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23.5: Fungal Infections of the Reproductive System - Biology

23.5: Fungal Infections of the Reproductive System - Biology


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Learning Objectives

  • Summarize the important characteristics of vaginal candidiasis

Only one major fungal pathogen affects the urogenital system. Candida is a genus of fungi capable of existing in a yeast form or as a multicellular fungus. Candida spp. are commonly found in the normal, healthy microbiota of the skin, gastrointestinal tract, respiratory system, and female urogenital tract (Figure (PageIndex{1})). They can be pathogenic due to their ability to adhere to and invade host cells, form biofilms, secrete hydrolases (e.g., proteases, phospholipases, and lipases) that assist in their spread through tissues, and change their phenotypes to protect themselves from the immune system. However, they typically only cause disease in the female reproductive tract under conditions that compromise the host’s defenses. While there are at least 20 Candida species of clinical importance, C. albicans is the species most commonly responsible for fungal vaginitis.

As discussed earlier, lactobacilli in the vagina inhibit the growth of other organisms, including bacteria and Candida, but disruptions can allow Candida to increase in numbers. Typical disruptions include antibiotic therapy, illness (especially diabetes), pregnancy, and the presence of transient microbes. Immunosuppression can also play a role, and the severe immunosuppression associated with HIV infection often allows Candida to thrive. This can cause genital or vaginal candidiasis, a condition characterized by vaginitis and commonly known as a yeast infection. When a yeast infection develops, inflammation occurs along with symptoms of pruritus (itching), a thick white or yellow discharge, and odor.

Other forms of candidiasis include cutaneous candidiasis (see Mycoses of the Skin) and oral thrush (see Microbial Diseases of the Mouth and Oral Cavity). Although Candida spp. are found in the normal microbiota, Candida spp. may also be transmitted between individuals. Sexual contact is a common mode of transmission, although candidiasis is not considered an STI.

Diagnosis of vaginal candidiasis can be made using microscopic evaluation of vaginal secretions to determine whether there is an excess of Candida. Culturing approaches are less useful because Candida is part of the normal microbiota and will regularly appear. It is also easy to contaminate samples with Candida because it is so common, so care must be taken to handle clinical material appropriately. Samples can be refrigerated if there is a delay in handling. Candida is a dimorphic fungus, so it does not only exist in a yeast form; cultivation can be used to identify chlamydospores and pseudohyphae, which develop from germ tubes (Figure (PageIndex{2})). The presence of the germ tube can be used in a diagnostic test in which cultured yeast cells are combined with rabbit serum and observed after a few hours for the presence of germ tubes. Molecular tests are also available if needed. The Affirm VPII Microbial Identification Test, for instance, tests simultaneously for the vaginal microbes C. albicans, G. vaginalis (see Bacterial Infections of the Urinary System), and Trichomonas vaginalis (see Protozoan Infections of the Urogenital System).

Topical antifungal medications for vaginal candidiasis include butoconazole, miconazole, clotrimazole, tioconazole, and nystatin. Oral treatment with fluconazole can be used. There are often no clear precipitating factors for infection, so prevention is difficult.

Exercise (PageIndex{1})

  1. What factors can lead to candidiasis?
  2. How is candidiasis typically diagnosed?

clinical focus - part 3

The Gram stain of Nadia’s vaginal smear showed that the concentration of lactobacilli relative to other species in Nadia’s vaginal sample was abnormally low. However, there were no clue cells visible, which suggests that the infection is not bacterial vaginosis. But a wet-mount slide showed an overgrowth of yeast cells, suggesting that the problem is candidiasis, or a yeast infection (Figure (PageIndex{3})). This, Nadia’s doctor assures her, is good news. Candidiasis is common during pregnancy and easily treatable.

Exercise (PageIndex{2})

Knowing that the problem is candidiasis, what treatments might the doctor suggest?

  • Candida spp. are typically present in the normal microbiota in the body, including the skin, respiratory tract, gastrointestinal tract, and female urogenital system.
  • Disruptions in the normal vaginal microbiota can lead to an overgrowth of Candida, causing vaginal candidiasis.
  • Vaginal candidiasis can be treated with topical or oral fungicides. Prevention is difficult.

Multiple Choice

Which oral medication is recommended as an initial topical treatment for genital yeast infections?

A. penicillin
B. acyclovir
C. fluconazole
D. miconazole

D

Fill in the Blank

The most common Candida species associated with yeast infections is _____.

C. albicans


Fungal Infections of the Reproductive System

Only one major fungal pathogen affects the urogenital system. Candida is a genus of fungi capable of existing in a yeast form or as a multicellular fungus. Candida spp. are commonly found in the normal, healthy microbiota of the skin, gastrointestinal tract, respiratory system, and female urogenital tract. They can be pathogenic due to their ability to adhere to and invade host cells, form biofilms, secrete hydrolases (e.g., proteases, phospholipases, and lipases) that assist in their spread through tissues, and change their phenotypes to protect themselves from the immune system. However, they typically only cause disease in the female reproductive tract under conditions that compromise the host’s defenses. While there are at least 20 Candida species of clinical importance, C. albicans is the species most commonly responsible for fungal vaginitis.

As discussed earlier, lactobacilli in the vagina inhibit the growth of other organisms, including bacteria and Candida, but disruptions can allow Candida to increase in numbers. Typical disruptions include antibiotic therapy, illness (especially diabetes), pregnancy, and the presence of transient microbes. Immunosuppression can also play a role, and the severe immunosuppression associated with HIV infection often allows Candida to thrive. This can cause genital or vaginal candidiasis, a condition characterized by vaginitis and commonly known as a yeast infection. When a yeast infection develops, inflammation occurs along with symptoms of pruritus (itching), a thick white or yellow discharge, and odor.

Other forms of candidiasis include cutaneous candidiasis and oral thrush. Although Candida spp. are found in the normal microbiota, Candida spp. may also be transmitted between individuals. Sexual contact is a common mode of transmission, although candidiasis is not considered an STI.

Diagnosis of vaginal candidiasis can be made using microscopic evaluation of vaginal secretions to determine whether there is an excess of Candida. Culturing approaches are less useful because Candida is part of the normal microbiota and will regularly appear. It is also easy to contaminate samples with Candida because it is so common, so care must be taken to handle clinical material appropriately. Samples can be refrigerated if there is a delay in handling. Candida is a dimorphic fungus, so it does not only exist in a yeast form cultivation can be used to identify chlamydospores and pseudohyphae, which develop from germ tubes. The presence of the germ tube can be used in a diagnostic test in which cultured yeast cells are combined with rabbit serum and observed after a few hours for the presence of germ tubes. Molecular tests are also available if needed. The Affirm VPII Microbial Identification Test, for instance, tests simultaneously for the vaginal microbes C. albicans, G. vaginalis, and Trichomonas vaginalis.

Topical antifungal medications for vaginal candidiasis include butoconazole, miconazole, clotrimazole, tioconazole, and nystatin. Oral treatment with fluconazole can be used. There are often no clear precipitating factors for infection, so prevention is difficult.


Chapter 20

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    CLINICAL FOCUS: Part 3

    The Gram stain of Nadia’s vaginal smear showed that the concentration of lactobacilli relative to other species in Nadia’s vaginal sample was abnormally low. However, there were no clue cells visible, which suggests that the infection is not bacterial vaginosis. But a wet-mount slide showed an overgrowth of yeast cells, suggesting that the problem is candidiasis, or a yeast infection (Figure 24.19). This, Nadia’s doctor assures her, is good news. Candidiasis is common during pregnancy and easily treatable.

    Jump to the next Clinical Focus box. Go back to the previous Clinical Focus box.


    Chancroid

    ​The sexually transmitted infection chancroid is caused by the gram-negative rod Haemophilus ducreyi. It is characterized by soft chancres (Figure 6) on the genitals or other areas associated with sexual contact, such as the mouth and anus. Unlike the hard chancres associated with syphilis, soft chancres develop into painful, open sores that may bleed or produce fluid that is highly contagious. In addition to causing chancres, the bacteria can invade the lymph nodes, potentially leading to pus discharge through the skin from lymph nodes in the groin. Like other genital lesions, soft chancres are of particular concern because they compromise the protective barriers of the skin or mucous membranes, making individuals more susceptible to HIV and other sexually transmitted diseases.

    Several virulence factors have been associated with H. ducreyi, including lipooligosaccharides, protective outer membrane proteins, antiphagocytic proteins, secretory proteins, and collagen-specific adhesin NcaA. The collagen-specific adhesion NcaA plays an important role in initial cellular attachment and colonization. Outer membrane proteins DsrA and DltA have been shown to provide protection from serum-mediated killing by antibodies and complement.

    H. ducreyi is difficult to culture thus, diagnosis is generally based on clinical observation of genital ulcers and tests that rule out other diseases with similar ulcers, such as syphilis and genital herpes. PCR tests for H. ducreyi have been developed in some laboratories, but as of 2015 none had been cleared by the US Food and Drug Administration (FDA). 3 Recommended treatments for chancroid include antibiotics such as azithromycin, ciprofloxacin, erythromycin and ceftriaxone. Resistance to ciprofloxacin and erythromycin has been reported. 4

    Figure 6. (a) A soft chancre on the penis of a man with chancroid. (b) Chancroid is caused by the gram-negative bacterium Haemophilus ducreyi, seen here in a gram-stained culture of rabbit blood. (credit a, b: modification of work by Centers for Disease Control and Prevention)​
    • What is the key difference between chancroid lesions and those associated with syphilis?
    • Why is it difficult to definitively diagnose chancroid?

    ​BACTERIAL REPRODUCTIVE TRACT INFECTIONS

    ​Many bacterial infections affecting the reproductive system are transmitted through sexual contact, but some can be transmitted by other means. In the United States, gonorrhea and chlamydia are common illnesses with incidences of about 350,000 and 1.44 million, respectively, in 2014. Syphilis is a rarer disease with an incidence of 20,000 in 2014. Chancroid is exceedingly rare in the United States with only six cases in 2014 and a median of 10 cases per year for the years 2010–2014. 5 Figure 7 summarizes bacterial infections of the reproductive tract.


    Discussion

    ‘Non‐immunological’ mechanisms such as thermoregulatory behaviour are increasingly appreciated as critical components of an animal's defence against pathogens (Thomas & Blanford 2003 Parker etਊl. 2011 De Roode & Lefèvre 2012). However, the adaptive significance of non‐immunological defences has been difficult to test. We find that when exposed to a common insect fungal pathogen, the fruit fly alters its temperature preference, which helps to mitigate the loss of fitness associated with infection.

    A Novel Mode of Immunity in Drosophila

    Despite being one of the most important model organisms for the study of temperature preference (Dillon etਊl. 2009) and innate immunity (Lemaitre & Hoffmann 2007), little is known about whether Drosophila employ thermoregulatory behaviour to fight infections. In contrast to the well𠄍ocumented phenomenon of behavioural fever (Watson 1993 Adamo 1998 Elliot, Blanford & Thomas 2002 Hunt etਊl. 2011), but consistent with other cases of behavioural anapyrexia (Müller & Schmid‐Hempel 1993 Zbikowska & Cichy 2012), we find that D. melanogaster infected with the fungus M. robertsii preferred colder temperatures compared with uninfected control animals. This switch in temperature preference bestows long‐term fitness benefits for the host, thus implying behavioural anapyrexia is host driven. Though lower temperatures reduced the growth rate of the fungus, we cannot rule out the possibility that this was not also advantageous to pathogen transmission and moving to a colder temperature could, for example, reduce predation of the fly, which could in turn increase the transmission success of the fungus. Further work will be required to investigate such possibilities. To a lesser degree, flies treated with a heat‐killed fungus also preferred colder temperatures. This suggests that the behavioural anapyrexia is host driven, because a dead pathogen would not be able to manipulate its host. It is possible that unknown factors associated with the presence of a dead fungus on the surface of the cuticle could induce a mild behavioural anapyrexia. Confirmation of the activation of other aspects of the immune system, such as antimicrobial peptides, would indicate the host has identified pathogenic material on its surface, thus supporting this behaviour is host driven.

    Behavioural anapyrexia by infected fruit flies directly enhances resistance against Metarhizium infections by placing the fungus in a suboptimal thermal environment reducing its germination success and vegetative growth (this study, Ouedraogo etਊl. 1997 Tefera & Pringle 2003਍imbi etਊl. 2004). Given the universal affect of temperature on microbial replication rates, anapyrexia is likely to act as a non‐specific mechanism of resistance that could be effective against numerous pathogens. However, in some cases the thermal response of an insect to infection varies depending on the susceptibility of the pathogen to temperature (Adamo 1998). There is a growing body of evidence to support an increase of immune gene expression at colder temperatures in Drosophila and other invertebrates (Linder, Owers & Promislow 2008 Murdock, Moller‐Jacobs & Thomas 2013 Sinclair etਊl. 2013). Although we did not investigate the possibility in this study, moving to the cold could further augment host immune function through its effect on immune gene expression. To date, many studies investigating thermal relationships of immune gene expression have focused on temperatures below the

    22 ଌ observed here for behavioural anapyrexia. It is important that future studies also consider temperatures and thermal regimes closer to those realistically experienced by fruit flies to fully understand the interactions between temperature and immune gene expression during an infection.

    Previous work suggests that tolerance to biotic and abiotic stress increases at colder temperatures (Sinclair etਊl. 2013). However, we found no evidence that the colder temperature enhances tolerance to fungal infection, which suggests that resistance and tolerance can vary independently in our system (Ayres & Schneider 2008). Our measure of tolerance, defined as age‐specific reaction norms between pathogen load and host mortality risk (Baucom & de Roode 2011), could be biased by cohort heterogeneity in resistance to infection if highly susceptible flies have higher pathogen loads than those that survive, which would make the correlation between observed pathogen load and mortality rate dependent on the severity of the infection. Measurements of fitness loss per individual could offer an alternative to our age‐specific mortality�sed measurements because it allows for individual, rather than cohort, measures of tolerance however, because it does not account for the sensitivity of reproductive output to temperature and cannot be measured in our system without destructive sampling, it could produce misleading results.

    The results we report here are based on the temperature preference of small cohorts of flies. The behaviour of animals, including D. melanogaster, can be influenced by collective group behaviour (Berdahl etਊl. 2013 Ramdya etਊl. 2014), and it is therefore important to note that we can only confidently state that the behavioural anapyrexia observed here applies to groups of fruit flies and the result for individual flies may differ, if, for example, an individual was searching for a mate. We hope this study will provide a foundation for future studies on thermal preferences in D. melanogaster during infection. To establish the extent of behavioural anapyrexia, further work exploring the incidence of cold‐seeking behaviour at additional time points throughout infection and with a range of infectious organisms, including other entomopathogenic fungus and bacterial pathogens, is required.

    Anapyrexia Mitigates the Reproductive Losses from Infection

    Previous work on non‐immunological defences has focused on survival and immunity in infected animals (Thomas & Blanford 2003 Parker etਊl. 2011 De Roode & Lefèvre 2012). To test whether behavioural responses are specific to infected animals, we need to evaluate not just whether infected animals benefit, but also whether they benefit appreciably more from inhabiting preferred temperatures than control animals. Though previous work has argued that behavioural fever and anapyrexia provide survival benefits for infected animals (Müller & Schmid‐Hempel 1993 Adamo 1998 Elliot, Blanford & Thomas 2002), we find that survival benefits are not sufficient to explain why infected animals prefer colder temperatures. While cold‐seeking behaviour indeed enhances the survival of Metarhizium‐infected fruit flies, uninfected control flies also receive survival benefit by residing at colder temperatures. The survival benefit of colder temperature does not derive from reduced rates of ageing (in control animals) or physiological decline (in infected animals). Instead, lower temperature greatly reduces the background risk of death, but its influence was relatively similar within each treatment.

    At the preferred cooler temperature, infected animals exhibited an increased LRS, but there was no evidence that they benefited more than control animals. Instead, we find that inhabiting cooler temperatures facilitates a shift in life‐history strategy that is specific to infected animals: enhanced late𠄊ge reproduction coming at a cost to early𠄊ge reproduction (supported by a three‐way interaction between temperature, infection and age). We found that infected fruit flies choose a temperature that reduces their fecundity immediately post‐infection (days 2𠄴 post‐infection), but provides enhanced reproduction at later time intervals (from day 6 onwards) both in terms of the number of eggs laid and the number of fecund days. Although it is important to note that reproductive output is not equivalent to reproductive effort, this finding is consistent with host‐mediated fecundity reduction strategy (Hurd 2001) and runs contrary to the strategy of fecundity compensation (Forbes 1993). As infected flies also achieved greater LRS at anapyrexia‐like temperature compared to those residing at the temperature preferred by control animals, our results highlight evidence of the costs of parasitism (e.g. a temporary reduction in host fecundity post‐infection) can be misleading. The adaptive values of fecundity compensation or reduction are likely to depend on the demography of the population. In particular, fecundity compensation might be maladaptive for declining populations associated with pathogen‐rich environments where late𠄊ge reproduction is likely to contribute more to overall fitness. Whereas a fecundity reduction strategy with relatively higher late𠄊ge reproduction is expected to be adaptive in declining populations such as those experiencing a high parasite burden (Charlesworth 1994 Brommer 2000).

    Anapyrexia is Costly for Fruit Flies

    A central concept in ecological immunology is that all host defence traits have costs which are traded off with other host life‐history traits (Sheldon & Verhulst 1996 Schmid‐Hempel 2003). This is an important prediction because in the absence of costs, we would expect defence traits to be constitutively expressed with minimal variation among individuals. We find that the anapyrexia‐like temperature significantly reduced early𠄊ge fecundity and intrinsic rate of increase, r in uninfected control flies. These are likely to represent significant fitness costs in growing populations where the intrinsic rate of increase is an appropriate measure of Darwinian fitness and to which early𠄊ge reproduction has a disproportionate contribution (Charlesworth 1994 Brommer 2000). Thus, poikilothermic animals in expanding populations are expected to favour fast development and early𠄊ge reproduction, both of which are positively influenced by ambient temperature (Taylor 1981 Huey etਊl. 1995 Dillon, Cahn & Huey 2007), in order to maximize their intrinsic rate of increase (Huey & Berrigan 2001).

    Previous studies using D. melanogaster indicate that adult flies have a strong temperature preference at approximately 24� ଌ (Sayeed & Benzer 1996 Dillon etਊl. 2009), we confirm this in uninfected control flies and show that they achieve higher intrinsic rates of increase at 25 ଌ than those kept at 22 ଌ. This is consistent with the previous finding that in Drosophila, r is maximized at 25 ଌ (Siddiqui & Barlow 1972 Martin & Huey 2008). In contrast, we found that LRS was not significantly different at the two temperatures in uninfected control treatments. Along with a recent study in nematodes (Anderson etਊl. 2011), our results suggest that at least in some populations of poikilotherms, the temperature preferences of uninfected animals might have evolved to maximize intrinsic rate of increase and not LRS. Together, these results suggest that if we only conduct our experiments under a single thermal condition, which does not represent the highly variable environment experienced by organisms under natural conditions, we may not be able to accurately assess the costs and benefits of immunity. In particular, phenotypes which result from genetic and environmental interactions may be missed (Moret & Schmid‐Hempel 2004 Lazzaro & Little 2009 Paaijmans etਊl. 2013).

    Conclusions

    Our findings show that fruit flies alter their temperature preference during an infection. This has implications for the reproductive success of fruit flies and may facilitate a mechanism for poikilotherms to tailor their life‐history strategies in response to infections. We demonstrate the importance of accounting for the thermal environment in studies of host–pathogen interactions and highlight that measuring classic fitness measures, LRS and r, within the same experiment can yield novel insights (Huey & Berrigan 2001 Anderson etਊl. 2011). Most importantly, we hope that these results stimulate further experimental work that directly assesses the importance of this mechanism in thermally variable environments including wild populations where poikilotherms are subject to fluctuating environmental temperatures. Recent studies suggest that behavioural thermoregulation will be a key mechanism for poikilothermic animals to buffer the impacts of global climate change (Kearney, Shine & Porter 2009 Gvozdík 2012). Moreover, given the recent global spread of fungal pathogens (Fisher etਊl. 2012), thermoregulatory behaviours are likely to play increasingly important roles in defending against these threats. Wild populations are also regularly under the threat of pathogenic exposure, and this can be variable in both the type of pathogen present and their virulence. We would expect that consequently the degree to which an infection, or more realistically, co‐infections of pathogens affect the fecundity and longevity of an individual is itself subject to great variability. The work we present here is an important step in our understanding of how an animal may mitigate these costs of infection.


    Anatomy and Physical Examination of the Stallion

    The Penis and Prepuce

    The penis of the stallion is composed of a root, a body, and a glans penis and is of the musculocavernous type ( Fig. 1-10 ). 1,3,5,6 The penis is supported at its root by the suspensory ligaments of the penis and the ischiocavernosus muscles. The penile root arises at the ischial arch in the form of two crura, which fuse distally to form the single and dorsal corpus cavernosum penis, and is enclosed by a thick tunica albuginea. The cavernous spaces making up the erectile tissue of the penis are the corpus cavernosum, corpus spongiosum, and corpus spongiosum glandis. Engorgement of these spaces with blood from branches of the internal and external pudendal arteries and obturator arteries is responsible for erection. 3,4 The cavernous spaces within the penis are continuous with the veins responsible for drainage. The corpus spongiosum originates at the pelvis at the bulb of the penis and distally surrounds the penile urethra within a groove on the ventral side of the penis. It continues distally over the free end of the penis to form the glans penis (corpus spongiosum glandis). The corpus spongiosum glandis is responsible for the distinct bell shape of the stallion’s penis that is seen following coitus. The urethral process is distinctly visible at the center of the glans penis and is surrounded by an invagination known as the fossa glandis. Accumulations of smegma secretions, known as “beans,” are lodged in the dorsal diverticulum of the fossa glandis, the urethral sinus. Careful examination and cleaning of this area are imperative during the reproductive evaluation of a stallion ( Figs. 1-11 and 1-12 ).

    The bulbospongiosus muscle lies ventral to the urethra and along the entire length of the penis ( Fig. 1-13 ). Arising as a direct continuation of the urethralis muscle, its smooth rhythmic contractions assist in moving the penile urethral contents (semen and urine) distally. Rhythmic pulsations of the bulbospongiosus muscle are distinctly felt during ejaculation if a hand is placed on the ventral aspect of the penis during collection. The paired retractor penis muscles also run ventrally along the length of the penis and attach at the glans penis. These smooth muscles function to return the penis to the sheath following detumescence.

    The prepuce is formed by a double fold of skin and resembles scrotal skin in that it is essentially hairless and well supplied with sebaceous and sweat glands. 5-7 It functions to contain and protect the non-erect penis. The external part of the prepuce, or sheath, begins at the scrotum and displays a marked raphe that is continuous with the scrotal raphe. This external layer extends some distance cranially before reflecting dorsocaudad to the abdominal wall to form the preputial orifice. 5 The internal layer of the prepuce extends caudad from the orifice to line the internal side of the sheath, then reflects craniad toward the orifice again before reflecting caudad to form the internal preputial fold and preputial ring (see Fig. 1-12 ). It is this additional internal fold that allows the marked lengthening (approximately by 50%) of the stallion’s penis during erection. During erection, the preputial orifice is visible at the base of the penis just in front of the scrotum, and the preputial ring is visible approximately midshaft of the penis ( Fig. 1-14 ). Located distal to the preputial ring during erection is the internal layer of the internal preputial fold.

    The penis and prepuce of a breeding stallion are best examined following teasing with an estrus mare, when the stallion can be observed to drop the penis and attain a full erection. The prepuce and penis should be free of vesicular, proliferative, or inflammatory lesions, such as those found in cases of coital exanthema, squamous cell carcinoma, or cutaneous habronemiasis. Removal of smegma accumulations may be required for a complete examination of the skin surfaces. Ultrasound of the penis of the stallion is not generally used in routine examination however, this modality may be useful in the diagnosis of suspected penile hematoma or fibrosis following injury.


    Notes on Systems Biology | Biotechnology

    The below mentioned article provides a note on systems biology.

    Systems biology is a new area of biology where an organism is viewed as an assem­bly of integrated and interacting networks of genes, proteins and biochemical reactions, which put life into the organism. Unlike molecular biology which focus on molecules, such as sequence of nucleotides and proteins, systems biology focus on systems that are composed of molecular components.

    Scope of Systems Biology:

    To understand the whole system of an organism follow­ing are the keys:

    1. Understanding structure of the system, such as gene regulatory and biochemical net­works, as well as physical structures.

    2. Understanding of dynamics of the system, both quantitative and qualitative analysis as well as construction of theory/model with powerful prediction capability.

    3. Understanding of control methods of the system.

    4. Understanding of design methods of the system.

    Goals and Approaches of Systems Biology:

    The fundamental characteristics of sys­tems biology are embodied in data and knowledge integration, the comprehensiveness of the data acquisition, and the ability to digitalize biological output. Integrative Biology and Digital Biology may be considered synonymous.

    Systems biology seeks to explain the biological phenomenon not on a gene-by-gene basis, but through the interaction of all the cellular and biochemical components in a cell or an organism. Systems biology is still in its infancy but that has to be explored and the area that we believe to be the main stream in biological sciences in this century (Fig. 23.4).

    The Institutes for Systems Biology, USA Ottawa Institute of Systems Biology, Canada, have been established to cater the needs of this new emerging discipline.

    Steps in Systems Biology:

    There are five simple steps to understand the systems biology :

    1. Defining of input and output of a system.

    2. Defining the relevant parts of the system under study.

    3. Different states of inputs are used and the relationship between these states and the output are quantified.

    4. The changes in system states are related to output using one of a. variety of mathe­matical tools, such as principal component analysis.

    5. With the help of a computer, the original network map is prepared on the basis of the results of the previous experiments.

    Systems Biology in Plant Science:

    The entire genome sequence of Arabidopsis and rice has been published in the year 2000 and 2005 respectively. The large scale c-DNA sequencing projects are rapidly progressing for plants like Medicago, corn, wheat, soya­-bean, sugarcane, poplar, etc.

    Functional genomics addresses the question what is the function of all these genes? Computational biology integrates data and ultimately helps us to understand the functioning of whole biological systems.

    Plant systems biology deals ‘ with the aspects like cell cycle, root development, cell death, bud formation, flower formation, leaf development, plant-microbe interactions, etc.

    Each system is highly com­plex, and biologists now have the tools at hand to view the global behaviour of their preferred model systems and to better select the genes that are likely to play key roles in the regulation of entire processes. Furthermore, cloning of ORFs (Open Reading Frames), promoters and making of new constructs can change or improve the gene expression which may be helpful.

    Significance of Systems Biology:

    With the development of new tools and techniques the complex system between genes, proteins and other metabolites can be understood they do not work in isolation, they interact among themselves in highly organized and complex ways.

    Systems biology deals with these complex interactions, which may be the biosynthetic pathways or translational modifications of proteins or the signal transduction pathway leading to expression of a set of specific genes (Fig. 23.5).

    For example, the immune system is not the result of a single mechanism or a set of genes instead, the inte­ractions of numerous genes, proteins, metabolisms and the organism’s external environ­ment, produce immune responses to fight infections and diseases. Thus, a study of all aspects of any system in an organism makes the subject of systems biology.


    23.5: Fungal Infections of the Reproductive System - Biology

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