Neglected Tropical Diseases (NTDs) are a group of parasitic and bacterial diseases that cause substantial illness for more than one billion people globally. Affecting the world’s poorest people, NTDs impair physical and cognitive development, contribute to mother and child illness and death, make it difficult to farm or earn a living, and limit productivity in the workplace. As a result, NTDs trap the poor in a cycle of poverty and disease.
More than 1 billion people—one-sixth of the world’s population—suffer from one or more Neglected Tropical Diseases (NTDs).
NTDs are a group of infectious diseases that are the source of tremendous suffering because of their disfiguring, debilitating, and sometimes deadly impact. They are called neglected because they have been largely wiped out in the more developed parts of the world and persist only in the poorest, most marginalized communities and conflict areas.
Social stigma is a major consequence of NTDs. In addition to causing physical and emotional suffering, these devastating diseases hamper a person’s ability to work, keep children out of school, and prevent families and communities from thriving.
Buruli ulcer is caused by a germ, Mycobacterium ulcerans, that belongs to the same family of organisms that cause leprosy and tuberculosis. As M. ulcerans produces a toxin – mycolactone – which destroys tissue, infection leads to destruction of skin and soft tissue with large ulcers usually on the legs or arms. Patients who are not treated early suffer long-term functional disability. Early diagnosis and treatment are the only ways to minimize morbidity and prevent disability.
In Africa, about 48% of those affected are children under 15 years, whereas in Australia, 10% are children under 15 years and in Japan, 19% are children under 15 years. No significant difference exists between the rates of affected males and affected females.
Lesions frequently occur in the limbs: 35% on the upper limbs, 55% on the lower limbs, and 10% on the other parts of the body.
In terms of severity, the disease has been classified into three categories: Category I single small lesion (32%), Category II non-ulcerative and ulcerative plaque and oedematous forms (35%) and Category III disseminated and mixed forms such as osteitis, osteomyelitis, joint involvement (33%). In Australia and Japan, most lesions (>90%) are diagnosed in Category I.
In all countries, at least 70% of all cases are diagnosed in the ulceration stage.
The exact mode of transmission of M. ulcerans is still unknown.
Signs and symptoms
Buruli ulcer often starts as a painless swelling (nodule). It can also initially present as a large painless area of induration (plaque) or a diffuse painless swelling of the legs, arms or face (oedema). Local immunosuppressive properties of the mycolactone toxin enable the disease to progress with no pain and fever. Without treatment or sometimes during antibiotics treatment, the nodule, plaque or oedema will ulcerate within 4 weeks with the classical, undermined borders. Occasionally, bone is affected causing gross deformities.
Chagas disease, also known as American trypanosomiasis, is a potentially life-threatening illness caused by the protozoan parasite, Trypanosoma cruzi or (T. cruzi).
It is found mainly in 21 Latin American countries1, where it is mostly vector-borne. The main vector involved in the transmission of the parasite to humans is a triatomine bug, also known as a ‘kissing bug’. An estimated 8 million people are infected worldwide, mostly in Latin America. Chagas disease is clinically curable if treatment is initiated at an early stage. Therefore universal access to prompt diagnosis and care is essential.
Once totally confined to the Region of the Americas, Chagas disease has spread to other continents over the last century mainly because of enhanced means of travel and global population movement to and from Latin America.
It is estimated that over 10 000 people die every year from clinical manifestations of Chagas disease, and more than 25 million people risk acquiring the disease.
Vector control remains the most useful method to prevent infection. Blood screening is vital to avoid infection through transfusion and organ transplantation. Screening and diagnosis in pregnant women and their children are essential control measures.
Chagas disease is named after Carlos Justiniano Chagas, a Brazilian doctor, who discovered the disease in 1909.
Dengue is fast emerging pandemic-prone viral disease in many parts of the world. Dengue flourishes in urban poor areas, suburbs and the countryside but also affects more affluent neighbourhoods in tropical and subtropical countries.
Dengue is a mosquito-borne viral infection causing a severe flu-like illness and, sometimes causing a potentially lethal complication called severe dengue. The incidence of dengue has increased 30-fold over the last 50 years. Up to 50-100 million infections are now estimated to occur annually in over 100 endemic countries, putting almost half of the world’s population at risk.
Severe dengue (previously known as dengue haemorrhagic fever) was first recognized in the 1950s during dengue epidemics in the Philippines and Thailand. Today it affects Asian and Latin American countries and has become a leading cause of hospitalization and death among children and adults in these regions.
The full life cycle of dengue fever virus involves the role of mosquito as a transmitter (or vector) and humans as the main victim and source of infection.
The dengue virus (DEN) comprises four distinct serotypes (DEN-1, DEN-2, DEN-3 and DEN-4) which belong to the genus Flavivirus, family Flaviviridae.
Distinct genotypes have been identified within each serotype, highlighting the extensive genetic variability of the dengue serotypes. Among them, “Asian” genotypes of DEN-2 and DEN-3 are frequently associated with severe disease accompanying secondary dengue infections.
The Aedes aegypti mosquito is the main vector that transmits the viruses that cause dengue. The viruses are passed on to humans through the bites of an infective female Aedes mosquito, which mainly acquires the virus while feeding on the blood of an infected person.
Once infected, humans become the main carriers and multipliers of the virus, serving as a source of the virus for uninfected mosquitoes. The virus circulates in the blood of an infected person for 2-7 days, at approximately the same time that the person develops a fever. Patients who are already infected with the dengue virus can transmit the infection via Aedes mosquitoes after the first symptoms appear (during 4-5 days; maximum 12).
In humans recovery from infection by one dengue virus provides lifelong immunity against that particular virus serotype. However, this immunity confers only partial and transient protection against subsequent infection by the other three serotypes of the virus. Evidence points to the fact that sequential infection increases the risk of developing severe dengue. The time interval between infections and the particular viral sequence of infections may also be of importance.
Echinococcosis is a parasitic disease that occurs in two main forms in humans: cystic echinococcosis (also known as hydatidosis) and alveolar echinococcosis, caused by the tapeworms Echinococcus granulosus and Echinococcus multilocularis, respectively.
Dogs, foxes and other carnivores harbour the adult worms in their intestine and evacuate the parasite eggs in their faeces. If the eggs are ingested by humans, they develop into larvae in several organs, mainly the liver and lungs.
Both cystic and alveolar echinococcosis are characterized by asymptomatic incubation periods that can last many years until the parasite larvae evolve and trigger clinical signs.
Both diseases can cause serious morbidity and death.
A number of herbivorous and omnivorous animals act as intermediate hosts of Echinococcus by ingesting parasite eggs in contaminated soil and developing parasitic larval stages in their viscera. Carnivores are definitive hosts of the parasite; they are infected through the consumption of viscera of intermediate hosts that harbour the parasite and also through scavenging infected carcases. Humans are accidental intermediate hosts and are unable to transmit the disease.
Transmission of cystic echinococcosis is principally maintained in a dog–sheep–dog cycle, although several other domestic animals may be involved including goats, swine, horses, cattle, camels and yaks. Transmission of alveolar echinococcosis usually occurs in a wildlife cycle among foxes, other carnivores and small mammals (mostly rodents). Domesticated dogs and cats can also be infected.
For both diseases, humans become infected through the ingestion of soil, water or food (e.g. green vegetables, berries) contaminated with the parasites’ eggs shed in the faeces of the carnivores, and also by hand-to-mouth transfer of eggs after contact with the contaminated fur of a carnivore, most commonly a dog.
Food borne Trematodes
Food borne Trematodes infections, or foodborne trematodiases, are a group of parasitic infections caused by trematodes (flatworms or “flukes”) that are acquired through ingestion of food contaminated with the larval stages of the parasite.
Transmission is linked to human behaviour patterns related to methods of producing, processing and preparing foods. In particular, dishes containing raw fish, crustaceans and plants are an established dietary tradition of many populations living in countries where these diseases are endemic. Foodborne trematodiases are thus sustained and perpetuated by entrenched cultural practices.
Foodborne trematode infections are all zoonotic infections; that is, diseases primarily affecting domestic or wild animals that may be transmitted to humans. Transmission occurs when humans enter the parasite’s biological cycle to replace its natural reservoir final animal host. Transmission cycles differ for each type of parasite, but they share some common characteristics: they are complex and involve one or two intermediate hosts, usually a mollusc and an animal species such as fish or crustaceans.
A significant number of trematode infections are transmitted by consuming contaminated food. Although most of these infections are only mildly pathogenic, severe pathology in humans is caused by four main genera: Clonorchis spp. (that cause clonorchiasis); Opisthorchis spp. (that cause opisthorchiasis); Fasciola spp. (that cause fascioliasis); and Paragonimus spp. (that cause paragonimiasis).
Guinea-worm disease is caused by the parasitic worm Dracunculus medinensis or “Guinea-worm”. This worm is the largest of the tissue parasite affecting humans. The adult female, which carries about 3 million embryos, can measure 600 to 800 mm in length and 2 mm in diameter. The parasite migrates through the victim’s subcutaneous tissues causing severe pain especially when it occurs in the joints. The worm eventually emerges (from the feet in most of the cases), causing an intensely painful oedema, a blister and an ulcer accompanied by fever, nausea and vomiting.
Infected persons try to relieve the burning sensation by immersing the infected part of their body in local water sources, usually ponds water. This also induces a contraction of the female worm at the base of the ulcer causing the sudden expulsion of hundreds of thousands of first stage larvae into the water. They move actively in the water.
For further development, these larvae need to be ingested by suitable species of voracious predatory crustacean, Cyclops or water fleas which measure 1–2 mm and widely abundant worldwide. In the cyclops, larvae develop to infective third-stage in 14 days at 26°C.
When a person drinks contaminated water from ponds or shallow open wells, the cyclops is dissolved by the gastric acid of the stomach and the larvae are released and migrate through the intestinal wall. After 100 days, the male and female meet and mate. The male becomes encapsulated and dies in the tissues while the female moves down the muscle planes. After about one year of the infection, the female worm emerges usually from the feet releasing thousands of larvae thus repeating the life cycle.
No drug is available to prevent or heal this parasitic disease – exclusively associated with drinking contaminated water. Dracunculiasis is, however, relatively easy to eliminate and eventually eradicate.
Guinea-worm disease is rarely fatal. Frequently, however, the patient remains sick for several months, mainly because:
- The emergence of the worm, sometimes several, is accompanied by painful oedema, intense generalised pruritus, blistering and an ulceration of the area from which the worm emerges.
- The migration and emergence of the worms occur in sensitive parts of the body, sometimes the articular spaces can lead to permanent disability.
- Ulcers caused by the emergence of the worm invariably develop secondary bacterial infections which exacerbate inflammation and pain resulting in temporary disability ranging from a few weeks to a few months.
- Accidental rupture of the worm in the tissue spaces can result in serious allergic reactions.
Leprosy, also known as Hansen’s disease, is a chronic infectious disease caused by Mycobacterium leprae. The disease mainly affects the skin, the peripheral nerves, mucosal surfaces of the upper respiratory tract and the eyes. Leprosy is known to occur at all ages ranging from early infancy to very old age. Leprosy is curable and early treatment averts most disabilities.
The exact mechanism of transmission of leprosy is not known. At least until recently, the most widely held belief was that the disease was transmitted by contact between cases of leprosy and healthy persons. More recently the possibility of transmission by the respiratory route is gaining ground. There are also other possibilities such as transmission through insects which cannot be completely ruled out.
Signs/symptoms and diagnosis
Clinical signs are easy to observe. In a country or area with a high incidence of leprosy, an individual should be regarded as having leprosy if he or she shows ONE of the following cardinal signs:
- skin lesion consistent with leprosy and with definite sensory loss, with or without thickened nerves
- positive skin smears
The skin lesion can be single or multiple, usually less pigmented than the surrounding normal skin. Sometimes the lesion is reddish or copper-coloured. A variety of skin lesions may be seen but macules (flat), papules (raised), or nodules are common. Sensory loss is a typical feature of leprosy. The skin lesion may show loss of sensation to pin pick and/or light touch. Thickened nerves, mainly peripheral nerve trunks constitute another feature of leprosy. A thickened nerve is often accompanied by other signs as a result of damage to the nerve. These may be loss of sensation in the skin and weakness of muscles supplied by the affected nerve. In the absence of these signs, nerve thickening by itself, without sensory loss and/or muscle weakness is often not a reliable sign of leprosy.
Leprosy can be classified on the basis of clinical manifestations and skin smear results. In the classification based on skin smears, patients showing negative smears at all sites are said to have paucibacillary leprosy (PB), while those showing positive smears at any site are said to have multibacillary leprosy (MB).
Lymphatic filariasis, commonly known as elephantiasis, is a painful and profoundly disfiguring disease. In communities where filariasis is transmitted, all ages are affected. While the infection may be acquired during childhood its visible manifestations may occur later in life, causing temporary or permanent disability. In endemic countries, lymphatic filariasis has a major social and economic impact with an estimated annual loss of $1 billion and impairing economic activity up to 88%
The disease is caused by three species of thread-like nematode worms, known as filariae – Wuchereria bancrofti, Brugia malayi and Brugia timori. Male worms are about 3–4 centimetres in length, and female worms 8–10 centimetres. The male and female worms together form “nests” in the human lymphatic system, the network of nodes and vessels that maintain the delicate fluid balance between blood and body tissues. The lymphatic system is an essential component of the body’s immune system.
Filarial infection can cause a variety of clinical manifestations, including lymphoedema of the limbs, genital disease (hydrocele, chylocele, and swelling of the scrotum and penis) and recurrent acute attacks, which are extremely painful and are accompanied by fever. The vast majority of infected people are asymptomatic, but virtually all of them have subclinical lymphatic damage and as many as 40% have kidney damage, with proteinuria and haematuria.
A blackfly (Simulium-damnosum) under microscope (x 100). a parasite comes out of one of its antena
The filarial worms (O. volvulus) are transmitted from person to person by the repeated bites of infected black flies (Simulium spp.) . These black flies breed in fast-flowing rivers and streams, mostly in remote villages located near fertile land where people rely on agriculture.
In human, female adult worms produce embryonic larvae (microfilariae) that migrate to the skin, eyes and other organs. A single female worm can release up to 1000 microfilariae larvae per day into the surrounding tissue. When a female black fly bites an infected person during a blood meal, it also ingests microfilariae which develop further into the infectious L3 stage and are then transmitted to the next human host during subsequent bites.
Photomicrograph of Onchocerca volvulus (adult worms)
Adult O. volvulus worms have the ability to live for fifteen years in the human body. Male and female worms are encapsulated in the subcutaneous fibrous tissue known as nodules.
Rabies is a zoonotic disease (a disease that is transmitted from animals to humans), caused by the rabies virus, of the Lyssavirus genus, within the family Rhabdoviridae. Domestic dogs are the most common reservoir of the virus, with more than 95% of human deaths caused by dog-mediated rabies.
The virus is transmitted in the saliva of rabid animals and generally enters the body via infiltration of virus-laden saliva from a rabid animal into a wound (e.g. scratches), or by direct exposure of mucosal surfaces to saliva from an infected animal (e.g. bites). The virus cannot infiltrate intact skin. Once the virus reaches the brain, it further replicates, resulting in presentation of clinical signs from the patient. There are two clinical manifestations of rabies – furious (classical or encephalitic) and paralytic. Furious rabies is most common form of human rabies, accounting for approximately 80% of cases.
With the exception of Antarctica, rabies is endemic on all continents. Of the tens of thousands of deaths occurring annually due to rabies, 95% of cases are reported in Asia and Africa.
Dog-mediated human rabies disproportionately affects poor rural communities, particularly children, with the majority (80%) of human deaths occurring in rural areas, where awareness and access to appropriate post-exposure prophylaxis is limited or non-existent.
The true burden of the disease is likely to be underestimated due to chronic underreporting and political neglect in many developing countries. Improved reporting systems are required to address the lack of accurate data and validate these estimates in a number of regions.
Rabies is a 100% vaccine-preventable disease. Countries embarking on rabies elimination programmes have successfully experienced marked reductions, often progressing to the elimination of rabies. Elimination programs often revolve around mass dog vaccination campaigns, where at least 70% of the dog population should be covered in order to break the cycle of transmission in dogs, and to humans.
Schistosomiasis is a disease of poverty that leads to chronic ill-health. Infection is acquired when people come into contact with fresh water infested with the larval forms (cercariae) of parasitic blood flukes, known as schistosomes. The microscopic adult worms live in the veins draining the urinary tract and intestines. Most of the eggs they lay are trapped in the tissues and the body’s reaction to them can cause massive damage.
Schistosomiasis affects almost 240 million people worldwide, and more than 700 million people live in endemic areas. The infection is prevalent in tropical and sub-tropical areas, in poor communities without potable water and adequate sanitation. Urogenital schistosomiasis is caused by Schistosoma haematobium and intestinal schistosomiasis by any of the organisms S. guineensis, S. intercalatum, S. mansoni, S. japonicum, and S. mekongi.
Several million people all over the world suffer from severe morbidity as a consequence of schistosomiasis.
The WHO strategy on use of anthelminthic drugs now makes it possible to control schistosomiasis in poor and marginalized communities, in conjunction with interventions against lymphatic filariasis, onchocerciasis and soil transmitted helminthiasis. In highly endemic areas, severe morbidity due to schistosomiasis can be prevented by regular treatment of at risk groups targeted based on community diagnosis based on sentinel groups. Praziquantel has been safely co-administered with albendazole and ivermectin, in areas where these drugs have been used separately for preventive chemotherapy.
Infection with T. solium can result in two distinct conditions: taeniasis and cysticercosis. While the adult tapeworm in the human intestine (taeniasis) does not have major health impacts, humans can also develop cysticercosis with tapeworm larvae (cysticerci) in the muscles, skin, eyes and the central nervous system, with possible devastating effects on health. When cysts develop in the brain, the condition is referred to as neurocysticercosis. Symptoms include severe headache, blindness, convulsions and epileptic seizures and can be fatal.
- solium also reduces the market value of pigs and makes pork unsafe to eat.
Taeniasis is acquired by humans through the inadvertent ingestion of tapeworm larvae (cysticerci) in undercooked pork. Once in the human body, cysticerci develop into adult tapeworms that live in the intestine and release egg-bearing gravid proglottids (segments) which are passed out with faeces.
Cysticercosis is acquired when worm proglottids or eggs are ingested and the developing larvae migrate through the body and form cysts in tissues. This is the case in pigs and cattle but it can also affect humans, usually when they swallow T. solium egg-contaminated soil, water or food (mainly vegetables) or through self-infection when hygiene practices, such as hand washing after the toilet, are unsufficient. When the central nervous system is affected by the larvae, the infection is called neurocysticercosis.
Trachoma is the leading infectious cause of blindness in the world. Infection spreads from person to person, particularly from child to child and from child to mother to child. The disease thrives especially in crowded living conditions where there are shortages of water, inadequate sanitation and where numerous eye-seeking flies are present. In affected communities, infection is often first encountered in infancy or childhood.
In affected communities, infection is often first encountered in infancy or childhood. With repeated infection over many years, the cumulative effect of many inflammatory episodes may cause the upper eyelid to turn inwards, so that the eyelashes rub on the eyeball, resulting in intense pain and scarring of the front of the eye. This is called trachomatous trichiasis, and ultimately leads to irreversible blindness.
The age at which people in a community start going blind from trachoma is related to the intensity of transmission of infection in the community.
Trachoma disease is usually clinically diagnosed. People are examined for clinical signs through the use of magnifiers (loupes). In most early stages, infection does not present visible signs of the disease. However, repeated infections cause scarring of the conjunctiva and it is during this phase that infected individuals get the feeling of irritation.
The WHO grading system for trachoma classifies the disease in 5 grades:
- Trachomatous Inflammation – Follicular (TF) – which mostly requires topical treatment.
- Trachomatous Inflammation – Intense (TI) – during which topical and systemic treatments are considered.
- Trachomatous Scarring (TS) – when scars are visible as in the tarsal conjunctiva and which may obscure tarsal blood vessels.
- Trachomatous Trichiasis (TT) – when an individual is referred for eyelid surgery; and
- Corneal Opacity – a stage during which a person is irreversibly blind.
In areas where trachoma is endemic, active (inflammatory) trachoma is common among preschool-aged children, with prevalence rates which can be as high as 60-90%. Infection becomes less frequent and shorter in duration with increasing age.
Infection is usually acquired through living in close proximity to others with active disease, and the family is the principal unit for transmission. An individual’s immune system can clear a single episode of infection, but in endemic communities, re-acquisition of the organism occurs frequently.
After years of repeated infection, the inside of the eyelid can become so severely scarred (trachomatous conjunctival scarring) that it turns inwards and causes the eye-lashes to rub against the eyeball (trachomatous trichiasis) resulting in constant pain and light intolerance; this and other alterations of the eye can lead to the scarring of the cornea. Left untreated, this condition leads to the formation of irreversible opacities, with resulting visual impairment or blindness. The age at which this occurs depends on several factors including local transmission intensity. In very highly endemic communities, it can occur in childhood, though onset between the ages of 30 and 40 years is more typical.
Visual impairment or blindness results in a worsening of the life experience of affected individuals and their families, who are normally already amongst the poorest of the poor. Women are blinded 2 to 3 times more often than men, probably due to their close contact with infected children and their resulting greater frequency of infection episodes themselves.
Environmental risk factors influencing the transmission of the disease include:
- poor hygiene;
- crowded households;
- water shortage; and
- inadequate latrines and sanitation facilities.
Trypanosomes are unicellular parasitic protozoa belonging to the Trypanosoma Genus of the Trypanosomatidae Class (Protozoa Kingdom). A large number of species and subspecies of trypanosomes have been described. Different species of trypanosomes infect a variety of different vertebrates, including animals and humans. Most species are transmitted by insects.
On the African continent a number of Trypanosoma species and subspecies are economically significant causing human and animal diseases which are an obstacle to human welfare, affecting cattle rearing and agricultural development.
Human African Trypanosomiasis or sleeping sickness, only occurs in Sub-Saharan Africa. It is caused by two subspecies of Trypanosoma brucei brucei, namely Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense. Wild and domestic animals can host these parasites and may represent under particular conditions an important reservoir of infection for the tsetse flies.
Animal African Trypanosomiasis is caused by other trypanosome species and subspecies then those affecting human beings. Trypanosoma brucei, Trypanosoma congolense, Trypanosoma equiperdum, Trypanosoma simiae, Trypanosoma suis and Trypanosoma vivax are some of the species and subspecies causing diseases in wild and domestic animals. These diseases bear different common names such as nagana, dourine and surra. All these diseases have an economic impact on the development of agriculture in Africa. Those affecting cattle are undoubtedly the most important economically since they are a major cause for reduced meat and milk production and draught power for agricultural production.
Occasional infections in humans with T. evansi, T lewisi, T. brucei brucei and, T congolense have been describing in human beings.
What is yaws?
Yaws is a poverty-related chronic skin disease that affects mainly children below 15 years of age (with a peak between 6 and 10 years).
It is caused by the bacterium – is a Treponema pallidumm subspecies pertenue and transmitted by skin contact. Yaws mainly affects the skin, but can also involve the bone and cartilage. The organism that causes yaws is closely related to the one that causes syphilis. Early detection and treatment can avoid gross disfigurement and disability which occur in about 10% of cases.
Yaws occurs in overcrowded communities, with limited access to basic amenities, such as water and sanitation, as well as health care.
Traditionally, laboratory-based serological tests such as Treponema pallidum particle agglutination (TPPA) and rapid plasma reagin (RPR) are widely used to diagnose treponemal infections (for example, syphilis and yaws). These tests cannot distinguish yaws from syphilis however, and the interpretation of results from these tests in adults who live in yaws endemic areas needs careful clinical assessment because of syphillis.
Rapid point-of-care tests that can be used in the field are widely available.
However, most of them are treponemal-based and cannot distinguish between past and current infection. Recently dual treponemal and nontreponemal rapid tests have become available, thus simplifying diagnosis in the field. These tests are able to detect both present and past infections to guide treatment of people with active infection.
Rapid point-of-care tests used in the field
Polymerase chain reaction (PCR) can be used to definitively confirm yaws by detecting the organisms in the skin lesions. It can also be used to monitor azithromycin resistance and this test will be very useful in the last phase of the eradication programme.
Either of 2 antibiotics – azithromycin or benzathine penicillin – may be used to treat yaws:
- Azithromycin (single oral dose) at 30 mg/kg (maximum 2 gm) is the preferred choice in the WHO “Yaws Eradication Strategy” (the Morges Strategy) because of the ease of administration and logistical consideration in large-scale treatment campaigns.
- Benzathine penicillin (single intramuscular dose) at 1.2 million units (adults) and 600 000 units (children). For patients allergic to penicillin and azithromycin, doxycycline 100mg (1 tab) orally, b.d. twice daily for 7 days may be used.
Before-after treatment with antibiotics
Soil transmitted helminthiasis.
Soil-transmitted helminthes infections are among the most common infections worldwide and affect the poorest and most deprived communities. They are transmitted by eggs present in human faeces which in turn contaminate soil in areas where sanitation is poor.
The main species that infect people are the roundworm (Ascaris lumbricoides), the whipworm (Trichuris trichiura) and the hookworms (Necator americanus and Ancylostoma duodenale).
Intestinal worms produce a wide range of symptoms including intestinal manifestations (diarrhoea, abdominal pain), general malaise and weakness. Hookworms cause chronic intestinal blood loss that result in anaemia.
Morbidity and symptoms
Morbidity is directly related to worm burden: the greater the number of worms in the infected person, the greater will be the severity of disease.
Soil-transmitted helminths impair the nutritional status of those infected in many ways, sometimes causing death by:
- negatively affecting nutritional status (causing intestinal bleeding, loss of appetite, diarrhoea or dysentery, and reducing absorption of micronutrients);
- worsening school performance;
- causing complications that require surgical intervention (i.e. intestinal obstruction and rectal prolapse).
Concomitant infections with other parasite species are frequent and may have additional effects on nutritional status and organ pathology.
Soil-transmitted helminths live in the intestine of infected individuals where they produce thousands of eggs each day that are passed in the faeces. Where the environmental conditions are favourable, the eggs develop into infective stages.
Humans become infected when ingesting infected eggs (Ascaris lumbricoides and Trichuris trichiura) or larvae (Ancylostoma duodenale) in contaminated food (e.g. vegetables that are not carefully cooked, washed or peeled), hands or utensils or through penetration of the skin by infective hookworm larvae in contaminated soil (Necator americanus and Ancylostoma duodenale).
Figure schematic life-cycle (source: helminth control in school age children)
There is no direct person-to-person transmission or infection from fresh faeces because eggs passed in faeces need about 3 weeks in the soil before they become infective.
Although strongyloidiasis has a similar route of infection as the other soil-transmitted helminthiases, it needs different diagnostic tools and different treatment. In areas where mass treatment with ivermectin has been used to control onchocerciasis or lymphatic filariasis, there has been a noticeable reduction in the prevalence of strongyloidiasis. The possibility of use this approach for the control of infection is presently under evaluation.