MicrobiologyBytes

Methicillin-resistant Staphylococcus aureus (MRSA), first identified in the 1960s, was initially considered to be a nosocomial pathogen (hospital acquired infection). Beginning in the late 20th century, a specific clone of MRSA known as USA300 emerged as a leading cause of community-acquired infection, but doubts remain as to where many cases of MRSA infection originate, and how to break the transmission of this dangerous strain.

A new study finds that 8% of hospital outpatients carrying methicillin-resistant MRSA lived with an MRSA-positive pet. When faced with chronic and or recurrent MRSA cases, physicians should consider the possibility of household pets as MRSA source. Patients should be informed of this possibility. Unnecessary close contact should be avoided and heightened hygiene practices should be instituted. Sampling/swabbing of all the human and animals in a household seems appropriate to identify unrecognized sources and break potential cycles of reinfection especially in cases involving immunocompromised patients.

Transmission of MRSA between Companion Animals and Infected Human Patients Presenting to Outpatient Medical Care Facilities. PLoS ONE 6(11): e26978. doi:10.1371/journal.pone.0026978
Methicillin-resistant Staphylococcus aureus (MRSA) is a significant pathogen in both human and veterinary medicine. The importance of companion animals as reservoirs of human infections is currently unknown. The companion animals of 49 MRSA-infected outpatients (cases) were screened for MRSA carriage, and their bacterial isolates were compared with those of the infected patients using Pulsed-Field Gel Electrophoresis (PFGE). Rates of MRSA among the companion animals of MRSA-infected patients were compared to rates of MRSA among companion animals of pet guardians attending a “veterinary wellness clinic” (controls). MRSA was isolated from at least one companion animal in 4/49 (8.2%) households of MRSA-infected outpatients vs. none of the pets of the 50 uninfected human controls. Using PFGE, patient-pets MRSA isolates were identical for three pairs and discordant for one pair (suggested MRSA inter-specie transmission p-value = 0.1175). These results suggest that companion animals of MRSA-infected patients can be culture-positive for MRSA, representing a potential source of infection or re-infection for humans. Further studies are required to better understand the epidemiology of MRSA human-animal inter-specie transmission.

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Parvoviruses are small non-enveloped, icosahedral DNA viruses with a diameter of 18–26 nm that encapsidate a single-stranded genome of approximately (~)5–6 kb. To date, there are a number of parvoviruses known to infect humans, including adeno-associated viruses (AAVs), parvovirus B19 (B19V), and two newly identified human parvoviruses, which are the human bocavirus (HBoV) and human parvovirus 4 (PARV4).

HBoV was firstly identified in respiratory samples from children with lower respiratory tract infections and subsequently proven epidemiologically to be associated with the diseases. PARV4 was initially found in a blood sample from an intravenous drug user with acute viral infection syndrome. Subsequently, the PARV4 genome was detected in human plasma pools at a low titer. PARV4 had also been found in the livers of hepatitis C virus-positive individuals and the bone marrow of HIV-positive individuals. Recently, PARV4 DNA was detected in cerebrospinal fluid of two children with encephalitis of unknown etiology – however, the disease association of PARV4 remains unclear.

HBoV has been classified as a member in the genus Bocavirus based on the similarity of its genome sequence with those of the two animal bocaviruses. However, the known PARV4 incomplete genome, which lacks information of the terminal repeats, does not show a close relationship to any of the known parvoviruses in the genera of the family Parvoviridae that have been classified to date. This has led to the proposed classification of the PARV4 and PARV4-like viruses as members in a new genus called Partetravirus in the family Parvoviridae by the International Committee on Taxonomy of Viruses (ICTV).

Little is known about the gene expression of PARV4 and the function of PARV4 proteins. Since the PARV4 has not been cultured in vitro, and the full-length genome with terminal repeats has not been sequenced, researchers profiled the gene expression of PARV4 by transfecting a replication-competent PARV4 genome. This study has revelealed for the first time the detailed transcription map of PARV4, which can be beneficial for subsequent study of PARV4 infection.

Molecular characterization of the newly identified human parvovirus 4 in the family Parvoviridae. Virology. Oct 30 2011
Human parvovirus 4 (PARV4) is an emerging human virus, and little is known about the molecular aspects of PARV4 apart from its incomplete genome sequence, which lacks information of the termini. We analyzed the gene expression profile of PARV4 using a nearly full-length HPV4 genome in a replication competent system in 293 cells. We found that PARV4 utilizes two promoters to transcribe non-structural protein- and structural protein-encoding mRNAs, respectively, which were polyadenylated at the right end of the genome. Three major proteins, including the large non-structural protein NS1a, whose mRNA is spliced, and capsid proteins VP1 and VP2, were detected. Additional functional analysis of the NS1a revealed its capability to induce cell cycle arrest at G2/M phase in ex vivo-generated human hematopoietic stem cells. Taken together, our characterization of the molecular features of PARV4 suggests that PARV4 represents a new genus in the family Parvoviridae.

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The fungus Candida albicans is often a benign member of the mucosal flora; however, it commonly causes mucosal disease with substantial morbidity and in vulnerable patients it causes life-threatening bloodstream infections. A striking feature of its biology is its ability to grow in yeast, pseudohyphal and hyphal forms. The hyphal form has an important role in causing disease by invading epithelial cells and causing tissue damage. This review describes our current understanding of the network of signal transduction pathways that monitors environmental cues to activate a programme of hypha-specific gene transcription, and the molecular processes that drive the highly polarized growth of hyphae.

Growth of Candida albicans hyphae. (October 2011) Nature Reviews Microbiology 9: 737-748 doi:10.1038/nrmicro2636

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I’ve written here before about how colony-collapse disorder (CCD) is affecting bees worldwide, but this new article from Trends in Microbiology is a good insight into the current state of knowledge:

Bees brought to their knees: microbes affecting honey bee health. Trends Microbiol. Oct 25 2011
The biology and health of the honey bee Apis mellifera has been of interest to human societies for centuries. Research on honey bee health is surging, in part due to new tools and the arrival of colony-collapse disorder (CCD), an unsolved decline in bees from parts of the United States, Europe, and Asia. Although a clear understanding of what causes CCD has yet to emerge, these efforts have led to new microbial discoveries and avenues to improve our understanding of bees and the challenges they face. Here we review the known honey bee microbes and highlight areas of both active and lagging research. Detailed studies of honey bee–pathogen dynamics will help efforts to keep this important pollinator healthy and will give general insights into both beneficial and harmful microbes confronting insect colonies.

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Listeria monocytogenes is responsible for the severe foodborne disease listeriosis. During pathogenesis, invasion of nonphagocytic cells by L. monocytogenes is crucial for crossing the host epithelial barriers and colonization of multiple organs including the liver. A new study investigated the role of the pore-forming toxin listeriolysin O (LLO) in L. monocytogenes entry into human hepatocytes.

LLO belongs to the largest family of bacterial pore-forming toxins called the cholesterol-dependent cytolysins and is a major virulence factor of L. monocytogenes. The research showed that LLO is required for efficient entry of L. monocytogenes into hepatocytes and shed light on the molecular processes involved in this activity. LLO induces tyrosine kinase(s), dynamin, and F-actin-dependent formation of an internalization vesicle. Similarly to LLO, the pore-forming toxin pneumolysin regulates bacterial entry into host cells. These findings indicate that host membrane perforation by a pore-forming toxin can be used as an invasion strategy by L. monocytogenes and raises the hypothesis that other bacteria may use a similar entry pathway.

The Pore-Forming Toxin Listeriolysin O Mediates a Novel Entry Pathway of L. monocytogenes into Human Hepatocytes. (2011)PLoS Pathog 7(11): e1002356. doi:10.1371/journal.ppat.1002356
Intracellular pathogens have evolved diverse strategies to invade and survive within host cells. Among the most studied facultative intracellular pathogens, Listeria monocytogenes is known to express two invasins-InlA and InlB-that induce bacterial internalization into nonphagocytic cells. The pore-forming toxin listeriolysin O (LLO) facilitates bacterial escape from the internalization vesicle into the cytoplasm, where bacteria divide and undergo cell-to-cell spreading via actin-based motility. In the present study we demonstrate that in addition to InlA and InlB, LLO is required for efficient internalization of L. monocytogenes into human hepatocytes (HepG2). Surprisingly, LLO is an invasion factor sufficient to induce the internalization of noninvasive Listeria innocua or polystyrene beads into host cells in a dose-dependent fashion and at the concentrations produced by L. monocytogenes. To elucidate the mechanisms underlying LLO-induced bacterial entry, we constructed novel LLO derivatives locked at different stages of the toxin assembly on host membranes. We found that LLO-induced bacterial or bead entry only occurs upon LLO pore formation. Scanning electron and fluorescence microscopy studies show that LLO-coated beads stimulate the formation of membrane extensions that ingest the beads into an early endosomal compartment. This LLO-induced internalization pathway is dynamin-and F-actin-dependent, and clathrin-independent. Interestingly, further linking pore formation to bacteria/bead uptake, LLO induces F-actin polymerization in a tyrosine kinase-and pore-dependent fashion. In conclusion, we demonstrate for the first time that a bacterial pathogen perforates the host cell plasma membrane as a strategy to activate the endocytic machinery and gain entry into the host cell.

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The native conformations of viruses and toxins are assembled to withstand harsh extracellular environments, yet they efficiently disassemble upon engaging a host cell. These reactions invariably allow the virus and toxin to gain host entry. How a stably assembled virus or toxin unravels as it encounters a host cell is remarkable. What driving force harbored in a host cell untangles the numerous covalent and noncovalent forces holding these toxic agents together? What precise function does disassembly serve?

Many viruses and toxins disassemble to enter host cells and cause disease. These conformational changes must be orchestrated temporally and spatially during entry to avoid premature disassembly leading to nonproductive pathways. Although viruses and toxins are evolutionarily distinct toxic agents, emerging findings in their respective fields have revealed that the cellular locations supporting disassembly, the host factors co-opted during disassembly, the nature of the conformational changes, and the physiological function served by disassembly are strikingly conserved. This review examines some of the shared disassembly principles observed in model viruses and toxins. Where appropriate, it underscores their differences, with the intention to draw together the fields of virus and toxin cell entry by using lessons gleaned from each field to inform and benefit one another.

How Viruses and Toxins Disassemble to Enter Host Cells. (2011) Annual Review of Microbiology 65: 287-305 doi: 10.1146/annurev-micro-090110-102855

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Social behaviors are most widely recognized in communication and cooperation observed in metazoans, ranging from navigation strategies and group hierarchies in insect communities to complex social networking in humans and other primates. However, communication and cooperation among individuals in a group also occurs at the cellular level, as illustrated in collective motility of migrating cells during wound healing, tissue morphogenesis and tumor metastases. Cell-cell communication and cooperative behavior is not restricted to higher animals and recent years have seen a surge in the study and understanding of social interactions and their underlying mechanisms in microbial systems.

Parasitic protozoa are etiologic agents of several major human maladies, including malaria, epidemic dysentery, Leishmaniasis and African sleeping sickness, that affect over half a billion people worldwide. Parasites also limit economic development in some of the poorest regions on the planet and are thus major contributors to the global human health and economic burden. Parasites have complex life cycles requiring transmission through multiple hosts, survival in diverse environments and a wide variety of cellular differentiation events. Hence there are numerous facets of parasite biology that may benefit from, or may even depend upon, social interactions. This review highlights recent work on social behavior in two well-studied parasites, Trypanosoma brucei that causes sleeping sickness and Plasmodium parasites that cause malaria. In addition to uncovering underappreciated aspects of parasite biology, these studies illustrate the potential for sociomicrobiology concepts to advance understanding of the biology, transmission and pathogenesis of parasitic protozoa.

Social parasites. Curr Opin Microbiol. Oct 21 2011
Protozoan parasites cause tremendous human suffering worldwide, but strategies for therapeutic intervention are limited. Recent studies illustrate that the paradigm of microbes as social organisms can be brought to bear on questions about parasite biology, transmission and pathogenesis. This review discusses recent work demonstrating adaptation of social behaviors by parasitic protozoa that cause African sleeping sickness and malaria. The recognition of social behavior and cell-cell communication as a ubiquitous property of bacteria has transformed our view of microbiology, but protozoan parasites have not generally been considered in this context. Works discussed illustrate the potential for concepts of sociomicrobiology to provide insight into parasite biology and should stimulate new approaches for thinking about parasites and parasite-host interactions.

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