5.6: How does code-switching come into play in the classroom?
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Written By: Trenice Durio
Learning Objectives
Upon reading this article, the reader will be able:
1.) To know the three types of code-switching: borrowing, calque, and intersentential.
2.) To use strategies/ activities to increase their students' abilities to code-switch effectively.
3.) To recognize the negative and positive aspects of code-switching.
What is Code-Switching?
Note
Definitions of Code-Switching
“consciously modifying speech to slip from one culture to another.”
(Haddock, 2008)
“change from lexical register to another”
(McCoy, 2006, p. 24)
“Shift in language that is guided by a shift in context”
(Knestrict & Schoensteadt, 2005, p. 177)
“use of complete sentences, phrases, and borrowed words from another language”
(Hughes, Shaunessy, and Brice, 2006, p. 8)
Code switching is the ability to recognize that different scenarios require a change in speech among multilingual groups. A person must identify that a change in a social situation has occurred in order to switch codes. Codes refer to different contexts of speech, such as formal vs. informal language or Spanish vs. English. Students who are bilingual or who come from different cultural backgrounds are noted for their ability to code switch. Since standard English is not their primary language, it takes these students added efforts to speak according to the standard Some are able to code switch fluently from one language to another, while some are unable to switch back and forth with ease. Unless a proper understanding of when and how to code switch is attained by the student, a lack of understanding will sometimes translate to a lack of knowledge. (Wheeler, 2008) For African-American students this lack of knowledge means “persistent over-representation in special education and remedial basic skills classes to under-representation in honor classes, to lagging SAT scores, to low high school graduation rates” (Wheeler, 2008).
Types of Code-Switching
There are three types of code-switching: borrowing, calque, and intersentential. The first type refers to using words from the secondary language in the same grammatical format, but words unavailable in the primary language (Hughes et al., 2006). Calque is literally translating a phrase without regard to proper context (Hughes et al., 2006). Third, intersentential is inserting an entire phrase from the secondary language into a conversation using the other language (Hughes et al., 2006). All types refer to switching back and forth from one language to another to communicate to others based on the situation.
Note
Types of Code-Switching
Borrowing : Saying "Bueno bye" (Spanish and English) instead of "Goodbye" (English) or "Buenos dias" (Spanish)
Calque : Saying "El lote deparquear" (Improper Spanish Translation) instead of "Parking lot" (English) or "Campo de estacionamiento" (Proper Spanish Translation)
Intersentential : Saying "Sientense, students" (Spanish and English) instead of "Sit down, students" (English) or "Sientense estudiantes" (Spanish)
Code-Switching As A Valuable Tool
For bilingual speakers, code-switching is a valuable tool for various reasons. It offers another language to use when words in the primary language are insufficient due to the speaker or listener’s limited English proficiency (Hughes et al., 2006). Since code-switching is motivated by situations, the speaker may use it to identify with a particular group of people (Hughes et al., 2006). Also, it can be a sociolinguistic tool, used for clarification, emphasis, separation from feelings, and achievement of a dramatic effect(Hughes et al., 2006). By giving the speaker more ways in which to communicate, code-switching is a useful tool in the bilingual community.
Code-Switching As a Negative Tool
Although code-switching can add to a student’s toolbox, it can also be a sign of delay in language ability. Bilingualism can be viewed as either a subtractive or an additive language process. Subtractive refers to increasing the fluency and vocabulary in one language while the ability in the other decreases(Hughes et al., 2006). Therefore, this process involves the replacement of one language for the other. The additive process is when the speaker holds on to the knowledge of the first language and adds on the skills of the second language(Hughes et al., 2006). Some people view code-switching as negative because they view it from the subtractive perspective, believing that the addition of a second language shows lack of knowledge. Also, a bias of which language is inserted into English is evident. For example, if a French phrase such as “je ne sais quoi” is used it shows academic achievement, while Spanish phrases such as “adios” signifies a lower status (Hughes et al., 2006). If a language is not used at a proper time or place, a student’s ability to communicate effectively may be misunderstood.
They’re Not Speaking Incorrectly!
A child says to his teacher, “I be doing my homework” or “Hola! How are you?” These examples both represent using vernacular language in an improper setting or lack of code switching (Wheeler, 2008). Teachers often identify this as speaking incorrect standard English. However, these students are not in fact making errors, but are simply speaking in their vernacular language. They were not attempting to communicate in Standard English, therefore the problem does not lie in correcting their speech, but teaching students an alternative means of communication (Wheeler, 2008). By knowing the focus of education, teachers are able to more effectively meet the students’ educational needs. To help teachers meet the needs of struggling students, Rebecca S. Wheeler designed a three-step strategy, including: Scientific Inquiry, Comparison and Contrast, and Code-Switching as Metacognition (2008). The first step, Scientific Inquiry, is to build a code-switching chart identifying grammar patterns in the student’s writings. The chart is divided into five sections: examine sentences, seek patterns, define the pattern, test the hypothesis, and write informal English pattern. This step identifies the area of struggle for students and the pattern they use in informal language. For example, instead of using “owner + ‘s + what is owned” (i.e. Leon’s ball) as in formal language, students may use “owner + what is used” (i.e. Leon ball) in their informal language (Wheeler, 2008, p. 56). After the pattern is defined, the next step, is to compare and contrast the Formal English with Informal English, using the chart. Now, the students can visually and audibly know the difference between the two forms of language. Lastly, in Code-Switching as Metacognition, the child practices code switching between the two. Students will identify the appropriate language for a given setting. Students can understand the two choices of formal and informal language and know the appropriate time to use each. (Wheeler, 2008) By giving students an alternative form of language and not changing their primary form of communication, teachers give students an additional tool in their education toolbox.
From the Perspective of a Teacher
In William McCoy's article, “Helping Students Find A Voice, by Giving Them the Words,” a teacher gives a personal account of how he succeeded at teaching 26 “at risk” students how to code-switch effectively. He believes it is the lack of understanding of their expectations and an insufficient academic vocabulary that causes students to fail in school. The first step in using the right words for a given setting is to know the audience (McCoy, 2006). He uses code-switching activities in his class, such as:
- Simulating a job interview with two applicants, one using slang and the other formal language. Through this activity, students understand that the type of language used has a strong impact on other’s perceptions of that person (McCoy, 2006).
- Writing a conversation in informal language on the board, and asking students to translate into the language used by professionals, such as a lawyer or professor (McCoy, 2006).
McCoy reports that at the beginning this exercise is a struggle for his students, but with practice their performance improves. After identifying the proper audience for a situation, students are to acknowledge the difference in situations and appropriate word usage. To teach this lesson, McCoy gives them a phrase like “I want some money,” and has them discuss how their speech would differ when robbing someone at a bank, asking for a raise at work, and requesting money from a parent. It is easy to see that each situation merits a different set of words by the speaker. Finally the students can use their knowledge and apply it to writing, focusing on having a purpose for their work. The goal is for the writer to have a thesis, support it with details, and recognize the opposing side's argument. As a result of McCoy’s work, he stated “I was reminded that students can succeed when given the tools and experiences to do so” (McCoy, 2006, p. 25). Without first identifying that students did not possess the skills to succeed, he would not be able to give them the tools needed for success.
References
Haddock, Captain. (2008). Obama's "code-switching" on education. Ed News Colorado . Sept. 12, 2008, ednewscolorado.org/blog/index.php/2008-04-15/obamas-code-switching-on-education/
Hughes, C. E., Shaunessy, E. S., & Brice, A.R. (2006). Code switching among bilingual and limited English proficient students: possible indicators of giftedness. Journal for the Education of the Gifted , 30 (1), 7-28.
Knestrict, T. & Schoensteadt L. (2005). Teaching social register and code switching in the classroom. Journal of Children & Poverty , 11 (2), 177-185.
McCoy, William. (2006). Helping students find a voice, by giving them the words. California English, 24-25.
Wheeler, R. S. (2008). Becoming adept at code-switching. Educational Leadership , 65 (7), 54-58.


6.11: Exercise - Combining Bins
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In the previous exercise, we took our original Rare and Frequent epochs and subdivided them according to whether the previous trial was Rare or Frequent, yielding four bins instead of two. We should be able to reconstruct our original two bins from the four new bins. However, there is a little trick that you need to know about.
Let’s start by thinking about how to reconstruct the original Rare bin, in which the preceding trial could be either Rare or Frequent. We could simply take Bin 1 (Rare preceded by Rare) and average it with Bin 2 (Rare preceded by Frequent). In ERP Bin Operations , we could implement this with the following equation:
bin5 = (bin1 + bin2) / 2 Label Rare preceded by Rare or Frequent
However, this would not give us the same waveforms that we obtained in our original analysis that disregarded whether the previous trial was Rare or Frequent. Can you figure out why?
The reason is that this equation gives Bins 1 and 2 equal weight in the new bin, but there were 6 trials with Bin 1 and 22 trials with Bin 2 (which you can see by typing ERP.ntrials in the Matlab Command Window). The equation above assumes that there were equal numbers of trials in each bin. To give each trial equal weight (which is what happened when the identity of the previous trial was disregarded by BINLISTER), we would need the following equation in ERP Bin Operations :
bin5 = (6*bin1 + 22*bin2) / 28 Label Rare preceded by Rare or Frequent
However, the exact equation would depend on how many trials were in Bins 1 and 2, which might vary across participants. To make this easier, ERP Bin Operations contains a function called wavgbin for performing weighted averaging , in which each bin is automatically weighted by the number of trials.
Let’s see how these different methods of averaging work. Make sure that the dataset from the previous exercise is loaded ( 12_P3_Sequential ). Select EEGLAB > ERPLAB > ERP Operations, ERP Bin Operations . In the equations panel, clear out any previous equations and enter the three following equations:
bin5 = (bin1 + bin2) / 2 Label Rare preceded by Rare or Frequent, equal weight
bin6 = (6*bin1 + 22*bin2) / 28 Label Rare preceded by Rare or Frequent, manually weighted
bin7 = wavgbin(bin1, bin2) Label Rare preceded by Rare or Frequent, automatically weighted
Make sure that the Mode is set to Modify existing ERPset , because we’re going to add these three bins to the four existing bins. Then click RUN .
Now plot Bins 5, 6, and 7. You can’t actually see the waveforms for Bin 6, because it’s identical to Bin 7, and the Bin 7 waveform exactly covers up the Bin 6 waveform. This shows that the wavgbin function is working properly. However, the P3b is slightly larger for these bins than for Bin 5. Why is that? You should be able to figure it out given what you know about the amplitude of the P3b in Bins 1 and 2 and the nature of the equations used for Bins 5, 6, and 7.
An obvious question is whether you should use unweighted averaging (as in Bin 5) or weighted averaging (as in Bins 6 and 7) when combining bins together. There isn’t a single answer to this question. If you’re trying to create something equivalent to what you would have gotten if you hadn’t subdivided the trials to begin with, then you’ll want to use weighted averaging. But beyond that, the answer will depend on the logic of your experimental design and your scientific questions.


Hydrogen Bonding
Skills to Develop
- Define and illustrate hydrogen bonds
It's a general rule that "hard" things like to bond with other hard things, and "soft" things like to bond with other soft things. (See the previous section for an explanation of hard and soft.) The reason for this is because hard-hard combinations are very favorable. Remember that hard means "hard to polarize", which usually means small and highly charged. Hard-hard combinations are based on strong Coulomb forces, between relatively big charges relatively close together.
Hydrogen bonds are a special case of hard-hard interaction that occurs in covalent molecules. Hydrogen that is bonded to very electronegative elements (N, O and F) will have a big δ+ (partial positive charge). N, O or F bonded to C or H will have a big δ- (partial negative charge). If the N, O or F has lone pairs, these can make interactions with a hydrogen on another molecule. The partial charges are pretty big, because of the big difference in electronegativity. Also, they can get very close together because these elements (especially H) are very small.
Hydrogen bonds are also an example of a dipole-dipole force, but they are extra big dipole-dipole forces because the charges are big (for partial charges) and the distances are short. They are also an example of Lewis acid-base interactions (because the electrons in the interaction come from a lone pair on N, O or F). And they are also an example of a HOMO/LUMO interaction. The H which is bound to a very electronegative atom has a low LUMO, because the energy match is bad between very different electronegativity atoms, leading to low splitting. The lone pair on the N, O or F is a high HOMO, because it is non-bonding, not bonding. These can then make a new bond.
Hydrogen bonds are very important. Because they are very strong, water is a liquid over a much wider temperature range than we would expect otherwise. Hydrogen bonds are also extremely important in biochemistry. They help hold proteins in their correct shape, help DNA store genetic information, and help enzymes make reactions go quickly.


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asylum
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legal protection extended by one country to citizens of another.
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chain migration
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the process of sequential migration from the same community of origin.
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circular migration
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repeated pattern of movement between locations, usually associated with work.
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cultural hybridity
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the exchange and innovation within cultures that is a product of migration and globalization.
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diaspora
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the movement and dispersal of large ethnic groups from their homelands because of warfare, institutionalized violence, or opportunity (usually education or employment).
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displacement
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migration due to persecution, conflict, or violence; involves refugees and those seeking asylum.
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environmental migration
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displacement caused by natural disasters, such as earthquakes, hurricanes, or droughts.
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epidemic
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a disease that spreads more than expected among a given group of people.
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forced labor
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the recruitment, transportation, transfer, and/or harboring of persons by means of threat or use of force or coercion for the purpose of financial exploitation.
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forced migration
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migration due to persecution, conflict, or violence; involves refugees and those seeking asylum.
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human trafficking
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the recruitment, transportation, transfer, and/or harboring of persons by means of threat or use of force or coercion for the purpose of exploitation. A form of modern slavery.
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immigrant
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an individual who moves permanently from one country to another.
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internal migration
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the domestic movement of people from rural to urban areas.
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labor migration
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the movement of people for the purpose of employment and/or economic stability.
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migrant
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a person who moves from their place of origin to reestablish a household.
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migration
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movement from one place to another that reestablishes a household, whether temporarily or permanently.
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modern slavery
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the recruitment, transportation, transfer, and/or harboring of persons by means of threat or use of force or coercion for the purpose of exploitation.
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pandemic
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an outbreak of a disease over a broad area.
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peasants
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a rural, subsistence-based agricultural class with limited landholdings.
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postcolonialism
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enduring politico-economic relationships between former colonizers and their former colonies that continue to have negative effects on the former colonies after independence.
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remittances
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transfers of money from workers back to their home countries, usually for their families.
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transnationalism
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the construction of social, economic, and political networks that originate in one country and then cross or transcend nation-state boundaries.


4.8: Case Questions
Open innovation means more than searching online for others who are attempting to solve the same problems you are and trying to take inspiration from other corporations and other entrepreneurs. It also involves forming partnerships, supporting new ventures, investing in business accelerators, and acquiring firms that innovate in ways that are valuable to your firm or to your entrepreneurial effort (assuming you can raise the capital to acquire a firm while you develop your invention). 7 Think of an example of a firm (other than Samsung, the example from Merit Morikawa’s article, and Apple, the “easy” answer) that has engaged in all of these practices. What seems to drive these different modes of open innovation? When are they most appropriate? When are they not appropriate ethically?
2 .Read this article to prepare for answering this question: https://www.brookings.edu/blog/brook...-are-we-ready/ . (Brennan Hoban. “Artificial Intelligence Will Disrupt the Future of Work. Are We Ready?” Brookings. May 23, 2018.)
Many signs point to growing automation across a variety of industries in the coming decades. In many cases, disruptive technologies will force people to innovate. Based on the DICEE innovation model, explain how humans will be needed on the design side of innovation to create human-centric products. In what ways can you create a career that is “disruption-proof”?


44.4C: Estuaries- Where the Ocean Meets Fresh Water
- Explain the ecology of estuaries
Estuaries: Where the Ocean Meets Fresh Water
Estuaries form a unique marine biome that occurs where a source of fresh water, such as a river, meets the ocean. Therefore, both fresh water and salt water are found in the same vicinity. Mixing results in a diluted (brackish) saltwater. Estuaries form protected areas where many of the young offspring of crustaceans, mollusks, and fish begin their lives. Salinity of estuaries is a very important factor that influences the organisms found there and their adaptations. The salinity, which varies, is based on the rate of flow of its freshwater sources. Once or twice a day, high tides bring salt water into the estuary. Low tides, occurring at the same frequency, reverse the current of salt water.
The short-term and rapid variation in salinity due to the mixing of fresh water and salt water is a difficult physiological challenge for the plants and animals that inhabit estuaries. Many estuarine plant species are halophytes: plants that can tolerate salty water on their roots or sea spray. In some halophytes, filters in the roots remove the salt from the water that the plant absorbs. Other plants are able to pump oxygen into their roots. Animals, such as mussels and clams, have developed behavioral adaptations that expend a lot of energy to function in this rapidly-changing environment. When these animals are exposed to low salinity, they stop feeding, close their shells, and switch from aerobic respiration (in which they use gills) to anaerobic respiration (a process that does not require oxygen). When high tide returns to the estuary, the salinity and oxygen content of the water increases, causing these animals to open their shells, begin feeding, and to return to aerobic respiration.
Key Points
- Estuaries acts as nursery grounds for crustaceans, mollusks, and fish.
- Salinity, regulated by the influx of seawater and outflow of freshwater once or twice each day, is a determining factor in the types of organisms that can live there.
- To deal with the short-term and rapid variation in salinity, estuary species have developed specialized adaptations that enable them to live with the salty conditions; as a result, most plant species found in estuaries are halophytes.
Key Terms
- brackish : salty or slightly salty, as a mixture of fresh and sea water, such as that found in estuaries
- halophyte : any plant that tolerates an environment having a high salt content
- estuary : coastal water body where ocean tides and river water merge


4.5: Introduction to Analyzing Data from Financial Statements
What you will learn to do: Analyze data from Financial Statements
The key financial statements of a company provide a snapshot of the financial position of the organization and this is extremely useful to the internal and external stakeholders of the business. However, the real power of financial statements lies in our ability to analyze the information on these financial statements to evaluate the past and present financial position of the company.
Financial statement analysis allows us to determine the health of the business in terms of how well it manages its inventories, expenses, revenues and debt. Analyzing these financial statements also gives us the ability to compare the financial health of the business against other companies in the same industry. In this section you will learn how companies report items such as inventories, assets, stockholder equity, revenues and expenses on their financial statements.


9: Power series methods
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- 9.1: Power Series
- Many functions can be written in terms of a power series. If we assume that a solution of a diﬀerential equation is written as a power series, then perhaps we can use a method reminiscent of undetermined coeﬃcients. That is, we will try to solve for the coefficients of the expansion . Before we can carry out this process, let us review some results and concepts about power series.
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- 9.3: Singular Points and the Method of Frobenius
- While behavior of ODEs at singular points is more complicated, certain singular points are not especially difficult to solve. Let us look at some examples before giving a general method. We may be lucky and obtain a power series solution using the method of the previous section, but in general we may have to try other things.
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- 9.E: Power series methods (Exercises)
- These are homework exercises to accompany Libl's "Differential Equations for Engineering" Textmap. This is a textbook targeted for a one semester first course on differential equations, aimed at engineering students. Prerequisite for the course is the basic calculus sequence.
Thumbnail: The sine function and its Taylor approximations around \(x_o=0\) of 5 th and 9 th degree.
Contributors and Attributions
- Jiří Lebl ( Oklahoma State University ).These pages were supported by NSF grants DMS-0900885 and DMS-1362337.


3.9.E: Problems on Boundedness and Diameters (Exercises)
Show that if a set \(A\) in a metric space is bounded, so is each subset \(B \subseteq A .\)
Prove that if the sets \(A_{1}, A_{2}, \ldots, A_{n}\) in \((S, \rho)\) are bounded, so is
\[
\bigcup_{k=1}^{n} A_{k}.
\]
Disprove this for infinite unions by a counterexample.
[Hint: By Theorem \(1,\) each \(A_{k}\) is in some \(G_{p}\left(\varepsilon_{k}\right),\) with one and the same center \(p\). If the number of the globes is finite, we can put max \(\left(\varepsilon_{1}, \ldots, \varepsilon_{n}\right)=\varepsilon,\) so \(G_{p}(\varepsilon)\) contains all \(A_{k} .\) Verify this in detail.
\(\Rightarrow 3 .\) From Problems 1 and 2 show that a set \(A\) in \((S, \rho)\) is bounded iff it is contained in a finite union of globes,
\[
\bigcup_{k=1}^{n} G\left(p_{k} ; \varepsilon_{k}\right).
\]
A set \(A\) in \((S, \rho)\) is said to be totally bounded iff for every \(\varepsilon>0\) (no matter how small), \(A\) is contained in a finite union of globes of radius \(\varepsilon\). By Problem 3, any such set is bounded. Disprove the converse by a counterexample.
[Hint: Take an infinite set in a discrete space.]
Show that distances between points of a globe \(\overline{G}_{p}(\varepsilon)\) never exceed 2\(\varepsilon\). (Use the triangle inequality!) Hence infer that \(d G_{p}(\varepsilon) \leq 2 \varepsilon\). Give an example where \(d G_{p}(\varepsilon)<2 \varepsilon .\) Thus the diameter of a globe may be less than twice its radius.
[Hint: Take a globe \(G_{p}\left(\frac{1}{2}\right)\) in a discrete space.]
Show that in \(E^{n}\left(* \text { as well as in } C^{n} \text { and any other normed linear space }\right.\) \(\neq\{0\}\) ), the diameter of a globe \(G_{p}(\varepsilon)\) always equals 2\(\varepsilon\) (twice its radius).
[Hint: By Problem \(5,2 \varepsilon\) is an upper bound of all \(\rho(\overline{x}, \overline{y})\) with \(\overline{x}, \overline{y} \in G_{p}(\varepsilon) .\)
To show that there is no smaller upper bound, prove that any number
\[
2 \varepsilon-2 r \quad(r>0)
\]
is exceeded by some \(\rho(\overline{x}, \overline{y}) ;\) e.g., take \(\overline{x}\) and \(\overline{y}\) on some line through \(\overline{p}\),
\[
\overline{\boldsymbol{x}}=\overline{\boldsymbol{p}}+\boldsymbol{t} \overrightarrow{\boldsymbol{u}},
\]
choosing suitable values for \(t\) to get \(\rho(\overline{x}, \overline{y})=|\overline{x}-\overline{y}|>2 \varepsilon-2 r . ]\)
Prove that in \(E^{n},\) a set \(A\) is bounded iff it is contained in an interval.
Prove that for all sets \(A\) and \(B\) in \((S, \rho)\) and each \(p \in S\)
\[
\rho(A, B) \leq \rho(A, p)+\rho(p, B).
\]
Disprove
\[
\rho(A, B)<\rho(A, p)+\rho(p, B)
\]
by an example.
Find \(\sup x_{n}, \inf x_{n}, \max x_{n},\) and \(\min x_{n}\) (if any) for sequences with general term
(a) \(n\);
(b) \((-1)^{n}\left(2-2^{2-n}\right)\);
(c) \(1-\frac{2}{n}\);
(d) \(\frac{n(n-1)}{(n+2)^{2}}\).
Which are bounded in \(E^{1} ?\)
Prove the following about lines and line segments.
(i) Show that any line segment in \(E^{n}\) is a bounded set, but the entire line is not.
(ii) Prove that the diameter of \(L(\overline{a}, \overline{b})\) and of \((\overline{a}, \overline{b})\) equals \(\rho(\overline{a}, \overline{b})\).
Let \(f : E^{1} \rightarrow E^{1}\) be given by
\[
f(x)=\frac{1}{x} \text { if } x \neq 0, \text { and } f(0)=0.
\]
Show that \(f\) is bounded on an interval \([a, b]\) iff 0\(\notin[a, b] .\) Is \(f\) bounded on \((0,1) ?\)
Prove the following:
(a) If \(A \subseteq B \subseteq(S, \rho),\) then \(d A \leq d B\).
(b) \(d A=0\) iff \(A\) contains at most one point.
(c) If \(A \cap B \neq \emptyset\), then
\[
d(A \cup B) \leq d A+d B.
\]
Show by an example that this may fail if \(A \cap B=\emptyset\).


12.6.S: Summary
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Summary
As computing and networking resources have become more and more an integral part of business, they have also become a target of criminals. Organizations must be vigilant with the way they protect their resources. The same holds true for us personally: as digital devices become more and more intertwined with our lives, it becomes crucial for us to understand how to protect ourselves.
Study Questions
- Briefly define each of the three members of the information security triad.
- What does the term authentication mean?
- What is multi-factor authentication?
- What is role-based access control?
- What is the purpose of encryption?
- What are two good examples of a complex password?
- What is pretexting?
- What are the components of a good backup plan?
- What is a firewall?
- What does the term physical security mean?
Exercises
- Describe one method of multi-factor authentication that you have experienced and discuss the pros and cons of using multi-factor authentication.
- What are some of the latest advances in encryption technologies? Conduct some independent research on encryption using scholarly or practitioner resources, then write a two- to three-page paper that describes at least two new advances in encryption technology.
- What is the password policy at your place of employment or study? Do you have to change passwords every so often? What are the minimum requirements for a password?
- When was the last time you backed up your data? What method did you use? In one to two pages, describe a method for backing up your data. Ask your instructor if you can get extra credit for backing up your data.
- Find the information security policy at your place of employment or study. Is it a good policy? Does it meet the standards outlined in the chapter?
- How are you doing on keeping your own information secure? Review the steps listed in the chapter and comment on how well you are doing.
- "Born to be breached" by Sean Gallagher on Nov 3 2012. Arstechnica . Retrieved from http://arstechnica.com/information-t...e-most-common/ on May 15, 2013. ↵
- SANS Institute. "A Short Primer for Developing Security Policies." Accessed from http://www.sans.org/security-resourc...icy_Primer.pdf on May 31, 2013. ↵
- Taken from SANS Institute's Mobile Device Checklist. You can review the full checklist at www.sans.org/score/checklists/mobile-device-checklist.xls . ↵


11.6: The Enlightenment
The Enlightenment
The Enlightenment was a philosophical movement in the eighteenth century composed of intellectuals who were greatly impressed with the achievements of the Scientific Revolution, and concerned with the idea of reason. They hoped that by using the scientific method, they could make progress toward a better society than the one they had inherited. Reason, natural law, hope, progress— these were common words to the thinkers of the time.
The Enlightenment was especially influenced by the ideas of two seventeenth-century Englishmen, Isaac Newton and John Locke. To Newton, the physical world and everything in it were like a giant machine (the Newtonian world-machine). If you could discover the natural laws that governed the physical world, then it was possible to discover the natural laws that governed human society.
John Locke (1632-1704)
John Locke’s theory of knowledge also greatly affected eighteenth-century intellectuals. In his Essay Concerning Human Understanding , Locke argued that every person was born with a blank mind (known as tabula rasa). Furthermore, he suggested that people were molded by the experiences they gained from the world around them.
John Locke's Kit-cat portrait by Godfrey Kneller, National Portrait Gallery, London Source: https://commons.wikimedia.org/wiki/F...ry,_London.JPG
Montesquieu (1689-1755)
Charles-Louis de Secondat, the Baron de Montesquieu, was a French noble. His most famous work, The Spirit of the Laws , was published in 1748. In this study of government, he tried to use the scientific method to find the natural laws that govern the social and political relationships of human beings.
Montesquieu identified three basic kinds of governments:
- republics, suitable for small states
- despotism, ideal for large states
- monarchies, appropriate for moderately sized states.
Montesquieu believed that England’s government had three branches: the executive (the monarch), the legislative (parliament), and the judicial (the courts of law). By separating the powers of each branch, he believed that each one would act as a check on the other. Because it prevents any one person or group from gaining too much power, he argued this system provides the greatest amount of freedom and security, not for the people, but for the state.
Jean-Jacques Rousseau (1712-1778)
By the mid-eighteenth century, a new group of philosophers had come of age. The most famous of this later generation was a man named Jean-Jacques Rousseau. As a young man, he wandered France and Italy holding various jobs. Eventually, he found himself in Paris where he became a member of the circle of philosophes.
In his Discourse on the Origins of the Inequality of Mankind, he argued that people adopted laws and government in order to preserve their private property. In the process of doing so, however, they had become enslaved by the government. What then, should people do in order to regain their freedom and throw off the chains of bondage?
In a famous work titled The Social Contract (1762), Rousseau suggested that an entire society agrees to be governed by the general will. If an individual wish to follow his/her own self-interest, they must be forced to abide by the will of the majority. In other words, liberty is achieved by being forced to follow what is best for the general will because it is what is best for the community at large.
Attribution: Material modified from CK-12 6.4 Absolutism and Enlightenment


5.10G: Benzoate Catabolism
- List a function of Rhodococcus in the scientific community
Key Points
- In the absence of water-splitting, photosynthesis is anoxygenic. Therefore, hydrogen production is sustained without inhibition from generated oxygen.
- Strains of Rhodococcus are applicably important owing to their ability to catabolize a wide range of compounds and produce bioactive steroids, acrylamide, and acrylic acid, and their involvement in fossil fuel biodesulfurization.
- The use of Rhodococcus is borne out of its ability to metabolize harmful environmental pollutants, such as toluene, naphthalene, herbicides, and PCBs.
Key Terms
- catabolism : Destructive metabolism, usually includes the release of energy and breakdown of materials.
- Rhodococcus : a genus of aerobic, nonsporulating, nonmotile Gram-positive bacteria closely related to Mycobacteria and Corynebacteria.
- benzoate : Any salt or ester of benzoic acid.
Benzoate catabolism is a series of chemical reactions resulting in the breakdown of benzoate. The purple non-sulphur (PNS) bacteria Rhodobacter sphaeroides is able to produce hydrogen from a wide range of organic compounds (chiefly organic acids) and light. The photo-system required for hydrogen production in Rhodobacter (PS-I) differ from its oxygenic photosystem (PS-II) due to the requirement of organic acids and the inability to oxidize water. In the absence of water-splitting, photosynthesis is anoxygenic. Therefore, hydrogen production is sustained without inhibition from generated oxygen. In PNS bacteria, hydrogen production is due to catalysis by nitrogenase. Hydrogenases are also present but the production of hydrogen by [FeFe]-hydrogenase is less than ten times the hydrogen uptake by [NiFe]-hydrogenase. Only under nitrogen-deficient conditions is nitrogenase activity sufficient to overcome uptake hydrogenase activity, resulting in net generation of hydrogen.
Rhodococcus is a genus of aerobic, nonsporulating, nonmotile Gram-positive bacteria closely related to Mycobacteria and Corynebacteria. While a few species are pathogenic, most are benign and have been found to thrive in a broad range of environments, including soil, water, and eukaryotic cells. Fully sequenced in October 2006, the genome is known to be 9.7 megabasepairs long and 67% G/C. Strains of Rhodococcus are applicably important owing to their ability to catabolize a wide range of compounds and produce bioactive steroids, acrylamide, and acrylic acid, and their involvement in fossil fuel biodesulfurization. This genetic and catabolic diversity is not only due to the large bacterial chromosome, but also to the presence of three large linear plasmids. Rhodococcus is also an experimentally advantageous system owing to a relatively fast growth rate and simple developmental cycle. However, as it stands now, Rhodococcus is not well characterized. Another important application of Rhodococcus comes from bioconversion, using biological systems to convert cheap starting material into more valuable compounds. This use of Rhodococcus is borne out of its ability to metabolize harmful environmental pollutants, such as toluene, naphthalene, herbicides, and PCBs. Rhodococci typically metabolize aromatic substrates by first oxygenating the aromatic ring to form a diol (two alcohol groups). Then, the ring is cleaved with intra/extradiol mechanisms, opening the ring and exposing the substrate to further metabolism. Since the chemistry here is very stereospecific, the diols are created with predictable chirality. While controlling the chirality of chemical reaction presents a significant challenge for synthetic chemists, biological processes can be used instead to faithfully produce chiral molecules in cases where direct chemical synthesis is infeasible or inefficient. An example of this is the use of Rhodococcus to produce indene, a precursor to the AIDS drug Crixivan TM , a protease inhibitor, and containing two of the five chiral centers needed in the complex.


4.22: Introduction to Financial Statements
What you will learn to do: Examine the elements of common financial statements
There are many ways that we can describe a business—by product, by target market or even by geographic location. However, simply describing a business gives us little information about the internal workings of the business and how efficiently it is managing its resources. This internal examination is accomplished by looking at a company’s financial statements. These statements are like a company report card. They tell external (and internal) stakeholders how well the company is managing its financial resources. In order to understand this financial report card it is necessary to first have a basic understanding of how companies account for all of the financial transactions of the business using the double entry accounting system.
Once you see how financial transactions effect the various accounts you can move on to reading and understanding the key financial statements of the business. Ultimately these financial statements will be used to create annual financial reports that investors can use to evaluate the overall financial health of the business. As you can imagine, creating these financial statements is an essential part of managing a business.


24.3: Bacterial Infections of the Gastrointestinal Tract
- Identify the most common bacteria that can cause infections of the GI tract
- Compare the major characteristics of specific bacterial diseases affecting the GI tract
A wide range of gastrointestinal diseases are caused by bacterial contamination of food. Recall that foodborne diseasecan arise from either infection or intoxication. In both cases, bacterial toxins are typically responsible for producing disease signs and symptoms. The distinction lies in where the toxins are produced. In an infection, the microbial agent is ingested, colonizes the gut, and then produces toxins that damage host cells. In an intoxication, bacteria produce toxins in the food before it is ingested. In either case, the toxins cause damage to the cells lining the gastrointestinal tract, typically the colon. This leads to the common signs and symptoms of diarrhea or watery stool and abdominal cramps, or the more severe dysentery. Symptoms of foodborne diseases also often include nausea and vomiting, which are mechanisms the body uses to expel the toxic materials.
Most bacterial gastrointestinal illness is short-lived and self-limiting; however, loss of fluids due to severe diarrheal illness can lead to dehydration that can, in some cases, be fatal without proper treatment. Oral rehydration therapy with electrolyte solutions is an essential aspect of treatment for most patients with GI disease, especially in children and infants.
Staphylococcal Food Poisoning
Staphylococcal food poisoning is one form of food intoxication. When Staphylococcus aureus grows in food, it may produce enterotoxins that, when ingested, can cause symptoms such as nausea, diarrhea, cramping, and vomiting within one to six hours. In some severe cases, it may cause headache, dehydration, and changes in blood pressure and heart rate. Signs and symptoms resolve within 24 to 48 hours. S. aureus is often associated with a variety of raw or undercooked and cooked foods including meat (e.g., canned meat, ham, and sausages) and dairy products (e.g., cheeses, milk, and butter). It is also commonly found on hands and can be transmitted to prepared foods through poor hygiene, including poor handwashing and the use of contaminated food preparation surfaces, such as cutting boards. The greatest risk is for food left at a temperature below 60 °C (140 °F), which allows the bacteria to grow. Cooked foods should generally be reheated to at least 60 °C (140 °F) for safety and most raw meats should be cooked to even higher internal temperatures (Figure \(\PageIndex{1}\)).
There are at least 21 Staphylococcal enterotoxins and Staphylococcal enterotoxin-like toxins that can cause food intoxication. The enterotoxins are proteins that are resistant to low pH, allowing them to pass through the stomach. They are heat stable and are not destroyed by boiling at 100 °C. Even though the bacterium itself may be killed, the enterotoxins alone can cause vomiting and diarrhea, although the mechanisms are not fully understood. At least some of the symptoms may be caused by the enterotoxin functioning as a superantigen and provoking a strong immune response by activating T cell proliferation.
The rapid onset of signs and symptoms helps to diagnose this foodborne illness. Because the bacterium does not need to be present for the toxin to cause symptoms, diagnosis is confirmed by identifying the toxin in a food sample or in biological specimens (feces or vomitus) from the patient. Serological techniques, including ELISA, can also be used to identify the toxin in food samples.
The condition generally resolves relatively quickly, within 24 hours, without treatment. In some cases, supportive treatment in a hospital may be needed.
How can S. aureus cause food intoxication?
Shigellosis (Bacillary Dysentery)
When gastrointestinal illness is associated with the rod-shaped, gram-negative bacterium Shigella , it is called bacillary dysentery, or shigellosis. Infections can be caused by S. dysenteriae , S. flexneri , S. boydii , and/or S. sonnei that colonize the GI tract. Shigellosis can be spread from hand to mouth or through contaminated food and water. Most commonly, it is transmitted through the fecal-oral route.
Shigella bacteria invade intestinal epithelial cells. When taken into a phagosome, they can escape and then live within the cytoplasm of the cell or move to adjacent cells. As the organisms multiply, the epithelium and structures with M cells of the Peyer’s patches in the intestine may become ulcerated and cause loss of fluid. Stomach cramps, fever, and watery diarrhea that may also contain pus, mucus, and/or blood often develop. More severe cases may result in ulceration of the mucosa, dehydration, and rectal bleeding. Additionally, patients may later develop hemolytic uremic syndrome (HUS), a serious condition in which damaged blood cells build up in the kidneys and may cause kidney failure, or reactive arthritis, a condition in which arthritis develops in multiple joints following infection. Patients may also develop chronic post-infection irritable bowel syndrome (IBS).
S. dysenteriae type 1 is able to produce Shiga toxin, which targets the endothelial cells of small blood vessels in the small and large intestine by binding to a glycosphingolipid. Once inside the endothelial cells, the toxin targets the large ribosomal subunit, thus affecting protein synthesis of these cells. Hemorrhaging and lesions in the colon can result. The toxin can target the kidney’s glomerulus, the blood vessels where filtration of blood in the kidney begins, thus resulting in HUS.
Stool samples, which should be processed promptly, are analyzed using serological or molecular techniques. One common method is to perform immunoassays for S. dysenteriae. (Other methods that can be used to identify Shigella include API test strips, Enterotube systems, or PCR testing. The presence of white blood cells and blood in fecal samples occurs in about 70% of patients 1 (Figure \(\PageIndex{2}\)). Severe cases may require antibiotics such as ciprofloxacin and azithromycin, but these must be carefully prescribed because resistance is increasingly common.
Compare and contrast Shigella infections and intoxications.
Salmonellosis
Salmonella gastroenteritis, also called salmonellosis, is caused by the rod-shaped, gram-negative bacterium Salmonella . Two species, S. enterica and S. bongori , cause disease in humans, but S. enterica is the most common. The most common serotypes of S. enterica are Enteritidis and Typhi. We will discuss typhoid fever caused by serotypes Typhi and Paratyphi A separately. Here, we will focus on salmonellosis caused by other serotypes.
Salmonella is a part of the normal intestinal microbiota of many individuals. However, salmonellosis is caused by exogenous agents, and infection can occur depending on the serotype, size of the inoculum, and overall health of the host. Infection is caused by ingestion of contaminated food, handling of eggshells, or exposure to certain animals. Salmonella is part of poultry’s microbiota, so exposure to raw eggs and raw poultry can increase the risk of infection. Handwashing and cooking foods thoroughly greatly reduce the risk of transmission. Salmonella bacteria can survive freezing for extended periods but cannot survive high temperatures.
Once the bacteria are ingested, they multiply within the intestines and penetrate the epithelial mucosal cells via M cells where they continue to grow (Figure \(\PageIndex{3}\)). They trigger inflammatory processes and the hypersecretion of fluids. Once inside the body, they can persist inside the phagosomes of macrophages. Salmonella can cross the epithelial cell membrane and enter the bloodstream and lymphatic system. Some strains of Salmonella also produce an enterotoxin that can cause an intoxication.
Infected individuals develop fever, nausea, abdominal cramps, vomiting, headache, and diarrhea. These signs and symptoms generally last a few days to a week. According to the Centers for Disease Control and Prevention (CDC), there are 1,000,000 cases annually, with 380 deaths each year. 2 However, because the disease is usually self-limiting, many cases are not reported to doctors and the overall incidence may be underreported. Diagnosis involves culture followed by serotyping and DNA fingerprinting if needed. Positive results are reported to the CDC. When an unusual serotype is detected, samples are sent to the CDC for further analysis. Serotyping is important for determining treatment. Oral rehydration therapy is commonly used. Antibiotics are only recommended for serious cases. When antibiotics are needed, as in immunocompromised patients, fluoroquinolones, third-generation cephalosporins, and ampicillin are recommended. Antibiotic resistance is a serious concern.
Typhoid Fever
Certain serotypes of S. enterica , primarily serotype Typhi ( S. typhi ) but also Paratyphi, cause a more severe type of salmonellosis called typhoid fever. This serious illness, which has an untreated mortality rate of 10%, causes high fever, body aches, headache, nausea, lethargy, and a possible rash.
Some individuals carry S. typhi without presenting signs or symptoms (known as asymptomatic carriers) and continually shed them through their feces. These carriers often have the bacteria in the gallbladder or intestinal epithelium. Individuals consuming food or water contaminated with these feces can become infected.
S. typhi penetrate the intestinal mucosa, grow within the macrophages, and are transported through the body, most notably to the liver and gallbladder. Eventually, the macrophages lyse, releasing S. typhi into the bloodstream and lymphatic system. Mortality can result from ulceration and perforation of the intestine. A wide range of complications, such as pneumonia and jaundice, can occur with disseminated disease.
S. typhi have Salmonella pathogenicity islands (SPIs) that contain the genes for many of their virulence factors. Two examples of important typhoid toxins are the Vi antigen, which encodes for capsule production, and chimeric A2B5 toxin, which causes many of the signs and symptoms of the acute phase of typhoid fever.
Clinical examination and culture are used to make the diagnosis. The bacteria can be cultured from feces, urine, blood, or bone marrow. Serology, including ELISA, is used to identify the most pathogenic strains, but confirmation with DNA testing or culture is needed. A PCR test can also be used, but is not widely available.
The recommended antibiotic treatment involves fluoroquinolones, ceftriaxone, and azithromycin. Individuals must be extremely careful to avoid infecting others during treatment. Typhoid fever can be prevented through vaccination for individuals traveling to parts of the world where it is common.
Why is serotyping particularly important in Salmonella infections and typhoid fever?
Mary Mallon was an Irish immigrant who worked as a cook in New York in the early 20 th century. Over seven years, from 1900 to 1907, Mallon worked for a number of different households, unknowingly spreading illness to the people who lived in each one. In 1906, one family hired George Soper, an expert in typhoid fever epidemics, to determine the cause of the illnesses in their household. Eventually, Soper tracked Mallon down and directly linked 22 cases of typhoid fever to her. He discovered that Mallon was a carrier for typhoid but was immune to it herself. Although active carriers had been recognized before, this was the first time that an asymptomatic carrier of infection had been identified.
Because she herself had never been ill, Mallon found it difficult to believe she could be the source of the illness. She fled from Soper and the authorities because she did not want to be quarantined or forced to give up her profession, which was relatively well paid for someone with her background. However, Mallon was eventually caught and kept in an isolation facility in the Bronx, where she remained until 1910, when the New York health department released her under the condition that she never again work with food. Unfortunately, Mallon did not comply, and she soon began working as a cook again. After new cases began to appear that resulted in the death of two individuals, the authorities tracked her down again and returned her to isolation, where she remained for 23 more years until her death in 1938. Epidemiologists were able to trace 51 cases of typhoid fever and three deaths directly to Mallon, who is unflatteringly remembered as “Typhoid Mary.”
The Typhoid Mary case has direct correlations in the health-care industry. Consider Kaci Hickox, an American nurse who treated Ebola patients in West Africa during the 2014 epidemic. After returning to the United States, Hickox was quarantined against her will for three days and later found not to have Ebola. Hickox vehemently opposed the quarantine. In an editorial published in the British newspaper The Guardian , 3 Hickox argued that quarantining asymptomatic health-care workers who had not tested positive for a disease would not only prevent such individuals from practicing their profession, but discourage others from volunteering to work in disease-ridden areas where health-care workers are desperately needed.
What is the responsibility of an individual like Mary Mallon to change her behavior to protect others? What happens when an individual believes that she is not a risk, but others believe that she is? How would you react if you were in Mallon’s shoes and were placed in a quarantine you did not believe was necessary, at the expense of your own freedom and possibly your career? Would it matter if you were definitely infected or not?
E. coli Infections
The gram-negative rod Escherichia coli is a common member of the normal microbiota of the colon. Although the vast majority of E. coli strains are helpful commensal bacteria, some can be pathogenic and may cause dangerous diarrheal disease. The pathogenic strains have additional virulence factors such as type 1 fimbriae that promote colonization of the colon or may produce toxins (see Virulence Factors of Bacterial and Viral Pathogens ). These virulence factors are acquired through horizontal gene transfer.
Extraintestinal disease can result if the bacteria spread from the gastrointestinal tract. Although these bacteria can be spread from person to person, they are often acquired through contaminated food or water. There are six recognized pathogenic groups of E. coli , but we will focus here on the four that are most commonly transmitted through food and water.
Enterotoxigenic E. coli (ETEC), also known as traveler’s diarrhea, causes diarrheal illness and is common in less developed countries. In Mexico, ETEC infection is called Montezuma’s Revenge. Following ingestion of contaminated food or water, infected individuals develop a watery diarrhea, abdominal cramps, malaise (a feeling of being unwell), and a low fever. ETEC produces a heat-stable enterotoxin similar to cholera toxin, and adhesins called colonization factors that help the bacteria to attach to the intestinal wall. Some strains of ETEC also produce heat-labile toxins. The disease is usually relatively mild and self-limiting. Diagnosis involves culturing and PCR. If needed, antibiotic treatment with fluoroquinolones, doxycycline, rifaximin, and trimethoprim-sulfamethoxazole (TMP/SMZ) may shorten infection duration. However, antibiotic resistance is a problem.
Enteroinvasive E. coli (EIEC) is very similar to shigellosis, including its pathogenesis of intracellular invasion into intestinal epithelial tissue. This bacterium carries a large plasmid that is involved in epithelial cell penetration. The illness is usually self-limiting, with symptoms including watery diarrhea, chills, cramps, malaise, fever, and dysentery. Culturing and PCR testing can be used for diagnosis. Antibiotic treatment is not recommended, so supportive therapy is used if needed.
Enteropathogenic E. coli (EPEC) can cause a potentially fatal diarrhea, especially in infants and those in less developed countries. Fever, vomiting, and diarrhea can lead to severe dehydration. These E. coli inject a protein (Tir) that attaches to the surface of the intestinal epithelial cells and triggers rearrangement of host cell actin from microvilli to pedestals. Tir also happens to be the receptor for Intimin, a surface protein produced by EPEC, thereby allowing E. coli to “sit” on the pedestal. The genes necessary for this pedestal formation are encoded on the locus for enterocyte effacement (LEE) pathogenicity island. As with ETEC, diagnosis involves culturing and PCR. Treatment is similar to that for ETEC.
The most dangerous strains are enterohemorrhagic E. coli (EHEC), which are the strains capable of causing epidemics. In particular, the strain O157:H7 has been responsible for several recent outbreaks. Recall that the O and H refer to surface antigens that contribute to pathogenicity and trigger a host immune response (“O” refers to the O-side chain of the lipopolysaccharide and the “H” refers to the flagella). Similar to EPEC, EHEC also forms pedestals. EHEC also produces a Shiga-like toxin. Because the genome of this bacterium has been sequenced, it is known that the Shiga toxin genes were most likely acquired through transduction (horizontal gene transfer). The Shiga toxin genes originated from Shigella dysenteriae . Prophage from a bacteriophage that previously infected Shigella integrated into the chromosome of E. coli . The Shiga-like toxin is often called verotoxin.
EHEC can cause disease ranging from relatively mild to life-threatening.  Although it is often self-limiting, it can lead to hemorrhagic colitis and profuse bleeding. One possible complication is HUS. Diagnosis involves culture, often using MacConkey with sorbitol agar to differentiate between E. coli O157:H7, which does not ferment sorbitol, and other less virulent strains of E. coli that can ferment sorbitol.
Serological typing or PCR testing also can be used, as well as genetic testing for Shiga toxin. To distinguish EPEC from EHEC, because they both form pedestals on intestinal epithelial cells, it is necessary to test for genes encoding for both the Shiga-like toxin and for the LEE. Both EPEC and EHEC have LEE, but EPEC lacks the gene for Shiga toxin. Antibiotic therapy is not recommended and may worsen HUS because of the toxins released when the bacteria are killed, so supportive therapies must be used. Table \(\PageIndex{1}\) summarizes the characteristics of the four most common pathogenic groups.
| Group | Virulence Factors and Genes | Signs and Symptoms | Diagnostic Tests | Treatment |
|---|---|---|---|---|
| Enterotoxigenic E. coli (ETEC) | Heat stable enterotoxin similar to cholera toxin | Relatively mild, watery diarrhea | Culturing, PCR | Self-limiting; if needed, fluoroquinolones, doxycycline, rifaximin, TMP/SMZ; antibiotic resistance is a problem |
| Enteroinvasive E. coli (EIEC) | Inv (invasive plasmid) genes | Relatively mild, watery diarrhea; dysentery or inflammatory colitis may occur | Culturing, PCR; testing for inv gene; additional assays to distinguish from Shigella | Supportive therapy only; antibiotics not recommended |
| Enteropathogenic E. coli (EPEC) | Locus of enterocyte effacement (LEE) pathogenicity island | Severe fever, vomiting, nonbloody diarrhea, dehydration; potentially fatal | Culturing, PCR; detection of LEE lacking Shiga-like toxin genes | Self-limiting; if needed, fluoroquinolones, doxycycline, rifaximin (TMP/SMZ); antibiotic resistance is a problem |
| Enterohemorrhagic E. coli (EHEC) | Verotoxin | May be mild or very severe; bloody diarrhea; may result in HUS | Culturing; plate on MacConkey agar with sorbitol agar as it does not ferment sorbitol; PCR detection of LEE containing Shiga-like toxin genes | Antibiotics are not recommended due to the risk of HUS |
Compare and contrast the virulence factors and signs and symptoms of infections with the four main E. coli groups.
Cholera and Other Vibrios
The gastrointestinal disease cholera is a serious infection often associated with poor sanitation, especially following natural disasters, because it is spread through contaminated water and food that has not been heated to temperatures high enough to kill the bacteria. It is caused by Vibrio cholerae serotype O1, a gram-negative, flagellated bacterium in the shape of a curved rod (vibrio). According to the CDC, cholera causes an estimated 3 to 5 million cases and 100,000 deaths each year. 4
Because V. cholerae is killed by stomach acid, relatively large doses are needed for a few microbial cells to survive to reach the intestines and cause infection. The motile cells travel through the mucous layer of the intestines, where they attach to epithelial cells and release cholera enterotoxin. The toxin is an A-B toxin with activity through adenylate cyclase (see Virulence Factors of Bacterial and Viral Pathogens ). Within the intestinal cell, cyclic AMP (cAMP) levels increase, which activates a chloride channel and results in the release of ions into the intestinal lumen. This increase in osmotic pressure in the lumen leads to water also entering the lumen. As the water and electrolytes leave the body, it causes rapid dehydration and electrolyte imbalance. Diarrhea is so profuse that it is often called “rice water stool,” and patients are placed on cots with a hole in them to monitor the fluid loss (Figure \(\PageIndex{4}\)).
Cholera is diagnosed by taking a stool sample and culturing for Vibrio . The bacteria are oxidase positive and show non-lactose fermentation on MacConkey agar. Gram-negative lactose fermenters will produce red colonies while non-fermenters will produce white/colorless colonies. Gram-positive bacteria will not grow on MacConkey. Lactose fermentation is commonly used for pathogen identification because the normal microbiota generally ferments lactose while pathogens do not. V. cholerae may also be cultured on thiosulfate citrate bile salts sucrose (TCBS) agar, a selective and differential media for Vibrio spp., which produce a distinct yellow colony.
Cholera may be self-limiting and treatment involves rehydration and electrolyte replenishment. Although antibiotics are not typically needed, they can be used for severe or disseminated disease. Tetracyclines are recommended, but doxycycline, erythromycin, orfloxacin, ciprofloxacin, and TMP/SMZ may be used. Recent evidence suggests that azithromycin is also a good first-line antibiotic. Good sanitation—including appropriate sewage treatment, clean supplies for cooking, and purified drinking water—is important to prevent infection (Figure \(\PageIndex{4}\))
V. cholera is not the only Vibrio species that can cause disease. V. parahemolyticus is associated with consumption of contaminated seafood and causes gastrointestinal illness with signs and symptoms such as watery diarrhea, nausea, fever, chills, and abdominal cramps. The bacteria produce a heat-stable hemolysin, leading to dysentery and possible disseminated disease. It also sometimes causes wound infections. V. parahemolyticus is diagnosed using cultures from blood, stool, or a wound. As with V. cholera , selective medium (especially TCBS agar) works well. Tetracycline and ciprofloxacin can be used to treat severe cases, but antibiotics generally are not needed.
Vibrio vulnificus is found in warm seawater and, unlike V. cholerae , is not associated with poor sanitary conditions. The bacteria can be found in raw seafood, and ingestion causes gastrointestinal illness. It can also be acquired by individuals with open skin wounds who are exposed to water with high concentrations of the pathogen. In some cases, the infection spreads to the bloodstream and causes septicemia. Skin infection can lead to edema, ecchymosis (discoloration of skin due to bleeding), and abscesses. Patients with underlying disease have a high fatality rate of about 50%. It is of particular concern for individuals with chronic liver disease or who are otherwise immunodeficient because a healthy immune system can often prevent infection from developing. V. vulnificus is diagnosed by culturing for the pathogen from stool samples, blood samples, or skin abscesses. Adult patients are treated with doxycycline combined with a third generation cephalosporin or with fluoroquinolones, and children are treated with TMP/SMZ.
Two other vibrios, Aeromonas hydrophila and Plesiomonas shigelloides , are also associated with marine environments and raw seafood; they can also cause gastroenteritis. Like V. vulnificus , A. hydrophila is more often associated with infections in wounds, generally those acquired in water. In some cases, it can also cause septicemia. Other species of Aeromonas can cause illness. P. shigelloides is sometimes associated with more serious systemic infections if ingested in contaminated food or water. Culture can be used to diagnose A. hydrophila and P. shigelloides infections, for which antibiotic therapy is generally not needed. When necessary, tetracycline and ciprofloxacin, among other antibiotics, may be used for treatment of A. hydrophila , and fluoroquinolones and trimethoprim are the effective treatments for P. shigelloides .
How does V. cholera infection cause rapid dehydration?
Campylobacter jejuni Gastroenteritis
Campylobacter is a genus of gram-negative, spiral or curved bacteria. They may have one or two flagella. Campylobacter jejuni gastroenteritis, a form of campylobacteriosis, is a widespread illness that is caused by Campylobacter jejuni . The primary route of transmission is through poultry that becomes contaminated during slaughter. Handling of the raw chicken in turn contaminates cooking surfaces, utensils, and other foods. Unpasteurized milk or contaminated water are also potential vehicles of transmission. In most cases, the illness is self-limiting and includes fever, diarrhea, cramps, vomiting, and sometimes dysentery. More serious signs and symptoms, such as bacteremia, meningitis, pancreatitis, cholecystitis, and hepatitis, sometimes occur. It has also been associated with autoimmune conditions such as Guillain-Barré syndrome, a neurological disease that occurs after some infections and results in temporary paralysis. HUS following infection can also occur. The virulence in many strains is the result of hemolysin production and the presence of Campylobacter cytolethal distending toxin (CDT), a powerful deoxyribonuclease (DNase) that irreversibly damages host cell DNA.
Diagnosis involves culture under special conditions, such as elevated temperature, low oxygen tension, and often medium supplemented with antimicrobial agents. These bacteria should be cultured on selective medium (such as Campy CV, charcoal selective medium, or cefaperazone charcoal deoxycholate agar) and incubated under microaerophilic conditions for at least 72 hours at 42 °C. Antibiotic treatment is not usually needed, but erythromycin or ciprofloxacin may be used.
Peptic Ulcers
The gram-negative bacterium Helicobacter pylori is able to tolerate the acidic environment of the human stomach and has been shown to be a major cause of peptic ulcers, which are ulcers of the stomach or duodenum. The bacterium is also associated with increased risk of stomach cancer (Figure \(\PageIndex{5}\)). According to the CDC, approximately two-thirds of the population is infected with H. pylori, but less than 20% have a risk of developing ulcers or stomach cancer. H. pylori is found in approximately 80% of stomach ulcers and in over 90% of duodenal ulcers. 5
H. pylori colonizes epithelial cells in the stomach using pili for adhesion. These bacteria produce urease, which stimulates an immune response and creates ammonia that neutralizes stomach acids to provide a more hospitable microenvironment. The infection damages the cells of the stomach lining, including those that normally produce the protective mucus that serves as a barrier between the tissue and stomach acid. As a result, inflammation (gastritis) occurs and ulcers may slowly develop. Ulcer formation can also be caused by toxin activity. It has been reported that 50% of clinical isolates of H. pylori have detectable levels of exotoxin activity in vitro . 6 This toxin, VacA, induces vacuole formation in host cells. VacA has no primary sequence homology with other bacterial toxins, and in a mouse model, there is a correlation between the presence of the toxin gene, the activity of the toxin, and gastric epithelial tissue damage.
Signs and symptoms include nausea, lack of appetite, bloating, burping, and weight loss. Bleeding ulcers may produce dark stools. If no treatment is provided, the ulcers can become deeper, more tissues can be involved, and stomach perforation can occur. Because perforation allows digestive enzymes and acid to leak into the body, it is a very serious condition.
To diagnose H. pylori infection, multiple methods are available. In a breath test, the patient swallows radiolabeled urea. If H. pylori is present, the bacteria will produce urease to break down the urea. This reaction produces radiolabeled carbon dioxide that can be detected in the patient’s breath. Blood testing can also be used to detect antibodies to H. pylori . The bacteria themselves can be detected using either a stool test or a stomach wall biopsy.
Antibiotics can be used to treat the infection. However, unique to H. pylori, the recommendation from the US Food and Drug Administration is to use a triple therapy. The current protocols are 10 days of treatment with omeprazole, amoxicillin, and clarithromycin (OAC); 14 days of treatment with bismuth subsalicylate, metronidazole, and tetracycline (BMT); or 10 or 14 days of treatment with lansoprazole, amoxicillin, and clarithromycin (LAC). Omeprazole, bismuth subsalicylate, and lansoprazole are not antibiotics but are instead used to decrease acid levels because H. pylori prefers acidic environments.
Although treatment is often valuable, there are also risks to H. pylori eradication. Infection with H. pylori may actually protect against some cancers, such as esophageal adenocarcinoma and gastroesophageal reflux disease. 7 8
How does H. pylori cause peptic ulcers?
Clostridium perfringens Gastroenteritis
Clostridium perfringens gastroenteritis is a generally mild foodborne disease that is associated with undercooked meats and other foods. C. perfringens is a gram-positive, rod-shaped, endospore-forming anaerobic bacterium that is tolerant of high and low temperatures. At high temperatures, the bacteria can form endospores that will germinate rapidly in foods or within the intestine. Food poisoning by type A strains is common. This strain always produces an enterotoxin, sometimes also present in other strains, that causes the clinical symptoms of cramps and diarrhea. A more severe form of the illness, called pig-bel or enteritis necroticans, causes hemorrhaging, pain, vomiting, and bloating. Gangrene of the intestines may result. This form has a high mortality rate but is rare in the United States.
Diagnosis involves detecting the C. perfringens toxin in stool samples using either molecular biology techniques (PCR detection of the toxin gene) or immunology techniques (ELISA). The bacteria itself may also be detected in foods or in fecal samples. Treatment includes rehydration therapy, electrolyte replacement, and intravenous fluids. Antibiotics are not recommended because they can damage the balance of the microbiota in the gut, and there are concerns about antibiotic resistance. The illness can be prevented through proper handling and cooking of foods, including prompt refrigeration at sufficiently low temperatures and cooking food to a sufficiently high temperature.
Clostridium difficile
Clostridium difficile is a gram-positive rod that can be a commensal bacterium as part of the normal microbiota of healthy individuals. When the normal microbiota is disrupted by long-term antibiotic use, it can allow the overgrowth of this bacterium, resulting in antibiotic-associated diarrhea caused by C. difficile . Antibiotic-associated diarrhea can also be considered a nosocomial disease. Patients at the greatest risk of C. difficile infection are those who are immunocompromised, have been in health-care settings for extended periods, are older, have recently taken antibiotics, have had gastrointestinal procedures done, or use proton pump inhibitors, which reduce stomach acidity and allow proliferation of C. difficile . Because this species can form endospores, it can survive for extended periods of time in the environment under harsh conditions and is a considerable concern in health-care settings.
This bacterium produces two toxins, Clostridium difficile toxin A (TcdA) and Clostridium difficile toxin B (TcdB). These toxins inactivate small GTP-binding proteins, resulting in actin condensation and cell rounding, followed by cell death. Infections begin with focal necrosis, then ulceration with exudate, and can progress to pseudomembranous colitis, which involves inflammation of the colon and the development of a pseudomembrane of fibrin containing dead epithelial cells and leukocytes (Figure \(\PageIndex{6}\)). Watery diarrhea, dehydration, fever, loss of appetite, and abdominal pain can result. Perforation of the colon can occur, leading to septicemia, shock, and death. C. difficile is also associated with necrotizing enterocolitis in premature babies and neutropenic enterocolitis associated with cancer therapies.
Diagnosis is made by considering the patient history (such as exposure to antibiotics), clinical presentation, imaging, endoscopy, lab tests, and other available data. Detecting the toxin in stool samples is used to confirm diagnosis. Although culture is preferred, it is rarely practical in clinical practice because the bacterium is an obligate anaerobe. Nucleic acid amplification tests, including PCR, are considered preferable to ELISA testing for molecular analysis.
The first step of conventional treatment is to stop antibiotic use, and then to provide supportive therapy with electrolyte replacement and fluids. Metronidazole is the preferred treatment if the C. difficile diagnosis has been confirmed. Vancomycin can also be used, but it should be reserved for patients for whom metronidazole was ineffective or who meet other criteria (e.g., under 10 years of age, pregnant, or allergic to metronidazole).
A newer approach to treatment, known as a fecal transplant, focuses on restoring the microbiota of the gut in order to combat the infection. In this procedure, a healthy individual donates a stool sample, which is mixed with saline and transplanted to the recipient via colonoscopy, endoscopy, sigmoidoscopy, or enema. It has been reported that this procedure has greater than 90% success in resolving C. difficile infections. 9
How does antibiotic use lead to C. difficile infections?
Foodborne Illness Due to Bacillus cereus
Bacillus cereus , commonly found in soil, is a gram-positive endospore-forming bacterium that can sometimes cause foodborne illness. B. cereus endospores can survive cooking and produce enterotoxins in food after it has been heated; illnesses often occur after eating rice and other prepared foods left at room temperature for too long. The signs and symptoms appear within a few hours of ingestion and include nausea, pain, and abdominal cramps. B. cereus produces two toxins: one causing diarrhea, and the other causing vomiting. More severe signs and symptoms can sometimes develop.
Diagnosis can be accomplished by isolating bacteria from stool samples or vomitus and uneaten infected food. Treatment involves rehydration and supportive therapy. Antibiotics are not typically needed, as the illness is usually relatively mild and is due to toxin activity.
Foodborne Illness Due to Yersinia
The genus Yersinia is best known for Yersinia pestis , a gram-negative rod that causes the plague. However, Y. enterocolitica and Y. pseudotuberculosis can cause gastroenteritis. The infection is generally transmitted through the fecal-oral route, with ingestion of food or water that has been contaminated by feces. Intoxication can also result because of the activity of its endotoxin and exotoxins (enterotoxin and cytotoxin necrotizing factor). The illness is normally relatively mild and self-limiting. However, severe diarrhea and dysentery can develop in infants. In adults, the infection can spread and cause complications such as reactive arthritis, thyroid disorders, endocarditis, glomerulonephritis, eye inflammation, and/or erythema nodosum. Bacteremia may develop in rare cases.
Diagnosis is generally made by detecting the bacteria in stool samples. Samples may also be obtained from other tissues or body fluids. Treatment is usually supportive, including rehydration, without antibiotics. If bacteremia or other systemic disease is present, then antibiotics such as fluoroquinolones, aminoglycosides, doxycycline, and trimethoprim-sulfamethoxazole may be used. Recovery can take up to two weeks.
Compare and contrast foodborne illnesses due to B. cereus and Yersinia .
Bacterial infections of the gastrointestinal tract generally occur when bacteria or bacterial toxins are ingested in contaminated food or water. Toxins and other virulence factors can produce gastrointestinal inflammation and general symptoms such as diarrhea and vomiting. Bacterial GI infections can vary widely in terms of severity and treatment. Some can be treated with antibiotics, but in other cases antibiotics may be ineffective in combating toxins or even counterproductive if they compromise the GI microbiota. Figure \(\PageIndex{7}\) and Figure \(\PageIndex{8}\) the key features of common bacterial GI infections.
At the hospital, Carli’s doctor began to think about possible causes of her severe gastrointestinal distress. One possibility was food poisoning, but no one else in her family was sick. The doctor asked about what Carli had eaten the previous day; her mother mentioned that she’d had eggs for lunch, and that they may have been a little undercooked. The doctor took a sample of Carli’s stool and sent it for laboratory testing as part of her workup. She suspected that Carli could have a case of bacterial or viral gastroenteritis, but she needed to know the cause in order to prescribe an appropriate treatment.
In the laboratory, technicians microscopically identified gram-negative bacilli in Carli’s stool sample. They also established a pure culture of the bacteria and analyzed it for antigens. This testing showed that the causative agent was Salmonella .
What should the doctor do now to treat Carli?
Key Concepts and Summary
- Major causes of gastrointestinal illness include Salmonella spp., Staphylococcus spp., Helicobacter pylori , Clostridium perfringens , Clostridium difficile , Bacillus cereus , and Yersinia bacteria.
- C. difficile is an important cause of hospital acquired infection.
- Vibrio cholerae causes cholera , which can be a severe diarrheal illness.
- Different strains of E. coli , including ETEC , EPEC , EIEC , and EHEC , cause different illnesses with varying degrees of severity.
- H. pylori is associated with peptic ulcers .
- Salmonella enterica serotypes can cause typhoid fever , a more severe illness than salmonellosis .
- Rehydration and other supportive therapies are often used as general treatments.
- Careful antibiotic use is required to reduce the risk of causing C. difficile infections and when treating antibiotic-resistant infections.
Footnotes
- 1 Jaya Sureshbabu. “Shigella Infection Workup.” Medscape . Updated Jun 28, 2016. http://emedicine.medscape.com/article/968773-workup .
- 2 Centers for Disease Control and Prevention. Salmonella . Updated August 25, 2016. https://www.cdc.gov/salmonella .
- 3 Kaci Hickox. “Stop Calling Me the ‘Ebola Nurse.’” The Guardian. November 17, 2014. www.theguardian.com/commentis...se-kaci-hickox.
- 4 Centers for Disease Control and Prevention. Cholera—Vibrio cholerae Infection . Updated November 6, 2014. http://www.cdc.gov/cholera/general . Accessed Sept 14, 2016.
- 5 Centers for Disease Control and Prevention. “ Helicobacter pylori : Fact Sheet for Health Care Providers.” Updated July 1998. www.cdc.gov/ulcer/files/hpfacts.pdf.
- 6 T. L. Cover. “The Vacuolating Cytotoxin of Helicobacter pylori .” Molecular Microbiology 20 (1996) 2: pp. 241–246. http://www.ncbi.nlm.nih.gov/pubmed/8733223 .
- 7 Martin J. Blaser. “Disappearing Microbiota: Helicobacter pylori Protection against Esophageal Adenocarcinoma.” Cancer Prevention Research 1 (2008) 5: pp. 308–311. http://cancerpreventionresearch.aacr....full.pdf+html .
- 8 Ivan F. N. Hung and Benjamin C. Y. Wong. “Assessing the Risks and Benefits of Treating Helicobacter pylori Infection.” Therapeutic Advances in Gastroenterology 2 (2009) 3: pp, 141–147. doi: 10.1177/1756283X08100279.
- 9 Faith Rohlke and Neil Stollman. “Fecal Microbiota Transplantation in Relapsing Clostridium difficile Infection,” Therapeutic Advances in Gastroenterology 5 (2012) 6: 403–420. doi: 10.1177/1756283X12453637.