MALARIA

Malaria is an infectious disease caused by

a parasite, it is spread by the bite of an infected mosquito. People catch malaria when the
parasite enters the blood. The parasite causes a deadly infection which kills many people
each year. The parasite that causes malaria is a protozoan called 'Plasmodium'. Protozoa
are organisms with only one cell, but they are not bacteria. Bacteria are smaller and simpler
than protozoans. People usually get malaria from the Anopheles or Culex mosquitoes: they
are the vectors of the disease. The Plasmodium gets into people by the bites of
mosquitoes. The Plasmodium is in the mosquito's special saliva. The mosquito's saliva
injects an anticoagulant into the person to prevent their blood from clotting. The person is
then infected with Plasmodium as a by-product. This makes the person have the disease
we call malaria. Only the female mosquito gives people malaria, because only the female
mosquito consumes blood. The male mosquito lives on the nectar of flowers. The female
uses blood as a source of protein for its eggs. Some people do not get malaria from
mosquitoes. A baby can get it while inside its mother. This is called maternal-foetal
transmission. People can also get malaria from a blood transfusion. This is when someone
gives blood to another person. Another way people can catch malaria is by using
a needle that someone with the disease used before them.

Signs and symptoms:

Malaria can cause jaundice, which causes the skin and the white areas of the eyes (sclerae)
to turn orange-yellow. This is caused by hyperbilirubinemia - too much bilirubin in the
blood. Bilirubin is a pigment which results when the body breaks down old red blood cells.
Symptoms are changes in someone's body that are signs for a disease. Most people who
get malaria get symptoms 10–30 days after they get infected (the Plasmodium gets in their
blood.) But some people can get symptoms after only a week, and some may be infected
with malaria and not have symptoms for a year.
The most common symptom of malaria is fever, when the body temperature is high. The
fever from malaria usually comes very suddenly. The people who have Malaria often feel
like they had influenza.
Symptoms of malaria are:

 Arthralgia (pain in joints)

 Headache (pain in head)
 Feeling very tired or sleepy
 Cough
 Chills (feeling very cold)
 Delirium (when people are very confused because of a disease. They may look drunk.
They may not be able to talk.)
 Coma (when people are not conscious. They look like they are asleep, but they cannot
be woken. )

Signs of malaria:

 Anaemia (low red blood cell levels in the blood)

 Diarrhoea
 Jaundice (yellow skin and eyes)
 Sweating
 Vomiting
 Fast heart rate
 Low blood pressure
 Enlarged organs. When something becomes enlarged or BIGGER than normal the word
often ends in -megaly.
 Hepatomegaly -enlarged liver, splenomegaly - enlarged spleen, or both
hepatosplenomegaly. When these organs become enlarged it may cause pain in
the right upper quadrant of the abdomen.

Complications are problems that happen because of a disease.

Pregnant women and young children have more complications. People who get malaria for
the first time have more complications. Falciparum malaria has the most complications.

Clinical diagnosis:
A clinical diagnosis is based on the signs and symptoms of a disease, it is a diagnosis
made without medical testing. In the case of malaria one of the main symptoms which may
lead to a clinical diagnosis of malaria is a fever. Any clinical diagnosis of malaria should be
confirmed by a trained professional based upon laboratory results as soon as it is
possible.

Malaria rapid diagnostic test

A Malaria rapid diagnostic test is a blood test which can confirm a diagnosis of malaria in
about twenty minutes. RDTs are not foolproof and have a number of drawbacks, and as
such a negative rapid diagnostic test should not be accepted at face-value and follow-up
with malaria microscopy is necessary.

Malaria microscopy
To see if patients have malaria, doctors may do a blood test. This test is called a Giemsa
blood smear. Blood is put on a slide which is a thin piece of glass. The Giemsa stain is put
on the slide. This stain helps doctors see the malaria. Then they look at the slide under
a microscope. The Plasmodium is seen in the red blood cells.

Treatment:
People with different kinds of malaria need different medicines. The medicine that works
for one kind of malaria may not for another kind. So it is very important to know
which species of Plasmodium the person has. If the species is not known, the person
should be given medicine and care like they have falciparum malaria – the worst kind. It is
also important to know where the person got malaria. Plasmodium in some places is
resistant to some medicines. So the medicines to treat malaria in Africa are different from
the medicines to treat malaria from South America.

Treatment of malaria other than falciparum:

Everywhere except New Guinea, the treatment is the same. In New Guinea most P. vivax is
resistant to chloroquine. It can be treated with quinine, but this medicine can make people
sick. Everywhere else, non-falciparum malaria is treated with chloroquine. Chloroquine kills
the Plasmodium in the blood. But the Plasmodium in the liver is not killed by
chloroquine. P. vivax and P. ovale both stay in the liver a long time. This is the dormant
phase. Another medicine must be given with chloroquine for P. vivax and P. ovale. This is
to kill the Plasmodium in the liver. The medicine used to kill malaria in the liver
is primaquine. In southeast Asia, some P. vivax is resistant to primaquine. Most other
places, primaquine works very well. Some people get very sick from primaquine. So people
have to be tested to see if they have G6PD-deficiency before they take primaquine.
Treatment of falciparum malaria:
Falciparum is the worst kind of malaria. People with falciparum malaria should be treated in
a hospital if they are:
 Very sick
 Children
 Pregnant
 Having malaria for the first time
 Not able to take medicines by mouth
Even people who are treated with medicines at home should stay with the doctor for 8
hours. This is to make sure they do not get sicker.It also makes sure they can take the
medicines by mouth. Malaria does not start to become a life-threatening disease until it has
been a couple of weeks after the bite without being treated. Falciparum malaria also has
more resistance to medicines. This makes it much harder to treat. Falciparum malaria is
always treated with two or more medicines. Doctors choose the medicines by where in the
world the person got malaria. Different places have P. falciparum that is resistant to
different medicines. The most important resistance is chloroquine-resistance. In some
places in the world, P. falciparum is killed by chloroquine. In some places it is chloroquine-
resistant. This means chloroquine does not kill it. In these places quinine can be used.
Quinine is taken by mouth.

How to prevent malaria:

There are three ways to prevent malaria:

 Control mosquitoes
 Keep mosquitoes from biting
 Take medicine to keep from getting sick after a bite, especially in those parts of the
world where people get malaria.
Control mosquitoes
Vector control is one way to stop malaria. Vector means an organism that carries
an infectious disease to another organism. For malaria, the vector is
the Anopheles mosquito.
The most used method of vector control is pesticides. These are chemicals that kill the
mosquito. The first pesticide used for vector control was DDT. DDT worked very well for
vector control. It killed mosquitoes. It did not make people very sick at the time it was used.
It did not cost very much money. Other chemicals for vector control had not been invented
yet.
In many places mosquitoes became resistant to DDT. This meant that DDT did not work
anymore in these areas. Scientists worried that DDT was making people and animals sick.
It killed a lot of wildlife too. DDT also stays in the environment for a long time. For these
reasons, people mostly use other chemicals for vector control.
Organophosphate or carbonate pesticides are used, like malathion or bendiocarb.
Vector control is not the only way to stop malaria. And DDT is not the only chemical that
can be used for vector control. The best way to stop malaria is to use a combination of
methods. In some places, DDT may be a useful part of a program to stop malaria. This is
why DDT is still allowed to be used for controlling malaria.

Keeping mosquitoes from biting:

The mosquito that carries malaria comes more at dawn (when the sun comes up) and dusk
(when the sun goes down.) Be most careful at these times. Wear long trousers and shirts
with long sleeves. Wear mosquitoes repellent (this is a chemical that mosquitoes do not
like, so they do not bite.) Mosquitoes will bite through thin cloth. So repellent should be
used on skin and clothes.
Pesticides can be used in rooms to kill mosquitoes. When sleeping outside, people use a
mosquito net. This is made from cloth that air can go through but keeps mosquitoes out. It
is put over a bed where people sleep to keep mosquitoes out. Sometimes people also use it
when they are not sleeping. It is best to use mosquito nets that have been treated with
Permethrin, which repels and kills mosquitoes.

Taking medicine to not get sick

People can take medicine when they are in a place where there is malaria. This reduces the
chances that they contract malaria. This is called prophylaxis.
Some people take prophylactic medicines for years. Many people in areas where there is
malaria do not have the money to buy this medicine.
People who live where there is no malaria usually have not had malaria. The first case
malaria is usually much worse. So people from places where there is no malaria may take
prophylactic medicines when they go to places where there is malaria. The kind of
prophylactic medicines people take depends on where they are. This is because not all
medicines work on the malaria in every place.
To make them work best, prophylactic medicines have to be taken the right way. The
medicine should start before going to an area with malaria. Most medicines should be
taken for 4 weeks after coming home. One medicine (Malarone) only needs to be used
for one week after coming home.

Resistance to malaria:
There are some children in Tanzania who are naturally immune to malaria. Researchers are
using this to develop a new vaccine. U.S. researchers have found the children produce
an antibody which attacks the malaria-causing parasite. Injecting a form of this antibody
into mice protected the animals from the disease. The researchers plan to do tests
on primates, including humans.
 DIARRHOEA

Diarrhoea, also spelled diarrhoea, is the

condition of having at least three loose or liquid bowel movements each day. It often lasts
for a few days and can result in dehydration due to fluid loss. Signs of dehydration often
begin with loss of the normal stretchiness of the skin and irritable behaviour. This can
progress to decreased urination, loss of skin color, a fast heart rate, and a decrease in
responsiveness as it becomes more severe. Loose but non-watery stools in babies who are
exclusively breastfed, however, are normal.
The most common cause is an infection of the intestines due to either a virus, bacteria,
or parasite - a condition also known as gastroenteritis. These infections are often acquired
from food or water that has been contaminated by faeces, or directly from another person
who is infected. The three types of diarrhoea are: short duration watery diarrhoea, short
duration bloody diarrhoea, and persistent diarrhoea (lasting more than two weeks). The
short duration watery diarrhoea may be due to an infection by cholera, although this is rare
in the developed world. If blood is present it is also known as dysentery. A number of non-
infectious causes can result in diarrhoea. These include lactose intolerance, irritable bowel
syndrome, non-celiac gluten sensitivity, celiac disease, inflammatory bowel
disease, hyperthyroidism, bile acid diarrhoea, and a number of medications. In most
cases, stool cultures to confirm the exact cause are not required.

Causes:
Sanitation
Poverty often leads to unhygienic living conditions, as in this community in the Indian
Himalayas. Such conditions promote contraction of diarrheal diseases, as a result of
poor sanitation and hygiene.
Open defecation is a leading cause of infectious diarrhoea leading to death.
Poverty is a good indicator of the rate of infectious diarrhoea in a population. This
association does not stem from poverty itself, but rather from the conditions under which
impoverished people live. The absence of certain resources compromises the ability of the
poor to defend themselves against infectious diarrhoea. "Poverty is associated with poor
housing, crowding, dirt floors, lack of access to clean water or to sanitary disposal of
faecal waste (sanitation), cohabitation with domestic animals that may carry human
pathogens, and a lack of refrigerated storage for food, all of which increase the frequency
of diarrhoea... Poverty also restricts the ability to provide age-appropriate, nutritionally
balanced diets or to modify diets when diarrhoea develops so as to mitigate and repair
nutrient losses. The impact is exacerbated by the lack of adequate, available, and
affordable medical care."[36]
Water
One of the most common causes of infectious diarrhoea, is a lack of clean water. Often,
improper faecal disposal leads to contamination of groundwater. This can lead to
widespread infection among a population, especially in the absence of water filtration or
purification. Human faeces contains a variety of potentially harmful human pathogens.[37]
Nutrition
Proper nutrition is important for health and functioning, including the prevention of
infectious diarrhoea. It is especially important to young children who do not have a fully
developed immune system. Zinc deficiency, a condition often found in children
in developing countries can, even in mild cases, have a significant impact on the
development and proper functioning of the human immune system. Indeed, this
relationship between zinc deficiency and reduced immune functioning corresponds with an
increased severity of infectious diarrhoea. Children who have lowered levels of zinc have a
greater number of instances of diarrhoea, severe diarrhoea, and diarrhoea associated with
fever. Similarly, vitamin A deficiency can cause an increase in the severity of diarrheal
episodes. However, there is some discrepancy when it comes to the impact of vitamin A
deficiency on the rate of disease. While some argue that a relationship does not exist
between the rate of disease and vitamin A status, others suggest an increase in the rate
associated with deficiency. Given that estimates suggest 127 million preschool children
worldwide are vitamin A deficient, this population has the potential for increased risk of
disease contraction.

Medications:
Some medications, such as the penicillum can cause diarrhea. Over 700 medications are
known to cause diarrhoea. The classes of medications that are known to cause diarrhea are
laxatives, antacids, heartburn medications, antibiotics, anti-neoplastic drugs, anti-
inflammatories as well as many dietary supplements.

Diagnostic approach:
The following types of diarrhoea may indicate further investigation is needed:

 In infants
 Moderate or severe diarrhoea in young children
 Associated with blood
 Continues for more than two days
 Associated non-cramping abdominal pain, fever, weight loss, etc.
 In travelers
 In food handlers, because of the potential to infect others;
 In institutions such as hospitals, child care centers, or geriatric and convalescent
homes.

Prevention:
Sanitation
Numerous studies have shown that improvements in drinking water and sanitation (WASH)
lead to decreased risks of diarrhoea. Such improvements might include for example use of
water filters, provision of high-quality piped water and sewer connections.
In institutions, communities, and households, interventions that promote hand
washing with soap lead to significant reductions in the incidence of diarrhea. The same
applies to preventing open defecation at a community-wide level and providing access
to improved sanitation. This includes use of toilets and implementation of the
entire sanitationchain connected to the toilets (collection, transport, disposal or reuse
of human excreta).
Hand washing
Basic sanitation techniques can have a profound effect on the transmission of diarrheal
disease. The implementation of hand washing using soap and water, for example, has been
experimentally shown to reduce the incidence of disease by approximately 42–48%. Hand
washing in developing countries, however, is compromised by poverty as acknowledged
by the CDC: "Handwashing is integral to disease prevention in all parts of the world;
however, access to soap and water is limited in a number of less developed countries. This
lack of access is one of many challenges to proper hygiene in less developed countries."
Solutions to this barrier require the implementation of educational programs that
encourage sanitary behaviours.
Water
Given that water contamination is a major means of transmitting diarrheal disease, efforts
to provide clean water supply and improved sanitation have the potential to dramatically
cut the rate of disease incidence. In fact, it has been proposed that we might expect an 88%
reduction in child mortality resulting from diarrheal disease as a result of improved water
sanitation and hygiene. Similarly, a meta-analysis of numerous studies on improving water
supply and sanitation shows a 22–27% reduction in disease incidence, and a 21–30%
reduction in mortality rate associated with diarrheal disease.
Chlorine treatment of water, for example, has been shown to reduce both the risk of
diarrheal disease, and of contamination of stored water with diarrheal pathogens.

Vaccination:
Immunization against the pathogens that cause diarrheal disease is a viable prevention
strategy, however it does require targeting certain pathogens for vaccination. In the case of
Rotavirus, which was responsible for around 6% of diarrheal episodes and 20% of diarrheal
disease deaths in the children of developing countries, use of a Rotavirus vaccine in trials
in 1985 yielded a slight (2-3%) decrease in total diarrheal disease incidence, while reducing
overall mortality by 6-10%. Similarly, a Cholera vaccine showed a strong reduction in
morbidity and mortality, though the overall impact of vaccination was minimal as Cholera is
not one of the major causative pathogens of diarrheal disease. Since this time, more
effective vaccines have been developed that have the potential to save many thousands of
lives in developing nations, while reducing the overall cost of treatment, and the costs to
society. A rotavirus vaccine decrease the rates of diarrhoea in a population. New vaccines
against rotavirus, Shigella, Enterotoxigenic Escherichia coli (ETEC), and cholera are under
development, as well as other causes of infectious diarrhoea.
Nutrition
Dietary deficiencies in developing countries can be combated by promoting better eating
practices. Zinc supplementation proved successful showing a significant decrease in the
incidence of diarrheal disease compared to a control group. The majority of the literature
suggests that vitamin A supplementation is advantageous in reducing disease
incidence. Development of a supplementation strategy should take into consideration the
fact that vitamin A supplementation was less effective in reducing diarrhoea incidence
when compared to vitamin A and zinc supplementation, and that the latter strategy was
estimated to be significantly more cost effective.
Breastfeeding
Breastfeeding practices have been shown to have a dramatic effect on the incidence of
diarrheal disease in poor populations. Studies across a number of developing nations have
shown that those who receive exclusive breastfeeding during their first 6 months of life are
better protected against infection with diarrheal diseases. One study in Brazil found that
non-breastfed infants were 14 times more likely to die from diarrhoea than exclusively
breastfed infants. Exclusive breastfeeding is currently recommended for the first six
months of an infant's life by the WHO, with continued breastfeeding until at least two years
of age.
Others
Probiotics decrease the risk of diarrhoea in those taking antibiotics.
Management
In many cases of diarrhoea, replacing lost fluid and salts is the only treatment needed. This
is usually by mouth – oral rehydration therapy – or, in severe cases, intravenously. Diet
restrictions such as the BRAT diet are no longer recommended. Research does not support
the limiting of milk to children as doing so has no effect on duration of diarrhoea. To the
contrary, WHO recommends that children with diarrhea continue to eat as sufficient
nutrients are usually still absorbed to support continued growth and weight gain, and that
continuing to eat also speeds up recovery of normal intestinal functioning. CDC
recommends that children and adults with cholera also continue to eat.
Medications such as loperamide (Imodium) and bismuth subsalicylate may be beneficial;
however they may be contraindicated in certain situations.
Fluids
Oral rehydration solution (ORS) slightly sweetened and salty water) can be used to prevent
dehydration. Standard home solutions such as salted rice water, salted yogurt drinks,
vegetable and chicken soups with salt can be given. Home solutions such as water in
which cereal has been cooked, unsalted soup, green coconut water, weak tea
(unsweetened), and unsweetened fresh fruit juices can have from half a teaspoon to full
teaspoon of salt (from one-and-a-half to three grams) added per liter. Clean plain water can
also be one of several fluids given. There are commercial solutions such as Pedialyte, and
relief agencies such as UNICEF widely distribute packets of salts and sugar. A WHO
publication for physicians recommends a homemade ORS consisting of one liter water with
one teaspoon salt (3 grams) and two tablespoons sugar (18 grams) added (approximately
the "taste of tears"). Rehydration Project recommends adding the same amount of sugar
but only one-half a teaspoon of salt, stating that this more dilute approach is less risky with
very little loss of effectiveness. Both agree that drinks with too much sugar or salt can
make dehydration worse.
Appropriate amounts of supplemental zinc and potassium should be added if available. But
the availability of these should not delay rehydration. As WHO points out, the most
important thing is to begin preventing dehydration as early as possible. In another example
of prompt ORS hopefully preventing dehydration, CDC recommends for the treatment of
cholera continuing to give Oral Rehydration Solution during travel to medical treatment.
Vomiting often occurs during the first hour or two of treatment with ORS, especially if a
child drinks the solution too quickly, but this seldom prevents successful rehydration since
most of the fluid is still absorbed. WHO recommends that if a child vomits, to wait five or
ten minutes and then start to give the solution again more slowly. Drinks especially high in
simple sugars, such as soft drinks and fruit juices, are not recommended in children under
5 years of age as they may increase dehydration. A too rich solution in the gut draws water
from the rest of the body, just as if the person were to drink sea water. Plain water may be
used if more specific and effective ORT preparations are unavailable or are not
palatable. Additionally, a mix of both plain water and drinks perhaps too rich in sugar and
salt can alternatively be given to the same person, with the goal of providing a medium
amount of sodium overall. A nasogastric tube can be used in young children to administer
fluids if warranted.
Eating
The WHO recommends a child with diarrhoea continue to be fed. Continued feeding speeds
the recovery of normal intestinal function. In contrast, children whose food is restricted
have diarrhoea of longer duration and recover intestinal function more slowly. The WHO
states "Food should never be withheld and the child's usual foods should not be diluted.
Breastfeeding should always be continued." And in the specific example of cholera, CDC
also makes the same recommendation. Breastfed infants with diarrhoea often choose to
breastfeed more, and should be encouraged to do so. In young children who are not
breast-fed and live in the developed world, a lactose-free diet may be useful to speed
recovery.
Medications
While antibiotics are beneficial in certain types of acute diarrhoea, they are usually not
used except in specific situations. There are concerns that antibiotics may increase the risk
of hemolytic uremic syndrome in people infected with Escherichia coli O157:H7. In
resource-poor countries, treatment with antibiotics may be beneficial. However, some
bacteria are developing antibiotic resistance, particularly Shigella. Antibiotics can also
cause diarrhoea, and antibiotic-associated diarrhoea is the most common adverse effect of
treatment with general antibiotics.
While bismuth compounds (Pepto-Bismol) decreased the number of bowel movements in
those with travelers' diarrhoea, they do not decrease the length of illness. Anti-motility
agents like loperamide are also effective at reducing the number of stools but not the
duration of disease. These agents should only be used if bloody diarrhoea is not present..
Bile acid sequestrants such as cholestyramine can be effective in chronic diarrhoea due
to bile acid malabsorption. Therapeutic trials of these drugs are indicated in chronic
diarrhoea if bile acid malabsorption cannot be diagnosed with a specific test, such
as SeHCAT retention.
 Amoebiasis

Amoebiasis, also known amoebic

dysentery, is an infection caused by any of the amoebas of
[3]
the Entamoeba group. Symptoms are most common during infection by Entamoeba
histolytica.[3] Amoebiasis can be present with no, mild, or severe symptoms.[3] Symptoms
may include abdominal pain, diarrhoea, or bloody diarrhea.[3] Complications can
include inflammation of the colon with tissue death or perforation, which may result
in peritonitis.[3] People affected may develop anemia due to loss of blood.
Cysts of Entamoeba can survive for up to a month in soil or for up to 45 minutes under
fingernails. Invasion of the intestinal lining can cause bloody diarrhea. If the parasite
reaches the bloodstream it can spread through the body, most frequently ending up in the
liver where it can cause amoebic liver abscesses. Liver abscesses can occur without
previous diarrhea. Diagnosis is typical by stool examination using a microscope, but may
not reliably exclude infection or separate between specific types. An increased white blood
cell count may be present in severe cases. The most accurate test is finding
specific antibodies in the blood, but it may remain positive following treatment. Bacterial
colitis can result in similar symptoms.
Prevention of amoebiasis is by improved sanitation, including separating food and water
from faeces.[3] There is no vaccine. There are two treatment options depending on the
location of the infection. Amoebiasis in tissues is treated with
either metronidazole, tinidazole, nitazoxanide, dehydroemetine or chloroquine, while
luminal infection is treated with diloxanide furoateor iodoquinoline. Effective treatment
against all stages of the disease may require a combination of medications. Infections
without symptoms do not require treatment but infected individuals can spread the parasite
to others and treatment can be considered. Treatment of other Entamoeba infections apart
from E. histolytica is not needed.
Amoebiasis is present all over the world. About 480 million people are infected with
amoebiasis and this results in the death of between 40,000–110,000 people a year. Most
infections are now believed due to E. dispar. E. dispar is more common in certain areas and
symptomatic cases may be less common than previously reported. The first case of
amoebiasis was documented in 1875 and in 1891 the disease was described in detail,
resulting in the terms amoebic dysentery and amoebic liver abscess. Further evidence from
the Philippines in 1913 found that upon swallowing cysts of E. histolytica volunteers
developed the disease.

Signs and symptoms:

Most infected people, about 90%, are asymptomatic, but this disease has the potential to
make the sufferer dangerously ill. It is estimated that about 40,000 to 100,000 people
worldwide die annually due to amoebiasis.
Infections can sometimes last for years. Symptoms take from a few days to a few weeks to
develop and manifest themselves, but usually it is about two to four weeks. Symptoms can
range from mild diarrhoea to severe dysentery with blood and mucus. The blood comes
from lesions formed by the amoebae invading the lining of the large intestine. In about 10%
of invasive cases the amoebae enter the bloodstream and may travel to other organs in the
body. Most commonly this means the liver, as this is where blood from the intestine
reaches first, but they can end up almost anywhere in the body.
Onset time is highly variable and the average asymptomatic infection persists for over a
year. It is theorized that the absence of symptoms or their intensity may vary with such
factors as strain of amoeba, immune response of the host, and perhaps
associated bacteria and viruses.
In asymptomatic infections the amoeba lives by eating and digesting bacteria and food
particles in the gut, a part of the gastrointestinal tract. It does not usually come in contact
with the intestine itself due to the protective layer of mucus that lines the gut. Disease
occurs when amoeba comes in contact with the cells lining the intestine. It then secretes
the same substances it uses to digest bacteria, which include enzymes that destroy cell
membranes and proteins. This process can lead to penetration and digestion of
human tissues, resulting first in flask-shaped ulcers in the intestine. Entamoeba
histolytica ingests the destroyed cells by phagocytosis and is often seen with red blood
cells (a process known as erythrophagocytosis) inside when viewed in stool samples.
Especially in Latin America, a granulomatous mass (known as an amoeboma) may form in
the wall of the ascending colon or rectum due to long-lasting immunological cellular
response, and is sometimes confused with cancer.
"Theoretically, the ingestion of one viable cyst can cause an infection."

Cause:
Amoebiasis is an infection caused by the amoeba Entamoeba histolytica. Likewise
amoebiasis is sometimes incorrectly used to refer to infection with other amoebae, but
strictly speaking it should be reserved for Entamoeba histolytica infection. Other amoebae
infecting humans include:
Parasites

 Dientamoeba fragilis, which causes Dientamoebiasis

 Entamoeba dispar
 Entamoeba hartmanni
 Entamoeba coli
 Entamoeba polecki
 Entamoeba bangladeshi
 Entamoeba moshkovskii
 Endolimax nana and
 Iodamoeba butschlii.
Except for Dientamoeba, the parasites above are not thought to cause disease.

 Free living amoebas. These species are often described as "opportunistic free-living
amoebas" as human infection is not an obligate part of their life cycle.
 Naegleria fowleri, which causes primary amoebic meningoencephalitis
 Acanthamoeba, which causes cutaneous amoebiasis and Acanthamoeba keratitis
 Balamuthia mandrillaris, which causes granulomatous amoebic encephalitis and
primary amoebic meningoencephalitis
 Sappinia diploidea
Life-cycle of the Entamoeba histolytica
Amoebiasis is usually transmitted by the fecal-oral route, but it can also be transmitted
indirectly through contact with dirty hands or objects as well as by anal-oral contact.
Infection is spread through ingestion of the cyst form of the parasite, a semi-dormant and
hardy structure found in feces. Any non-encysted amoebae, or trophozoites, die quickly
after leaving the body but may also be present in stool: these are rarely the source of new
infections. Since amoebiasis is transmitted through contaminated food and water, it is
often endemic in regions of the world with limited modern sanitation systems, including
México, Central America, western South America, South Asia, and western and
southern Africa.
Amoebic dysentery is often confused with "traveler's diarrhea" because of its prevalence in
developing nations. In fact, most traveler's diarrhea is bacterial or viral in origin.
Diagnosis:
With colonoscopy it is possible to detect small ulcers of between 3–5mm, but diagnosis
may be difficult as the mucous membrane between these areas can look either healthy or
inflamed.
Asymptomatic human infections are usually diagnosed by finding cysts shed in the stool.
Various flotation or sedimentation procedures have been developed to recover the cysts
from fecal matter and stains help to visualize the isolated cysts for microscopic
examination. Since cysts are not shed constantly, a minimum of three stools are examined.
In symptomatic infections, the motile form (the trophozoite) is often seen in fresh
feces. Serological tests exist, and most infected individuals (with symptoms or not) test
positive for the presence of antibodies. The levels of antibody are much higher in
individuals with liver abscesses. Serology only becomes positive about two weeks after
infection. More recent developments include a kit that detects the presence of amoeba
proteins in the faeces, and another that detects ameba DNA in feces. These tests are not in
widespread use due to their expense.
Microscopy is still by far the most widespread method of diagnosis around the world.
However it is not as sensitive or accurate in diagnosis as the other tests available. It is
important to distinguish the E. histolytica cyst from the cysts of nonpathogenic intestinal
protozoa such as Entamoeba coli by its appearance. E. histolytica cysts have a maximum
of four nuclei, while the commensal Entamoeba coli cyst has up to 8 nuclei. Additionally,
in E. histolytica, the endosome is centrally located in the nucleus, while it is usually off-
center in Entamoeba coli. Finally, chromatoidal bodies in E. histolytica cysts are rounded,
while they are jagged in Entamoeba coli. However, other species, Entamoeba disparand E.
moshkovskii, are also commensals and cannot be distinguished from E. histolytica under
the microscope. As E. dispar is much more common than E. histolytica in most parts of the
world this means that there is a lot of incorrect diagnosis of E. histolytica infection taking
place. The WHO recommends that infections diagnosed by microscopy alone should not be
treated if they are asymptomatic and there is no other reason to suspect that the infection
is actually E. histolytica. Detection of cysts or trophozoites stools under microscope may
require examination of several samples over several days to determine if they are present,
because cysts are shed intermittently and may not show up in every sample.
Typically, the organism can no longer be found in the feces once the disease goes extra-
intestinal. Serological tests are useful in detecting infection by E. histolytica if the
organism goes extra-intestinal and in excluding the organism from the diagnosis of other
disorders. An Ova & Parasite (O&P) test or an E. histolytica fecal antigen assay is the
proper assay for intestinal infections. Since antibodies may persist for years after clinical
cure, a positive serological result may not necessarily indicate an active infection. A
negative serological result however can be equally important in excluding suspected tissue
invasion by E. histolytica.
Prevention:
To help prevent the spread of amoebiasis around the home:

 Wash hands thoroughly with soap and hot running water for at least 10 seconds after
using the toilet or changing a baby's diaper, and before handling food.
 Clean bathrooms and toilets often; pay particular attention to toilet seats and taps.
 Avoid sharing towels or face washers.
To help prevent infection:

 Avoid raw vegetables when in endemic areas, as they may have been fertilized using
human faeces.
 Boil water or treat with iodine tablets.
 Avoid eating street foods especially in public places where others are sharing sauces in
one container
Good sanitary practice, as well as responsible sewage disposal or treatment, are necessary
for the prevention of E. histolytica infection on an endemic level. E.histolytica cysts are
usually resistant to chlorination, therefore sedimentation and filtration of water supplies
are necessary to reduce the incidence of infection.
E. histolytica cysts may be recovered from contaminated food by methods similar to those
used for recovering Giardia lamblia cysts from feces. Filtration is probably the most
practical method for recovery from drinking water and liquid foods. E. histolytica cysts
must be distinguished from cysts of other parasitic (but nonpathogenic) protozoa and from
cysts of free-living protozoa as discussed above. Recovery procedures are not very
accurate; cysts are easily lost or damaged beyond recognition, which leads to many falsely
negative results in recovery tests.
Treatment:
E. histolytica infections occur in both the intestine and (in people with symptoms) in tissue
of the intestine and/or liver. As a result, two different classes of drugs are needed to treat
the infection, one for each location. Such anti-amoebic drugs are known as amoebicides.
Prognosis:
In the majority of cases, amoebas remain in the gastrointestinal tract of the hosts. Severe
ulceration of the gastrointestinal mucosal surfaces occurs in less than 16% of cases. In
fewer cases, the parasite invades the soft tissues, most commonly the liver. Only rarely are
masses formed (amoebomas) that lead to intestinal obstruction.(Mistaken for Ca caecum
and appendicular mass) Other local complications include bloody diarrhea, pericolic and
pericaecal abscess.
Complications of hepatic amoebiasis includes subdiaphragmatic abscess, perforation of
diaphragm to pericardium and pleural cavity, perforation to abdominal cavital (amoebic
peritonitis) and perforation of skin (amoebiasis cutis).
Pulmonary amoebiasis can occur from hepatic lesion by haemotagenous spread and also
by perforation of pleural cavity and lung. It can cause lung abscess, pulmono pleural
fistula, empyema lung and broncho pleural fistula. It can also reach the brain through blood
vessels and cause amoebic brain abscess and amoebic meningoencephalitis. Cutaneous
amoebiasis can also occur in skin around sites of colostomy wound, perianal region,
region overlying visceral lesion and at the site of drainage of liver abscess.
Urogenital tract amoebiasis derived from intestinal lesion can cause amoebic
vulvovaginitis (May's disease), rectovesicle fistula and rectovaginal fistula.
Entamoeba histolytica infection is associated with malnutrition and stunting of growth.
Epidemiology:
In 2010 it caused about 55,000 deaths worldwide down from 68,000 in 1990. [19] In older
textbooks it is often stated that 10% of the world's population is infected with Entamoeba
histolytica. It is now known that at least 90% of these infections are due to E.
dispar. Nevertheless, this means that there are up to 50 million true E. histolytica infections
and approximately seventy thousand die each year, mostly from liver abscesses or other
complications. Although usually considered a tropical parasite, the first case reported (in
1875) was actually in St Petersburg in Russia, near the Arctic Circle. Infection is more
common in warmer areas, but this is both because of poorer hygiene and the parasitic
cysts surviving longer in warm moist conditions.
History:
Amoebiasis was first described by Losh in 1875, in northern Russia. The most dramatic
incident in the US was the Chicago World's Fair outbreak in 1933 caused by contaminated
drinking water. There were more than a thousand cases, with 98 deaths. It has been known
since 1897 that at least one non-disease-causing species of Entamoeba existed
(Entamoeba coli), but it was first formally recognized by the WHO in 1997 that E.
histolytica was two species, despite this having first been proposed in 1925. In addition to
the now-recognized E. dispar evidence shows there are at least two other species
of Entamoeba that look the same in humans – E. moshkovskii and Entamoeba
bangladeshi. The reason these species haven't been differentiated until recently is because
of the reliance on appearance.
Joel Connolly of the Chicago Bureau of Sanitary Engineering brought the outbreak to an
end when he found that defective plumbing permitted sewage to contaminate drinking
water. In 1998 there was an outbreak of amoebiasis in the Republic of Georgia. Between 26
May and 3 September 1998, 177 cases were reported, including 71 cases of intestinal
amoebiasis and 106 probable cases of liver abscess.
The Nicobarese people have attested to the medicinal properties found in Glochidion
calocarpum, a plant common to India, saying that its bark and seed are most effective in
curing abdominal disorders associated with amoebiasis.
 Filariasis

Filariasis is a parasitic disease caused by

an infection with roundworms of the Filarioidea type. These are spread by blood-
feeding black flies and mosquitoes. This disease belongs to the group of diseases
called helminthiases.
Eight known filarial nematodes use humans as their definitive hosts. These are divided into
three groups according to the niche they occupy in the body:

 Lymphatic filariasis is caused by the worms Wuchereria bancrofti, Brugia malayi,

and Brugia timori. These worms occupy the lymphatic system, including the lymph
nodes; in chronic cases, these worms lead to the syndrome of elephantiasis.
 Subcutaneous filariasis is caused by Loa loa (the eye worm), Mansonella streptocerca,
and Onchocerca volvulus. These worms occupy the subcutaneous layer of the skin, in
the fat layer. L. loa causes Loa loa filariasis, while O. volvulus causes river blindness.
 Serous cavity filariasis is caused by the worms Mansonella perstans and Mansonella
ozzardi, which occupy the serous cavityof the abdomen. Dirofilaria immitis, or the dog
heartworm rarely infects humans.
The adult worms, which usually stay in one tissue, release early larval forms known
as microfilariae into the host's bloodstream. These circulating microfilariae can be taken up
with a blood meal by the arthropod vector; in the vector, they develop into infective larvae
that can be transmitted to a new host.
Individuals infected by filarial worms may be described as either "microfilaraemic" or
"amicrofilaraemic", depending on whether microfilariae can be found in their peripheral
blood. Filariasis is diagnosed in microfilaraemic cases primarily through direct observation
of microfilariae in the peripheral blood. Occult filariasis is diagnosed in amicrofilaraemic
cases based on clinical observations and, in some cases, by finding a circulating antigen in
the blood.

Signs and symptoms:

The most spectacular symptom of lymphatic filariasis is elephantiasis – edema with
thickening of the skin and underlying tissues—which was the first disease discovered to be
transmitted by mosquito bites. Elephantiasis results when the parasites lodge in
the lymphatic system.
Elephantiasis affects mainly the lower extremities, while the ears, mucous membranes,
and amputation stumps are affected less frequently. However, different species of filarial
worms tend to affect different parts of the body; Wuchereria bancrofti can affect the legs,
arms, vulva, breasts, and scrotum (causing hydrocele formation), while Brugia timori rarely
affects the genitals. Those who develop the chronic stages of elephantiasis are usually free
from microfilariae (amicrofilaraemic), and often have adverse immunological reactions to
the microfilariae, as well as the adult worms.
The subcutaneous worms present with rashes, urticarial papules, and arthritis, as well as
hyper- and hypopigmentation macules. Onchocerca volvulus manifests itself in the eyes,
causing "river blindness" (onchocerciasis), one of the leading causes of blindness in the
world. Serous cavity filariasis presents with symptoms similar to subcutaneous filariasis, in
addition to abdominal pain, because these worms are also deep-tissue dwellers.

Cause:
Human filarial nematode worms have complicated life cycles, which primarily consists of
five stages. After the male and female worms mate, the female gives birth to live
microfilariae by the thousands. The microfilariae are taken up by the vector insect
(intermediate host) during a blood meal. In the intermediate host, the microfilariae molt and
develop into third-stage (infective) larvae. Upon taking another blood meal, the vector
insect injects the infectious larvae into the dermis layer of the skin. After about one year,
the larvae molt through two more stages, maturing into the adult worms.

Diagnosis:
Microfilaria of Dirofilaria immitis (Heartworms) in a lymph node of a dog with lymphoma.
This baby nematode is in a pillow of intermediate-to-large, immature lymphocytes,
exhibiting multiple criteria of cancer.
Filariasis is usually diagnosed by identifying microfilariae on Giemsa stained, thin and
thick blood film smears, using the "gold standard" known as the finger prick test. The
finger prick test draws blood from the capillaries of the finger tip; larger veins can be used
for blood extraction, but strict windows of the time of day must be observed. Blood must
be drawn at appropriate times, which reflect the feeding activities of the vector insects.
Examples are W. bancrofti, whose vector is a mosquito; night is the preferred time for
blood collection. Loa loa's vector is the deer fly; daytime collection is preferred. This
method of diagnosis is only relevant to microfilariae that use the blood as transport from
the lungs to the skin. Some filarial worms, such as M. streptocerca and O. volvulus,
produce microfilarae that do not use the blood; they reside in the skin only. For these
worms, diagnosis relies upon skin snips and can be carried out at any time.

Concentration methods:
Various concentration methods are applied: membrane filter, Knott's concentration
method, and sedimentation technique.
Polymerase chain reaction (PCR) and antigenic assays, which detect circulating filarial
antigens, are also available for making the diagnosis. The latter are particularly useful in
amicrofilaraemic cases. Spot tests for antigen[4] are far more sensitive, and allow the test to
be done anytime, rather in the late hours.
Lymph node aspirate and chylous fluid may also yield microfilariae. Medical imaging, such
as CT or MRI, may reveal "filarial dance sign" in the chylous fluid; X-ray tests can show
calcified adult worms in lymphatics. The DEC provocation test is performed to obtain
satisfying numbers of parasites in daytime samples. Xenodiagnosis is now obsolete, and
eosinophilia is a nonspecific primary sign.

Treatment:
The recommended treatment for people outside the United States is albendazole combined
with ivermectin. A combination of diethylcarbamazine and albendazole is also effective.
Side effects of the drugs include nausea, vomiting, and headaches. [8] All of these
treatments are microfilaricides; they have no effect on the adult worms. While the drugs are
critical for treatment of the individual, proper hygiene is also required.
Different trials were made to use the known drug at its maximum capacity in absence of
new drugs. In a study from India, it was shown that a formulation of albendazole had better
anti-filarial efficacy than albendazole itself.
In 2003, the common antibiotic doxycycline was suggested for treating
elephantiasis. Filarial parasites have symbiotic bacteria in the genus Wolbachia, which live
inside the worm and seem to play a major role in both its reproduction and the
development of the disease. This drug has shown signs of inhibiting the reproduction of
the bacteria, further inducing sterility. Clinical trials in June 2005 by the Liverpool School of
Tropical Medicine reported an eight-week course almost completely eliminated
microfilaraemia.
Society and culture
Research teams
In 2015 William C. Campbell and Satoshi Ōmura were Co-awarded half of that year's Nobel
prize in Physiology or Medicine for the discovery of the drug avermectin, which, in the
further developed form ivermectin, has decreased the occurrence of lymphatic filariasis.
Prospects for elimination
Filarial diseases in humans offer prospects for elimination by means of vermicidal
treatment. If the human link in the chain of infection can be broken, then notionally the
disease could be wiped out in a season. In practice it is not quite so simple, and there are
complications in that multiple species overlap in certain regions and double infections are
common. This creates difficulties for routine mass treatment because people with
onchocerciasis in particular react badly to treatment for lymphatic filariasis.

Other animals:
Filariasis can also affect domesticated animals, such as cattle, sheep, and dogs.
Cattle

 Verminous hemorrhagic dermatitis is a clinical disease in cattle due to Parafilaria

bovicola.
 Intradermal onchocerciasis of cattle results in losses in leather due to Onchocerca
dermata, O. ochengi, and O. dukei. O. ochengi is closely related to human O.
volvulus (river blindness), sharing the same vector, and could be useful in human
medicine research.
 Stenofilaria assamensis and others cause different diseases in Asia, in cattle and zebu.
Horses

 "Summer bleeding" is hemorrhagic subcutaneous nodules in the head and upper

forelimbs, caused by Parafilaria multipapillosa (North Africa, Southern and Eastern
Europe, Asia and South America).
Dogs

 Heart filariasis is caused by Dirofilaria immitis.