People become infected by swallowing the mature parasite; this normally occurs through the ingestion of contaminated food or water. The infected host then produces an immature form  of the parasite in their feces, and when the parasite matures, it is capable of infecting its next host, via food or water containing the parasite. [ citation needed ]


At time of excretion, the immature  oocyst  usually contains one  sporoblast  (more rarely two). In further maturation after excretion, the sporoblast divides in two, so the oocyst now contains two sporoblasts. The sporoblasts secrete a cyst wall, thus becoming sporocysts; and the sporocysts divide twice to produce four sporozoites each. Infection occurs by ingestion of sporocyst-containing oocysts: the sporocysts excyst in the small intestine and release their sporozoites, which invade the epithelial cells and initiate  schizogony . Upon rupture of the  schizonts , the  merozoites  are released, invade new  epithelial cells , and continue the cycle of asexual multiplication.  Trophozoites  develop into  schizonts  which contain multiple merozoites. After a minimum of one week, the sexual stage begins with the development of male and female gametocytes.  Fertilization  results in the development of oocysts that are excreted in the stool.  Cystoisospora belli  infects both humans and animals. [ citation needed ]


Microscopic demonstration of the large typically shaped oocysts is the basis for diagnosis. Because the oocysts may be passed in small amounts and intermittently, repeated stool examinations and concentration procedures are recommended. If stool examinations are negative, examination of  duodenal  specimens by biopsy or string test (Enterotest) may be needed. The oocysts can be visualized on wet mounts by microscopy with bright-field, differential interference contrast (DIC), and  epifluorescence . They can also be stained by modified  acid-fast stain . [ citation needed ]


Typical laboratory analyses include: [ citation needed ]


Avoiding food or water that may be contaminated with stools can help prevent the infection of  Cystoisospora  (Isosporiasis). Good hand-washing, and personal-hygiene practices should be used as well. One should wash their hands with soap and warm water after using the toilet, changing diapers, and before handling food (CDC.gov). [ 1 ]  It is also important to teach children the importance of washing their hands, and how to properly wash their hands. [ citation needed ]


The treatment of choice is  trimethoprim-sulfamethoxazole  (Bactrim). [ 3 ]


While isosporiasis occurs throughout the world, it is more common in tropical and subtropical areas. Cystoisospora infections are more common in individuals with compromised immune systems, such as HIV or leukemia. [ citation needed ]


Parasitic worms , also known as  helminths , [ 1 ]  are a  polyphyletic  group of large  macroparasites ; adults can generally be seen with the naked eye. Many are  intestinal worms  that are  soil-transmitted  and  infect  the  gastrointestinal tract . Other parasitic worms such as   schistosomes  reside in blood vessels.


Some parasitic worms, including  leeches  and  monogeneans , are  ectoparasites  –  thus, they are not classified as helminths, which are  endoparasites .


Parasitic worms live in and feed in living  hosts . They receive  nourishment  and protection while disrupting their hosts' ability to absorb  nutrients . This can cause weakness and  disease  in the host, and poses a global health and economic problem. [ 2 ]  Parasitic worms cannot reproduce entirely within their host's body; they have a life cycle that includes some stages that need to take place outside of the host. [ 3 ]  Helminths are able to survive in their mammalian hosts for many years due to their ability to manipulate the host's  immune response  by secreting immunomodulatory products. [ 4 ]  All parasitic worms produce  eggs  during reproduction. These eggs have a strong shell that protects them against a range of environmental conditions. The eggs can therefore survive in the environment for many months or years.


Many of the worms referred to as helminths are intestinal parasites. An infection by a helminth is known as  helminthiasis , helminth infection, or intestinal worm infection. There is a naming convention which applies to all helminths: the ending "-asis" (or in veterinary science: "-osis") is added at the end of the name of the worm to denote the infection with that particular worm. [ citation needed ]  For example,  Ascaris  is the name of a type of helminth, and  ascariasis  is the name of the infection caused by that helminth.


Helminths are a group of organisms which share a similar form but are not necessarily  evolutionarily related . The term "helminth" is an artificial term. [ 5 ] [ 6 ]  There is no real consensus on the taxonomy (or groupings) of the helminths, particularly within the  nematodes . [ 7 ]  The term "helminth" contains a number of  phyla , many of which are completely unrelated. However, for practical considerations the term is currently used to describe four phyla with superficial similarities:  Annelida  (ringed or segmented worms),  Platyhelminthes  ( flatworms ),  Nematoda  (roundworms), and  Acanthocephala  (thorny-headed worms). [ 7 ]  The phylum  Platyhelminthes  includes two classes of worms of particular medical significance: the  cestodes  (tapeworms) and the  trematodes  (flukes and  blood flukes ), depending on whether or not they have segmented bodies. [ 1 ] [ 8 ]


There may be as many as 300,000 species of parasites affecting vertebrates, [ 9 ]  and as many as 300 affecting humans alone. [ 10 ]


Helminths of importance in the  sanitation  field are the human parasites, and are classified as  Nemathelminthes  (nematodes) and  Platyhelminthes , depending on whether they possess a round or flattened body, respectively. [ 8 ]


Ringworm  (dermatophytosis) is actually caused by various  fungi , and not by a parasitic worm. [ 11 ] [ 12 ]


The  lifetime  of adult worms varies tremendously from one species to another but is generally in the range of 1 to 8 years (see following table). This lifetime of several years is a result of their ability to manipulate the immune response of their hosts by secreting immunomodulatory products. [ 4 ]


Helminths can be either hermaphroditic (having the sex organs of both sexes), like tapeworms and flukes (not including the blood fluke), or have their sexes differentiated, like the roundworms. [ 13 ]  All helminths produce eggs (also called ova) for reproduction. [ 14 ]


Generally, thousands or even hundreds of thousands of eggs are produced each time the female worm deposits its eggs - a process called  oviposition . There is a large variation in the number of eggs produced by different species of worm at one time; it varies in the range of 3,000 to 700,000. The frequency of egg deposition from an adult helminth is generally daily, and can occur up to six times per day for some  Taenia  species. Adult trematodes lay smaller numbers of eggs compared to cestodes or nematodes. However, the egg develops into a  miracidia  from which thousands of  cercariae , or swimming larvae, develop. This means that one egg may produce thousands of adult worms. [ 15 ]  Helminth eggs remain viable for 1–2 months in crops and for many months in soil, fresh water, and  sewage , or even for several years in  feces ,  fecal sludge  (historically called  night soil ), and  sewage sludge  – a period that is much longer compared to other microorganisms. [ 16 ] [ 17 ]


Helminth eggs are resistant to various environmental conditions due to the composition of the egg shell. Each helminth egg species has 3 to 4 layers with different physical and chemical characteristics: [ 13 ]


Larvae hatch from eggs, either inside or outside the host, depending on the type of helminth. For eggs in moist soil at optimal temperature and oxygen levels, the embryo develops into an infective larva after 2 to 4 weeks, named "second-stage larva". Once ingested by a host, this larva has the ability to get out of the egg, hatch in the small intestine and migrate to different organs. These infective larvae (or "infective eggs") may remain viable in soil for two years or longer. [ 22 ]


The process of larval maturation in the host can take from about two weeks up to four months, depending on the helminth species. [ citation needed ]


The following table shows the principal morphological and reproductive distinctions for three helminth groups:


Fasciola hepatica


Number of species


Registered > 25,000 [ 24 ]


Hymenolepis nana


Taenia solium  / Taenia saginata


Ascaris lumbricoides


Hookworm


Trichuris trichiura


Some days (eggs can survive for months) [ 26 ]


9–15 days [ 23 ]


18 days to several weeks [ 27 ]


1–2 days [ 28 ]


15–30 days [ 29 ]


After hatching, the larvae develop into cysticercoid, which can survive for years in an animal [ 26 ]


5–7 weeks as  cercariae  in snails and longer periods in wet environments as encysted  metacercariae [ 15 ]


10–14 days [ 27 ]


5–10 days (after maturing can survive for weeks outside the host) [ 28 ]


60–70 days (from hatching to mature state) [ 29 ]


5–6 days [ 23 ]


2 months (from cysticercoid to adult) [ 26 ]


3–4 months [ 15 ]


2–3 months [ 27 ]


2–8 weeks [ 23 ]  (can become dormant for months)


4–6 weeks


Several years [ 26 ]


8–10 years [ 23 ]


1–2 years [ 27 ]


Several years [ 28 ]


1 year [ 29 ]


up to 6 times a day [ 26 ]


daily [ 27 ]


daily [ 28 ]


daily [ 29 ]


50,000-100,000 [ 26 ]


200,000 [ 27 ] [ 22 ]  to 250,000 or more [ 23 ]


5,000-10,000 [ 23 ]


3,000-20,000 [ 29 ]


Draft genomes for all categories of helminth have been sequenced in recent years and are available through the ParaSite sub-portal of  WormBase . [ 30 ]


Parasitic worms have been used as a medical treatment for various diseases, particularly those involving an overactive  immune response . [ 31 ]  As  humans  have evolved with parasitic worms, proponents argue they are needed for a healthy immune system. [ 31 ]  Scientists are looking for a connection between the prevention and control of parasitic worms and the increase in  allergies  such as hay-fever in developed countries. [ 31 ]  Removal of parasitic worms from areas is correlated with an increase in autoimmune disorders in those areas. [ 32 ]  Parasitic worms may be able to damp down the immune system of their host, making it easier for them to live in the intestine without coming under attack. [ 31 ]  This may be one mechanism for their proposed medicinal effect. [ citation needed ]


One study suggests a link between the rising rates of  metabolic syndrome  in the developed worlds and the largely successful efforts of Westerners to eliminate intestinal parasites.  The work suggests eosinophils (a type of white blood cell) in fat tissue play an important role in preventing insulin resistance by secreting interleukin 4, which in turn switches  macrophages  into "alternative activation".  Alternatively-activated macrophages are important to maintaining glucose homeostasis (i.e., blood sugar regulation).  Helminth infection causes an increase in eosinophils.  In the study, the authors fed rodents a high-fat diet to induce metabolic syndrome, and then injected them with helminths.  Helminth infestation improved the rodents' metabolism. [ 33 ]   The authors concluded:


Although sparse in blood of persons in developed countries, eosinophils are often elevated in individuals in rural developing countries where intestinal parasitism is prevalent and metabolic syndrome rare.  We speculate that eosinophils may have evolved to optimize metabolic homeostasis during chronic infections by ubiquitous intestinal parasites…. [ 33 ]


For medical purposes, the exact number of helminth eggs is less important and therefore most  diagnoses  are made simply by identifying the appearance of the  worm  or eggs in  feces . Due to the large quantity of eggs laid,  physicians  can  diagnose  using as few as one or two  fecal smears . [ citation needed ]  The  Kato technique  (also called the Kato-Katz technique) is a laboratory method for preparing human stool samples prior to searching for parasite eggs.  Eggs per gram  is a laboratory test that determines the number of eggs per gram of feces in patients suspected of having a parasitological infection, such as schistosomiasis. [ citation needed ]


Helminth eggs can reach the soil when polluted  wastewater ,  sewage sludge  or  human waste  are used as  fertilizer . Such soil is often characterized by moist and warm conditions. Therefore, the risk of using contaminated wastewater and sludge in agricultural fields is a real problem, especially in poor countries, where this practice is prevalent. [ 18 ] [ 34 ]  Helminth eggs are regarded as the main biological health risk when applying sewage sludge, fecal sludge or fecal matter on agricultural soils. [ 16 ]  The eggs are the infective stage of the helminths’ life cycle for causing the disease  helminthiasis . [ citation needed ]


Due to this strong shell, helminth eggs or ova remain viable in soil, fresh water and sewage for many months. In feces, fecal sludge and sewage sludge they can even remain viable for several years. [ 16 ] [ 17 ]  Helminth eggs of concern in  wastewater  used for  irrigation  have a size between 20 and 90 μm and a relative density of 1.06–1.23. [ 18 ]   It is very difficult to inactivate helminth eggs, unless temperature is increased above 40 °C or moisture is reduced to less than 5%. [ 18 ]  Eggs that are no longer viable do not produce any larvae. In the case of  Ascaris lumbricoides  (giant roundworm), which has been considered the most resistant and common helminth type, fertilized eggs deposited in soil are resistant to desiccation but are, at this stage of development, very sensitive to environmental temperatures: The reproduction of a fertilized egg within the eggshell develops at an environmental soil temperature about 25 °C which is lower than the body temperature of the host (i.e., 37 °C for humans). [ 22 ]  However, development of the larvae in the egg stops at temperatures below 15.5 °C, and eggs cannot survive temperatures much above 38 °C. If the temperature is around 25 °C, the infectiousness occurs after nearly 10 days of incubation. [ 8 ] [ 35 ] [ 36 ]


Processes that remove particles, such as sedimentation, filtration or  coagulation-flocculation  physically remove helminth eggs from wastewater (but do not inactivate them). [ 37 ] [ 38 ]  Therefore,  waste stabilization ponds  (lagoons), storage basins,  constructed wetlands , rapid filtration or  upflow anaerobic sludge blanket  (UASB) reactors can be used.


Helminth ova cannot be inactivated with chlorine, UV light or ozone (in the latter case at least not with economical doses because >36 mg/L ozone are needed with 1 hour contact time). [ citation needed ]


Helminth ova can be inactivated in  sewage sludge treatment  if the temperature is increased over 40 °C or moisture is reduced to less than 5%. [ 18 ]  Best results can be obtained when both of these conditions are met together for an extended period of time. [ 39 ]  Details about the contact time under these conditions and other related environmental factors are generally not well-defined for every type of helminth egg species. [ 8 ]  Helminth eggs are considered highly resistant biological structures. [ 18 ]


The eggs from  helminths  (parasitic worms) are a commonly used indicator organism to assess the safety of  sanitation  and  wastewater  reuse systems (such schemes are also called  reuse of human excreta ). [ 40 ] : 55   This is because they are the most resistant  pathogens  of all types of pathogens (pathogens can be  viruses ,  bacteria ,  protozoa  and helminths). [ 41 ]  It means they are relatively hard to destroy through conventional treatment methods. They can survive for 10–12 months in tropical climates. [ 41 ]  These eggs are also called  ova  in the literature. [ 42 ]


Helminth eggs that are found in wastewater and sludge stem from soil-transmitted helminths (STHs) which include  Ascaris lumbricoides  (Ascaris),  Anclostoma duodenale ,  Necator americanus  (hookworm), and  Trichuris trichiura  (whipworm). [ 43 ]  Ascaris and whipworm that are identified in reusable wastewater systems can cause certain diseases and complications if ingested by humans and pigs. [ 44 ]  Hookworms will plant and hatch their larvae into the soil where they grow until maturity. Once the hookworm eggs are fully developed, they infect organisms by crawling through the organism’s skin. [ 45 ]


The presence or absence of viable helminth eggs ("viable" meaning that a larva would be able to hatch from the egg) in a sample of dried fecal matter,  compost  or  fecal sludge  is often used to assess the efficiency of diverse wastewater and sludge treatment processes in terms of pathogen removal. [ 40 ] : 55   In particular, the number of viable  Ascaris  eggs is often taken as an indicator for all helminth eggs in treatment processes as they are very common in many parts of the world and relatively easy to identify under the microscope. However, the exact inactivation characteristics may vary for different types of helminth eggs. [ 46 ]


For the purpose of setting treatment standards and reuse legislation, it is important to be able to determine the amount of helminth eggs in an environmental sample with some accuracy. The detection of viable helminth eggs in samples of wastewater, sludge or fresh feces (as a diagnostic tool for the infection  helminthiasis ) is not straight forward. In fact, many laboratories in developing countries lack the right equipment or skilled staff required to do so. An important step in the analytical methods is usually the concentration of the eggs in the sample, especially in the case of wastewater samples. A concentration step may not be required in samples of dried feces, e.g. samples collected from  urine-diverting dry toilets . [ citation needed ]


Proctitis  or  anusitis  is an  inflammation  of the  anus  and the lining of the  rectum , affecting only the last 6 inches of the rectum.


A common symptom is a continual urge to have a bowel movement—the rectum could feel full or have constipation. Another is tenderness and mild irritation in the rectum and anal region. A serious symptom is pus and blood in the  discharge , accompanied by cramps and pain during the bowel movement. If there is severe bleeding,  anemia  can result, showing symptoms such as pale skin, irritability, weakness, dizziness, brittle nails, and shortness of breath. [ citation needed ]


Symptoms are ineffectual straining to empty the bowels,  diarrhea ,  rectal bleeding  and possible discharge, a feeling of not having adequately emptied the bowels, involuntary spasms and cramping during bowel movements, left-sided abdominal pain, passage of mucus through the rectum, and anorectal pain.


Gonorrhea   (Gonococcal proctitis)


Chlamydia   (chlamydia proctitis)


Herpes Simplex Virus 1 and 2   (herpes proctitis)


Syphilis   (syphilitic proctitis)


Proctitis has many possible causes. It may occur idiopathically (idiopathic proctitis, that is, arising spontaneously or from an unknown cause). Other causes include damage by irradiation (for example in radiation therapy for  cervical cancer  and prostate cancer) or as a  sexually transmitted infection , as in  lymphogranuloma venereum  and  herpes proctitis . Studies suggest a celiac disease-associated "proctitis" can result from an intolerance to  gluten . [ 1 ] [ 2 ]


A common cause is engaging in  anal sex  with partner(s) infected with sexual transmitted diseases in  men who have sex with men . [ 3 ] [ 4 ]  Shared enema usage has been shown to facilitate the spread of  Lymphogranuloma venereum  proctitis. [ 5 ]


Doctors can diagnose proctitis by looking inside the rectum with a  proctoscope  or a  sigmoidoscope . A  biopsy  is taken, in which the doctor scrapes a tiny piece of tissue from the rectum, and this tissue is then examined by microscopy. The physician may also take a stool sample to test for infections or bacteria. If the physician suspects that the patient has Crohn's disease or ulcerative colitis, colonoscopy or barium  enema  X-rays are used to examine areas of the intestine.


Treatment for proctitis varies depending on severity and the cause. For example, the physician may prescribe antibiotics for proctitis caused by bacterial infection. If the proctitis is caused by Crohn's disease or ulcerative colitis, the physician may prescribe the drug  5-aminosalicyclic acid  (5ASA) or  corticosteroids  applied directly to the area in enema or  suppository  form, or taken orally in pill form. Enema and suppository applications are usually more effective, but some patients may require a combination of oral and rectal applications.


Another treatment available is that of fiber supplements such as  Metamucil .  Taken daily these may restore regularity and reduce pain associated with proctitis.


Chronic radiation proctitis is usually treated first-line with sucralfate enemas. These are non-invasive and are effective in diffuse, distal disease. Other treatments may include mesalamine suppositories, vitamin E, hyperbaric oxygen, or short chain fatty acid enemas; however these treatments are only supported by observational or anecdotal evidence.


Reactive arthritis , previously known as  Reiter's syndrome , [ 1 ]  is a form of  inflammatory   arthritis [ 2 ]  that develops in response to an  infection  in another part of the body (cross-reactivity). Coming into contact with  bacteria  and developing an infection can trigger the disease. [ 3 ]  By the time a person presents with symptoms, the "trigger" infection has often been cured or is in  remission  in chronic cases, thus making determination of the initial cause difficult.


The arthritis often is coupled with other characteristic symptoms; this was previously called  Reiter's syndrome ,  Reiter's disease  or  Reiter's arthritis .  The condition was renamed to reactive arthritis because of  Hans Reiter 's war crimes with the  Nazi Party .


The manifestations of reactive arthritis include the following triad of symptoms: an inflammatory arthritis of large joints, inflammation of the eyes in the form of  conjunctivitis  or  uveitis , and  urethritis  in men or  cervicitis  in women. Arthritis occurring alone following sexual exposure or enteric infection is also known as reactive arthritis. Affected people may present with mucocutaneous lesions, as well as  psoriasis -like skin lesions such as  circinate balanitis , and  keratoderma blennorrhagicum .  Enthesitis  can involve the Achilles tendon resulting in heel pain. [ 4 ]  Not all affected persons have all the manifestations.


The clinical pattern of reactive arthritis commonly consists of an  inflammation  of fewer than five joints which often includes the knee or  sacroiliac joint . The arthritis may be "additive" (more joints become inflamed in addition to the primarily affected one) or "migratory" (new joints become inflamed after the initially inflamed site has already improved). [ 5 ] [ 6 ]


Reactive arthritis is an  RF-seronegative ,  HLA-B27 -linked arthritis [ 7 ]  often precipitated by genitourinary or gastrointestinal  infections . The most common triggers are intestinal infections (with  Salmonella ,  Shigella  or  Campylobacter ) and sexually transmitted infections (with  Chlamydia trachomatis ); [ 8 ]  however, it also can happen after  group A streptococcal infections . [ 9 ] [ 10 ]


It most commonly strikes individuals aged 20–40 years of age, is more common in men than in women, and more common in white than in black people. This is owing to the high frequency of the HLA-B27 gene in the white population. [ 11 ] [ 12 ]  It can occur in epidemic form. Patients with  HIV  have an increased risk of developing reactive arthritis as well.


Numerous cases during World Wars I and II focused attention on the triad of arthritis, urethritis, and conjunctivitis (often with additional mucocutaneous lesions), which at that time was also referred to as  Fiessenger–Leroy–Reiter syndrome . [ 13 ]


Reactive arthritis is associated with the  HLA-B27  gene on chromosome 6 and by the presence of  enthesitis  as the basic pathologic lesion [ 16 ]  and is triggered by a preceding  infection . The most common triggering infection in the US is a genital infection with  Chlamydia trachomatis . Other bacteria known to cause reactive arthritis which are more common worldwide are  Ureaplasma urealyticum ,  Salmonella  spp.,  Shigella  spp.,  Yersinia  spp., and  Campylobacter  spp. [ 17 ]  A bout of  food poisoning  or a  gastrointestinal  infection may also precede the disease (the last four  genera  of bacteria mentioned above are enteric bacteria). [ 18 ]   Shigella  is the most common organism causing reactive arthritis following diarrhea.  Chlamydia trachomatis  is the most common cause of reactive arthritis following urethritis.  Ureaplasma  and  mycoplasma  are rare causes. There is some circumstantial evidence for other organisms causing the disease, but the details are unclear. [ 18 ]


Reactive arthritis usually manifests about 1–3 weeks after a known infection. The mechanism of interaction between the infecting organism and the host is unknown. Synovial fluid cultures are negative, suggesting that reactive arthritis is caused either by an autoimmune response involving cross-reactivity of bacterial antigens with joint tissues or by bacterial antigens that have somehow become deposited in the joints. [ citation needed ]


There are few clinical symptoms, but the clinical picture is dominated by arthritis in one or more joints, resulting in pain, swelling, redness, and heat sensation in the affected areas.


The  urethra ,  cervix  and the  throat  may be swabbed in an attempt to  culture  the causative organisms. Cultures may also be carried out on  urine  and  stool  samples or on fluid obtained by  arthrocentesis .


Tests for  C-reactive protein  and  erythrocyte sedimentation rate  are non-specific tests that can be done to corroborate the diagnosis of the syndrome.
A blood test for the genetic marker  HLA-B27  may also be performed. About 75 percent of all the patients with reactive arthritis have this gene.


Although there are no definitive criteria to diagnose the existence of reactive arthritis, the  American College of Rheumatology  has published  sensitivity and specificity  guidelines. [ 19 ]


The main goal of treatment is to identify and eradicate the underlying infectious source with the appropriate  antibiotics  if still present. Otherwise, treatment is symptomatic for each problem. Nonspecific urethritis may be treated with a short course of  tetracycline .  Analgesics , particularly  NSAIDs , are used.  Steroids ,  sulfasalazine  and  immunosuppressants  may be needed for patients with severe reactive symptoms that do not respond to any other treatment. Local  corticosteroids  are useful in the case of  iritis . [ citation needed ]


Reactive arthritis may be self-limiting, frequently recurring, chronic or progressive. Most patients have severe symptoms lasting a few weeks to six months. 15 to 50 percent of cases involve recurrent bouts of arthritis. Chronic arthritis or sacroiliitis occurs in 15–30 percent of cases. Repeated attacks over many years are common, and patients sometimes end up with chronic and disabling  arthritis ,  heart disease ,  amyloid  deposits,  ankylosing spondylitis ,  immunoglobulin A   nephropathy , cardiac conduction abnormalities, or  aortitis  with  aortic regurgitation . [ 20 ]  However, most people with reactive arthritis can expect to live  normal life spans  and maintain a near-normal lifestyle with modest adaptations to protect the involved organs.


Because women may be underdiagnosed, the exact incidence of reactive arthritis is difficult to estimate. A few studies have been completed, though. In  Norway  between 1988 and 1990, the incidence was 4.6 cases per 100,000 for chlamydia-induced reactive arthritis and 5 cases per 100,000 for that induced by  enteric bacteria . [ 21 ]  In 1978 in  Finland , the annual incidence was found to be 43.6 per 100,000. [ 22 ]


When reactive arthritis appears in a triad that also includes ophthalmic and urogenital manifestations, the  eponym  "Reiter's syndrome" is often applied; [ citation needed ]  German physician  Hans Conrad Julius Reiter  described the condition in a soldier he treated during  World War I .


A number of physicians have suggested that the eponym is undeserved. Reiter's  Nazi Party  affiliation, and in particular his involvement in forced human experimentation in the  Buchenwald concentration camp  (which, after his capture at the end of  World War II , resulted in his  prosecution in Nuremberg  as a  war criminal ), have come to overshadow his medical accomplishments. Furthermore, he was not the first physician to make associations between the arthritis and other symptoms—the names arthritis urethritica, venereal arthritis and polyarteritis enterica had previously been applied—and the full triad was described by another physician in the 19th century. [ 23 ]


The  Simple Clinical Colitis Activity Index  ( SCCAI ) is a diagnostic tool and questionnaire used to assess the severity of  symptoms  in people who suffer from  ulcerative colitis . It was created in 1998 and is still used to assess the severity of symptoms. [ 1 ]  It is also used for research purposes to determine the efficacy of various treatments aimed at relieving symptoms. [ 2 ]   The calculated score ranges from 0 to 19, where active disease is a score of 5 or higher. [ citation needed ]


The score is determined by asking the person with colitis questions regarding: [ citation needed ]


The  soil-transmitted helminths  (also called  geohelminths ) are a group of  intestinal parasites  belonging to the  phylum   Nematoda  that are transmitted primarily through contaminated soil. They are so called because they have a direct  life cycle  which requires no  intermediate hosts  or  vectors , and the  parasitic infection  occurs through  faecal  contamination of soil, foodstuffs and water supplies. The adult forms are essentially  parasites  of humans, causing  soil-transmitted helminthiasis  (STH), but also infect  domesticated   mammals . The  juveniles  are the infective forms and they undergo tissue-migratory stages during which they invade vital organs such as  lungs  and  liver . Thus the disease manifestations can be both local and systemic. The geohelminths together present an enormous infection burden on humanity, amounting to 135,000 deaths every year, and persistent infection of more than two billion people. [ 1 ] [ 2 ]


Soil-transmitted helminths are typically from the following  families  of  nematodes , namely: [ citation needed ]


Soil-transmitted helminthiasis is a collective name for the diseases caused by ascaris, whipworm and hookworms in humans. It includes species-specific diseases such as [ citation needed ]


Soil-transmitted helminthiasis is classified as one of the  neglected tropical diseases  projected to be controlled/eradicated by 2020 through the  London Declaration on Neglected Tropical Diseases . [ 4 ]


This is caused by  Strongyloides stercoralis . Even though the disease is principally a soil-transmitted helminthiasis, the infection being mediated through contaminated soil, it is however generally omitted in clinical practices and control programmes because of its (allegedly) relatively less significant influence on health and socio-economic conditions. Also it is not restricted to humans, as it is common in  pets . But there is an emerging hyperinfection syndrome caused by  S. stercoralis , which exhibits a high  mortality rate  (15% to 87%). [ 5 ] [ 6 ]


Geohelminth infection is a major health problem particularly in  rural areas  of  developing countries  like  Subsaharan Africa ,  India  and other  Southeast Asian  countries. It is an important cause of  morbidity  in  school age  children who harbour the highest intensity of worm infestation. Some of the significant morbidity attributed to intestinal  helminthiasis  are  malnutrition ,  growth retardation ,  anaemia ,  vitamin A deficiency  and  impaired intellectual performance . [ 2 ] [ 7 ]


The World Health Organization is promoting the control of  soil transmitted helminthiasis with large scale, regular distribution of anthelminthics (albendazole or mebendazole) to the population groups more at risk of morbidity (children and women of reproductive age). The number of school-age children treated with PC has progressed steadily from less than 120 million in 2008 to over 450 million in 2018 and is in contiuous espansion. [ 8 ]


Anguillula stercoralis   Bavay, 1876


Strongyloides stercoralis  is a  human pathogenic   parasitic   roundworm  causing the disease  strongyloidiasis . Its common name in the US is  threadworm . In the UK and Australia, however, the term  threadworm  can also refer to  nematodes  of the genus  Enterobius , otherwise known as  pinworms . [ 2 ]


The  Strongyloides stercoralis  nematode can parasitize humans. The adult parasitic stage lives in tunnels in the  mucosa  of the small  intestine . The genus  Strongyloides  contains 53 species, [ 3 ] [ 4 ]  and  S. stercoralis  is the  type species .  S. stercoralis  has been reported in other  mammals , including  cats  and  dogs . However, it seems that the species in dogs is typically not  S. stercoralis , but the related species  S. canis .  Non-human primates  are more commonly infected with  S. fuelleborni  and  S. cebus , although  S. stercoralis  has been reported in captive primates. Other species of  Strongyloides  that are naturally parasitic in humans, but with restricted distributions, are  S. fuelleborni fuelleborni  in  central Africa  and  S. fuelleborni kellyi  in  Papua New Guinea . [ 5 ]


S. stercoralis  infection is associated with fecal contamination of soil or water. Hence, it is a very rare infection in developed economies. In developing countries, it is less prevalent in urban areas than in rural areas (where sanitation standards are poor).  S. stercoralis  can be found in areas with tropical and subtropical climates. [ 6 ]


Strongyloidiasis was first described in the 19th century in French soldiers returning home from expeditions in  Indochina . Today, the countries of the old Indochina ( Vietnam ,  Cambodia , and  Laos ) still have endemic strongyloidiasis, with the typical prevalences being 10% or less. Regions of  Japan  used to have endemic strongyloidiasis, but control programs have eliminated the disease. Strongyloidiasis appears to have a high prevalence in some areas of  Brazil  and  Central America . It is endemic in  Africa , but the prevalence is typically low (1% or less). Pockets have been reported from rural  Italy , but the current status is unknown. In the  Pacific islands , strongyloidiasis is rare, although some cases have been reported from  Fiji . In tropical  Australia , some rural and remote  Australian Aboriginal  communities have very high prevalences of strongyloidiasis. [ 7 ]


In some African countries (e.g.,  Congo ),  S. fuelleborni  was more common than  S. stercoralis  in parasite surveys from the 1970s, but the current status is unknown. In  Papua New Guinea ,  S. stercoralis  is endemic, but prevalence is low. However, in some areas, another species,  S. kellyi , [ 8 ]  is a very common parasite of children in the  New Guinea Highlands  and  Western Province . [ 8 ]


Knowledge of the geographic distribution of strongyloidiasis is of significance to travelers who may acquire the parasite during their stays in endemic areas.


Because strongyloidiasis could theoretically be transmittable through unsanitary bedclothes care must be taken never to use unclean hotel bed sheets in endemic areas. Using plastic slippers when showering may be very important when travelling in tropical regions.


Estimates of the number of people infected vary with one estimate putting the figure at 370 million worldwide. [ 9 ] [ 10 ]  Local prevalence can exceed 40% in some tropical and subtropical countries. [ 11 ]


The life cycle of this parasite is more complex than that of most  nematodes , with its alternation between free-living and parasitic cycles, and its potential for autoinfection (the parasite has the ability to complete its life cycle without the involvement of another host) and multiplication within the  host . The parasitic cycle is  homogonic , while the free-living cycle is heterogonic. The heterogonic life cycle is advantageous to the parasite because it allows reproduction in the absence of a host.


In the free-living cycle, the  rhabditiform   larvae  passed in the  stool  can either molt twice and become infective filariform larvae (direct development) or molt four times and become free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch. In the direct development, first-stage larvae (L1) transform into infective larvae (IL) via three molts. The indirect route results first in the development of free-living adults that mate; the female lays eggs, which hatch and then develop into IL. The direct route gives IL faster (three days) versus the indirect route (seven to 10 days). However, the indirect route results in an increase in the number of IL produced. Speed of development of IL is traded for increased numbers. The free-living males and females of  S. stercoralis  die after one generation; they do not persist in the soil. The latter, in turn, can either develop into a new generation of free-living adults or develop into infective  filariform  larvae. The filariform larvae penetrate the human host skin to initiate the parasitic cycle.
Upon contact with contaminated soil, infectious larvae contained in the soil can penetrate the skin.


Some of the larvae enter the superficial veins and are carried in the blood to the lungs, where they enter the  alveoli . They are then coughed up and swallowed into the gut, where they parasitise the intestinal mucosa of the  duodenum  and  jejunum . In the small intestine, they molt twice and become adult female worms. The females live threaded in the  epithelium  of the small intestine and, by  parthenogenesis , produce eggs, which yield rhabditiform larvae. Only females will reach reproductive adulthood in the intestine. Female strongyloids reproduce through parthenogenesis. The eggs hatch in the intestine and young larvae are then excreted in the feces. It takes about two weeks to reach egg development from the initial skin penetration. By this process,  S. stercoralis  can cause both respiratory and gastrointestinal symptoms. The worms also participate in autoinfection, in which the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may follow the previously described route, being carried successively to the lungs, the bronchial tree, the  pharynx , and the small intestine, where they mature into adults; or they may disseminate widely in the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in  Strongyloides stercoralis  and  Capillaria philippinensis  infections. [ citation needed ]   In the case of  Strongyloides , autoinfection may explain the possibility of persistent infections for many years in persons not having been in an endemic area and of hyperinfections in immunodepressed individuals.


Strongyloides  is thought to be attracted to humans via paired thermosensory neurons. [ 12 ]  While  S. stercoralis  is attracted to chemicals such as carbon dioxide or sodium chloride, these chemicals are not specific. Larvae have been thought to locate their hosts via chemicals in the skin, the predominant one being  urocanic acid , a  histidine  metabolite on the uppermost layer of skin that is removed by sweat or the daily skin-shedding cycle. [ 13 ]  Urocanic acid concentrations can achieve at least fivefold greater levels on the foot sole than any other part of the human body. [ 13 ] [ 14 ] [ verification needed ]


Dogs can act as a host for this parasite both in the wild and in the laboratory, but  transmission from dog to human  has been difficult to prove. Molecular genetic analyses have shown that there are two populations of this parasite in dogs, one of which (type B) is exclusive to dogs and a second (type A) that is common to dogs and humans. [ 15 ] [ 16 ]  These two genotypes may be separate species. The identity of the genes suggests that dog to human transmission may occur.


Whereas males grow to only about 0.9  mm  (0.04  in ) in length, females can grow from 2.0 to 2.5 mm (0.08 to 0.10 in). Both sexes also possess a tiny buccal capsule and cylindrical esophagus without a posterior bulb. [ 17 ]  In the free-living stage, the esophagi of both sexes are rhabditiform. Males can be distinguished from females by two structures: the  spicules  and  gubernaculum .


An unusual feature of  S. stercoralis  is autoinfection. Only one other species in the genus  Strongyloides ,  S. felis , has this trait. Autoinfection is the development of L1 into small infective larvae in the gut of the host. These autoinfective larvae penetrate the wall of the lower ileum or colon or the skin of the perianal region, enter the circulation again, travel to the lungs, and then to the small intestine, thus repeating the cycle. Autoinfection makes strongyloidiasis due to  S. stercoralis  an infection with several unusual features.


Persistence of infection is the first of these important features. Because of autoinfection, humans have been known to still be infected up to 65 years after they were first exposed to the parasite (e.g.,  World War II  or  Vietnam War  veterans). Once a host is infected with  S. stercoralis , infection is lifelong unless effective treatment eliminates all adult parasites and migrating autoinfective larvae.


Many people infected are asymptomatic at first. Symptoms include  dermatitis : swelling, itching,  larva currens , and mild hemorrhage at the site where the skin has been penetrated. Spontaneous scratch-like lesions may be seen on the face or elsewhere. If the parasite reaches the lungs, the chest may feel as if it is burning, and wheezing and coughing may result, along with pneumonia-like symptoms ( Löffler's syndrome ). The intestines could eventually be invaded, leading to burning pain, tissue damage, sepsis, and ulcers. Stools may have yellow  mucus  with a recognizable smell. Chronic  diarrhea  can be a symptom. [ 18 ]  In severe cases, edema may result in obstruction of the intestinal tract, as well as loss of  peristaltic  contractions. [ 19 ]


Strongyloidiasis in immunocompetent individuals is usually an indolent disease. However, in immunocompromised individuals, it can cause a hyperinfective syndrome (also called disseminated strongyloidiasis) due to the reproductive capacity of the parasite inside the host. This hyperinfective syndrome can have a mortality rate close to 90% if disseminated. [ 20 ] [ 21 ] [ 22 ]


Immunosuppressive drugs, especially corticosteroids and agents used for tissue transplantation, can increase the rate of autoinfection to the point where an overwhelming number of larvae migrate through the lungs, which in many cases can prove fatal. In addition, diseases such as  human T-lymphotropic virus 1 , which enhance the Th1 arm of the immune system and lessen the Th2 arm, increase the disease state. [ 21 ]  Another consequence of autoinfection is the autoinfective larvae can carry gut bacteria back into the body. About 50% of people with hyperinfection present with bacterial disease due to enteric bacteria. Also, a unique effect of autoinfective larvae is larva currens due to the rapid migration of the larvae through the skin. Larva currens appears as a red line that moves rapidly (more than 5 cm or 2 in per day), and then quickly disappears. It is pathognomonic for autoinfective larvae and can be used as a diagnostic criterion for strongyloidiasis due to  S. stercoralis .


Locating juvenile larvae, either rhabditiform or filariform, in recent stool samples will confirm the presence of this parasite. [ 23 ]  Other techniques used include direct fecal smears, culturing fecal samples on  agar  plates, serodiagnosis through  ELISA , and duodenal fumigation. Still, diagnosis can be difficult because of the day-to-day variation in juvenile parasite load.


Ideally, prevention, by improved sanitation (proper disposal of feces), practicing good hygiene (washing of hands), etc., is used before any drug regimen is administered.


Ivermectin  is the drug of choice for treatment, due to its low side effect profile. [ 24 ]   Albendazole  is also effective in treating strongyloidiasis.  Mebendazole  has a much higher failure rate in clinical practice than albendazole or ivermectin. [ 25 ]  However, these drugs have little effect on the autoinfective larvae. Hence, repeat treatments with ivermectin or albendazole must be administered to kill newly matured parasites that have developed from the autoinfective larvae. This means a full treatment dose every two weeks until all larvae capable of maturing into adults have been extirpated. Follow-up stool samples, potential additional treatment, and blood tests are necessary to ensure a cure. [ 26 ]


This parasite depends on chemical cues to find a potential host. It uses sensor neurons of class AFD to identify cues excreted by the host. [ 27 ]  S. stercoralis  is attracted to nonspecific attractants of warmth, carbon dioxide, and sodium chloride. Urocanic acid, a component of skin secretions in mammals, is a major chemoattractant. Larvae of  S. stercoralis  are strongly attracted to this compound. [ 13 ]  This compound can be suppressed by metal ions, suggesting a possible strategy for preventing infection.


Strongyloidiasis  is a  human parasitic disease  caused by the  nematode  called  Strongyloides stercoralis , or sometimes the closely related  S. fülleborni . These  helminths  belong to a group of  nematodes  called  roundworms . These intestinal worms can cause a number of symptoms in people, principally skin symptoms,  abdominal pain ,  diarrhea  and  weight loss , but also many other specific and vague symptoms in disseminated disease, and severe life-threatening conditions through hyperinfection. In some people, particularly those who require  corticosteroids  or other immunosuppressive medication,  Strongyloides  can cause a  hyperinfection syndrome  that can lead to death if untreated. The diagnosis is made by blood and stool tests. The medication  ivermectin  is widely used to treat strongyloidiasis.


Strongyloidiasis is a type of  soil-transmitted helminthiasis . Low estimates postulate it to affect 30–100 million people worldwide, [ 1 ]  mainly in tropical and subtropical countries, while higher estimates conservatively extrapolate that infection is upwards to or above 370 million people. [ 2 ]   It belongs to the group of  neglected tropical diseases , and worldwide efforts are aimed at eradicating the infection. [ 3 ]


Strongyloides  infection occurs in five forms. As the infection continues and the larvae mature, there may be respiratory symptoms ( Löffler's syndrome ). The infection may then become chronic with mainly digestive symptoms. There may be respiratory, skin, and digestive symptoms of reinfection (when larvae migrate through the body) from the skin to the lungs and finally to the small intestine. Finally, the hyperinfection syndrome causes symptoms in many organ systems, including the  central nervous system . [ 4 ] [ 5 ]


Frequently  asymptomatic .  Gastrointestinal system   symptoms  include abdominal  pain  and  diarrhea  and/or conversely  constipation .   Pulmonary  symptoms (including  Löffler's syndrome ) can occur during pulmonary migration of the filariform larvae.   Pulmonary infiltrate  may be present through radiological investigation.   Dermatologic  manifestations include  urticarial   rashes  in the buttocks and waist areas as well as  larva currens . [ 6 ]   Eosinophilia  is generally present. Strongyloidiasis can become chronic and then become completely asymptomatic. [ citation needed ]


Disseminated strongyloidiasis occurs when patients with chronic strongyloidiasis become  immunosuppressed . There is a distinction to be made between dissemination and hyperinfection. It is mainly a semantic distinction. There can be mild dissemination where the worm burden is relatively lower yet causes insidious symptoms, or extreme dissemination that the term hyperinfection is used to describe.  Thus hyperinfection of varying levels of severe dissemination may present with abdominal pain, distension,  shock , pulmonary and neurologic  complications ,  sepsis ,  haemorrhage ,  malabsorption , and depending on the combination, degree, number, and severity of symptoms, is potentially fatal.   The worms enter the bloodstream from the bowel wall, simultaneously allowing entry of bowel bacteria such as  Escherichia coli . This may cause symptoms such as  sepsis  (bloodstream infection), [ 7 ]  and the bacteria may spread to other organs where they may cause localized infection such as  meningitis . [ 8 ]   Dissemination without hyperinfection may present to a lesser degree the above and many other symptoms. [ citation needed ]


Dissemination can occur many decades after the initial infection [ 9 ]  and has been associated with high dose  corticosteroids ,  organ transplant , any other instances and causes of immunosuppression,  HIV , [ 10 ] [ 11 ]  lepromatous  leprosy , tertiary  syphilis ,  aplastic anemia , malnutrition, advanced  tuberculosis  and  radiation poisoning . [ 12 ]   It is often recommended that patients being started on immunosuppression be screened for chronic strongyloidiasis; however, this is often impractical (screen tests are sometimes unavailable) and in developed countries, the prevalence of chronic strongyloidiasis is minimal, so screening is usually not cost-effective, except in endemic areas.  The reality of global travel and the need for modern advanced healthcare, even in the so-called "developed world", necessitates that in non-endemic areas there is easily accessible testing and screening for neglected tropical diseases such as strongyloidiasis. [ citation needed ]


There is not necessarily any eosinophilia in the disseminated disease. The absence of eosinophilia in an infection limited to the gastrointestinal tract may indicate a poor prognosis. [ 13 ]  Eosinophilia is often absent in disseminated infection. Steroids will also suppress eosinophilia while leading to dissemination and potential hyperinfection. [ citation needed ]


Escalated disseminated infections caused by immunosuppression can result in a wide variety and variable degree of disparate symptoms depending on the condition and other biological aspects of the individual, that may emulate other diseases or diagnoses. In addition to the many palpable gastrointestinal and varied other symptoms drastic  cachexia  amidst lassitude is often present, although severe disseminated infections can occur in individuals without weight loss regardless of  body mass index . [ citation needed ]


Diagnosis  rests on the  microscopic  identification of larvae (rhabditiform and occasionally filariform) in the stool or  duodenal  fluid. Examination of many samples may be necessary, and not always sufficient, because direct stool examination is relatively  insensitive , with a single sample only able to detect larvae in about 25% of cases. [ 14 ]  It can take 4 weeks from initial infection to the passage of larvae in the stool. [ citation needed ]


The stool can be examined in  wet mounts : [ citation needed ]


Culture techniques are the most sensitive, but are not routinely available in the West.  In the UK, culture is available at either of the Schools of Tropical Medicine in Liverpool or London. The direct examination must be done on a stool sample that is freshly collected and not allowed to cool down, because  hookworm  eggs hatch on cooling and the larvae are very difficult to distinguish from  Strongyloides . [ citation needed ]


Finding  Strongyloides  in the stool is negative in up to 70% of tests. It is important to undergo frequent stool sampling and duodenal biopsy if a severe infection is suspected. The duodenal fluid can be examined using techniques such as the  Enterotest string  or duodenal aspiration. [ 15 ]   Larvae may be detected in  sputum  from patients with disseminated strongyloidiasis. [ citation needed ]


Given the poor ability of stool examination to diagnose  Strongyloides , detecting  antibodies  by  ELISA  can be useful. [ 16 ]  Serology can cross-react with other parasites, remain positive for years after successful treatment or be falsely negative in immunocompromised patients. [ 14 ] [ 17 ]  Infected patients will also often have an elevated  eosinophil  count, with an average of absolute eosinophil count of 1000 in one series. [ 18 ]   Eosinophilia of a gastrointestinal infection may fluctuate in response to larval output, or may be permanently lacking in some disseminated infections. Hence lack of eosinophilia is not evidence of the absence of infection. The combination of clinical suspicion, a positive antibody, and peripheral eosinophilia can strongly suggest Stronglyoides infection. [ citation needed ]


It would be useful to have significant advances in the sensitivity of the means of diagnosis, as it would also solve the challenging problem of proof of cure. If a definitive diagnosis is solved then it stands to reason that proof of cure becomes easily realizable. [ 19 ]


The consensus drug of choice for the treatment of uncomplicated strongyloidiasis is  ivermectin . However, even if it is considered the main drug of choice, recent studies have illustrated the challenges in ivermectin curing strongyloidiasis. [ 20 ]  Ivermectin does not kill the  Strongyloides  larvae, only the adult worms, therefore repeat dosing may be necessary to properly eradicate the infection. There is an auto-infective cycle of roughly two weeks during which ivermectin should be re-administered; however, additional dosing may still be necessary as it will not kill  Strongyloides  in the blood or larvae deep within the bowels or diverticula. [ 21 ]  Other drugs that can be effective are  albendazole  and  thiabendazole  (25 mg/kg twice daily for 5 days—400 mg maximum (generally)). [ 11 ]   All patients who are at risk of disseminated strongyloidiasis should be treated. The optimal duration of treatment for patients with disseminated infections is not clear. [ 10 ]


Treatment of strongyloidiasis can be difficult and if ceasing treatment before being entirely cleared  Strongyloides  via the autoinfective cycle has been known to live in individuals for decades; [ 22 ]  even after initial or inadequate sustained treatment. Continued treatment, blood, and stool monitoring thus may be necessary even if symptoms temporarily resolve. As cited earlier, since some infections are insidiously asymptomatic, and relatively expensive bloodwork is often inconclusive via false-positives or false-negatives, [ 23 ]  just as stool samples can be unreliable in diagnoses, [ 24 ]  there is yet, unfortunately, no real gold standard for proof of cure, mirroring the lack of an efficient and reliable methodology of diagnosis. [ 4 ] [ 19 ] [ 25 ]  An objective eradication standard for strongyloidiasis is elusive given the high degree of suspicion needed to even begin treatment, the sometimes difficulty of the only definitive diagnostic criteria of detecting and isolating larvae or adult  Strongyloides , the importance of early diagnosis, particularly before steroid treatments, [ 26 ]  and the very wide variability and exclusion/inclusion of differing collections of diffuse symptoms. Disregarding mis-ascribing bonafide delusional parasitosis disorders, [ 27 ] [ 28 ] [ 29 ]  strongyloidiasis should be more well known among medical professionals and have serious consideration for broad educational campaigns in effected geographic locales both within the semi-tropical developed world and otherwise, as well as in the tropical developing world where, among many other neglected tropical diseases, it is endemic. [ 30 ] [ 31 ]


Government programs are needed to help decontaminate endemic areas and to help affected populations from infection. [ 32 ]  Furthermore, progress is required in establishing financial support to facilitate and cover affordable medications for individuals in affected at-risk regions and communities to help continue treatments. [ 33 ]


There are conflicting reports on effective drug treatments. Ivermectin ineffectiveness and rising  drug resistance  have been documented. [ 34 ] [ 35 ]  Albendazole is noted by the  WHO  as being the least effective. [ 36 ]   Thiabendazole can have severe side effects and is unavailable in many countries. [ 37 ]  Major inroads are required to advance the development of successful medications and drug protocols for strongyloidiasis and other neglected tropical diseases. [ 38 ]


Contagiousness via textiles, unlike  Enterobius vermicularis , is unfounded. As is, generally speaking, person-to-person contagiousness of asymptomatic and disseminated infection. It has rarely been transmitted through organ transplantation. [ 39 ]  Married  Vietnam War  veterans who were infected, yet never developed significant hyperinfection, lived for multiple decades with non-debilitating disseminated infection, without treatment, with wives who failed to ever contract infection. [ 40 ]   Contraction occurs overwhelmingly from skin exposure to any contaminated soil, contaminated potting soil, contaminated waters, lack of sanitation, or environmental factors as potential vectors. Nearly never to extraordinarily very rarely documented is a transmission from person to person (besides from infected male homosexual sex), other than closeness of contact to the productive coughing of a very ill hyperinfected individual. It has been shown possible to occur in that situation, or potentially other similar scenarios, it is speculated via pulmonary secretions of a direly hyperinfected individual. In which case treatment for others may be indicated, if deemed necessary by proximity, symptoms, precautions, probable exposures to the same vectors, or through screening of serology and stool samples, until infection is eradicated. [ 41 ]


Before administering steroids at least somewhat screening for infection in even remotely potentially susceptible individuals to prevent escalating the infection is advised. As not doing so in certain cohorts can have extremely high mortality rates from inadvertently caused hyperinfection via immunosuppression of application of certain steroids. Thus extreme caution with respect to  iatrogenic  risks is crucial to avoiding deaths or other adverse consequences in treatment, that of course prefigures a correct diagnosis. [ 42 ] [ 43 ]  People with high exposure to  Strongyloides stercoralis  may mitigate the risk of strongyloidiasis hyperinfection associated with corticosteroid treatment, with the presumptive use of ivermectin. Such hyperinfection has been a particular concern during the  COVID-19 pandemic  because of the use of corticosteroids to treat COVID-19. The CDC and other international bodies recommend the use of ivermectin for refugees from areas that have a risk of strongyloidiasis. [ 44 ]


During the 1940s, the treatment of choice was enteric-coated tablets of 60 mg  gentian violet , three times daily, for 16 days. [ 45 ]   The cure rate was reported to be only about 50 to 70 percent, requiring repeat courses.  It is possible the cure rate was even less than that published in the literature, due to the difficulty in positively diagnosing infection. [ citation needed ]


Low estimates postulate it to affect 30–100 million people worldwide, [ 1 ]  mainly in tropical and subtropical countries, while higher estimates conservatively extrapolate that infection is upwards to or above 370 million people. [ 2 ]   It belongs to the group of  neglected tropical diseases , and worldwide efforts are aimed at eradicating the infection. [ 3 ]


The disease was first recognized in 1876 by the  French  physician Louis Alexis Normand, working in the naval hospital in  Toulon ; he identified the adult worms and sent them to  Arthur René Jean Baptiste Bavay , affiliated with France's Superior Council on Health, who observed that these were the adult forms of the larvae found in the stool. In 1883 the  German  parasitologist  Rudolf Leuckart  made initial observations on the life cycle of the parasite, and Belgian physician Paul Van Durme (building on observations by the German parasitologist  Arthur Looss ) described the mode of infection through the skin. The German parasitologist  Friedrich Fülleborn  described autoinfection and the way by which strongyloidiasis involves the intestine. Interest in the condition increased in the 1940s when it was discovered that those who had acquired the infection abroad and then received immunosuppression developed hyperinfestation syndrome. [ 46 ]


Travelers' diarrhea  ( TD ) is a stomach and intestinal infection. TD is defined as the passage of unformed  stool  (one or more by some definitions, three or more by others) while traveling. [ 2 ] [ 3 ]  It may be accompanied by abdominal cramps, nausea, fever, headache and bloating. [ 3 ]  Occasionally  dysentery  may occur. [ 5 ]  Most travelers recover within three to four days with little or no treatment. [ 3 ]  About 12% of people may have symptoms for a week. [ 3 ]


Bacteria  are responsible for more than half of cases, [ 3 ]  typically via  foodborne illness  and  waterborne diseases . The bacteria  enterotoxigenic  Escherichia coli  (ETEC) are typically the most common except in  Southeast Asia , where  Campylobacter  is more prominent. [ 2 ] [ 3 ]  About 10 to 20 percent of cases are due to  norovirus . [ 3 ]   Protozoa  such as  Giardia  may cause longer term disease. [ 3 ]  The risk is greatest in the first two weeks of travel and among young adults. [ 2 ]  People affected are more often from the  developed world . [ 2 ]


Recommendations for prevention include eating only properly cleaned and cooked food, drinking  bottled water , and frequent  hand washing . [ 4 ]  The  oral cholera vaccine , while effective for  cholera , is of questionable use for travelers'  diarrhea . [ 6 ]  Preventive  antibiotics  are generally discouraged. [ 3 ]  Primary treatment includes rehydration and replacing lost salts ( oral rehydration therapy ). [ 3 ] [ 4 ]  Antibiotics are recommended for significant or persistent symptoms, and can be taken with  loperamide  to decrease diarrhea. [ 3 ]  Hospitalization is required in less than 3 percent of cases. [ 2 ]


Estimates of the percentage of people affected range from 20 to 50 percent among travelers to the  developing world . [ 3 ]  TD is particularly common among people traveling to Asia (except for Japan and Singapore), the Middle East, Africa, Latin America, and Central and South America. [ 4 ] [ 7 ]  The risk is moderate in  Southern Europe , and Russia. [ 8 ]  TD has been linked to later  irritable bowel syndrome  and  Guillain–Barré syndrome . [ 2 ] [ 3 ]  It has colloquially been known by a number of names, including " Montezuma 's revenge," “ mummy  tummy” [ 9 ]  and " Delhi  belly". [ 10 ]


The onset of TD usually occurs within the first week of travel, but may occur at any time while traveling, and even after returning home, depending on the incubation period of the infectious agent. [ 11 ]  Bacterial TD typically begins abruptly, but  Cryptosporidium  may incubate for seven days, and  Giardia  for 14 days or more, before symptoms develop. Typically, a traveler experiences four to five loose or watery bowel movements each day. Other commonly associated symptoms are abdominal cramping, bloating, fever, and  malaise . Appetite may decrease significantly. [ 12 ]   Though unpleasant, most cases of TD are mild, and resolve in a few days without medical intervention. [ 13 ]


Blood or  mucus  in the diarrhea, significant abdominal pain, or high fever suggests a more serious cause, such as  cholera , characterized by a rapid onset of weakness and torrents of watery diarrhea with flecks of mucus (described as "rice water" stools). Medical care should be sought in such cases; dehydration is a serious consequence of cholera, and may trigger serious  sequelae —including, in rare instances, death—as rapidly as 24 hours after onset if not addressed promptly. [ 13 ]


Infectious agents  are the primary cause of travelers' diarrhea.  Bacterial enteropathogens  cause about 80% of cases.   Viruses  and  protozoans  account for most of the rest. [ 12 ]


The most common causative agent isolated in countries surveyed has been  enterotoxigenic  Escherichia coli  (ETEC). [ 12 ]  Enteroaggregative  E. coli  is increasingly recognized. [ 13 ]   Shigella   spp.  and  Salmonella  spp. are other common bacterial pathogens.   Campylobacter ,  Yersinia ,  Aeromonas , and  Plesiomonas  spp. are less frequently found. Mechanisms of action vary: some bacteria release  toxins  which bind to the intestinal wall and cause diarrhea; others damage the intestines themselves by their direct presence. [ citation needed ]


Brachyspira pilosicoli  pathogen also appears to be responsible for many chronic intermittent watery diarrhea and is only diagnosed through colonic biopsies and microscopic discovery of a false brush border  [ 14 ]  on H&E or Warthin silver stain: its brush-border is stronger and longer that Brachyspira aalborgi's brush-border. It is unfortunately often not diagnosed as coproculture does not allow growth and 16S PCR panel primers do not match Brachyspira sequences. [ 15 ]


While viruses are associated with less than 20% of adult cases of travelers' diarrhea, they may be responsible for nearly 70% of cases in infants and children. Diarrhea due to viral agents is unaffected by antibiotic therapy, but is usually self-limited. [ 13 ]   Protozoans such as  Giardia lamblia ,  Cryptosporidium  and  Cyclospora cayetanensis  can also cause diarrhea. Pathogens commonly implicated in travelers' diarrhea appear in the table in this section. [ 13 ] [ 16 ]


A subtype of travelers' diarrhea afflicting hikers and campers, sometimes known as  wilderness diarrhea , may have a somewhat different frequency of distribution of pathogens. [ 17 ]


The primary source of infection is ingestion of  fecally  contaminated food or water. Attack rates are similar for men and women. [ 12 ]


The most important determinant of risk is the traveler's destination. High-risk destinations include  developing countries  in Latin America, Africa, the Middle East, and Asia. [ 12 ]  Among backpackers, additional risk factors include drinking untreated surface water and failure to maintain personal hygiene practices and clean cookware. [ 18 ]  Campsites often have very primitive (if any) sanitation facilities, making them potentially as dangerous as any developing country. [ citation needed ]


Although travelers' diarrhea usually resolves within three to five days (mean duration: 3.6 days), in about 20% of cases, the illness is severe enough to require bedrest, and in 10%, the illness duration exceeds one week. [ 13 ]   For those prone to serious infections, such as   bacillary dysentery ,  amoebic dysentery , and  cholera , TD can occasionally be life-threatening. [ 13 ]   Others at higher-than-average risk include young adults,  immunosuppressed  persons, persons with  inflammatory bowel disease  or  diabetes , and those taking  H2 blockers  or  antacids . [ 12 ]


Travelers often get diarrhea from eating and drinking foods and beverages that have no adverse effects on local residents. This is due to  immunity  that develops with constant, repeated exposure to pathogenic organisms. The extent and duration of exposure necessary to acquire immunity has not been determined; it may vary with each individual organism. A study among expatriates in Nepal suggests that immunity may take up to seven years to develop—presumably in adults who avoid deliberate pathogen exposure. [ 19 ]
Conversely, immunity acquired by American students while living in Mexico disappeared, in one study, as quickly as eight weeks after cessation of exposure. [ 20 ]


Recommendations include avoidance of questionable foods and drinks, on the assumption that TD is fundamentally a  sanitation  failure, leading to bacterial contamination of drinking water and food. [ 12 ]  While the effectiveness of this strategy has been questioned, given that travelers have little or no control over sanitation in hotels and restaurants, and little evidence supports the contention that food vigilance reduces the risk of contracting TD, [ 21 ]  guidelines continue to recommend basic, common-sense precautions when making food and beverage choices: [ 3 ]


If handled properly, thoroughly cooked fresh and packaged foods are usually safe. [ 12 ]  Raw or undercooked meat and seafood should be avoided.  Unpasteurized  milk, dairy products, mayonnaise, and pastry icing are associated with increased risk for TD, as are foods and beverages purchased from street vendors and other establishments where unhygienic conditions may be present. [ 13 ]


Although safe bottled water is now widely available in most remote destinations, travelers can treat their own water if necessary, or as an extra precaution. [ 13 ]
Techniques include boiling, filtering, chemical treatment, and ultraviolet light; boiling is by far the most effective of these methods. [ 22 ]  Boiling rapidly kills all active bacteria, viruses, and protozoa. Prolonged boiling is usually unnecessary; most microorganisms are killed within seconds at water temperature above 55–70 °C (131–158 °F). [ 23 ] [ 24 ]  The second-most effective method is to combine filtration and chemical disinfection. [ 25 ]   Filters eliminate most bacteria and protozoa, but not viruses. Chemical treatment with halogens—chlorine bleach, tincture of iodine, or commercial tablets—have low-to-moderate effectiveness against protozoa such as  Giardia , but work well against bacteria and viruses.
UV light is effective against both viruses and cellular organisms, but only works in clear water, and it is ineffective unless manufacturer's instructions are carefully followed for maximum water depth/distance from UV source, and for dose/exposure time. Other claimed advantages include short treatment time, elimination of the need for boiling, no taste alteration, and decreased long-term cost compared with bottled water. The effectiveness of UV devices is reduced when water is muddy or turbid; as UV is a type of light, any suspended particles create shadows that hide microorganisms from UV exposure. [ 26 ]


Bismuth subsalicylate  four times daily reduces rates of travelers' diarrhea. [ 2 ] [ 27 ]  Though many travelers find a four-times-per-day regimen inconvenient, lower doses are not effective. [ 2 ] [ 27 ]  Potential side effects include black tongue, black stools, nausea, constipation, and  ringing in the ears . Bismuth subsalicylate should not be taken by those with  aspirin  allergy, kidney disease, or  gout , nor concurrently with certain antibiotics such as the  quinolones , and should not be taken continuously for more than three weeks. [ medical citation needed ]  Some countries do not recommend it due to the risk of rare but serious side effects. [ 27 ]


A  hyperimmune bovine colostrum  to be taken by mouth is marketed in Australia for prevention of ETEC-induced TD. As yet, no studies show efficacy under actual travel conditions. [ 3 ]


Though effective, antibiotics are not recommended for the prevention of TD in most situations because of the risk of allergy or adverse reactions to the antibiotics, and because intake of preventive antibiotics may decrease the effectiveness of such drugs should a serious infection develop subsequently. Antibiotics can also cause  vaginal yeast infections , or overgrowth of the bacterium  Clostridioides difficile , leading to  pseudomembranous colitis  and its associated severe, unrelenting diarrhea. [ 28 ]


Antibiotics may be warranted in special situations where benefits outweigh the above risks, such as immunocompromised travelers, chronic intestinal disorders, prior history of repeated disabling bouts of TD, or scenarios in which the onset of diarrhea might prove particularly troublesome. Options for prophylactic treatment include the  fluoroquinolone  antibiotics (such as  ciprofloxacin ),  azithromycin , and  trimethoprim/sulfamethoxazole , though the latter has proved less effective in recent years. [ 29 ]   Rifaximin  may also be useful. [ 27 ] [ 30 ]   Quinolone antibiotics may bind to metallic cations such as bismuth, and should not be taken concurrently with bismuth subsalicylate. Trimethoprim/sulfamethoxazole should not be taken by anyone with a history of  sulfa  allergy. [ medical citation needed ]


The  oral cholera vaccine , while effective for prevention of cholera, is of questionable use for prevention of TD. [ 6 ]  A 2008 review found tentative evidence of benefit. [ 31 ]  A 2015 review stated it may be reasonable for those at high risk of complications from TD. [ 3 ]  Several vaccine candidates targeting ETEC or  Shigella  are in various stages of development. [ 32 ] [ 33 ]


One 2007 review found that  probiotics  may be safe and effective for prevention of TD, while another review found no benefit. [ 2 ]  A 2009 review confirmed that more study is needed, as the evidence to date is mixed. [ 27 ]


Most cases of TD are mild and resolve in a few days without treatment, but severe or protracted cases may result in significant fluid loss and dangerous  electrolytic imbalance . Dehydration due to diarrhea can also alter the effectiveness of medicinal and contraceptive drugs. Adequate fluid intake ( oral rehydration therapy ) is therefore a high priority. Commercial rehydration drinks [ 34 ]  are widely available; alternatively, purified water or other clear liquids are recommended, along with salty crackers or  oral rehydration salts  (available in stores and pharmacies in most countries) to replenish lost electrolytes. [ 12 ]  Carbonated water or soda, left open to allow dissipation of the carbonation, is useful when nothing else is available. [ 13 ]   In severe or protracted cases, the oversight of a medical professional is advised. [ citation needed ]


If diarrhea becomes severe (typically defined as three or more loose stools in an eight-hour period), especially if associated with nausea, vomiting, abdominal cramps, fever, or blood in stools, medical treatment should be sought. Such patients may benefit from antimicrobial therapy. [ 12 ]   A 2000 literature review found that antibiotic treatment shortens the duration and severity of TD; most reported side effects were minor, or resolved on stopping the antibiotic. [ 35 ]


The antibiotic recommended varies based upon the destination of travel. [ 36 ]   Trimethoprim–sulfamethoxazole  and  doxycycline  are no longer recommended because of high levels of resistance to these agents. [ 12 ]  Antibiotics are typically given for three to five days, but single doses of  azithromycin  or  levofloxacin  have been used. [ 37 ]   Rifaximin  and  rifamycin  are approved in the U.S. for treatment of TD caused by ETEC. [ 38 ] [ 39 ]  If diarrhea persists despite therapy, travelers should be evaluated for bacterial strains resistant to the prescribed antibiotic, possible viral or parasitic infections, [ 12 ]  bacterial or amoebic dysentery,  Giardia , helminths, or cholera. [ 13 ]


Antimotility drugs such as  loperamide  and  diphenoxylate  reduce the symptoms of diarrhea by slowing transit time in the gut. They may be taken to slow the frequency of stools, but not enough to stop bowel movements completely, which delays expulsion of the causative organisms from the intestines. [ 12 ]  They should be avoided in patients with fever, bloody diarrhea, and possible inflammatory diarrhea. [ 40 ]  Adverse reactions may include nausea, vomiting, abdominal pain, hives or rash, and loss of appetite. [ 41 ]  Antimotility agents should not, as a rule, be taken by children under age two. [ 42 ] [ 43 ]


An estimated 10 million people—20 to 50% of international travelers—develop TD each year. [ 12 ]   It is more common in the developing world, where rates exceed 60%, but has been reported in some form in virtually every travel destination in the world. [ 44 ]


Moctezuma's revenge  is a colloquial term for travelers' diarrhea contracted in Mexico. The name refers to  Moctezuma II  (1466–1520), the  Tlatoani  (ruler) of the  Aztec  civilization who was  overthrown  by the Spanish conquistador  Hernán Cortés  in the early 16th century, thereby bringing large portions of what is now Mexico and Central America under the rule of the  Spanish crown . The relevance being that Cortés and his soldiers carried the  smallpox  virus, which Mexicans had never been exposed to. The resulting infection reduced the population of  Tenochtitlan  by 40 percent in 1520 alone. [ 45 ]


Wilderness diarrhea , also called wilderness-acquired diarrhea (WAD) or backcountry diarrhea, refers to diarrhea among backpackers, hikers, campers and other outdoor recreationalists in wilderness or backcountry situations, either at home or abroad. [ 17 ]   It is caused by the same fecal microorganisms as other forms of travelers' diarrhea, usually bacterial or viral. Since wilderness campsites seldom provide access to sanitation facilities, the infection risk is similar to that of any developing country. [ 18 ]   Water treatment, good hygiene, and dish washing have all been shown to reduce the incidence of WAD. [ 46 ] [ 47 ]


This article incorporates  public domain material  from websites or documents of the  Centers for Disease Control and Prevention .


Trichinosis , also known as  trichinellosis , is a  parasitic disease  caused by  roundworms  of the  Trichinella  genus. [ 1 ]  During the initial infection, invasion of the  intestines  can result in  diarrhea ,  abdominal pain , and  vomiting . [ 1 ]  Migration of  larvae  to muscle, which occurs about a week after being infected, can cause  swelling  of the face,  inflammation of the whites of the eyes ,  fever ,  muscle pains , and a  rash . [ 1 ]  Minor infection may be  without symptoms . [ 1 ]  Complications may include  inflammation of heart muscle ,  central nervous system  involvement, and  inflammation of the lungs . [ 1 ]


Trichinosis is mainly spread when undercooked meat containing  Trichinella   cysts  is eaten. [ 1 ]  In North America this is most often bear, but infection can also occur from pork, boar, and dog meat. [ 7 ]  Several  species  of  Trichinella  can cause disease, with  T. spiralis  being the most common. [ 1 ]  After the infected meat has been eaten, the larvae are released from their cysts in the stomach. [ 1 ]  They then invade the wall of the  small intestine , where they develop into adult worms. [ 1 ]  After one week, the females release new larvae that migrate to  voluntarily controlled muscles , where they form cysts. [ 1 ]  The diagnosis is usually based on symptoms and confirmed by finding specific  antibodies in the blood , or larvae on  tissue biopsy . [ 1 ]


The best way to prevent trichinosis is to fully cook meat. [ 3 ]  A  food thermometer  can verify that the temperature inside the meat is high enough. [ 3 ]  Infection is typically treated with antiparasitic medication such as  albendazole  or  mebendazole . [ 4 ]  Rapid treatment may kill adult worms and thereby stop further worsening of symptoms. [ 4 ]  Both medications are considered safe but have been associated with side effects such as  bone marrow suppression . [ 4 ]  Their use during pregnancy or in children under the age of 2 years is poorly studied but appears to be safe. [ 4 ]  Treatment with steroids is sometimes also required in severe cases. [ 4 ]  Without treatment, symptoms typically resolve within three months. [ 5 ]


Worldwide, about 10,000 infections occur a year. [ 6 ]  At least 55 countries including the United States, China, Argentina, and Russia have had recently documented cases. [ 5 ]  While the disease occurs in the tropics, it is less common there. [ 5 ]  Rates of trichinosis in the United States have decreased from about 400 cases per year in the 1940s to 20 or fewer per year in the 2000s. [ 6 ] [ 8 ]  The risk of death from infection is low. [ 5 ]


The great majority of trichinosis infections have either minor or no symptoms and no complications. [ 9 ]  The two main phases for the infection are enteral (affecting the intestines) and parenteral (outside the intestines). The symptoms vary depending on the phase, species of  Trichinella , the quantity of encysted larvae ingested, age, sex, and host immunity. [ 10 ]


A large burden of adult worms in the intestines promotes symptoms such as  nausea ,  heartburn ,  dyspepsia , and  diarrhea  from two to seven days after infection, while small worm burdens generally are asymptomatic.  Eosinophilia  presents early and increases rapidly. [ 11 ]


The severity of symptoms caused by larval migration from the intestines depends on the number of larvae produced. As the larvae migrate through tissue and vessels, the body's inflammatory response results in  edema , muscle pain, fever, and weakness. A classic sign of trichinosis is  periorbital edema , swelling around the eyes, which may be caused by  vasculitis .  Splinter hemorrhage  in the nails is also a common symptom. [ 12 ]


They may very rarely cause enough damage to produce serious neurological deficits (such as  ataxia  or  respiratory paralysis ) from worms entering the  central nervous system  (CNS), which is compromised by trichinosis in 10–24% of reported cases of  cerebral venous sinus thrombosis , a very rare form of stroke (three or four cases per million annual incidence in adults). [ 13 ]  Trichinosis can be fatal depending on the severity of the infection; death can occur 4–6 weeks after the infection, [ 14 ]  and is usually caused by  myocarditis ,  encephalitis , or  pneumonia . [ 15 ]


The classical agent is  T. spiralis  (found worldwide in many carnivorous and omnivorous animals, both domestic and  sylvatic  (wild), [ citation needed ]  but seven primarily sylvatic species of  Trichinella  also are now recognized:


The typical lifecycle for  T. spiralis  involves humans, pigs, and rodents. A pig becomes infected when it eats infectious cysts in raw meat, often porcine  carrion  or a  rat  ( sylvatic cycle ). A human becomes infected by consuming raw or undercooked infected pork (domestic cycle). In the stomach, the  cysts  from infected undercooked meat are acted on by  pepsin  and  hydrochloric acid , which help release the larvae from the cysts into the  stomach . [ 10 ]  The larvae then migrate to the  small intestine , and burrow into the  intestinal mucosa , where they molt four times before becoming adults. [ 10 ]


Thirty to 34 hours after the cysts were originally ingested, the adults mate, and within five days produce larvae. [ 10 ]  Adult worms can only reproduce for a limited time because the  immune system  eventually expels them from the small intestine. [ 10 ]  The larvae then use their piercing mouthpart, called the "stylet", to pass through the  intestinal mucosa  and enter the  lymphatic vessels , and then enter the  bloodstream . [ 20 ]


The larvae travel by  capillaries  to various organs, such as the  retina ,  myocardium , or  lymph nodes ; however, only larvae that migrate to  skeletal muscle  cells survive and  encyst . [ 14 ]  The larval host cell becomes a  nurse cell , in which the larva will be encapsulated, potentially for the life of the host, waiting for the host to be eaten. The development of a capillary network around the nurse cell completes encystation of the larva. Trichinosis is not soil-transmitted, as the  parasite  does not lay eggs, nor can it survive long outside a host. [ 5 ] [ 21 ]


Diagnosis of trichinosis is confirmed by a combination of exposure history, clinical diagnosis, and laboratory testing. [ citation needed ]


An epidemiological investigation can be done to determine a patient's exposure to raw infected meat. Often, an infection arises from home preparation of contaminated meat, in which case microscopy of the meat may be used to determine the infection. Exposure determination does not have to be directly from a laboratory-confirmed infected animal. Indirect exposure criteria include the consumption of products from a laboratory-confirmed infected animal or sharing of a common exposure with a laboratory-confirmed infected human. [ 14 ]


Clinical presentation of the common trichinosis symptoms may also suggest infection. These symptoms include eye puffiness,  splinter hemorrhage , nonspecific  gastroenteritis , and muscle pain. [ 14 ]  The case definition for trichinosis at the European Center for Disease Control states, "at least three of the following six:  fever , muscle soreness and pain,  gastrointestinal symptoms , facial  edema ,  eosinophilia , and subconjunctival, subungual, and retinal  hemorrhages ." [ 14 ]


Blood tests and  microscopy  can be used to aid in the diagnosis of trichinosis. Blood tests include a complete blood count for eosinophilia,  creatine phosphokinase  activity, and various immunoassays such as  ELISA  for larval antigens. [ 14 ]


Laws and rules for food producers may improve food safety for consumers, such as the rules established by the  European Commission  for inspections, rodent control, and improved hygiene. [ 14 ]  A similar protocol exists in the United States, in the  USDA  guidelines for farms and slaughterhouse responsibilities in inspecting pork. [ 22 ]


Public education about the dangers of consuming raw and undercooked meat, especially pork, may reduce infection rates. Hunters are also an at-risk population due to their contact and consumption of wild game, including bears. As such, many states, such as New York, require the completion of a course in such matters before a hunting license can be obtained. [ 23 ]


Testing methods are available for both individual carcasses and monitoring of the herds. [ 24 ]  Artificial digestion method is usually used for the testing of individual carcasses, while the testing for specific antibodies is usually used for herd monitoring. [ 24 ]


Larvae may be killed by the heating or  irradiation  of raw meat. Freezing is normally only effective for  T. spiralis , since other species, such as  T. nativa , are freeze-resistant and can survive long-term freezing. [ 14 ]


Pork can be safely cooked to a slightly lower temperature, provided that the internal meat temperature is at least as hot for at least as long as listed in the  USDA  table below. [ 25 ]  Nonetheless, allowing a  margin of error  for variation in internal temperature within a particular cut of pork, which may have bones that affect temperature uniformity, is prudent. In addition, kitchen thermometers have measurement errors that must be considered. Pork may be cooked for significantly longer and at a higher uniform internal temperature than listed below to be safe. [ 26 ]


Unsafe and unreliable methods of cooking meat include the use of microwave ovens, curing, drying, and smoking, as these methods are difficult to standardize and control. [ 14 ]


Incidence of infection can be reduced by: [ citation needed ]


The US  Centers for Disease Control and Prevention  makes the following recommendation: "Curing (salting), drying, smoking, or microwaving meat does not consistently kill infective worms." [ 27 ]
However, under controlled commercial food processing conditions, some of these methods are considered effective by the USDA. [ 28 ]


The USDA Animal and Plant Health Inspection Service (APHIS) is responsible for the regulations concerning the importation of swine from foreign countries. The Foreign Origin Meat and Meat Products, Swine section covers swine meat (cooked, cured, dried, and fresh). APHIS developed the National Trichinae Certification Program; this is a voluntary "preharvest" program for U.S. swine producers "that will provide documentation of swine management practices" to reduce the incidence of  Trichinella  in swine. [ 29 ]  The CDC reports 0.013% of U.S. swine are infected with  Trichinella . [ 29 ]


As with most diseases, early treatment is better and decreases the risk of developing the disease. If larvae do encyst in skeletal muscle cells, they can remain infectious for months to years. [ 14 ]


Early administration of  anthelmintics , such as  mebendazole  or  albendazole , decreases the likelihood of larval encystation, particularly if given within three days of infection. [ 12 ]  However, most cases are diagnosed after this time. [ 14 ]   In humans, mebendazole (200–400 mg three times a day for three days) or albendazole (400 mg twice a day for 8–14 days) is given to treat trichinosis. [ 30 ]  These drugs prevent newly hatched larvae from developing, but should not be given to pregnant women or children under two years of age. [ 10 ]


Medical references from the 1940s described no specific treatment for trichinosis at the time, but intravenous injection of calcium salts was found to be useful in managing symptoms related to severe toxemia from the infection. [ 31 ]


After infection,  steroids , such as  prednisone , may be used to relieve muscle pain associated with larval migration. [ citation needed ]


Researchers trying to develop a vaccine for  Trichinella  have tried using either "larval extracts, excretory-secretory antigen, DNA, or recombinant antigen protein." [ 32 ]  Currently, no marketable vaccine is available for trichinosis, but experimental mouse studies have suggested possibilities.


About 11 million humans are infected with  Trichinella ;  T. spiralis  is the species responsible for most of these infections. [ 36 ]  Infection was once very common, but this disease is now rare in the  developed world , but two known outbreaks occurred in 2015. In the first outbreak, around 40 people were infected in Liguria, Italy, during a New Year's Eve celebration. [ 37 ] [ 38 ]  The second outbreak in France was associated with pork sausages from  Corsica , which were eaten raw, affecting 14 people in total. [ 39 ]
The incidence of trichinosis in the U.S. has decreased dramatically in the past century from an average of 400 cases per year mid-20th century down to an annual average of 20 cases per year (2008–10). [ 8 ]  The number of cases has decreased because of legislation prohibiting the feeding of raw meat garbage to hogs, increased commercial and home freezing of pork, and the public awareness of the danger of eating raw or undercooked pork products. [ 40 ]


China reports around 10,000 cases every year and is the country with the highest number of cases. [ 14 ] [ dubious  –  discuss ]  In China, between 1964 and 1998, over 20,000 people became infected with trichinosis, and more than 200 people died. [ 32 ]


Trichinosis is common in developing countries where meat fed to pigs is raw or undercooked, but infections also arise in developed countries in Europe where raw or undercooked pork, wild boar, and horse meat may be consumed as delicacies. [ 14 ]


In the  developing world , most infections are associated with undercooked pork. For example, in  Thailand , between 200 and 600 cases are reported annually around the  Thai New Year . This is mostly attributable to a particular delicacy,  larb , which calls for undercooked pork as part of the recipe. [ citation needed ]


In parts of Eastern Europe, the  World Health Organization  reports, some swine herds have trichinosis infection rates above 50%, with correspondingly large numbers of human infections. [ 41 ]


Historically, pork products were thought to have the most risk of infecting humans with  T. spiralis . However, a trichinosis surveillance conducted between 1997 and 2001 showed a higher percentage of cases caused by consumption of wild game (the sylvatic transmission cycle). This is thought to be due to the Federal Swine Health Protection Act (Public Law 96-468) that was passed by Congress in 1980. Before this act, swine were fed garbage that could potentially be infected by  T. spiralis . This act was put in place to prevent trichinella-contaminated food from being given to swine. Additionally, other requirements were put in place, such as rodent control, limiting commercial swine contact with wildlife, maintaining good hygiene, and removing dead pigs from pens immediately. [ 42 ]


Between 2002 and 2007, 11 trichinosis cases were reported to the CDC each year on average in the United States, and 2008–10 averaged 20 cases per year; [ 8 ]  these were mostly the result of consuming undercooked game (sylvatic transmission) or home-reared pigs (domestic transmission). [ citation needed ]


The  kashrut  and  halal  dietary laws of  Judaism  and  Islam  prohibit eating pork. In the 19th century, when the association between trichinosis and undercooked pork was first established, this association was suggested to be the reason for the prohibition, reminiscent of the earlier opinion of medieval  Jewish  philosopher  Maimonides  that food forbidden by Jewish law was "unwholesome". This theory was controversial and eventually fell out of favor. [ 43 ]


The disappearance of the pathogen from domestic pigs has led to a relaxation of legislation and control efforts by veterinary public health systems. Trichinosis has lately been thought of as a re-emerging  zoonosis , supplemented by the increased distribution of meat products, political changes, a changing climate, and increasing  sylvatic  transmission. [ 44 ]


Major sociopolitical changes can produce conditions that favor the resurgence of  Trichinella  infections in swine and, consequently, in humans. For instance, "the overthrow of the social and political structures in the 1990s" in Romania led to an increase in the incidence rate of trichinosis. [ 45 ]


As early as 1835, trichinosis was known to have been caused by a parasite, but the mechanism of infection was unclear at the time. A decade later,  American  scientist  Joseph Leidy  pinpointed undercooked meat as the primary vector for the parasite, and two decades afterward, this hypothesis was fully accepted by the scientific community. [ 46 ]


The circumstances surrounding the first observation and identification of  T. spiralis  are controversial, due to a lack of records. In 1835,  James Paget , a first-year medical student, first observed the larval form of  T. spiralis , while witnessing an autopsy at St. Bartholomew’s Hospital in London. Paget took a special interest in the presentation of muscle with white flecks, described as a "sandy diaphragm".  Although Paget is most likely the first person to have noticed and recorded these findings, the parasite was named and published in a report by his professor,  Richard Owen , who is now credited for the discovery of the  T. spiralis  larval form. [ 20 ] [ 47 ]


A series of experiments conducted between 1850 and 1870 by the German researchers  Rudolf Virchow ,  Rudolf Leuckart , and  Friedrich Albert von Zenker , which involved feeding infected meat to a dog and performing the subsequent necropsy, led to the discovery of the lifecycle of  Trichinella . Through these experiments, Virchow was able to describe the development and infectivity of  T. spiralis . [ 48 ]


The  International Commission on Trichinellosis  (ICT) was formed in Budapest in 1958. Its mission is to exchange information on the epidemiology, biology, pathophysiology, immunology, and clinical aspects of trichinosis in humans and animals. Prevention is a primary goal. Since the creation of the ICT, its members (more than 110 from 46 countries) have regularly gathered and worked together during meetings held every four years: the  International Conference on Trichinellosis . [ citation needed ]


Ascaris trichiura   Linnaeus, 1771


Trichuris trichiura ,  Trichocephalus trichiuris  or  whipworm , is a  parasitic   roundworm  (a type of  helminth ) that causes  trichuriasis  (a type of  helminthiasis  which is one of the  neglected tropical diseases ) when it infects a human  large intestine . It is commonly known as the  whipworm  which refers to the shape of the worm; it looks like a  whip  with wider "handles" at the posterior end. [ 2 ]  The helminth is also known to cause  rectal prolapse .


The female  T. trichiura  produces 2,000–10,000 single-celled eggs per day. [ 3 ]  Eggs are deposited from human feces to soil where, after two to three weeks, they become embryonated and enter the "infective" stage. These embryonated infective eggs are ingested by hand-mouth or through  fomites  and hatch in the human  small intestine , exploiting the intestinal microflora as a stimulus to hatching. [ 4 ]  This is the location of growth and molting. The infective  larvae  penetrate the  villi  and continue to develop in the small intestine. The young worms move to the  caecum  and penetrate the  mucosa , and there they complete development as adult worms in the  large intestine . The life cycle from the time of ingestion of eggs to the development of mature worms takes approximately three months. During this time, there may be limited signs of infection in stool samples, due to a lack of egg production and shedding. The female  T. trichiura  begin to lay eggs after three months of maturity. Worms commonly live for about one year, [ 5 ]  during which time females can lay up to 20,000 eggs per day.


Recent studies using genome-wide scanning revealed that two quantitative trait loci on  chromosome 9  and  chromosome 18  may be responsible for a genetic predisposition or susceptibility to infection of  T. trichiura  by some individuals. [ 6 ]


Trichuris trichiura  has a narrow anterior esophageal end and shorter and thicker posterior end. These pinkish-white worms are threaded through the  mucosa . They attach to the host through their slender anterior end and feed on tissue secretions instead of blood. Females are larger than males; approximately 35–50 mm long compared to 30–45 mm. [ 7 ]  The females have a bluntly round posterior end compared to their male counterparts with a coiled posterior end. Their characteristic eggs are barrel-shaped and brown, and have bipolar protuberances.