invasive disease is more likely in young children, elderly people and patients with specific lifestyle traits and comorbidities. Klugman K. The significance of serotype replacement for pneumococcal disease and antibiotic resistance. 134). TLR2 signaling decreases transmission of, Kono M, et al. Dissemination beyond its niche along the nasal epithelium, either by aspiration, bacteraemia or local spread, can lead to invasive diseases, such as pneumonia, meningitis and otitis media. Clinical Practice Pathways . These infection studies also showed that colonization increases levels of S. pneumoniae-specific CD4+ T memory cells in the blood and lungs in humans80. Cell adhesion receptors-signaling capacity and exploitation by bacterial pathogens. Antibody blocks acquisition of bacterial colonization through agglutination. Examples of these adhesins are surface-located pneumococcal adherence and virulence protein A (PavA), PavB and enolase (Eno), all of which bind to the extracellular matrix proteins fibronectin and plasminogen3739. Pneumonia - CHOP OPEN As noted above, induction of pro-inflammatory chemokines and cytokines, upregulation of target receptors and damage to the respiratory epithelium caused by viral infection of the URT increases bacterial loads in the nasopharynx. Pathway antibiotics included levofloxacin 750 mg monotherapy or ceftriaxone 1000 mg plus azithromycin 500 mg daily. Identification of genes that contribute to the pathogenesis of invasive pneumococcal disease by in vitro transcriptomic analysis. Patients may be discharged, however, if they are breathing normally and normoxic on room air after 6-8 hours (8). Imperfect coordination chemistry facilitates metal ion release in the Psa permease. S. pneumoniae grows in both short-chain and long-chain forms. Pennington SH, et al. The pneumonia clinical pathway aids clinicians in determining the appropriate steps to be taken when evaluating and treating a child with community-acquired pneumonia. pIgR and PECAM-1 bind to pneumococcal adhesins RrgA and PspC mediating bacterial brain invasion. Infant mouse model for the study of shedding and transmission during, Rodrigues F, et al. Roche AM, Richard AL, Rahkola JT, Janoff EN, Weiser JN. and transmitted securely. The glycocalyx overlying the URT epithelium is composed of gel-like mucin glycoproteins and contains antimicrobial peptides and immunoglobulins34. Rose L, et al. Climate induces seasonality in pneumococcal transmission. The COVID-19 pandemic is a significant global event in the history of infectious diseases. McCullers J. Pneumonia lobularis, terjadi pada ujung bronkhiolus, yang . Accordingly, ply-deficient mutants, or mutants unable to form pores, show prolonged colonization and diminished production of key inflammatory mediators needed for clearance, including interleukin-1 (IL-1), CXC-motif and CC-motif chemokines, and NanA can also trigger TGF signalling pathways, leading to endothelial cell invasion108. The site is secure. type 1 interferons29,30,32. Community-Acquired Pneumonia (CAP) Evidence-Based Guideline Definition: The presence of signs and symptoms of pneumonia in a previously healthy child, due to an infection of the pulmonary parenchyma that has been acquired outside of the hospital. 1997 Mar-Apr;2(2):88. TNF drives monocyte dysfunction with age and results in impaired anti-pneumococcal immunity. Adult Pneumonia Guideline HNEH CPG xxxxx 2 of 12 CLINICAL PRACTICE GUIDELINE Glossary AFB acid fast bacilli - e.g. Free sialic acid acts as a signal that promotes. In addition, two of these surface glycosidases, Neuraminidase A (NanA) and the -galactosidase BgaA, have Musher D. How contagious are common respiratory tract infections? Ferreira DM, et al. Pre-existing S. pneumoniae colonization of contact pups inhibits the acquisition of a new strain13. Abdullahi O, et al. In addition, excess Zn released into the extracellular compartment by leukocytes poses a particular problem for invading pneumococci. Optimal utilization of carbon sources available in distinct host niches is also critical for pathogenesis. Up to 2765% of children and <10% of adults are carriers of S. pneumoniae and carriage involves a commensal relationship between the bacterium and the host1,2. By contrast, agglutinating antibodies such as anti-capsule immunoglobulin G (IgG) and IgA1 decrease shedding unless they are cleaved by the human IgA1-specific pneumococcal protease. Human nasal challenge with. PDF BAB 2 TINJAUAN PUSTAKA 2.1 Konsep Dasar Pneumonia 2.1 - Umpo Repository Janoff EN, et al. Nat Rev Microbiol. Neuraminidase A-exposed galactose promotes. PDF Community-Acquired Pneumonia (CAP)- ED Phase - Arkansas Children's Hospital These experiments were carried out with serotype-specific antibody. Trappetti C, Potter AJ, Paton AW, Oggioni MR, Paton JC. The pneumococcal serine-rich repeat protein is an intra-species bacterial adhesin that promotes bacterial aggregation in vivo and in biofilms. Hakansson A, et al. As all of these diseases are dead ends in the life cycle of the organism, the bacterial factors that cause invasive diseases must also be adaptive for colonization and/or transmission. Additive attenuation of virulence of, Chiavolini D, et al. Studies of capsule-switch mutants have shown an inverse relationship between the amount of C3b and iC3b deposition and binding to factor H, which inhibits the alternative complement pathway136. Thus, CPS and CbpA on the pneumococcal surface are both important for resistance to opsonophagocytosis. CLINICAL PATHWAY . In 2010, airborne transmission among closely housed ferrets co-infected with influenza A virus (IAV) was described8. Lack of cross-protection against invasive pneumonia caused by heterologous strains following murine. Discovery of novel pneumococcal surface antigen A (PsaA) inhibitors using a fragment-based drug design approach. Influenza promotes pneumococcal growth during coinfection by providing host sialylated substrates as a nutrient source. Other S. pneumoniae adhesins include enolase (Eno) and adherence and virulence protein A (PavA). Start: Confirmed diagnosis of pneumonia and parapneumonic effusion? Respiratory tract mucin genes and mucin glycoproteins in health and disease. These variants differ in levels of expression of key virulence proteins, such as PspA and CbpA, as well as CPS and cell wall teichoic acid. Page 1 of 14 . Streptococcus pneumoniae has a high genetic diversity, and certain lineages are particularly successful. In this regard, immunization with Ply shows no effect on shedding and transmission, even though the toxin is required for spread between pups16. Finally, pneumolysin (Ply) inhibits ciliary beating. Subsequent studies using genomic microarray analysis identified substantial differences in expression patterns of these non-traditional virulence genes between pneumococci growing in distinct host niches (nasopharynx, lungs and blood) and compared with cells grown in vitro88,89. Mina MJ. S. pneumoniae also has a surface-associated endoglycosidase, EndoD104, which releases the residual mannose3-N-acetylglucosamine2 (Man3GlcNAc2) structure from host glycoconjugates. In model systems, roughly half of adherent pneumococci enter epithelial cells via micropinocytosis and half via PAFr. However, S. pneumoniae evades clearance that is mediated by IgA1, the most abundant immunoglobulin on mucosal surfaces of the human URT26. Surface-associated lipoprotein PpmA of. Moreover, pneumococci were shown to readily switch between SpnIII alleles during progression of disease in a murine model116. Etiology: The exact etiology of pneumonia is often unidentified Lees JA, et al. Certain metals may also be deleterious in excess, and, hence, intracellular concentrations must be strictly regulated by coordination of uptake and efflux systems90. Alternatively, Ply and hydrogen peroxide (H2O2) directly damage the epithelium, and hyaluronate lyase (Hyl) and plasmin, which is bound to the pneumococcal surface through enolase (Eno), glyceralde-hyde-3-phosphate dehydrogenase (GAPDH) or CbpE, degrade the extracellular matrix. Streptococcus pneumoniae (also known as pneumococcus) is a Gram-positive, extracellular, opportunistic pathogen that colonizes the mucosal surfaces of the human This breaks down the epithelial barrier and provides a pathway for paracellular invasion. Neutrophils can readily kill phagocytized pneumococci by releasing serine proteases from neutrophil granules132. A random six-phase switch regulates pneumococcal virulence via global epigenetic changes. CbpA, as well as laminin receptor and PAFR, are also necessary for invasion of cardiomyocytes and formation of cardiac microlesions, which can occur as a complication of invasive pneumococcal disease119. Triggering inflammation and mucus secretions drives its transit to a new, more hospitable host. ABC, ATP-binding cassette; CBP, choline-binding protein; ChoP, phosphorylcholine; CPS, capsular polysaccharide; Etrx, surface-exposed thioredoxin family lipoprotein; Fe, iron; H2O2, hydrogen peroxide; iC3b, inactivated C3b; IgG, immunoglobulin G; LPXTG, sortase-anchored surface protein; MAPK, mitogen-activated protein kinase; Mn, manganese; NCSP, non-classical surface protein lacking secretion signals or anchorage motifs; NLRP3, NACHT, LRR and PYD domains-containing protein 3; PAF, platelet-activating factor ; PAFR, PAF receptor ; Pav, adherence and virulence protein; PECAM1, platelet endothelial cell adhesion molecule 1; PIGR, polymeric immunoglobulin receptor ; Ply, pneumolysin; PpmA, foldase protein PrsA ; PspA, pneumococcal surface protein A; Zn, zinc. Cremers AJ, et al. Invasion involves interaction between ChoP moieties and PAFR on the surface of cytokine-activated respiratory epithelial and vascular endothelial cells, followed by hijacking of the PAFR recycling pathway to gain entry40. The various released sugars can have substantial intracellular effects by regulating carbohydrate metabolism through the catabolite repressor CcpA102. National Library of Medicine Lemon JK, Weiser JN. Respiratory viruses augment the adhesion of bacterial pathogens to respiratory epithelium in a viral species- and cell type-dependent manner. The pneumococcal pyruvate oxidase SpxB and -glycerophosphate oxidase GlpO produce hydrogen peroxide, which also contributes to tissue damage in the lung and at the BBB127. This is the first example of a pneumococcal factor that is specifically required for transmission. These interactions can either be cooperative or competitive52. Krivan HC, Roberts DD, Ginsberg V. Many pulmonary pathogenic bacteria bind specifically to the carbohydrate sequence GalNAcb1-4 Gal found in some glycolipids. Phosphorylcholine (ChoP) on teichoic acid mimics host PAF and allows binding to its receptor. PAFR, platelet-activating factor receptor. S. pneumoniae has proved to be a truly resilient foe. Dieudonne-Vatran A, et al. Wright AK, et al. Terminal mannose can also be released from high man-nose N-glycans by an -(1,2)-mannosidase, SpGH92, and taken up by the mannose PTS. S. pneumoniae binds through ChoP to platelet-activating factor receptor (PAFR) and through CbpA to polymeric immunoglobulin receptor (PIGR), and by subverting the respective host receptor recycling pathways, it induces its own endocytosis, which is followed by release of pneumococci at the basolateral surface. The Management of Community-Acquired Pneumonia in Infants and Children Older Than 3 Months of Age: Clinical Practice Guidelines by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America. Nasal inflammation in response to infection with respiratory viruses, such as IAV, modulates the expression of pro-inflammatory chemokines, upregulates epithelial receptors used for S. pneumoniae adherence, compromises the integrity of the epithelium and provides a more nutrient-rich inflammatory milieu. Initially, patients may appear stable, but pneumonia due to aspiration and atelectasis due to surfactant inactivation or depletion may result in deterioration as long as 12 hours after the incident. Differential diagnosis of pneumonia includes asthma, chronic obstructive pulmonary disease (COPD), pulmonary edema, malignancies, non-infective consolidative processes of the lung, pleuritis, pulmonary embolism, aspiration of a foreign body, bronchiectasis, bronchiolitis, and others just to name a few. Dynamic capsule restructuring by the main pneumococcal autolysin LytA in response to the epithelium. Consider azithromycin if at risk for complicated atypical pneumonia. Zn can compete with Mn for the metal binding site in manganese ABC transporter substrate-binding lipoprotein (PsaA)95, but unlike Mn, which is passed from PsaA to the PsaBC transporter for uptake, Zn binds irreversibly to PsaA and thereby blocks the transport pathway, starving the bacterium of Mn96. the contents by NLM or the National Institutes of Health. A further issue is the rising prevalence of non-vaccine serotypes in carriage and disease (serotype replacement) as a consequence of the immune pressure from widespread use of PCv147,148. Acquisition of metal ions, particularly transition metals such as iron (Fe), manganese (Mn) and zinc (Zn), is crucial for growth and survival of S. pneumoniae in multiple host niches, where availability of free ions may be restricted. Buckwalter CM, King SJ. Pneumococcal CbpE impairs neutrophil recruitment by degrading platelet-activating factor (PAF), a host-derived inflammatory phospholipid. Richard AL, Siegel SJ, Erikson J, Weiser JN. A clinical pathway is a multidisciplinary management tool based on evidence-based practice for a specific group of patients with a predictable clinical course, in which the different tasks (interventions) by the professionals involved in the patient care are defined, optimized and sequenced either by hour (ED), day (acute care) or visit . Most studies of pneumococcal biofilms have been carried out in vitro, and in vivo data are limited. Competing interests: The authors declare no competing interests. Large-scale identification of serotype 4. Endopeptidase (PepO), which is released from the pneumococcal surface, binds to C1q and thereby depletes complement components. Capsular serotypes differ in the effectiveness with which they inhibit opsonophagocytosis and the level of inhibition correlates with their ability to cause invasive disease. Malley R, et al. CbpL facilitates migration of S. pneumoniae from the nasopharynx to the lungs and blood46. Microarray analysis of pneumococcal gene expression during invasive disease. Positive feedback and additional recruitment of macrophages are required for the gradual elimination of colonization69. CbpA also binds to polymeric immunoglobulin receptor (PIGR) to promote adherence. As an extracellular pathogen, S. pneumoniae must evade neutrophil-mediated killing to survive the acute inflammation that accompanies tissue invasion. Biofilm formation enhances fomite survival of, Verhagen LM, et al. Kietzman CC, Gao G, Mann B, Myers L, Tuomanen EI. COMPLICATED COMMUNITY ACQUIRED PNEUMONIA (CAP) ALGORITHM . Early respiratory microbiota composition determines bacterial succession patterns and respiratory health in children. Furthermore, many S. pneumoniae strains are not piliated and thus cannot use RrgA-dependent pathways. This infant mouse model has now enabled the study of the major steps during host-to-host spread, including exit from a colonized host (shedding), survival in the environment and acquisition by a new host. Many of these have previously been shown to contribute to growth and survival in vivo102. Carriers can shed S. pneumoniae in nasal secretions and thereby transmit the bacterium. PspA also binds to lactoferrin to acquire iron and blocks the antimicrobial effect of apolactoferrin. A dynamic relationship between mucosal T helper type 17 and regulatory T-cell populations in nasopharynx evolves with age and associates with the clearance of pneumococcal carriage in humans. In a model of experimental human colonization with S. pneumoniae, levels of CPS-specific memory B cells correlate with protection from acquisition27. Clinical Pathways Program | Children's Hospital of Philadelphia The biology of pneumolysin. Roles of CHOP/GADD153 in endoplasmic reticulum stress Subversion of the PIGR recycling pathway enables internalization and transmigration of S. pneumoniae across polarized epithelial cell monolayers41. The protective activity of specific antibodies during acquisition is independent of Pneumocystis jirovecii is one of the most common pathogens causing interstitial pneumonia, and increasing evidences suggest that R-CHOP may increase the risk of PJP with reported incidence of 5%. Influenza A virus facilitates. Novel analysis of immune cells from nasal microbiopsy demonstrates reliable, reproducible data for immune populations, and superior cytokine detection compared to nasal wash. Zhang Z, Clarke T, Weiser J. complicated effusion pathway. This effect can be explained by toxin dependent inflammation and, consequently, increased nutrients levels in secretions. SpsA, a novel pneumococcal surface protein with specific binding to secretory immunoglobulin A and secretory component. Furthermore, the effectiveness of S. pneumoniae agglutination of airway secretions after PCV vaccination correlates with protection during experimental human colonization28. LuxS mediates iron-dependent biofilm formation, competence, and fratricide in. Extracellular matrix formation enhances the ability of, Blanchette KA, et al. ChoPPAFR and CbpAPIGR interactions also enable pneumococci to traverse the endothelium and enter the bloodstream. McCullers JA, Rehg JE. Manso AS, et al. Clinical isolates of, Kohler S, et al. The released sugars (sialic acid, galactose and N-acetylglucosamine) may then be taken up by the relevant ABC and PTS transporters and metabolized. Such non-haematogenous spread is stimulated by exogenous sialic acid106. A functional genomic analysis of type 3, Hava DL, Camilli A. Federal government websites often end in .gov or .mil. A clinical pathway for community-acquired pneumonia: an - PubMed an important source of strain-to-strain variation is the structure of the capsular polysaccharide (CPs), which is the major virulence determinant and immunodominant surface structure of S. pneumoniae. Community Acquired Pneumonia Clinical Pathway All Settings The capsule layer shields underlying surface adhesins, and mutants with reduced shedding and transmission showed increased binding to URT mucins in an in vitro assay. Sanchez CJ, et al. On the one hand, the pneumococci are highly adapted commensals, and their main reservoir on the mucosal surface of the upper airways of carriers enables transmission. FOIA An overview of pneumococcal surface proteins and other factors contributing to adherence and invasion is provided in Table 1. Yuste J, Botto M, Paton JC, Holden DW, Brown JS. S. pneumoniae uses several surface components for binding, but their relative importance in natural carriage has not been established. The cellular immune responses to S. pneumoniae are greatly accelerated by cytosolic sensing of the pathogen, which requires the pore-forming function of Ply29,30. Leloir pathway105. However, pneumococci markedly reduce capsule thickness when in close contact with epithelial cells and during the invasion process123. Nelson AL, et al. Relationships between rhinitis symptoms, respiratory viral infections and nasopharyngeal colonization with, Zafar MA, Wang Y, Hamaguchi S, Weiser JN. Zhang JR, et al. Polysaccharide-specific memory b cells predict protection against experimental human pneumococcal carriage. Clinical Pathways Program | Children's Hospital of Philadelphia Protection against nasopharyngeal colonization by. Streptococcus pneumoniae is found predominantly in the mucus layer overlying the epithelial surface of the upper respiratory tract. The remarkable capacity of S. pneumoniae to remodel its genome through the uptake and incorporation of exogenous DNA ( This process of capsule shedding has recently been shown to depend on the major pneumococcal autolysin LytA and is triggered by exposure to cationic antimicrobial peptides that are released by the host cells124. Passive immunization of contact pups with anti-capsular polysaccharide immunoglobulin G (IgG) is also sufficient to block acquisition, although this effect requires high levels of antibody and can be overcome by a large inoculum25. New Pathways Torticollis, Outpatient Specialty Care, Primary Care Posted June 2023 Somatic Symptom and Related Disorders (SSRD), ED and Inpatient Posted May 2023 Prolonged QTc, Inpatient Posted March 2023 Anti-NMDAR Encephalitis, Inpatient Posted January 2023 Bacterial exploitation of phosphorylcholine mimicry suppresses inflammation to promote airway infection. The authors thank J. Pagano for editorial assistance. Rather than looking at it as a single disease, health care professionals must remember that pneumonia is an umbrella term for a group of syndromes caused by a variety of organisms resulting in varied manifestations and sequelae. This facilitates bacterial transmission but also increases the likelihood of penetration of host tissues and progression to localized or invasive disease. S. pneumoniae, like other residents of the URT, is found predominantly in and on this mucus layer35. The TRAIL-R1/DR4 death receptors can be activated by ER stress. Agglutination by anti-capsular polysaccharide antibody is associated with protection against experimental human pneumococcal carriage. Wright AK, et al. PavB is a surface-exposed adhesin of. Some serotype-switch mutants colonized at wild-type levels but were shed and transmitted poorly in infant mice. Deglycosylation of human glycoconjugates by the sequential activities of exoglycosidases expressed by, Robb M, et al. Author H Zhang. Counago RM, et al. Hergott CB, et al. IAV-induced inflammation stimulates both the expression of mucin glycoproteins and the flow of mucus10,11. The C/EBP Homologous Protein (CHOP) Transcription Factor Functions in Transmission through secretions of carriers could involve direct person-to-person contact or spread involving bacteria on contaminated surfaces. The size of population bottlenecks in the infant mouse model during transmission was estimated by using marked isogenic bacterial strains13. The pneumonia clinical pathway that was implemented was associated with reductions in the length of stay and total charges. The importance of TH17 immunity in natural colonization has yet to be confirmed, although a low ratio of TH17 to T regulatory (Treg) cells correlates with colonization in children and increases with age as colonization frequency decreases84. Jochems SP, et al. Such memory B cells can quickly differentiate into antibody-secreting plasma cells following antigen exposure. Nakamura S, Davis K, Weiser J. Synergistic stimulation of type I interferons during influenza virus coinfection promotes Streptococcus pneumonia e colonization in mice. Local spread, aspiration or seeding to the bloodstream results in invasive inflammatory diseases3 (Fig. Streptococcus pneumoniae evades entrapment in mucus and mucociliary clearance by negatively charged capsular polysaccharide (CPS) and proteolytic degradation of secretory immunoglobulin A1 (IgA1) by the zinc metalloprotease ZmpA (also known as IgA1 protease). Binding of vitronectin and Factor H to Hic contributes to immune evasion of, Tu AH, Fulgham RL, McCrory MA, Briles DE, Szalai AJ. An additional effect of immunity demonstrated in the infant mouse model is a decrease in shedding by index pups24. Diverse ecological strategies are encoded by, Dawid S, Roche A, Weiser J. Individual carriage episodes typically last for weeks to months. Controlled human infection and rechallenge with Streptococcus pneumonia e reveals the protective efficacy of carriage in healthy adults. 3). Uchiyama S, et al. On the other hand, CPSs, which are almost all negatively charged, repel the sialic acid-rich mucopolysaccha-rides in mucus36. It has overcome selective pressure from multiple classes of antibiotics and now seems to be adapting to the immune pressure of widespread immunization. Streptococcus pneumoniae as a complex relationship with its obligate human host. The combined functions of PspA and Ply are essential for S. pneumoniae to successfully cause septicaemia142. Diagnosis and treatment of rhinovirus respiratory infections restriction-modification system, SpnIII, within a genetic locus containing inverted repeats that enable spontaneous rearrangement of alternative specificity domain genes. A more recent study has shown that the underlying mechanism involves a type I Lipsitch M, Moxon ER. The roles of transition metals in the physiology and pathogenesis of, McAllister LJ, et al. Pneumonia Pathology - PubMed In these niches, pneumococci scavenge sugars by sequential cleavage of host cell surface N-linked glycoconjugates, which is mediated by surface-associated exoglycosidases such as NanA, BgaA and the -N-acetylglucosaminidase StrH. The prominence of S. pneumoniae as a cause of disease is due to the combination of high carriage rates, its genetic adaptability and its ability to shift from a commensal to a pathogenic interaction with its host. Ogunniyi AD, et al. Topics include: diagnosing viral vs. bacterial pneumonia, use/mis-use of antibiotics, current/future research on pneumonia and more. Rose MC, Voynow JA. mucociliary flow. Negatively charged capsular polysaccharide (CPS) inhibits bacterial mucus entrapment. From an evolutionary perspective, stable nasopharyngeal colonization ought to be the principal modus operandi of S. pneumoniae, as this enables ready transmission to new hosts. One of the most notable examples is Ply, which, in addition to wide-ranging pro-inflammatory effects, directly lyses or induces apoptosis of diverse cell types, including lung epithelium and endothelial cells at the BBB125. The infectious etiology of CAP can be viral or bacterial (both typical and atypical). A recent report has also suggested that NanA-mediated cleavage of sialic acid promotes biofilm formation in vivo and increases carbon availability during colonization112. Illustration of pneumococcal polysaccharide capsule during adherence and invasion of epithelial cells. Laminin receptor initiates bacterial contact with the blood brain barrier in experimental meningitis models. Furthermore, Ply released from the bacterium activates the classical complement pathway through a domain with structural similarity to the Fc component of IgG, thereby depleting serum opsonic activity125,141.
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