巢寄生行为

巢寄生是一种鸟类将卵产在其它鸟的鸟巢中,由义亲代为孵化和育雏的一种特殊的繁殖行为。照片中所示的草地鹨（Ａｎｔｈｕｓｐｒａｔｅｎｓｉｓ）喂食大杜鹃,就是一种种间巢寄生类型。大杜鹃是现有巢寄生鸟类８０多种中最典型的一种鸟,它可把卵寄生在１２５种其它鸟类的巢中。巢寄生行为表现在：宿主的选择,大杜鹃在繁殖期寻找与孵化期和育雏期相似、雏鸟食性基本相同、卵形与颜色易仿的宿主,多为雀形目鸟类。寄生时间上,大杜鹃多在宿主开始孵卵之前,乘宿主离巢外出时快速寄生产卵。巢寄生的协同进化,表现在宿主卵的形态特征上。寄生…     

巢寄生的协同进化

巢寄生现象一直是鸟类学专家探讨的热点问题,对于协同进化的问题又有许多不同理论。从宿主的2种对待寄生卵的行为出发,对于巢寄生协同进化的各种理论做了简单的归纳。其中宿主的拒卵行为被认为是一种适应性的表现,这导致和寄生鸟的进化竞争。而对宿主接受卵的行为却有2种不同的观点,即进化滞后说和进化平衡说,这2种学说从不同的方面都能解释宿主接受卵的行为。关于巢寄生的协同进化问题还需要进一步的研究和更多的实例证明．     

大杜鹃对北红尾鸲的放牧行为

在宿主的寄生防御压力下,鸟类巢寄生者通常会进化出一系列有效的寄生行为以提高其自身的繁殖适合度。以往研究发现,部分巢寄生者可能具有类似人类的"放牧"行为,即通过破坏或捕食不适合寄生的宿主巢,促使其重新筑巢以获取新的寄生机会。然而,对于其野外行为事件的报道并不多见。2018年5至8月,在贵州六枝地区,通过对宿主北红尾鸲(Phoenicurusauroreus)的巢进行录像监控,首次记录到大杜鹃(Cuculus canorus)对正在孵卵的北红尾鸲的放牧行为。进一步查阅了大杜鹃寄生系统中已有的放牧案例,说明放牧行为很可能是大杜鹃普遍采用的一种寄生策略。     

中杜鹃捕食比氏鹟莺的卵

许多杜鹃在产下寄生卵之前通常会先叼走或吃掉宿主的1~2枚卵,这说明杜鹃不仅是寄生性繁殖的鸟类,同时可能也是潜在的捕食者。关于杜鹃对其宿主巢捕食的动机,一般认为一是由于杜鹃发现宿主巢时,已不适合寄生,将其捕食或毁坏可迫使宿主重新筑巢,从而杜鹃会获得寄生机会;二则可能由于宿主识别并拒绝了寄生卵,一些杜鹃会通过捕食或破坏宿主的巢,作为对宿主的一种惩罚性报复。2015年6月,在贵州宽阔水自然保护区,通过录像首次记录到中杜鹃(Cuculus saturatus)捕食整巢比氏鹟莺(Seicercus latouchei)卵的行为,表明中杜鹃不仅是许多宿主鸟类的巢寄生者,同时也可能是其巢捕食者。     

鸟类卵色的进化

鸟类学家提出了多种假说用于解释鸟类卵色的多态性,然而,不同学者的观点和研究结果不尽相同。本文从捕食者、警戒色、太阳辐射和巢寄生角度综述了各种假说和研究,探讨鸟类卵色的进化。     

北京小龙门东方中杜鹃多重寄生冕柳莺的报道

多重巢寄生是1只或多只寄生性鸟类在1个宿主巢内产2枚或多枚卵的特殊行为方式。对于雏鸟具有排他性的杜鹃而言,多重寄生被认为是种内个体之间或种间的一种竞争,但相关报道较少。通过野外观察和分子生物学检测技术,我们在北京小龙门国家森林公园确定了一个被东方中杜鹃(Cuculus optatus)多重寄生的冕柳莺(Phylloscopus coronatus)巢。     

小杜鹃对小鳞胸鹪鹛的巢寄生

鸟类的巢寄生现象一直被作为生物协同演化的典型模式系统之一。对杜鹃选择宿主及其巢寄生情况进行调查和观测,能够为协同演化研究提供重要基础资料。2015年7月,我们在四川省雷波县发现一个被杜鹃寄生的鸟巢。通过野外观测和分子生物学检测,确定宿主为小鳞胸鹪鹛(Pnoepyga pusilla),而寄生者为小杜鹃(Cuculus poliocephalus)。     

大杜鹃对家燕的巢寄生

了解杜鹃(Cuculus spp.)对不同宿主鸟类的巢寄生,是研究杜鹃与其宿主之间协同进化的重要基础资料。大杜鹃(Cuculus canorus)和家燕(Hirundo rustica)分布遍及全国,且为同域分布,但两者之间的寄生现象尚未有过系统调查。2012年和2014年4~8月,对繁殖于吉林市昌邑区桦皮厂镇(34°58′44.18″N,126°13′26.83″E,海拔184 m)和海南岛的家燕种群进行调查,结果表明,吉林市昌邑区桦皮厂镇家燕种群的寄生率为2.4%(1/42),而在海南岛所调查的1 719个家燕巢未发现杜鹃寄生现象。同时在网络上搜集家燕巢寄生的报道案例,共记录到13巢家燕被大杜鹃寄生繁殖,均发生在北方的家燕种群。     

长白山中华秋沙鸭的种内巢寄生

雁形目鸟类的种内巢寄生现象十分普遍,但有关中华秋沙鸭(Mergussquamatus)的种内巢寄生现象未见报道。2019年4和5月,从长白山1个中华秋沙鸭人工巢的视频监控发现,1只雌鸭在亲鸟孵卵时强行进入巢箱趴卧约29 min。其后根据该巢窝卵数的增加、超常窝卵数和窝卵不同步孵化3个指标,确认该巢存在种内巢寄生现象。宿主对进入巢内寄生的个体表现出强烈的攻击行为,但对寄生卵未表现出明显的拒卵行为。由于区域内仍有较多巢箱未被利用,中华秋沙鸭的种内巢寄生行为是否源于对有限巢址资源的竞争,有待进一步研究。     

三个东方大苇莺种群大杜鹃寄生率的变异

东方大苇莺Acrocephalus orientalis是大杜鹃Cuculus canorus的主要寄主之一。本文对东方大苇莺的3个地理种群进行杜鹃寄生率的时空比较。发现不同东方大苇莺种群被大杜鹃的巢寄生率在21.4%和65.5%之间,差异显著;不过,地理位置相近的两个种群在巢寄生率上则没有显著差异。另外,同一地理种群的巢寄生率年间也存在显著差异。     

Virulence, drug sensitivity and transmission success in the rodent malaria, Plasmodium chabaudi

Here, we test the hypothesis that virulent malaria parasites are less susceptible to drug treatment than less virulent parasites. If true, drug treatment might promote the evolution of more virulent parasites (defined here as those doing more harm to hosts). Drug-resistance mechanisms that protect parasites through interactions with drug molecules at the sub-cellular level are well known. However, parasite phenotypes associated with virulence might also help parasites survive in the presence of drugs. For example, rapidly replicating parasites might be better able to recover in the host if drug treatment fails to eliminate parasites. We quantified the effects of drug treatment on the in-host survival and between-host transmission of rodent malaria (Plasmodium chabaudi) parasites which differed in virulence and had never been previously exposed to drugs. In all our treatment regimens and in single- and mixed-genotype infections, virulent parasites were less sensitive to pyrimethamine and artemisinin, the two antimalarial drugs we tested. Virulent parasites also achieved disproportionately greater transmission when exposed to pyrimethamine. Overall, our data suggest that drug treatment can select for more virulent parasites. Drugs targeting transmission stages (such as artemisinin) may minimize the evolutionary advantage of virulence in drug-treated infections.     

Comparison of in vitro-cultured and wild-type Perkinsus marinus. I. Pathogen virulence

Perkinsus marinus is a highly contagious pathogen of the eastern oyster Crassostrea virginica. Until recently, transmission studies have employed wild-type parasites isolated directly from infected oysters. Newly developed methods to propagate P. marinus in vitro have led to using cultured parasites for infection studies, but results suggest that cultured parasites are less virulent than wild-type parasites In this paper, we report results of experiments designed to quantify differences between wild-type and cultured P. marinus virulence and to test the following hypotheses: (1) in vitro-cultured parasites are less virulent than wild-type parasites; (2) virulence decreases gradually during in vitro culture; (3) virulence of in vitro cultures can be restored by in vivo passage; (4) virulence changes with culture phase. Our results demonstrate that parasites freshly isolated from infected hosts are much more virulent than those propagated in culture, indicating a potential deficiency in the culture medium used. Virulence was lost immediately in culture and, for that reason, the practice of repassing cultured cells through the host to restore virulence does not work for P. marinus. Virulence was also associated with culture phase: log-phase parasites were significantly more virulent than those obtained from lag- or stationary-phase cultures.     

Inter‐specific brood parasitism and the evolution of avian reproductive strategies

Avian brood parasitism is a potent selective agent modulating host behaviors and morphology, although its role in determining diversification of avian breeding strategies remains elusive. Hitherto, the study of selection of brood parasites on host breeding strategies has been based on single reproductive trait approaches, which neglect that evolutionary responses to brood parasites may involve co‐ordinated changes in several aspects of reproduction. Here I consider covariation among reproductive traits to test whether parental breeding strategies of hosts of brown headed cowbird (BHC hereafter) in North America and the common cuckoo (CC hereafter) in Europe, two parasites with contrasting level of virulence, have evolved in response to brood parasitism. The effect of parasitism on avian breeding strategies differed between continents. Long term exposure to BHC parasitism selected for a lower breeding investment in North America, but not so CC parasitism in Europe. These results suggest a key role of parasite virulence on the evolution of avian breeding strategies and that brood parasitism has selected for a co‐ordinated breeding strategy of reducing parasitism costs by shortening and fractioning reproductive events within a single season in North America.     

Selection for plasmid post-segregational killing depends on multiple infection: evidence for the selection of more virulent parasites through parasite-level competition

Is the virulence of parasites an outcome of optimized infection? Virulence has often been considered an inevitable consequence of parasite reproduction when the cost incurred by the parasite in reducing the fitness of its current host is offset by increased infection of new hosts. More recent models have focused on how competition occurring between parasites during co-infection might effect selection of virulence. For example, if co-infection was common, parasites with higher intrinsic growth rates might be selected, even at the expense of being optimally adapted to infect new hosts. If growth rate is positively correlated with virulence, then competition would select increased virulence. We tested these models using a plasmid-encoded virulence determinant. The virulence determinant did not contribute to the plasmid's reproduction within or between hosts. Despite this, virulent plasmids were more successful than avirulent derivatives during selection in an environment allowing within-host competition. To explain these findings we propose and test a model in which virulent parasites are selected by reducing the reproduction of competitors.     

The evolution of acceptance and tolerance in hosts of avian brood parasites

Avian brood parasites lay their eggs in the nests of their hosts, which rear the parasite's progeny. The costs of parasitism have selected for the evolution of defence strategies in many host species. Most research has focused on resistance strategies, where hosts minimize the number of successful parasitism events using defences such as mobbing of adult brood parasites or rejection of parasite eggs. However, many hosts do not exhibit resistance. Here we explore why some hosts accept parasite eggs in their nests and how this is related to the virulence of the parasite. We also explore the extent to which acceptance of parasites can be explained by the evolution of tolerance; a strategy in which the host accepts the parasite but adjusts its life history or other traits to minimize the costs of parasitism. We review examples of tolerance in hosts of brood parasites (such as modifications to clutch size and multi‐broodedness), and utilize the literature on host–pathogen interactions and plant herbivory to analyse the prevalence of each type of defence (tolerance or resistance) and their evolution. We conclude that (i) the interactions between brood parasites and their hosts provide a highly tractable system for studying the evolution of tolerance, (ii) studies of host defences against brood parasites should investigate both resistance and tolerance, and (iii) tolerance and resistance can lead to contrasting evolutionary scenarios.     

Of mice and worms: are co-infections with unrelated parasite strains more damaging to definitive hosts?

Intraspecific competition between co-infecting parasites can influence the amount of virulence, or damage, they do to their host. Kin selection theory dictates that infections with related parasite individuals should have lower virulence than infections with unrelated individuals, because they benefit from inclusive fitness and increased host longevity. These predictions have been tested in a variety of microparasite systems, and in larval stage macroparasites within intermediate hosts, but the influence of adult macroparasite relatedness on virulence has not been investigated in definitive hosts. This study used the human parasite Schistosoma mansoni to determine whether definitive hosts infected with related parasites experience lower virulence than hosts infected with unrelated parasites, and to compare the results from intermediate host studies in this system. The presence of unrelated parasites in an infection decreased parasite infectivity, the ability of a parasite to infect a definitive host, and total worm establishment in hosts, impacting the less virulent parasite strain more severely. Unrelated parasite co-infections had similar virulence to the more virulent of the two parasite strains. We combine these findings with complementary studies of the intermediate snail host and describe trade-offs in virulence and selection within the life cycle. Damage to the host by the dominant strain was muted by the presence of a competitor in the intermediate host, but was largely unaffected in the definitive host. Our results in this host–parasite system suggest that unrelated infections may select for higher virulence in definitive hosts while selecting for lower virulence in intermediate hosts.     

Case-control studies on host factors in severe malaria

Although molecular biology has illustrated the phenotypic heterogeneity of Plasmodium falciparum, there are still no specific markers of virulence. As parasite virulence is an important determinant of severe malaria, the choice of comparison groups in the study of host factors influencing severity is a delicate issue. Ignoring parasite factors in the selection of controls potentially leads to biased comparisons between a majority of cases with virulent parasites and a majority of controls with non-virulent parasites. This article discusses how to avoid this virulence bias in the absence of specific markers of virulence.     

Within-host parasite cooperation and the evolution of virulence

Infections by multiple genotypes are common in nature and are known to select for higher levels of virulence for some parasites. When parasites produce public goods (PGs) within the host, such co-infections have been predicted to select for lower levels of virulence. However, this prediction is based on simplifying assumptions regarding epidemiological feedbacks on the multiplicity of infections (MOI). Here, we analyse the case of parasites producing a PG (for example, siderophore-producing bacteria) using a nested model that ties together within-host and epidemiological processes. We find that the prediction that co-infection should select for less virulent strains for PG-producing parasites is only valid if both parasite transmission and virulence are linear functions of parasite density. If there is a trade-off relationship such that virulence increases more rapidly than transmission, or if virulence also depends on the total amount of PGs produced, then more complex relationships between virulence and the MOI are predicted. Our results reveal that explicitly taking into account the distribution of parasite strains among hosts could help better understand the selective pressures faced by parasites at the population level.     

Plasmodium berghei: Isolation and maintenance of an irradiation attenuated strain in the nude mouse

An attenuated strain of malaria causing limited parasitemia in mice was derived from a highly virulent strain of Plasmodium berghei (NK65) which produced 100% lethality in mice. A pool of mouse blood infected with the original highly virulent P. berghei was exposed to 40 Krad irradiation and parasites were inoculated into nude mice as well as into thymus competent normal littermates. Thymus competent mice showed no parasitemia, while one out of the five nude mice inoculated with the irradiated parasites developed a slow and progressive parasitemia. These parasites induced a self-limiting parasitemia in thymus competent mice, even when a large inoculum was administered. Maintenance of the low virulence strain required passage through nude mice. After 50 passages at two weekly intervals, reversion to virulence did not occur. A single vaccination with the attenuated strain induced immunity in mice against a challenge inoculation with the original virulent strain. Specific IgG persisted at high titer for more than 9 weeks in mice receiving a single inoculation of the attenuated strain.