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Some studies reported up to 80% of patients with irritable bowel syndrome (IBS) have SIBO (using the hydrogen breath test). Subsequent studies demonstrated statistically significant reduction in IBS symptoms following therapy for SIBO.
There is a lack of consensus however, regarding the suggested link between IBS and SIBO. Other authors concluded that the abnormal breath results so common in IBS patients do not suggest SIBO, and state that "abnormal fermentation timing and dynamics of the breath test findings support a role for abnormal intestinal bacterial distribution in IBS." There is general consensus that breath tests are abnormal in IBS; however, the disagreement lies in whether this is representative of SIBO. More research is needed to clarifiy this possible link.
The common routes of transmission for the disease-causing bacteria are fecal-oral, person-to-person sexual contact, ingestion of contaminated food (generally unpasteurized (raw) milk and undercooked or poorly handled poultry), and waterborne (i.e., through contaminated drinking water). Contact with contaminated poultry, livestock, or household pets, especially puppies, can also cause disease.
Animals farmed for meat are the main source of campylobacteriosis. A study published in PLoS Genetics (September 26, 2008) by researchers from Lancashire, England, and Chicago, Illinois, found that 97 percent of campylobacteriosis cases sampled in Lancashire were caused by bacteria typically found in chicken and livestock. In 57 percent of cases, the bacteria could be traced to chicken, and in 35 percent to cattle. Wild animal and environmental sources were accountable for just three percent of disease.
The infectious dose is 1000–10,000 bacteria (although ten to five hundred bacteria can be enough to infect humans). "Campylobacter" species are sensitive to hydrochloric acid in the stomach, and acid reduction treatment can reduce the amount of needed to cause disease.
Exposure to bacteria is often more common during travelling, and therefore campylobacteriosis is a common form of travelers' diarrhea.
Enteroinvasive "Escherichia coli" (EIEC) is a type of pathogenic bacteria whose infection causes a syndrome that is identical to shigellosis, with profuse diarrhea and high fever. EIEC are highly invasive, and they use adhesin proteins to bind to and enter intestinal cells. They produce no toxins, but severely damage the intestinal wall through mechanical cell destruction.
It is closely related to "Shigella".
After the "E. coli" strain penetrates through the epithelial wall, the endocytosis vacuole gets lysed, the strain multiplies using the host cell machinery, and extends to the adjacent epithelial cell. In addition, the plasmid of the strain carries genes for a type III secretion system that is used as the virulent factor. Although it is an invasive disease, the invasion usually does not pass the submucosal layer. The similar pathology to shigellosis may be because both strains of bacteria share some virulent factors. The invasion of the cells can trigger a mild form of diarrhea or dysentery, often mistaken for dysentery caused by "Shigella" species. The illness is characterized by the appearance of blood and mucus in the stools of infected individuals or a condition called colitis.
Dysentery caused by EIEC usually occurs within 12 to 72 hours following the ingestion of contaminated food. The illness is characterized by abdominal cramps, diarrhea, vomiting, fever, chills, and a generalized malaise. Dysentery caused by this organism is generally self-limiting with no known complications.
Enterovirulent classes of "E. coli" are referred to as the EEC group (enterovirulent "E. coli"):
1. Enteroinvasive "E. coli" (EIEC) invades (passes into) the intestinal wall to produce severe diarrhea.
2. Enterohemorrhagic "E. coli" (EHEC): A type of EHEC, "E. coli" 0157:H7, can cause bloody diarrhea and hemolytic uremic syndrome (anemia and kidney failure).
3. Enterotoxigenic "E. coli" (ETEC) produces a toxin that acts on the intestinal lining, and is the most common cause of traveler's diarrhea.
4. Enteropathogenic "E. coli" (EPEC) can cause diarrhea outbreaks in newborn nurseries.
5. Enteroaggregative "E. coli" (EAggEC) can cause acute and chronic (long-lasting) diarrhea in children.
It is currently unknown what foods may harbor EIEC, but any food contaminated with human feces from an ill individual, either directly or via contaminated water, could cause disease in others. Outbreaks have been associated with hamburger meat and unpasteurized milk.
Fibromyalgia is a poorly understood pain condition. Lactulose breath testing has shown that patients with fibromyalgia have a more pronounced degree of abnormal results compared to both IBS patients and the general population. This study also demonstrated positive correlation between the amount of pain and the degree of abnormality on the breath test. A subsequent study also demonstrated increased prevalence of intestinal hyperpermeability, which some believe occurs commonly with SIBO.
The World Health Organization recommends the following:
- Food should be properly cooked and hot when served.
- Consume only pasteurized or boiled milk and milk products, never raw milk products.
- Make sure that ice is from safe water.
- If you are not sure of the safety of drinking water, boil it, or disinfect it with chemical disinfectant.
- Wash hands thoroughly and frequently with soap, especially after using the toilet and after contact with pets and farm animals.
- Wash fruits and vegetables thoroughly, especially if they are to be eaten raw. Peel fruits and vegetables whenever possible.
- Food handlers, professionals and at home, should observe hygienic rules during food preparation.
- Professional food handlers should immediately report to their employer any fever, diarrhea, vomiting or visible infected skin lesions.
To date, the precise causative factor has not been verified, and the disease has been attributed by various sources to viruses, parasites, bacteria, use of antibiotics and sulfonamides, and heavy metal poisoning. Other possible causes include peracute salmonellosis, clostridial enterocolitis, and endotoxemia. "Clostridium difficile" toxins isolated in the horse have a genotype like the current human "epidemic strain", which is associated with human "C. difficile"-associated disease of greater than historical severity. "C. difficile" can cause pseudomembranous colitis in humans, and in hospitalized patients who develop it, fulminant "C. difficile" colitis is a significant and increasing cause of death.
Horses under stress appear to be more susceptible to developing colitis X. Disease onset is often closely associated with surgery or transport. Excess protein and lack of cellulose content in the diet (a diet heavy on grain and lacking adequate hay or similar roughage) is thought to be the trigger for the multiplication of clostridial organisms. A similar condition may be seen after administration of tetracycline or lincomycin to horses. These factors may be one reason the condition often develops in race horses, having been responsible for the deaths of the Thoroughbred filly Landaluce,
the Quarter Horse stallion Lightning Bar,
and is one theory for the sudden death of Kentucky Derby winner Swale.
The link to stress suggests the condition may be brought on by changes in the microflora of the cecum and colon that lower the number of anaerobic bacteria, increase the number of Gram-negative enteric bacteria, and decrease anaerobic fermentation of soluble carbohydrates, resulting in damage to the cecal and colonic mucosa and allowing increased absorption of endotoxins from the lumen of the gut.
The causative agent may be "Clostridium perfringens", type A, but the bacteria are recoverable only in the preliminary stages of the disease.
The suspect toxin could also be a form of "Clostridium difficile". In a 2009 study at the University of Arizona, "C. difficile" toxins A and B were detected, large numbers of "C. difficile" were isolated, and genetic characterization revealed them to be North American pulsed-field gel electrophoresis type 1, polymerase chain reaction ribotype 027, and toxinotype III. Genes for the binary toxin were present, and toxin negative-regulator tcdC contained an 18-bp deletion. The individual animal studied in this case was diagnosed as having peracute typhlocolitis, with lesions and history typical of those attributed to colitis X.
Use of antibiotics may also be associated with some forms of colitis-X. In humans, "C. difficile" is the most serious cause of antibiotic-associated diarrhea, often a result of eradication of the normal gut flora by antibiotics. In one equine study, colitis was induced after pretreatment with clindamycin and lincomycin, followed by intestinal content from horses which had died from naturally occurring idiopathic colitis. (A classic adverse effect of clindamycin in humans is "C. difficile"-associated diarrhea.) In the experiment, the treated horses died. After necropsy, "Clostridium cadaveris" was present, and is proposed as another possible causative agent in some cases of fatal colitis.
In Germany, 90% of cases of infectious enteritis are caused by four pathogens, Norovirus, Rotavirus, "Campylobacter" and "Salmonella". Other common causes of infectious enteritis include bacteria such as "Shigella" and "E. coli," as well as viruses such as adenovirus, astrovirus and calicivirus. Other less common pathogens include "Bacillus cereus, Clostridium perfringens, Clostridium difficile" and "Staphylococcus aureus".
"Campylobacter jejuni" is one of the most common sources of infectious enteritis, and the most common bacterial pathogen found in 2 year old and smaller children with diarrhoea. It has been linked to consumption of contaminated water and food, most commonly poultry and milk. The disease tends to be less severe in developing countries, due to the constant exposure which people have with the antigen in the environment, leading to early development of antibodies.
Rotavirus is responsible for infecting 140 million people and causing 1 million deaths each year, mostly in children younger than 5 years. This makes it the most common cause of severe childhood diarrhoea and diarrhea-related deaths in the world. It selectively targets mature enterocytes in the small intestine, causing malabsorption, as well as inducing secretion of water. It has also been observed to cause villus ischemia, and increase intestinal motility. The net result of these changes is induced diarrhoea.
Enteritis necroticans is an often fatal illness, caused by β-toxin of "Clostridium perfringens". This causes inflammation and segments of necrosis throughout the gastrointestinal tract. It is most common in developing countries, however has also been documented in post-World War II Germany. Risk factors for enteritis necroticans include decreased trypsin activity, which prevent intestinal degradation of the toxin, and reduced intestinal motility, which increases likelihood of toxin accumulation.
Crohn's disease – also known as regional enteritis, it can occur along any surface of the gastrointestinal tract. In 40% of cases it is limited to the small intestine.
Coeliac disease – caused by an autoimmune reaction to gluten by genetically predisposed individuals.
Eosinophilic enteropathy – a condition where eosinophils build up in the gastrointestinal tract and blood vessels, leading to polyp formation, necrosis, inflammation and ulcers. It is most commonly seen in patients with a history of atopy, however is overall relatively uncommon.
Colitis X, equine colitis X or peracute toxemic colitis is a catchall term for various fatal forms of acute or peracute colitis found in horses, but particularly a fulminant colitis where clinical signs include sudden onset of severe diarrhea, abdominal pain, shock, and dehydration. Death is common, with 90% to 100% mortality, usually in less than 24 hours. The causative factor may be "Clostridium difficile", but it also may be caused by other intestinal pathogens. Horses under stress appear to be more susceptible to developing colitis X, and like the condition pseudomembranous colitis in humans, there also is an association with prior antibiotic use. Immediate and aggressive treatment can sometimes save the horse, but even in such cases, 75% mortality is considered a best-case scenario.
The risk of acquiring infectious diarrhea in the wilderness arises from inadvertent ingestion of pathogens. Various studies have sought to estimate diarrhea attack rates among wilderness travelers, and results have ranged widely. The variation of diarrhea rate between studies may depend on the time of year, the location of the study, the length of time the hikers were in the wilderness,
the prevention methods used, and the study methodology.
The National Outdoor Leadership School (NOLS), which emphasizes strict hand-washing techniques, water disinfection and washing of common cooking utensils in their programs, reports that gastrointestinal illnesses occurred at a rate of only 0.26 per 1000 program days. In contrast, a survey of long-distance Appalachian Trail hikers found more than half the respondents reported at least one episode of diarrhea that lasted an average of two days. (Infectious diarrhea may last longer than an average of two days; certain forms of non-infectious diarrhea, caused by diet change etc., can be of very brief duration). Analysis of this survey found occurrence of diarrhea was positively associated with the duration of exposure in the wilderness. During any given four-week period, as many as 7.2% of Americans may experience some form of infectious or non-infectious diarrhea. A number of behaviors each individually reduced the incidence of diarrhea: treating water; routinely washing hands with soap and water after defecation and urination; cleaning cooking utensils with soap and warm water; and taking multi-vitamins.
A variety of pathogens can cause infectious diarrhea, and most cases among backpackers appear to be caused by bacteria from feces. A study at Grand Teton National Park found 69% of diarrhea affected visitors had no identifiable cause, that 23% had diarrhea due to "Campylobacter" and 8% of patients with diarrhea had giardiasis. Campylobacter enteritis occurred most frequently in young adults who had hiked in wilderness areas and drunk untreated surface water in the week prior. Another study tested 35 individuals before and after a trip to the Desolation Wilderness of California. Giardia cysts were found in fecal samples from two people after the trip, but they were asymptomatic. A third person was empirically treated for symptoms of giardiasis.
Fecal-oral transmission may be the most common vector for wilderness acquired diarrhea. There are differing opinions regarding the importance of routine disinfection of water during relatively brief backcountry visits.
One study suggests that on very long trips in the wilderness, taking multivitamins may reduce the incidence of diarrhea.
There are several populations that have a higher risk for contracting coccidioidomycosis and developing the advanced disseminated version of the disease. Populations with exposure to the airborne arthroconidia working in agriculture and construction have a higher risk. Outbreaks have also been linked to earthquakes, windstorms and military training exercises where the ground is disturbed. Historically an infection is more likely to occur in males than females, although this could be attributed to occupation rather than gender specific. Women who are pregnant and immediately postpartum are at a high risk of infection and dissemination. There is also an association between stage of pregnancy and severity of the disease, with third trimester women being more likely to develop dissemination. Presumably this is related to highly elevated hormonal levels, which stimulate growth and maturation of spherules and subsequent release of endospores. Certain ethnic populations are more susceptible to disseminated coccioidomycosis. The risk of dissemination is 175 times greater in Filipinos and 10 times greater in African Americans than non-Hispanic whites. Individuals with a weakened immune system are also more susceptible to the disease. In particular, individuals with HIV and diseases that impair T-cell function. Individuals with pre-existing conditions such as diabetes are also at a higher risk. Age also affects the severity of the disease, with more than one third of deaths being in the 65-84 age group.
Dysentery results from viral, bacterial, or parasitic infestations. These pathogens typically reach the large intestine after entering orally, through ingestion of contaminated food or water, oral contact with contaminated objects or hands, and so on.
Each specific pathogen has its own mechanism or pathogenesis, but in general, the result is damage to the intestinal lining, leading to the inflammatory immune response. This can cause elevated temperature, painful spasms of the intestinal muscles (cramping), swelling due to water leaking from capillaries of the intestine (edema), and further tissue damage by the body's immune cells and the chemicals, called cytokines, which are released to fight the infection. The result can be impaired nutrient absorption, excessive water and mineral loss through the stools due to breakdown of the control mechanisms in the intestinal tissue that normally remove water from the stools, and in severe cases, the entry of pathogenic organisms into the bloodstream.
Extensive cellular damage or death is required to cause bleeding. Bacteria can do this either by invading into intestinal mucosa or by secreting toxins that cause cell death. Bacterial infections that cause bloody diarrhea are typically classified as being either invasive or toxogenic. Invasive species cause damage directly by invading into the mucosa. The toxogenic species do not invade, but cause cellular damage by secreting toxins, resulting in bloody diarrhea. This is also in contrast to toxins that cause watery diarrhea, which usually do not cause cellular damage, but rather they take over cellular machinery for a portion of life of the cell.
Some microorganisms – for example, bacteria of the genus "Shigella" – secrete substances known as cytotoxins, which kill and damage intestinal tissue on contact. Shigella is thought to cause bleeding due to invasion rather than toxin, because even non-toxogenic strains can cause dysentery, but E. coli with shiga-like toxins do not invade the intestinal mucosa, and are therefore toxin dependent. Viruses directly attack the intestinal cells, taking over their metabolic machinery to make copies of themselves, which leads to cell death.
Definitions of dysentery can vary by region and by medical specialty. The U. S. Centers for Disease Control and Prevention (CDC) limits its definition to "diarrhea with visible blood". Others define the term more broadly. These differences in definition must be taken into account when defining mechanisms. For example, using the CDC definition requires that intestinal tissue be so severely damaged that blood vessels have ruptured, allowing visible quantities of blood to be lost with defecation. Other definitions require less specific damage.
Dysentery may also be caused by shigellosis, an infection by bacteria of the genus "Shigella", and is then known as bacillary dysentery (or Marlow syndrome). The term "bacillary dysentery" etymologically might seem to refer to any dysentery caused by any bacilliform bacteria, but its meaning is restricted by convention to "Shigella" dysentery.
The CDC recommends hand-washing and avoiding potentially contaminated food and untreated water.
Boiling suspect water for one minute is the surest method to make water safe to drink and kill disease-causing microorganisms such as "Giardia lamblia" if in doubt about whether water is infected. Chemical disinfectants or filters may be used.
According to a review of the literature from 2000, there is little evidence linking the drinking of water in the North American wilderness and Giardia. CDC surveillance data (for 2005 and 2006) reports one outbreak (6 cases) of waterborne giardiasis contracted from drinking wilderness river water in Colorado. However, less than 1% of reported giardiasis cases are associated with outbreaks.
Person-to-person transmission accounts for the majority of "Giardia" infections and is usually associated with poor hygiene and sanitation. "Giardia" is found on the surface of the ground, in the soil, in undercooked foods, and in water, and on hands without proper cleaning after handling infected feces. Water-borne transmission is associated with the ingestion of contaminated water. In the U.S., outbreaks typically occur in small water systems using inadequately treated surface water. Venereal transmission happens through fecal-oral contamination. Additionally, diaper changing and inadequate hand washing are risk factors for transmission from infected children. Lastly, food-borne epidemics of "Giardia" have developed through the contamination of food by infected food-handlers.
Some intestinal parasitic infections may play a role in irritable bowel syndrome and other long-term sequelae.
The newborn`s exposure to the maternal vaginal bacterial flora which contains aerobic and anaerobic bacterial flora can lead to the development of anaerobic bacterial infection. These infections include cellulitis of the site of fetal monitoring (caused by "Bacterodes" spp.), bacteremia, aspiration pneumonia (caused by "Bacterodes" spp.), conjunctivitis (caused by clostridia,) omphalitis (caused by mixed flora), and infant botulism. Clostridial species may play a role in necrotizing enterocolitis. Management of these infection necessitates treating of the underlying condition(s) when present, and administration of proper antimicrobial therapy
Coccidiosis is a significant disease for chickens, especially affecting the young chicks. It can be fatal or leave the bird with compromised digestion. There are chick feed mixes that contain a coccidiostat to manage exposure levels and control disease. In an outbreak, coccidiocidal medications are given. Examples are toltrazuril (Baycox) or amprolium. After multiple infections, surviving chickens become resistant to the coccidia.
The disease is regarded as extremely rare, with an incidence (new number of cases per year) of one case per million people. The patients are predominantly male (86% in a survey of American patients), although in some countries the rate of women receiving a diagnosis of Whipple's disease has increased in recent years. It occurs predominantly in those of Caucasian ethnicity, suggesting a genetic predisposition in that population.
"T. whipplei" appears to be an environmental organism that is commonly present in the gasterointestinal tract but remains asymptomatic. Several lines of evidence suggest that some defect—inherited or acquired—in immunity is required for it to become pathogenic. The possible immunological defect may be specific for "T. whipplei", since the disease is not associated with a substantially increased risk of other infections.
The disease is usually diagnosed in middle age (median 49 years). Studies from Germany have shown that age at diagnosis has been rising since the 1960s.
Condition predisposing to anaerobic infections include: exposure of a sterile body location to a high inoculum of indigenous bacteria of mucous membrane flora origin, inadequate blood supply and tissue necrosis which lower the oxidation and reduction potential which support the growth of anaerobes. Conditions which can lower the blood supply and can predispose to anaerobic infection are: trauma, foreign body, malignancy, surgery, edema, shock, colitis and vascular disease. Other predisposing conditions include splenectomy, neutropenia, immunosuppression, hypogammaglobinemia, leukemia, collagen vascular disease and cytotoxic drugs and diabetes mellitus. A preexisting infection caused by aerobic or facultative organisms can alter the local tissue conditions and make them more favorable for the growth of anaerobes. Impairment in defense mechanisms due to anaerobic conditions can also favor anaerobic infection. These include production of leukotoxins (by "Fusobacterium" spp.), phagocytosis intracellular killing impairments (often caused by encapsulated anaerobes and by succinic acid ( produced by "Bacteroides" spp.), chemotaxis inhibition (by "Fusobacterium, Prevotella" and "Porphyromonas" spp.), and proteases degradation of serum proteins (by Bacteroides spp.) and production of leukotoxins (by "Fusobacterium" spp.).
The hallmarks of anaerobic infection include suppuration, establishment of an abscess, thrombophlebitis and gangrenous destruction of tissue with gas generation. Anaerobic bacteria are very commonly recovered in chronic infections, and are often found following the failure of therapy with antimicrobials that are ineffective against them, such as trimethoprim–sulfamethoxazole (co-trimoxazole), aminoglycosides, and the earlier quinolones.
Some infections are more likely to be caused by anaerobic bacteria, and they should be suspected in most instances. These infections include brain abscess, oral or dental infections, human or animal bites, aspiration pneumonia and lung abscesses, amnionitis, endometritis, septic abortions, tubo-ovarian abscess, peritonitis and abdominal abscesses following viscus perforation, abscesses in and around the oral and rectal areas, pus-forming necrotizing infections of soft tissue or muscle and postsurgical infections that emerge following procedures on the oral or gastrointestinal tract or female pelvic area. Some solid malignant tumors, ( colonic, uterine and bronchogenic, and head and neck necrotic tumors, are more likely to become secondarily infected with anaerobes. The lack of oxygen within the tumor that are proximal to the endogenous adjacent mucosal flora can predispose such infections.
Carrión's disease, or Oroya fever, or Peruvian wart is a rare infectious disease found only in Peru, Ecuador, and Colombia. It is endemic in some areas of Peru, is caused by infection with the bacterium "Bartonella bacilliformis", and transmitted by sandflies of genus "Lutzomyia".
Cat scratch disease occurs worldwide. Cats are the main reservoir of "Bartonella henselae", and the bacterium is transmitted to cats by the cat flea "Ctenocephalides felis". Infection in cats is very common with a prevalence estimated between 40-60%, younger cats being more commonly infective. Cats usually become immune to the infection, while dogs may be very symptomatic. Humans may also acquire it through flea or tick bites from infected dogs, cats, coyotes, and foxes.
Trench fever, produced by "Bartonella quintana" infection, is transmitted by the human body louse "Pediculus humanus corporis". Humans are the only known reservoir. Thorough washing of clothing may help to interrupt the transmission of infection.
A possible role for ticks in transmission of "Bartonella" species remains to be elucidated; in November 2011, "Bartonella rochalimae", "B. quintana", and "B. elizabethae" DNA was first reported in "Rhipicephalus sanguineus" and "Dermacentor nitens" ticks in Peru.
Fever and sickness behavior and other signs of infection are often taken to be due to them. However, they are evolved physiological and behavioral responses of the host to clear itself of the infection. Instead of incurring the costs of deploying these evolved responses to infections, the body opts to tolerate an infection as an alternative to seeking to control or remove the infecting pathogen.
Subclinical infections are important since they allow infections to spread from a reserve of carriers. They also can cause clinical problems unrelated to the direct issue of infection. For example, in the case of urinary tract infections in women, this infection may cause preterm delivery if the person becomes pregnant without proper treatment.
An animal infected with Valley fever cannot transmit the disease to other animals.
In dogs, the most common symptom of coccidioidomycosis is a chronic cough, which can be dry or moist. Other symptoms include fever (in approximately 50% of cases), weight loss, anorexia, lethargy, and depression. The disease can disseminate throughout the dog's body, most commonly causing osteomyelitis (infection of the bone marrow), which leads to lameness. Dissemination can cause other symptoms, depending on which organs are infected. If the fungus infects the heart or pericardium, it can cause heart failure and death.
In cats, symptoms may include skin lesions, fever, and loss of appetite, with skin lesions being the most common.
Other species in which Valley fever has been found include livestock such as cattle and horses; llamas; marine mammals, including sea otters; zoo animals such as monkeys and apes, kangaroos, tigers, etc.; and wildlife native to the geographic area where the fungus is found, such as cougars, skunks, and javelinas.
The most common medications used to treat coccidian infections are in the sulfonamide antibiotic family.
Depending on the pathogen and the condition of the animal, untreated coccidiosis may clear of its own accord, or become severe and damaging, and sometimes cause death.
Treatment of infections caused by "Bartonella" species include:
Some authorities recommend the use of azithromycin.