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Clinical case study clostridium perfringens
Infection of clostridium perfringens in human
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Clostridium perfringens, formally known as C. welchii or Bacillus welchii, is a gram-positive, rod-shaped, anaerobic, spore forming bacterium. The first association C. perfringens had with gastrointestinal disease was in the 1920s (Songer, 1996). The next case was post-World War 1, in Germany, in the 1940s, when it caused gangrene of the bowel, enteritis necroticans. Since then, C. perfringens has been the most commonly associated with gas gangrene (Lawrence et al., 1997). In 1950, there was a confirmed food poisoning case that linked back to C. perfringens (McDonel, 1986). It was not until the late 1970s that there was a relationship made between equine enteric disease and C. perfringens. However, it was not extensively studied until 1977, …show more content…
perfringens type A in the feces of racehorses suffering from colitis in comparison to the lower levels detected in healthy horses (Borriello, 1995). Currently, C. perfringens is associated with causing severe colitis in horses, yet can sometimes be ingested without causing any harm. Therefore, it is vital to understand what type of strain and toxins are causing gastrointestinal diseases and how to control and prevent them.
C. perfringens, Bacteria (Domain), Firmicutes (Phylum), Clostridia (Class), Clostridiales (Order), Clostridiaceae (Family), Clostridium (Genus), C. perfringens (Species), is found in the intestinal tract as well as decaying vegetation, marine sediment, and soil (Herholz et al., 1999). This bacterium is a mesophile with optimum growing temperatures at 37° C. It is non-motile, but has the ability to
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perfringens is the most common cause of foodborne illness in the United States, with a million cases each year (CDC, 2014). C. perfringens is able to produce up to 15 different toxins, making it versatile. These toxins are used to isolate the five different types of C. perfringes: type A, B, C, D, and E. The four toxins that are primarily used to isolate the different types include alpha, beta, epsilon, and iota-toxins. Type A is the most common and most variable, and subdivided into entertoxigenic and non-enterotoxigenic strains (Herholz et al., 1999). Enterotoxigenic type A and C are associated with equine enterocolitis, gas gangrene, infections, avian and canine necrotic enteritis, colitis in horses, and diarrhea in pigs (Divers and Ball, 1996). Types B, C, D, and E can cause severe enteritis, dysentery, toxemia, and high mortality rates in young lambs, calves, pigs, and foals. Types B, C, D, and E have been intermittently associated with foal enterocolitis, and equine antibiotic associated diarrhea (Divers and Ball, 1996). Even though the alpha toxin is noted to be relatively nonpathogenic, the beta2 toxin plays a significant role in digestive disease, specifically, enterocolitis in equine (Herholz et al., 1999). This is mainly due to the C. perfringens entertoxin (CPE), the main virulence factor that initiates many critical gastrointestinal diseases across species (Herholz et al. 1999). CPE works in a four-step mechanism against membrane action (CDC, 2014). First,
Clostridium difficile, otherwise known as C. diff, is a species of spore-forming, anaerobic, gram-positive bacteria that is known to cause watery diarrhea. 1 The genus name, Clostridium refers to the spindle shape of the organism while Difficile means difficult in Latin due to the fact that this organism thrives in unfavorable conditions and is very difficult to isolate.4 The incidence of getting CDI has increased over the years due to new strains of increased toxin production of the bacteria and increased resistance to antibiotics.2 It is a gastrointestinal infection, and the most common cause of infectious diarrhea.1 C. difficile was first identified in the feces of healthy newborns back in the 1930’s and by 1935, it was considered normal flora. 2 During 1974, researchers conducted that about 21% of patients that were treated with an antibiotic called clindamyacin reported diarrhea and about 10% of them reported to have conducted pseudomembranous colitis as a side effect of this treatment. 2 It was in 1978 where C. diff had been known to cause anti-biotic associated diarrhea and pseudomembranous colitis. 2 It is known to form spores that resist many disinfectants; it also survives for several months on different surfaces.1 It is a common form of a nosocomial infection and the prevalence of becoming infected with C. diff is about 0-15% in a health care setting. 3 The spores survive well in environments such as soil, water and animals and is distributed worldwide. 4 CDI produces two toxins (Toxin A and B), which are cytotoxic and cause tissue necrosis.4
These biochemical tests are process of elimination that relies on the bacteria’s ability to breakdown certain kinds of food sources, their respiratory abilities and other biochemical conditions found in nature. The results of these tests prove that the unknown organism is Citrobacter freundii hereby referred to as C. freundii. C. freundii is a member of the Enterobacteriaceae family, like all the other unknowns given in this test. The species is a facultative anaerobic and is a gram-negative bacilli.
Bordetella pertussis is a highly communicable agent and is transmitted person-to-person via airborne droplets or direct contact with discharges from the respiratory mucous membranes of an infected person. This small, gram-negative coccobacillus is non-motile, aerobic and fastidious. B. pertussis colonizes the respiratory tract including the mouth, nose, throat and beginning of the lungs of young children worldwide. The bacteria bind to ciliated cells in the respiratory mucosa by producing adhesions. Filamentous hemagglutinin on the cell surface and pertussis toxin (Ptx) both help the bacteria in binding. Filamentous hemagglutinin binds to the galactose residues on the glycolipid of the ciliated cells. Ptx, in its cell-bound form, binds to the glycolipid lactosylceramide, which is also found on the ciliated cells. Ptx binds to the surface of phagocytes as well, causing phagocytosis of the bacteria. This mechanism may lead to enhanced survival as an intracellular parasite. Adding to its many purposes, Ptx deregulates the host cell adenylate cyclase activity. The A subunit of this AB toxin, affects the G protein responsible for inhibiting adenylate cyclase. This leads to an increase in cyclic adenosine monophosphate (cAMP) creating detrimental metabolic changes in the host cells.
For the disease to occur, Bordetella pertussis evades the host immune system and is disseminate in the lower respiratory tract. Inhaled bacteria droplets then attach to the ciliated epithelial cells in the nasal-pharynx and trachea. It is at this point that Bordetella pertussis produces virulent factors that are classified into two; adhesins and toxins. Adhesins mediate bacterial attachment to the epithelial cells while toxins that mediate the host immune system. Adhesins include; filamentous haemagglutinin, fimbriae and pertactin while toxins include pertussis toxin, tracheal cytotoxin and adenylate cyclase toxin(1). To understand the role of these virulence factors in whooping cough disease, a mouse model has been used (2).
As stated in Chan-Tack and Bartlett’s article Botulism, “The incidence of foodborne botulism is approximately 24 cases per year. The incidence of wound botulism is 3 cases per year. The incidence of infant botulism is 71 cases per year, with a mean age of 3 months.” (2010). In addition, in merely fifteen percent of the Clostridium botulinium outbreaks are the toxin type undetermined. The first case descriptions of botulism were reported by Dr. Justinus Kerner, a German physician, in 1822. He had conducted experiments on himself and laboratory animals, which gave him this case findings (Taillac, & Kim, 2010).
Among hospitalized patients around the world, Clostridium difficile is the primary source of infectious diarrhea. Previously, continuously unbalanced intestinal microbiota, usually due to antimicrobials, was deemed a precondition of developing the infection. However, recently, there have been alterations in the biology from virtually infecting the elderly population exclusively, wherein the microbiota in their guts have been interrupted by antimicrobials, to currently infecting individuals within of all age groups displaying no recent antimicrobial use. Furthermore, recent reports have confirmed critical occurrences among groups previously assumed to be of minimal risk—pregnant women, children, and individuals with no previous exposure to antimicrobials, for instance. Unfortunately, this Gram-positive, toxin-producing anaerobic bacterium is estimated to cost US critical care facilities $800 million per year at present, suggesting the need for effective measures to eliminate this nosocomial infection (Yakob, Riley, Paterson, & Clements, 2013).
The majority of clinical cases of laminitis occur in pastures where there is an accumulation of rapidly fermentable non-structural carbohydrates (NSC) such as fructans, simple sugars or starches (Geor, 2010). Pasture-associated laminitis has major economic and welfare implications in the equine sector. Increased risk factors include insulin resistance, increased insulin secretory response, hypertriglyceridaemia and obesity (Asplin, et al., 2007; Carter, et al., 2009 and de Laat, et al., 2010). Insulin resistance has been associated with a number of problems in the horse, most notably laminitis.
Some strains of this microorganism produce C. perfringens enterotoxin (CPE), a group of toxins that cause a variety of adverse effects in the host. Strains of C. perfringens are classified as 5 biotypes, A – E, depending on the production of four major enterotoxins (α, β, ε and ι). In addition, strains of C. perfringens may also produce a number of other toxins including neuraminidase, hyaluronidase, and collagenase. For example, α-toxin, produced by C. perfringens type A, is primarily responsible for the production of gas gangrene. However, only roughly 5% of C. perfringens carry the CPE gene that codes for the production of these toxins. CPE is inactivated at 74oC.
More precisely DON is classified as type-B trichothecene [20]. It is produced by Fusarium culmorum and F. graminearum [(Maresca, 2013). DON contamination is observed worldwide, within cereal crops such as wheat, maize or barley being most frequently affected (Richard, 2007). Furthermore, silage contamination is regularly observed (Tangni et al., 2013). Cold and wet weather conditions favour DON production (Lindblad et al., 2012) and it was found that the timing of the rainfall is more influential than the amount of precipitation (Mesterházy, 2002). In animal husbandry, DON, also known as vomitoxin, is primarily known for causing feed refusal and emesis in pigs (Pestka, 2007). This mycotoxin also alters the immune response and the intestinal functions (Pestka, 2007). DON may be produced together with two acetylated derivatives, 3-AcDON and 15-AcDON, that have differential toxicity on pig intestine (Behrens et al., 2015). Poultry are not as sensitive to DON and feed refusal is only observed at very high concentrations (16–20 mg/kg feed) (Whitlow and Hagler, 2002). Ruminants are the least sensitive animal species to DON, a fact that is attributed to the capacity of rumen microflora to detoxify this mycotoxin (Fink-Gremmels,
Clostridium tetani is a Gram-positive bacteria. Gram-positive bacteria retain a crystal violet stain in their thick peptidoglycan. C. tetani are bacillus-shaped organisms. Typically bacillus shaped organisms are shaped like rods, however, C. tetani, although bacillus, tend to have a drumstick-like shape. This drumstick shaping is due to terminal spores formed by the bacteria. Spores are dormant forms of an organism. The spores germinate and swell within the cell, imparting the bacteria’s drumstick shape.1 Clostridium tetani are also anaerobic, meaning that they cannot survive in the presence of oxygen. The organisms are very sensitive to heat, however, the spores that they produce can become rather resistant to heat and antiseptics.2 C. tetani spores are pervasive throughout nature. The natural habitat of C. tetani consists of areas that are damp and warm. Common sources for these bacteria include soil, manure, animal intestines, and feces.3 Generally, C. tetani spores can survive for months in their natural environment. However, under the proper environmental conditions, the spores can survive for years.4
However, health concerned organizations want to ban the use of these products due to the increasing fears that they can cause harm to the consumers. For over 50 years, antibiotics have been added to the food of animals such as poultry, cattle and pigs. The main purpose for doing so is to lower the risk of disease in animals. Farm animals are housed together in overcrowded areas, which are very dirty. The hygiene level can get to such a poor state that they are often in contact with their own excreta as well as excreta of the other animals they are housed with and because of tight single air space they share, the likelihood of catching diseases from one another is further increased and very often a whole heard can be infected at one time.
E. coli are bacteria that can cause an infection in various parts of your body, including your intestines. E. coli bacteria normally live in the intestines of people and animals. Most types of E. coli do not cause infections, but some produce a poison (toxin) that can cause diarrhea. Depending on the toxin, this can cause mild or severe diarrhea.
Clostridium Perfringens is one of the most common agents of Gas Gangrene and food poisoning. C. Perfringens cannot spread from person to person nor can it produce within itself in a human’s body. The most common way to be infected with C. Perfringens is by consuming large amounts of the bacteria from under cooked foods. In some cases C. Perfringens is not too severe, and is commonly mistaken to be the 24 - hour flu (Clark, 2015). The most common sources of where C. Perfringens grows in foods such as beef, poultry, gravies and soups. The spores from C. perfringens is found all around the environment such as sewages, dust, and soil. It takes many bacteria to infect food and cause illness in the human body. From the temperature
“People can become infected with antibiotic bacteria from a variety of resources. [such as] meat or other foods. if not properly cooked [and] workers who have contact with animals at factory farms.” (Gale, 2013). The fact that there are chances for people to get sick from their most desired foods shows how bad factory farming can be.
The most commonly recognized food borne infections are those caused by the bacteria Campylobacter, Salmonella, and E. coli 0157:H7, and by a group of viruses called Calicivirus, also know as the Norwalk viruses. “Thousands of types of bacteria are naturally present in our environment, but not all bacteria cause disease in humans.” (Schmutz 1)