Impacts of brood parasitism by shiny cowbird Molothrus bonariensis on the breeding success of a small host, the black-backed water tyrant Fluvicola albiventer.

The shiny cowbird Molothrus bonariensis parasitizes many species with different life-history traits and has a detrimental effect on the survival of the progeny of the hosts. In response, hosts have developed numerous antiparasitic defenses. Here, we examined the effects of brood parasitism by shiny cowbird on the clutch and brood sizes (83 nests) in a small host, the black-backed water tyrant Fluvicola albiventer. We also studied whether the death of parasite nestlings was related to the care of the foster parents and whether the host had any antiparasitic defense against the shiny cowbird. Our results indicate that brood parasitism significantly decreased the host hatching and fledging successes. The majority of nest failures (57%) were caused by brood parasitism. Shiny cowbird parasitism occurred in 52% of nests and the intensity of parasitism was 1.23 ± 0.53 eggs per parasitized nest. Of the total host eggs, 54% were damaged. During the incubation stage, 20 nests (47%) were abandoned because of egg punctures by shiny cowbirds females. Only two parasitic fledglings were recorded, while the remaining nestlings either died from starvation (n = 12) or predation (n = 3). Foster parents abandoned parasitic nestlings between 5 and 10 days old. Our findings demonstrate that the shiny cowbird has very low rates of fledging success when parasitizing black-backed water tyrant. Also, parasitism had a high reproductive cost in the black-backed water tyrant because a very low proportion (7%) of the parasitized nests (n = 43) were successful.

Acute Necrotizing Ulcerative Gingivitis: A Case Report.

Compared to other conditions found in the necrotizing periodontal diseases group, acute necrotizing ulcerative gingivitis (ANUG) is a definite and specific disease. This illness has a long history that originates from the time of Hippocrates and is also referred to by several synonyms. ANUG occurs less commonly than other oral disorders, even though it is typically not rare. It starts suddenly, advances quickly, and finally results in significant loss of alveolar bone and soft tissue. Viral microorganisms and weakened host defenses have been linked to the etiology and pathophysiology of ANUG. In situations where there is psychological and physiological stress, the incidence of ANUG rises. In developed nations, the incidence of ANUG has declined and, in some cases, gone extinct due to the development of antibiotics and improved nutritional status. However, due to the persistently low nutritional status, the illness continues to be a frequently diagnosed clinical lesion in developing nations. This case report presents the case of a 24-year-old ANUG patient and the sequential treatment of this patient.

Urban living can rescue Darwin's finches from the lethal effects of invasive vampire flies.

Human activity changes multiple factors in the environment, which can have positive or negative synergistic effects on organisms. However, few studies have explored the causal effects of multiple anthropogenic factors, such as urbanization and invasive species, on animals and the mechanisms that mediate these interactions. This study examines the influence of urbanization on the detrimental effect of invasive avian vampire flies (Philornis downsi) on endemic Darwin's finches in the Galápagos Islands. We experimentally manipulated nest fly abundance in urban and non-urban locations and then characterized nestling health, fledging success, diet, and gene expression patterns related to host defense. Fledging success of non-parasitized nestlings from urban (79%) and non-urban (75%) nests did not differ significantly. However, parasitized, non-urban nestlings lost more blood, and fewer nestlings survived (8%) compared to urban nestlings (50%). Stable isotopic values (δ15 N) from urban nestling feces were higher than those from non-urban nestlings, suggesting that urban nestlings are consuming more protein. δ15 N values correlated negatively with parasite abundance, which suggests that diet might influence host defenses (e.g., tolerance and resistance). Parasitized, urban nestlings differentially expressed genes within pathways associated with red blood cell production (tolerance) and pro-inflammatory response (innate immunological resistance), compared to parasitized, non-urban nestlings. In contrast, parasitized non-urban nestlings differentially expressed genes within pathways associated with immunoglobulin production (adaptive immunological resistance). Our results suggest that urban nestlings are investing more in pro-inflammatory responses to resist parasites but also recovering more blood cells to tolerate blood loss. Although non-urban nestlings are mounting an adaptive immune response, it is likely a last effort by the immune system rather than an effective defense against avian vampire flies since few nestlings survived.

Abscisic Acid: A Potential Secreted Effector Synthesized by Phytophagous Insects for Host-Plant Manipulation.

Abscisic acid (ABA) is an isoprenoid-derived plant signaling molecule involved in a wide variety of plant processes, including facets of growth and development as well as responses to abiotic and biotic stress. ABA had previously been reported in a wide variety of animals, including insects and humans. We used high-performance liquid chromatography-electrospray ionization tandem mass spectrometry (HPLC-(ESI)-MS/MS) to examine concentrations of ABA in 17 species of phytophagous insects, including gall- and non-gall-inducing species from all insect orders with species known to induce plant galls: Thysanoptera, Hemiptera, Lepidoptera, Coleoptera, Diptera, and Hymenoptera. We found ABA in insect species in all six orders, in both gall-inducing and non-gall-inducing species, with no tendency for gall-inducing insects to have higher concentrations. The concentrations of ABA in insects often markedly exceeded those typically found in plants, suggesting it is highly improbable that insects obtain all their ABA from their host plant via consumption and sequestration. As a follow-up, we used immunohistochemistry to determine that ABA localizes to the salivary glands in the larvae of the gall-inducing Eurosta solidaginis (Diptera: Tephritidae). The high concentrations of ABA, combined with its localization to salivary glands, suggest that insects are synthesizing and secreting ABA to manipulate their host plants. The pervasiveness of ABA among both gall- and non-gall-inducing insects and our current knowledge of the role of ABA in plant processes suggest that insects are using ABA to manipulate source-sink mechanisms of nutrient allocation or to suppress host-plant defenses. ABA joins the triumvirate of phytohormones, along with cytokinins (CKs) and indole-3-acetic acid (IAA), that are abundant, widespread, and localized to glandular organs in insects and used to manipulate host plants.

Manipulation of host immune defenses by effector proteins delivered from multiple secretion systems of Salmonella and its application in vaccine research.

Salmonella is an important zoonotic bacterial species and hazardous for the health of human beings and livestock globally. Depending on the host, Salmonella can cause diseases ranging from gastroenteritis to life-threatening systemic infection. In this review, we discuss the effector proteins used by Salmonella to evade or manipulate four different levels of host immune defenses: commensal flora, intestinal epithelial-mucosal barrier, innate and adaptive immunity. At present, Salmonella has evolved a variety of strategies against host defense mechanisms, among which various effector proteins delivered by the secretory systems play a key role. During its passage through the digestive system, Salmonella has to face the intact intestinal epithelial barrier as well as competition with commensal flora. After invasion of host cells, Salmonella manipulates inflammatory pathways, ubiquitination and autophagy processes with the help of effector proteins. Finally, Salmonella evades the adaptive immune system by interfering the migration of dendritic cells and interacting with T and B lymphocytes. In conclusion, Salmonella can manipulate multiple aspects of host defense to promote its replication in the host.

Elevated nest temperature has opposing effects on host species infested with parasitic nest flies.

Environmental factors, such as elevated temperature, can have varying effects on hosts and their parasites, which can have consequences for the net outcome of this relationship. The individual direct effects of temperature must be disentangled to determine the net-effect in host-parasite relationships, yet few studies have determined the net-effects in a multi-host system. To address this gap, we experimentally manipulated temperature and parasite presence in the nests of two host species infested by parasitic blowflies (Protocalliphora sialia). We conducted a factorial experiment by increasing temperature (or not) and removing all parasites (or not) in the nests of eastern bluebirds (Sialia sialis) and tree swallows (Tachycineta bicolor). We then measured nestling morphometrics, blood loss, and survival and quantified parasite abundance. We predicted that if temperature had a direct effect on parasite abundance, then elevated temperature would cause similar directional effects on parasite abundance across host species. If temperature had a direct effect on hosts, and therefore an indirect effect on the parasite, parasite abundance would differ across host species. Swallow nests with elevated temperature had fewer parasites compared to nests without temperature manipulation. In contrast, bluebird nests with elevated temperatures had more parasites compared to nests without temperature manipulation. The results of our study demonstrate that elevated temperature can have differential effects on host species, which can impact infestation susceptibility. Furthermore, changing climates could have complex net-effects on parasite fitness and host health across multi-host-parasite interactions.

Altered transcriptional responses in the lungs of aged mice after influenza infection.

BACKGROUND: Influenza causes a serious infection in older individuals who are at the highest risk for mortality from this virus. Changes in the immune system with age are well known. This study used transcriptomic analysis to evaluate how aging specifically affects the functional host response to influenza in the lung. Adult (12-16 weeks) and aged (72-76 weeks) mice were infected with influenza and lungs were processed for RNA analysis. RESULTS: Older mice demonstrated a delayed anti-viral response on the level of transcription compared to adults, similar to the immunologic responses measured in prior work. The transcriptional differences, however, were evident days before observable differences in the protein responses described previously. The transcriptome response to influenza in aged mice was dominated by immunoglobulin genes and B cell markers compared to adult animals, suggesting immune dysregulation. Despite these differences, both groups of mice had highly similar transcriptional responses involving non-immune genes one day after inoculation and T cell genes during resolution. CONCLUSIONS: These results define a delayed and dysregulated immune response in the lungs of aged mice infected with influenza. The findings implicate B cells and immunoglobulins as markers or mechanisms of immune aging. In addition to discovering new therapeutic targets, the findings underscore the value of transcription studies and network analysis to characterize complex biological processes, and serve as a model to analyze the susceptibility of the elderly to infectious agents.

Under the Radar: Strategies Used by Helicobacter pylori to Evade Host Responses.

The body depends on its physical barriers and innate and adaptive immune responses to defend against the constant assault of potentially harmful microbes. In turn, successful pathogens have evolved unique mechanisms to adapt to the host environment and manipulate host defenses. Helicobacter pylori (Hp), a human gastric pathogen that is acquired in childhood and persists throughout life, is an example of a bacterium that is very successful at remodeling the host-pathogen interface to promote a long-term persistent infection. Using a combination of secreted virulence factors, immune subversion, and manipulation of cellular mechanisms, Hp can colonize and persist in the hostile environment of the human stomach. Here, we review the most recent and relevant information regarding how this successful pathogen overcomes gastric epithelial host defense responses to facilitate its own survival and establish a chronic infection.

Viral Decoys: The Only Two Herpesviruses Infecting Invertebrates Evolved Different Transcriptional Strategies to Deflect Post-Transcriptional Editing.

The highly versatile group of Herpesviruses cause disease in a wide range of hosts. In invertebrates, only two herpesviruses are known: the malacoherpesviruses HaHV-1 and OsHV-1 infecting gastropods and bivalves, respectively. To understand viral transcript architecture and diversity we first reconstructed full-length viral genomes of HaHV-1 infecting Haliotis diversicolor supertexta and OsHV-1 infecting Scapharca broughtonii by DNA-seq. We then used RNA-seq over the time-course of experimental infections to establish viral transcriptional dynamics, followed by PacBio long-read sequencing of full-length transcripts to untangle viral transcript architectures at two selected time points. Despite similarities in genome structure, in the number of genes and in the diverse transcriptomic architectures, we measured a ten-fold higher transcript variability in HaHV-1, with more extended antisense gene transcription. Transcriptional dynamics also appeared different, both in timing and expression trends. Both viruses were heavily affected by post-transcriptional modifications performed by ADAR1 affecting sense-antisense gene pairs forming dsRNAs. However, OsHV-1 concentrated these modifications in a few genomic hotspots, whereas HaHV-1 diluted ADAR1 impact by elongated and polycistronic transcripts distributed over its whole genome. These transcriptional strategies might thus provide alternative potential roles for sense-antisense transcription in viral transcriptomes to evade the host's immune response in different virus-host combinations.

Rickettsia-host interaction: strategies of intracytosolic host colonization.

Bacterial infection is a highly complex biological process involving a dynamic interaction between the invading microorganism and the host. Specifically, intracellular pathogens seize control over the host cellular processes including membrane dynamics, actin cytoskeleton, phosphoinositide metabolism, intracellular trafficking and immune defense mechanisms to promote their host colonization. To accomplish such challenging tasks, virulent bacteria deploy unique species-specific secreted effectors to evade and/or subvert cellular defense surveillance mechanisms to establish a replication niche. However, despite superficially similar infection strategies, diverse Rickettsia species utilize different effector repertoires to promote host colonization. This review will discuss our current understandings on how different Rickettsia species deploy their effector arsenal to manipulate host cellular processes to promote their intracytosolic life within the mammalian host.

The Micro-Immunotherapy Medicine 2LEID Exhibits an Immunostimulant Effect by Boosting Both Innate and Adaptive Immune Responses.

This study aimed at evaluating the effects of the micro-immunotherapy medicine (MIM) 2LEID, both in vitro and in vivo, on several components of the innate and adaptive immune system. MIM increased the phagocytic activity of macrophages, and it augmented the expression of the activation markers CD69 and HLA-DR in NK cells and monocytes/macrophages, respectively. The effect of MIM was evaluated in a model of respiratory infection induced by influenza A virus administration to immunocompetent mice in which it was able to improve neutrophil recruitment within the lungs (p = 0.1051) and slightly increased the circulating levels of IgM (p = 0.1655). Furthermore, MIM stimulated the proliferation of CD3-primed T lymphocytes and decreased the secretion of the immunosuppressive cytokine IL-10 in CD14+-derived macrophages. Human umbilical vein endothelial cells were finally used to explore the effect of MIM on endothelial cells, in which it slightly increased the expression of immune-related markers such as HLA-I, CD137L, GITRL, PD-L1 and ICAM-1. In conclusion, the present study suggests that MIM might be a promising nonspecific (without antigen specificity) immunostimulant drug in preventing and early treating respiratory infections, but not only exclusively, as it would gently support several facets of the immune system and host defenses.

SERINC5 Inhibits HIV-1 Infectivity by Altering the Conformation of gp120 on HIV-1 Particles.

SERINC5 is a 10-transmembrane-domain cellular protein that is incorporated into budding HIV-1 particles and reduces HIV-1 infectivity by inhibiting virus-cell fusion. HIV-1 susceptibility to SERINC5 is determined by sequences in the viral Env glycoprotein gp120, and the antiviral effect of SERINC5 is counteracted by the viral accessory protein Nef. While the precise mechanism by which SERINC5 inhibits HIV-1 infectivity is unclear, previous studies have suggested that SERINC5 affects Env conformation. To define the effects of SERINC5 on Env conformation, we quantified the binding of HIV-1 particles to immobilized Env-specific monoclonal antibodies. We observed that SERINC5 reduced the binding of HIV-1 particles bearing a SERINC5-susceptible Env to antibodies that recognize the V3 loop, a soluble CD4 (sCD4)-induced epitope, and an N-linked glycan. In contrast, SERINC5 did not alter the capture of HIV-1 particles bearing the SERINC5-resistant Env protein. Moreover, the effect of SERINC5 on antibody-dependent virus capture was abrogated by Nef expression. Our results indicate that SERINC5 inhibits HIV-1 infectivity by altering the conformation of gp120 on virions and/or physical masking of specific HIV-1 Env epitopes.IMPORTANCE SERINC5 is a host cell protein that inhibits the infectivity of HIV-1 by a novel and poorly understood mechanism. Here, we provide evidence that the SERINC5 protein alters the conformation of the HIV-1 Env proteins and that this action is correlated with SERINC5's ability to inhibit HIV-1 infectivity. Defining the specific effects of SERINC5 on the HIV-1 glycoprotein conformation may be useful for designing new antiviral strategies targeting Env.

A tradeoff between tolerance and resistance to a major fungal pathogen in elite wheat cultivars.

Tolerance and resistance represent two strategies that hosts evolved to protect themselves from pathogens. Tolerance alleviates the reduction in host fitness due to infection without reducing a pathogen's growth, whereas resistance reduces pathogen growth. We investigated the tolerance of wheat to the major fungal pathogen Zymoseptoria tritici in 335 elite wheat cultivars. We used a novel digital phenotyping approach that included 11 152 infected leaves and counted 2069 048 pathogen fruiting bodies. We discovered a new component of tolerance that is based on the relationship between the green area remaining on a leaf and the number of pathogen fruiting bodies. We found a negative correlation between tolerance and resistance among intolerant cultivars, presenting the first compelling evidence for a tradeoff between tolerance and resistance to plant pathogens. Surprisingly, the tradeoff arises due to limits in the host resources available to the pathogen and not due to metabolic constraints, contrary to what ecological theory suggests. The mechanism underlying this tradeoff may be relevant for many plant diseases in which the amount of host resources available to the pathogen can limit the pathogen population. Our analysis indicates that European wheat breeders may have selected for tolerance instead of resistance to an important pathogen.

Analysis of Leukocyte Behaviors on Microfluidic Chips.

The orchestration of massive leukocytes in the immune system protects humans from invading pathogens and abnormal cells in the body. So far, researches focusing on leukocyte behaviors are performed based on both in vivo and in vitro models. The in vivo animal models are usually less controllable due to their extreme complexity and nonignorable species issue. Therefore, many researchers turn to in vitro models. With the advances in micro/nanofabrication, the microfluidic chip has emerged as a novel platform for model construction in multiple biomedical research fields. Specifically, the microfluidic chip is used to study leukocyte behaviors, due to its incomparable advantages in high throughput, precise control, and flexible integration. Moreover, the small size of the microstructures on the microfluidic chip can better mimic the native microenvironment of leukocytes, which contributes to a more reliable recapitulation. Herein are reviewed the recent advances in microfluidic chip-based leukocyte behavior analysis to provide an overview of this field. Detailed discussions are specifically focused on host defense against pathogens, immunodiagnosis, and immunotherapy studies on microfluidic chips. Finally, the current technical challenges are discussed, as well as possible innovations in this field to improve the related applications.

Widespread occurrence of the antifungal cutaneous bacterium Janthinobacterium lividum on Andean water frogs threatened by fungal disease.

Amphibian diversity has declined due to the infectious disease chytridiomycosis, caused by the fungal pathogen Batrachochytrium dendrobatidis (Bd). Coexistence between amphibian hosts and this pathogen in some locations is attributed to the presence of the cutaneous bacterium Janthinobacterium lividum (Jliv). This microbe inhibits the growth of Bd on the host, reduces morbidity, and improves survival. Andean water frogs in the genus Telmatobius seem to be particularly vulnerable to the disease yet populations of T. intermedius and T. marmoratus persist in southern and central Peru. We investigated the presence of Jliv on these 2 frog species and assessed the relationship of Jliv presence with prevalence and intensity of Bd infection. By sampling 125 frogs from 7 streams (3323-3950 m a.s.l.) and 27 from a city market, we found spatial variation in the mutualism among populations (range 0-40% proportion of Jliv-positives). Overall, 57% of frogs were infected with Bd, 12.5% of frogs hosted both Jliv and Bd, while 7.2% hosted just Jliv. We found that the probability of an individual being infected with Bd was independent of the presence of Jliv; however, we did detect a protective effect of Jliv with respect to intensity of infection. The extent of Jliv distribution in the high Andes stands in stark contrast to the rarity of Jliv on frogs in lower elevation cloud forest biomes.

The Pathogenesis of Staphylococcus aureus Eye Infections.

Staphylococcus aureus is a major pathogen of the eye able to infect the tear duct, eyelid, conjunctiva, cornea, anterior and posterior chambers, and the vitreous chamber. Of these infections, those involving the cornea (keratitis) or the inner chambers of the eye (endophthalmitis) are the most threatening because of their potential to cause a loss in visual acuity or even blindness. Each of these ocular sites is protected by the constitutive expression of a variety of antimicrobial factors and these defenses are augmented by a protective host response to the organism. Such infections often involve a predisposing factor that weakens the defenses, such as the use of contact lenses prior to the development of bacterial keratitis or, for endophthalmitis, the trauma caused by cataract surgery or intravitreal injection. The structural carbohydrates of the bacterial surface induce an inflammatory response able to reduce the bacterial load, but contribute to the tissue damage. A variety of bacterial secreted proteins including alpha-toxin, beta-toxin, gamma-toxin, Panton-Valentine leukocidin and other two-component leukocidins mediate tissue damage and contribute to the induction of the inflammatory response. Quantitative animal models of keratitis and endophthalmitis have provided insights into the S. aureus virulence and host factors active in limiting such infections.

Simultaneous RNA-seq based transcriptional profiling of intracellular Brucella abortus and B. abortus-infected murine macrophages.

Brucella is a zoonotic pathogen that survives within macrophages; however the replicative mechanisms involved are not fully understood. We describe the isolation of sufficient Brucella abortus RNA from primary host cell environment using modified reported methods for RNA-seq analysis, and simultaneously characterize the transcriptional profiles of intracellular B. abortus and bone marrow-derived macrophages (BMM) from BALB/c mice at 24 h (replicative phase) post-infection. Our results revealed that 25.12% (801/3190) and 16.16% (515/3190) of the total B. abortus genes were up-regulated and down-regulated at >2-fold, respectively as compared to the free-living B. abortus. Among >5-fold differentially expressed genes, the up-regulated genes are mostly involved in DNA, RNA manipulations as well as protein biosynthesis and secretion while the down-regulated genes are mainly involved in energy production and metabolism. On the other hand, the host responses during B. abortus infection revealed that 14.01% (6071/43,346) of BMM genes were reproducibly transcribed at >5-fold during infection. Transcription of cytokines, chemokines and transcriptional factors, such as tumor necrosis factor (Tnf), interleukin-1α (Il1α), interleukin-1ß (Il1ß), interleukin-6 (Il6), interleukin-12 (Il12), chemokine C-X-C motif (CXCL) family, nuclear factor kappa B (Nf-κb), signal transducer and activator of transcription 1 (Stat1), that may contribute to host defense were markedly induced while transcription of various genes involved in cell proliferation and metabolism were suppressed upon B. abortus infection. In conclusion, these data suggest that Brucella modulates gene expression in hostile intracellular environment while simultaneously alters the host pathways that may lead to the pathogen's intracellular survival and infection.

Two Synechococcus genes, Two Different Effects on Cyanophage Infection.

Synechococcus is an abundant marine cyanobacterium that significantly contributes to primary production. Lytic phages are thought to have a major impact on cyanobacterial population dynamics and evolution. Previously, an investigation of the transcriptional response of three Synechococcus strains to infection by the T4-like cyanomyovirus, Syn9, revealed that while the transcript levels of the vast majority of host genes declined soon after infection, those for some genes increased or remained stable. In order to assess the role of two such host-response genes during infection, we inactivated them in Synechococcus sp. strain WH8102. One gene, SYNW1659, encodes a domain of unknown function (DUF3387) that is associated with restriction enzymes. The second gene, SYNW1946, encodes a PIN-PhoH protein, of which the PIN domain is common in bacterial toxin-antitoxin systems. Neither of the inactivation mutations impacted host growth or the length of the Syn9 lytic cycle. However, the DUF3387 mutant supported significantly lower phage DNA replication and yield of phage progeny than the wild-type, suggesting that the product of this host gene aids phage production. The PIN-PhoH mutant, on the other hand, allowed for significantly higher Syn9 genomic DNA replication and progeny production, suggesting that this host gene plays a role in restraining the infection process. Our findings indicate that host-response genes play a functional role during infection and suggest that some function in an attempt at defense against the phage, while others are exploited by the phage for improved infection.

The Effect of Short-Term Hyperglycemia on the Innate Immune System.

BACKGROUND: Diabetes mellitus increases the susceptibility to infection by altering both the innate and the adaptive immune systems. Hyperglycemia has been associated with adverse outcomes in hospitalized patients, especially critically ill patients; these poor outcomes are explained in part by hospital-associated infections. MATERIALS AND METHODS: PubMed, EMBASE and Google Scholar were searched to identify studies published between 1970 and 2014 reporting short-term effects of hyperglycemia on the innate immune system. MeSH database search terms included hyperglycemia, immune system, inflammation, inflammation mediators, neutrophils, endothelial dysfunction, complement system proteins and diabetes. Pertinent articles reported studies in healthy volunteers and diabetic patients, using in vitro laboratory experiments, and with animal models. RESULTS: Hyperglycemia activates protein kinase C, and this inhibits neutrophil migration, phagocytosis, superoxide production and microbial killing. High glucose concentrations decrease the formation of neutrophil extracellular traps. Hyperglycemia can also induce Toll-like receptor expression and inhibit neutrophil function and apoptosis. High glucose concentrations decrease vascular dilation and increase permeability during the initial inflammatory responses, possibly through protein kinase C activation. Hyperglycemia can cause direct glycosylation of proteins and alter the tertiary structure of complement; these changes inhibit immunoglobulin-mediated opsonization of bacteria and complement fixation to bacteria and decreases phagocytosis. Hyperglycemia also stimulates the production and release of cytokines. Several trials have demonstrated that better glycemic control reduces nosocomial infections in critically ill patients and surgical site infections. CONCLUSIONS: In summary, acute hyperglycemia can significantly alter innate immune responses to infection, and this potentially explains some of the poor outcomes in hospitalized patients who develop hyperglycemia.

BEHAVIORAL DEFENSES AGAINST AVIAN BROOD PARASITISM IN SYMPATRIC AND ALLOPATRIC HOST POPULATIONS.

The brown-headed cowbird (Molothrus ater) is a widespread, obligate brood parasite of North American passerine birds. In southern Manitoba, where hosts are sympatric with cowbirds, American robins (Turdus migratorius) ejected parasitic eggs from all experimentally parasitized clutches (N = 25) and no eggs were accepted for more than four days. In contrast, robins in northern Manitoba, an area where cowbirds do not breed, accepted parasitic eggs in 33% of nests (N = 18) for at least five days. Acceptance of experimental cowbird eggs by a second host, the yellow warbler (Dendroica petechia), was similar in allopatric (100% of 20 nests) and sympatric (88.6% of 35 nests) populations, but models of a female cowbird elicited greater nest defense by warblers in the area of sympatry. Neither host rejected eggs of conspecifics, thus, rejection of cowbird eggs was not an epiphenomenon of conspecific brood parasitism. These results support the hypothesis that recognition of cowbirds and their eggs evolved as adaptations to counter cowbird parasitism and not some other selection pressure. The expression of anti-parasite defenses by some individuals within allopatric populations further suggests these traits may be controlled genetically but persist in such areas either through the continued introgression of rejecter genes from sympatric populations or because of the low cost of rejection behavior when parasitism is absent or rare.