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Zoonotic Parasitic Diseases: Emerging issues and Problems
Several hundred infectious diseases are classified as zoonotic diseases as they are caused by
bacteria, virus, fungi or parasites that can be transmitted from animals to humans. These zoonotic
diseases include many of the classic infectious diseases such as rabies and ricketsia (e.g. Rocky
Mountain Spotted Fever), as well as most of the “new” emerging infectious diseases such as HIV,
SARS. Zoonotic infections can be significant pathogens, with a more severe outcome, in patients
with various forms of immune suppression due to infection, i.e. HIV, or immune suppressive drugs.
A number of parasitic zoonoses such as cryptosporidiosis, toxoplasmosis and leishmaniasis have
gained in importance as human pathogens due to their ability to cause disease in patients with
immune suppression due to HIV. The majority of the classic parasitic diseases due to helminthes,
trematodes, cestodes and protozoa are zoonotic.
There are increasing numbers of cases of zoonotic infections being recognized. A number of factors
underlie this emergence of zoonotic disease including overpopulation, disruptions due to military
action, mass migrations of populations due to natural or man-made disasters, the migration of
populations into large urban centers, and inadequate food and water supplies. The clearing of new
areas for the cultivation of food and other land uses has resulted in human settlement in areas were
animal populations and parasites were previously isolated from humans. In addition, displacement
and stress of wildlife through development as well as global warming. can lead to epidemics of
wildlife disease with resultant overflow infections into domestic animals and humans as well as
bring additional zoonotic infections into contact with human hosts. The use of bushmeat as a food
source has been linked to the emergence of several zoonotic diseases such as SARS and HIV.
Worldwide tourism and adventure travel has resulted in the exposure of new groups to “exotic”
zoonotic pathogens. The popularity of exotic pets has resulted in several reports of zoonotic
infections, such as human Monkeypox transmission linked to Prairie dogs which were infected due
to exposure to an exotic rodent while being housed at an animal dealer’s facility. Advances in
medical progress such as xenotranplantation or the use of various animal cells in the production of
therapeutic agents has the potential to result in the emergence of new zoonotic infections. Both
organ transplantation and blood transfusion have been associated with the transmission of zoonotic
infections such as Leishmaniasis and Trypanosoma cruzi due to these infections being present in
donors.
As pointed out in article on emerging parasitic zoonoses, emerging infectious diseases are
dominated by zoonoses and the majority of these infections originate in wildlife. While protozoa are
more likely to account for emerging parasitic infections, there are clear examples of metazoan
infections as emerging or re-emerging diseases. Interactions of wildlife and human populations often
drive this process as illustrated by the increase in Echinococus multilocularis in Europe as a
consequence of control of rabies in the red fox population leading to an increase in these animals in
urban centers. The fox population may also play a role in increased exposure to Toxocara canis and
other parasites. Control and prevention of these zoonotic diseases is complex and requires an
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integrative multidisciplinary approach grounded in careful epidemiological studies understanding
the variables that influence disease emergence and transmission. For example, culling of infected
dogs does not reduce the risk of human infection from Leishmania, but providing insecticide collars
has been demonstrated to be an effective strategy.
A comprehensive review of the phylogeny and biology of Babesia spp. These Ixodid tick-borne
zoonotic infectious diseases associated with infection of erythrocytes resulting in cell lysis leading
to anemia, hyperbillirubinuria, hemoglobinuria and other disease manifestations. There are over
100 Babesia spp. that have been recognized, infecting many mammalian and some avian species, of
these the Babesia microti complex, Babesia divergens, Babesia bovis, Babesia canis, Babesia
duncani, Babesia enatorum. Blood transfusion has been recognized as an increasing source of
transmission and immune compromised patients have been demonstrated to have persistent
infections with non-classical presentations. Increases in wildlife animal reservoirs and the expansion
of urban environments into undeveloped areas have resulted in increases in these illnesses and the
recognition of new species of Babesia that can infect humans.
A comprehensive review of the species and genotypes ofCryptosporidium and Giardia as they relate
to the zoonotic potential of these pathogenic protozoa.Cryptosporidium oocysts are often found in
water supplies and molecular studies have been applied to allow species recognition, enabling
studies of the zoonotic potential of the 18 Cryptosporidium spp. currently recognized. Host-adapted
genotypes of various Cryptosporidium spp. have been described and characterized. Of
these, Cryptosporidium parvum has a broad host range and molecular studies suggest zoonotic
human transmission occurs. In contrast, studies on Giardia have suggested that zoonotic
transmission is not as common as previously suggested. Overall, they point out the utility of
molecular epidemiological tools in dissecting the presence of anthroponotic as well as zoonotic
transmission of these parasites.
The epidemiology of Toxoplasma gondii infection in animals and humans in the United States of
America. It has been 100 years since the discovery of this pathogenic protozoan associated with
infections in both immune competent and immune compromised hosts. It is one of the most
ubiquitous zoonotic infections being transmitted through meat via tissue cysts containing
bradyzoites and through the contamination of both food and water by oocysts shed by cats.
Given the complex relationships between humans, domestic animals and wildlife, as well as the
profound alternations in the environment due to human interventions, we can expect to see changes
in the epidemiology of zoonotic parasitic infections with increasing importance being paid to the
emergence of these zoonotic infections. Control strategies for these emerging infections will require
the use of molecular techniques and traditional epidemiological investigations to define the problem,
and management strategies that will be effective for these infections.
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Tick paralysis
Tick paralysis is the only tick-borne disease that is not caused by an infectious organism. The
illness is caused by a neurotoxinproduced in the tick's salivary gland. After prolonged attachment,
the engorged tick transmits the toxin to its host. The incidence of tick paralysis is unknown. Patients
can experience severe respiratory distress (similar to anaphylaxis).
Signs and symptoms
Tick paralysis results from inoculation of a toxin from tick salivary glands during a blood meal. The
toxin causes symptoms within 2–7 days, beginning with weakness in both legs that progresses
to paralysis. The paralysis ascends to the trunk, arms, and head within hours and may lead
to respiratory failure and death. The disease can present as acuteataxia without muscle weakness.
Electromyographic (EMG) studies usually show a variable reduction in the amplitude of compound
muscle action potentials, but no abnormalities of repetitive nerve stimulation studies. These appear
to result from a failure of acetylcholine release at the motor nerve terminal level.
Pathogenesis
Tick paralysis is believed to be due to toxins found in the tick's saliva that enter the bloodstream
while the tick is feeding. The two ticks most commonly associated with North American tick
paralysis are the Rocky Mountain wood tick (Dermacentor andersoni) and the American dog tick
(Dermacentor variabilis); however, 43 tick species have been implicated in human disease around
the world. Most North American cases of tick paralysis occur from April to June, when
adult Dermacentor ticks emerge from hibernation and actively seek hosts. In Australia, tick
paralysis is caused by the tick Ixodes holocyclus. 20 fatal cases were reported in Australia.
Although tick paralysis is of concern in domestic animals and livestock in the United States as well,
human cases are rare and usually occur in children under the age of 10.
Tick paralysis occurs when an engorged and gravid (egg-laden) female tick produces a neurotoxin in
its salivary glands and transmits it to its host during feeding. Experiments have indicated that the
greatest amount of toxin is produced between the fifth and seventh day of attachment (often
initiating or increasing the severity of symptoms), although the timing may vary depending on the
species of tick.
Unlike babesiosis, which are caused by the systemic proliferation and expansion of parasites in
their hosts long after the offending tick is gone, tick paralysis is chemically induced by the tick and
therefore usually only continues in its presence. Once the tick is removed, symptoms usually
diminish rapidly. However, in some cases, profound paralysis can develop and even become fatal
before anyone becomes aware of a tick's presence.
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Diagnostic tests
Diagnosis is based on symptoms and upon finding an embedded tick, usually on the scalp.
Treatment
Removal of the embedded tick usually results in resolution of symptoms within several hours to
days. If the tick is not removed, the toxin can be fatal, with reported mortality rates of 10–12
percent, usually due to respiratory paralysis. The tick is best removed by grasping the tick as close to
the skin as possible and pulling in a firm steady manner.
Unlike the other species of ticks, the toxin of Ixodes holocyclus (Australian Paralysis Tick) will not
resolve itself and will be fatal if medical assistant is not immediately sought after pulling the tick off
of the animal. Contrary to popular belief, if the head detaches from the body while being pulled off,
leaving the head will not inject more venom. The head may cause a skin irritation but it will not
inject any more venom. Once the tick is removed, place it in a clear bag, so the vet can identify it.
Water and food can worsen the results of the animal as the venom can prevent the animal from
swallowing properly. If you find an Australian Paralysis Tick on your animal, immediately remove
the tick and seek veterinary assistance even if you do not think the tick has been on the animal long
enough to inject venom.
Prevention
No human vaccine is currently available for any tick-borne disease, except for tick-borne
encephalitis. Individuals should therefore take precautions when entering tick-infested areas,
particularly in the spring and summer months. Preventive measures include avoiding trails that are
overgrown with bushy vegetation, wearing light-coloured clothes that allow one to see the ticks
more easily, and wearing long pants and closed-toe shoes. Young children may be especially
vulnerable to these adverse effects. Permethrin, which can only be applied to clothing, is much more
effective in preventing tick bites. Permethrin is not a repellent but rather an insecticide; it causes
ticks to curl up and fall off the protected clothing.
Toxoplasmosis
Toxoplasmosis is a parasitic disease caused by Toxoplasma gondii. ] Infections with toxoplasmosis
usually cause no symptoms in adult humans.[ ] Occasionally there may be a few weeks or months of
mild flu-like illness such as muscle aches and tender lymph nodes.[ ] In a small number of people,
eye problems may develop. In those with a weak immune system, severe symptoms such
asseizures and poor coordination may occur. If infected during pregnancy, a condition known as
congenital toxoplasmosis may affect the child.[ ]
Toxoplasmosis is usually spread by eating poorly cooked food that contains cysts, exposure to
infected cat feces, and from a mother to a child during pregnancy if the mother becomes infected.
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Rarely the disease may be spread by a blood transfusion. It is not otherwise spread between people.
]
The parasite is only known to reproduce sexually in the cat family. However, it can infect most
types of warm-blooded animals, including humans. ] Diagnosis is typically by testing the blood
for antibodies or by testing theamniotic fluid for the parasite's DNA.[ ]
Prevention is by properly preparing and cooking food. It is also recommended that pregnant women
not clean cat litter boxes. ]Treatment of otherwise healthy people is usually not needed. During
pregnancy spiramycin or pyrimethamine/sulfadiazine and folinic acid may be used for treatment.[ ]
Up to half of the world's population are infected by toxoplasmosis but have no symptoms.[ ] In the
United States about 23% are affected ] and in some areas of the world this is up to 95%.[ ] About
200,000 cases of congenital toxoplasmosis occur a year.[ ]Charles Nicolle and Louis Manceaux first
described the organism in 1908. In 1941 transmission during pregnancy from a mother to a child
was confirmed.[ ]
Signs and symptoms[ ]
Infection has three stages:
Acute toxoplasmosis[ ]
Acute toxoplasmosis is often asymptomatic in healthy adults. However, symptoms may manifest
and are often influenza-like: swollen lymph nodes, headaches, fever, and fatigue,[ ] or muscle
aches and pains that last for a month or more. Rarely will a human with a fully functioning immune
system develop severe symptoms following infection. People with weakened immune systems are
likely to experience headache, confusion, poor coordination, seizures, lung problems that may
resemble tuberculosis or Pneumocystis jiroveci pneumonia (a common opportunistic infection that
occurs in people with AIDS), or blurred vision caused by severe inflammation of the retina (ocular
toxoplasmosis)[ ] Young children and immunocompromised people, such as those with HIV/AIDS,
those taking certain types of chemotherapy, or those who have recently received an organ transplant,
may develop severe toxoplasmosis. This can cause damage to the brain (encephalitis) or the eyes
(necrotizing retinochoroiditis).[ ] Infants infected via placental transmission may be born with either
of these problems, or with nasal malformations, although these complications are rare in newborns.
The toxoplasmictrophozoites causing acute toxoplasmosis are referred to as tachyzoites, and are
typically found in bodily fluids.
Swollen lymph nodes are commonly found in the neck or under the chin, followed by the armpits
and the groin. Swelling may occur at different times after the initial infection, persist, and recur for
various times independently of antiparasitic treatment.[ ] It is usually found at single sites in adults,
but in children, multiple sites may be more common. Enlarged lymph nodes will resolve within one
to two months in 60% of cases. However, a quarter of those affected take two to four months to
return to normal, and 8% take four to six months. A substantial number (6%) do not return to normal
until much later.[ ]
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Latent toxoplasmosis[ ]
Due to its asymptomatic nature, it is easy for a host to become infected with Toxoplasma gondii and
develop toxoplasmosis without knowing it. Although mild, flu-like symptoms occasionally occur
during the first few weeks following exposure, infection with T. gondii produces no readily
observable symptoms in healthy human adults. In most immunocompetent people, the infection
enters a latent phase, during which only bradyzoites (tissue cysts) are present;[ ] these tissue cysts
and even lesions can occur in the retinas, alveolar lining of the lungs (where an acute infection may
mimic a Pneumocystis jirovecii infection), heart, skeletal muscle, and the central nervous
system (CNS), including the brain.[ ] Cysts form in the CNS (brain tissue) upon infection with T.
gondii and persist for the lifetime of the host.[ ] Most infants who are infected while in the womb
have no symptoms at birth, but may develop symptoms later in life.[ ]
Reviews of serological studies have estimated that 30–50% of the global population has been
exposed to and may be chronically infected with latent toxoplasmosis, although infection rates differ
significantly from country to country. This latent state of infection has recently been associated
with numerous disease burdens,[ ] neural alterations, and subtle gender-dependent behavioral
changes in immunocompetent humans.
Cutaneous toxoplasmosis[ ]
While rare, skin lesions may occur in the acquired form of the disease,
including roseola and erythema multiforme-like eruptions, prurigo-like nodules, urticaria, and
maculopapular lesions. Newborns may have punctate macules, ecchymoses, or “blueberry muffin”
lesions. Diagnosis of cutaneous toxoplasmosis is based on the tachyzoite form of T. gondii being
found in the epidermis.[ ] It is found in all levels of the epidermis, is about 6 μm by 2 μm and bowshaped, with the nucleus being one-third of its size. It can be identified by electron microscopy or
by Giemsa staining tissue where the cytoplasm shows blue, the nucleus red.[ ]
life cycle
In its life cycle, T. gondii adopts several forms.[ ] Tachyzoites are responsible for acute infection;
they divide rapidly and spread through the tissues of the body. After proliferating, tachyzoites
convert into bradyzoites, which take the form of latent intracellular tissue cysts that form mainly in
the tissues of the muscles and brain. The transformation into cysts is in part triggered by the pressure
of the host immune system.[ ] The bradyzoites are not responsive to antibiotics. The bradyzoites,
once formed, can remain in the tissues for the lifespan of the host. In a healthy host, if some
bradyzoites convert back into active tachyzoites, the immune system will quickly destroy them.
However, in immunocompromised individuals, or in fetuses, which lack a developed immune
system, the tachyzoites can run rampant and cause significant neurological damage.[ ]
The parasite’s survival is dependent on a balance between host survival and parasite proliferation.[
]
T. gondii achieves this balance by manipulating the host’s immune response, reducing the host’s
immune response and enhancing the parasite’s reproductive advantage. ] Once it infects a normal
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host cell, it resists damage caused by the host’s immune system, and changes the host's immune
processes.
As it forces its way into the host cell, the parasite forms a parasitophorous vacuole (PV) membrane
from the membrane of the host cell. The PV encapsulates the parasite, and is both resistant to the
activity
of
the
endolysosomal
system,
and
can
take
control
of
the
host’s mitochondria and endoplasmic reticulum. .
T. gondii also has the ability to initiate autophagy of the host’s cells.[ ] This leads to a decrease in
healthy, uninfected cells, and consequently fewer host cells to attack the infected cells. Research by
Wang et al finds that infected cells lead to higher levels of autophagosomes in normal and infected
cells.[ ] Their research reveals that T. gondiicauses host cell autophagy using a calcium-dependent
pathway.[ ] Another study suggests that the parasite can directly affect calcium being released from
calcium stores, which are important for the signalling processes of cells.[ ]
The mechanisms above allow T. gondii to persist in a host. Some limiting factors for the toxoplasma
is that its influence on the host cells is stronger in a weak immune system and is quantity-dependent,
so a large number of T. gondii per host cell cause a more severe effect.[ ] The effect on the host also
depends on the strength of the host immune system. Immunocompetent individuals do not normally
show severe symptoms or any at all, while fatality or severe complications can result in
immunocompromised individuals.[ ]
It should be noted that since the parasite can change the host’s immune response, it may also have
an effect, positive or negative, on the immune response to other pathogenic threats.[ ] This includes,
but is not limited to, the responses to infections by Helicobacter felis, Leishmania major, or other
parasites, such as Nippostrongylus brasiliensis.[ ]
Transmission[ ]
Toxoplasmosis is generally transmitted through an oral route, by accidentally ingesting toxoplama
gondii cysts, but can be transmitted congenitally, passed from mother to fetus through the placenta.[
Oral transmission may occur through:



Ingestion of raw or partly cooked meat, especially pork, lamb, or venison
containing Toxoplasma cysts: Infection prevalence in countries where undercooked meat is
traditionally eaten has been related to this transmission method. Tissue cysts may also be
ingested during hand-to-mouth contact after handling undercooked meat, or from using knives,
utensils, or cutting boards contaminated by raw meat.[ ]
Ingestion of unwashed fruits or vegetables that have been in contact with contaminated soil
containing infected cat feces.[ ]
Ingestion of contaminated cat feces: This can occur through hand-to-mouth contact following
gardening, cleaning a cat's litter box, contact with children's sandpits; the parasite can survive in
the environment for over a year.[ ]
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Cats excrete the pathogen in their feces for a number of weeks after contracting the disease,
generally by eating an infected rodent. Even then, cat feces are not generally contagious for the first
day or two after excretion, after which the cyst 'ripens' and becomes potentially pathogenic.[40]
Pregnancy precautions[ ]
Congenital toxoplasmosis is a specific form of toxoplasmosis in which an unborn fetus is infected
via the placenta.[ ] Congenital toxoplasmosis is associated with fetal death and abortion, and in
infants, it is associated with neurologic deficits, neurocognitive deficits, and chorioretinitis.[ ] A
positive antibody titer indicates previous exposure and immunity, and largely ensures the unborn
fetus' safety. A simple blood draw at the first prenatal doctor visit can determine whether or not a
woman has had previous exposure and therefore whether or not she is at risk. If a woman receives
her first exposure to T. gondii while pregnant, the fetus is at particular risk.[ ]
For pregnant women with negative antibody titers, indicating no previous exposure to T. gondii,
serology testing as frequent as monthly is advisable as treatment during pregnancy for those women
exposed to T. gondii for the first time dramatically decreases the risk of passing the parasite to the
fetus. Since a baby's immune system does not develop fully for the first year of life, and the resilient
cysts that form throughout the body are very difficult to eradicate with antiprotozoans, an infection
can be very serious in the young.
Despite these risks, pregnant women are not routinely screened for toxoplasmosis in most countries,
for reasons of cost-effectiveness and the high number of false positivesgenerated; Portugal, ] France,
]
Austria, ] Uruguay, ] and Italy[ ] are notable exceptions, and some regional screening programmes
operate in Germany, Switzerland andBelgium.[ ] As invasive prenatal testing incurs some risk to
the fetus (18.5 pregnancy losses per toxoplasmosis case prevented),[ ] postnatal or neonatal screening
is preferred. The exceptions are cases where fetal abnormalities are noted, and thus screening can be
targeted.[ ]
Pregnant women should avoid handling raw meat, drinking raw milk (especially goat milk) and be
advised to not eat raw or undercooked meat regardless of type.[ ] Because of the obvious relationship
between Toxoplasma and cats it is also often advised to avoid exposure to cat feces, and refrain from
gardening (cat feces are common in garden soil) or at least wear gloves when so engaged. [ ] Most
cats are not actively shedding oocysts, since they get infected in the first six months of their life,
when they shed oocysts for a short period of time (1–2 weeks.)[ ] However, these oocysts get buried
in the soil, sporulate and remain infectious for periods ranging from several months to more than a
year.[ ] Numerous studies have shown living in a household with a cat is not a significant risk factor
for T. gondii infection, though living with several kittens has some significance.[ ]
In 2006, a Czech research team[ ] discovered women with high levels of toxoplasmosis antibodies
were significantly more likely to have baby boys than baby girls. In most populations, the birth rate
is around 51% boys, but women infected with T. gondii had up to a 72% chance of a boy. In mice,
the sex ratio was higher in early latent toxoplasmosis and lower in later latent toxoplasmosis.[ ]
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Rodent behavior[ ]
Infection with T. gondii has been shown to alter the behavior of mice and rats in ways thought to
increase the rodents’ chances of being preyed upon by cats. Infected rodents show a reduction in
their innate aversion to cat odors; while uninfected mice and rats will generally avoid areas marked
with cat urine or with cat body odor, this avoidance is reduced or eliminated in infected
animals. Moreover, some evidence suggests this loss of aversion may be specific to feline odors:
when given a choice between two predator odors (cat or mink), infected rodents show a significantly
stronger preference to cat odors than do uninfected controls.
In rodents, T. gondii–induced behavioral changes occur through epigenetic remodeling in neurons
associated observed behaviors; for example, it modifies epigenetic methylation to induce
hypomethylation of arginine vasopressin-related genes in the medial amygdala to greatly decrease
predator aversion. Similar epigenetically-induced behavioral changes have also been observed in
mouse models of addiction, where changes in the expression of histone-modifying enzymes via gene
knockout or enzyme inhibition in specific neurons produced alterations in drug-related
behaviors. Widespread histone-lysine acetylation in cortical astrocytes appears to be another
epigenetic mechanism employed by T. gondii.
T. gondii-infected rodents show a number of behavioral changes beyond altered responses to cat
odors. Rats infected with the parasite show increased levels of activity and
decreased neophobic behavior.[ ] Similarly, infected mice show alterations in patterns
of locomotion and exploratory behavior during experimental tests. These patterns include traveling
greater distances, moving at higher speeds, accelerating for longer periods of time, and showing a
decreased pause-time when placed in new arenas.[ ] Infected rodents have also been shown to have
lower anxiety, using traditional models such as elevated plus mazes, open field arenas, and social
interaction tests.
Diagnosis[ ]
Diagnosis of toxoplasmosis in humans is made by biological, serological, histological, or molecular
methods, or by some combination of the above.[ ] Toxoplasmosis can be difficult to distinguish
from primary central nervous system lymphoma. It mimics several other infectious diseases so
clinical signs are non-specific and are not sufficiently characteristic for a definite diagnosis. As a
result, the diagnosis is made by a trial of therapy (pyrimethamine, sulfadiazine, and folinic
acid (USAN: leucovorin)), if the drugs produce no effect clinically and no improvement on repeat
imaging.
T. gondii in may also be detected in blood, amniotic fluid, or cerebrospinal fluid by
using polymerase chain reaction.[ ] T. gondii may exist in a host as an inactive cyst that would likely
evade detection.
Serological testing can detect T. gondii antibodies in the blood serum, using methods including
the Sabin–Feldman dye test (DT), the indirect hemagglutination assay, the indirect fluorescent
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antibody assay (IFA), the direct agglutination test, the latex agglutination test (LAT), the enzymelinked immunosorbent assay (ELISA), and the immunosorbent agglutination assay test (IAAT).[ ]
The most commonly used tests to measure IgG antibody are the DT, the ELISA, the IFA, and the
modified direct agglutination test.[ ] IgG antibodies usually appear within a week or two of infection,
peak within one to two months, then decline at various rates.[ ] Toxoplasma IgG antibodies generally
persist for life, and therefore may be present in the bloodstream as a result of either current or
previous infection.[ ]
To some extent, acute toxoplasmosis infections can be differentiated from chronic infections using
an IgG avidity test, which is a variation on the ELISA. In the first response to infection, toxoplasmaspecific IgG has a low affinity for the toxoplasma antigen; in the following weeks and month, IgG
affinity for the antigen increases. Based on the IgG avidity test, if the IgG in the infected individual
has a high affinity, it means that the infection began three to five months before testing. This is
particularly useful in congenital infection, where pregnancy status and gestational age at time of
infection determines treatment.[ ]
In contrast to IgG, IgM antibodies can be used to detect acute infection, but generally not chronic
infection.[ ] The IgM antibodies appear sooner after infection than the IgG antibodies and disappear
faster than IgG antibodies after recovery.[ ] In most cases, T. gondii-specific IgM antibodies can first
be detected approximately a week after acquiring primary infection, and decrease within one to six
months; 25% of those infected are negative for T. gondii-specific IgM within seven months.[
]
However, IgM may be detectable months or years after infection, during the chronic phase, and
false positives for acute infection are possible.[ ] The most commonly used tests for the measurement
of IgM antibody are double-sandwich IgM-ELISA, the IFA test, and the immunosorbent
agglutination assay (IgM-ISAGA). Commercial test kits often have low specificity, and the reported
results are frequently misinterpreted.[ ]
Congenital toxoplasmosis[ ]
Recommendations for the diagnosis of congenital toxoplasmosis include: prenatal diagnosis based
on testing of amniotic fluid and ultrasound examinations; neonatal diagnosis based on molecular
testing of placenta and cord blood and comparative mother-child serologic tests and a clinical
examination
at
birth;
and
early
childhood
diagnosis
based
onneurologic and ophthalmologic examinations and a serologic survey during the first year of life.[
]
During pregnancy, serological testing is recommended at three week intervals.[ ]
Even though diagnosis of toxoplasmosis heavily relies on serological detection of specific antiToxoplasma immunoglobulin, serological testing has limitations. For example, it may fail to detect
the active phase of T. gondii infection because the specific anti-Toxoplasma IgG or IgM may not be
produced until after several weeks of infection. As a result, a pregnant woman might test negative
during the active phase of T. gondii infection leading to undetected and therefore untreated
congenital toxoplasmosis.[ ] Also, the test may not detect T. gondii infections in
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immunocompromised patients because the titers of specific anti-Toxoplasma IgG or IgM may not
rise in this type of patient.
Many PCR-based techniques have been developed to diagnose toxoplasmosis using clinical
specimens that include amniotic fluid, blood, cerebrospinal fluid, and tissue biopsy. The most
sensitive PCR-based technique is nested PCR, followed by hybridization of PCR products.[ ] The
major downside to these techniques is that they are time consuming and do not provide quantitative
data.[ ]
Real-time PCR is useful in pathogen detection, gene expression and regulation, and allelic
discrimination. This PCR technique utilizes the 5' nuclease activity of Taq DNA polymerase to
cleave a nonextendible, fluorescence-labeled hybridization probe during the extension phase of
PCR.[ ] A second fluorescent dye, e.g., 6-carboxy-tetramethyl-rhodamine, quenches the fluorescence
of the intact probe. ] The nuclease cleavage of the hybridization probe during the PCR releases the
effect of quenching resulting in an increase of fluorescence proportional to the amount of PCR
product, which can be monitored by a sequence detector.[ ]
Toxoplasmosis cannot be detected with immunostaining. Lymph nodes affected
by Toxoplasma have characteristic changes, including poorly demarcated reactive germinal centers,
clusters of monocytoid B cells, and scattered epithelioid histiocytes.
Treatment[ ]
Treatment is often only recommended for people with serious health problems, such as people
with HIV whose CD4 counts are under 200 cells/mm3, because the disease is most serious when
one's immune system is weak. Trimethoprim/sulfamethoxazole is the drug of choice to prevent
toxoplasmosis, but not for treating active disease. A new study (May 2012) shows a promising new
way to treat the active and latent form of this disease using two endochin-like quinolones.[ ]
Cryptosporidiosis
Cryptosporidiosis, also known as crypto, ] is a parasitic disease caused by Cryptosporidium, a
genus of protozoan parasites in the phylum Apicomplexa. It affects the distal small intestine and can
affect the respiratory tract in both immunocompetent (i.e., individuals with a normal
functioning immune system) and immunocompromised (e.g., persons with HIV/AIDS) individuals,
resulting in watery diarrhea with or without an unexplained cough.[ ] In immunocompromised
individuals, the symptoms are particularly severe and can be fatal. It is primarily spread through
the fecal-oral route, often through contaminated water; recent evidence suggests that it can also be
transmitted via fomites in respiratory secretions.[ ]
Cryptosporidium is the organism most commonly isolated in HIV-positive patients presenting with
diarrhea.[ ]Despite not being identified until 1976, it is one of the most common waterborne diseases
and is found worldwide. The parasite is transmitted by environmentally hardy microbial
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cysts (oocysts) that, once ingested, exist in the small intestine and result in an infection of
intestinal epithelial tissue.
Signs and symptoms[ ]
Cryptosporidiosis may occur as an asymptomatic infection, an acute infection (i.e., duration shorter
than 2 weeks), recurrent acute infections in which symptoms reappear following a brief period of
recovery for up to 30 days, and a chronic infection (i.e., duration longer than 2 weeks) in which
symptoms are severe and persistent. It may be fatal in individuals with a severely
compromised immune system. Symptoms usually appear 5–10 days after infection (range: 2–28
days) and normally last for up to 2 weeks in immunocompetent individuals (i.e., individuals with a
normal functioning immune system); symptoms are usually more severe and persist longer
in immunocompromisedindividuals . Following the resolution of diarrhea, symptoms can reoccur
after several days or weeks due to reinfection. Based upon one clinical trial, the likelihood of reinfection is high in immunocompetent adults.
In immunocompetent individuals, cryptosporidiosis is primarily localized to the distal small
intestine and sometimes the respiratory tract as well. In immunocompromised persons,
cryptosporidiosis
may
disseminate
to
other
organs,
including
the hepatobiliary
system, pancreas, upper gastrointestinal tract, and urinary bladder; pancreatic and biliary infection
can involve acalculous cholecystitis, sclerosing cholangitis, papillary stenosis, or pancreatitis.
Intestinal cryptosporidiosis[ ]
Common signs and symptoms of intestinal cryptosporidiosis include:








Moderate to severe watery diarrhea, sometimes contains mucus and rarely contains blood
or leukocytes[ ]
 In
very
severe
cases,
diarrhea
may
be
profuse
and cholera-like
with malabsorption and hypovolemia
Low-grade fever
Crampy abdominal pain
Dehydration
Weight loss
Fatigue[ ]
Nausea and vomiting – suggests upper GI tract involvement[ ] and may lead to respiratory
cryptosporidiosis
Epigastric or right upper quadrant tenderness ]
Less common or rare signs and symptoms include:

Reactive arthritis (may affect the hands, knees, ankles, and feet)[ ]

Jaundice – suggests hepatobiliary involvement
12
Ascites – suggests pancreatic involvement[
Respiratory cryptosporidiosis[ ]

Symptoms of upper respiratory cryptosporidiosis include:



Inflammation of the nasal mucosa, sinuses, larynx, or trachea[
Nasal discharge[ ]
Voice change[2] (e.g., hoarseness)[ ]
Symptoms of lower respiratory cryptosporidiosis include:

Cough


Shortness of breath
Fever[ ]

Hypoxemia[ ]
Cause[ ]
Cryptosporidium is
a
genus
of protozoan pathogens which
is
categorized
under
the phylum Apicomplexa. Other apicomplexan pathogens include the malaria parasite Plasmodium,
and Toxoplasma, the causative agent of toxoplasmosis. A number of Cryptosporidium infect
mammals. In humans, the main causes of disease are C. parvum and C. hominis(previously C.
parvum genotype 1). C. canis, C. felis, C. meleagridis, and C. muris can also cause disease in
humans.Cryptosporidium is capable of completing its life cycle within a single host, resulting in
microbial cyst stages that are excreted in feces and are capable of transmission to a new host via
the fecal-oral route. Other vectors of disease transmission also exist.
The pattern of Cryptosporidium life cycle fits well with that of other intestinal homogeneous
coccidian genera of the suborderEimeriina: macro- and microgamonts develop independently; a
microgamont gives rise to numerous male gametes; and oocysts serving for parasites' spreading in
the environment. Electron microscopic studies made from the 1970s have shown the intracellular,
although extracytoplasmic localization of Cryptosporidium species.
These species possess a number of unusual features:




an endogenous phase of development in microvilli of epithelial surfaces
two morphofunctional types of oocysts
the smallest number of sporozoites per oocyst
a multi-membraneous "feeder" organelle
DNA studies suggest a relationship with the gregarines rather than the coccidia.[ ] The taxonomic
position of this group has not yet been finally agreed upon.
13
The genome of Cryptosporidium parvum was sequenced in 2004 and was found to be unusual
amongst Eukaryotes in that the mitochondria seem not to contain DNA.[ ] A closely related
species, C. hominis, also has its genome sequence available.[ ] CryptoDB.org is a NIH-funded
database that provides access to the Cryptosporidium genomics data sets.
Transmission[ ]
Infection is through contaminated material such as earth, water, uncooked or crosscontaminated food that has been in contact with the feces of an infected individual or animal.
Contact must then be transferred to the mouth and swallowed. It is especially prevalent amongst
those in regular contact with bodies of fresh water including recreational water such as swimming
pools. Other potential sources include insufficiently treated water supplies, contaminated food, or
exposure to feces.[ ] The high resistance of Cryptosporidiumoocysts to disinfectants such
as chlorine bleach enables them to survive for long periods and still remain infective.[ ] Some
outbreaks have happened in day care related to diaper changes.[ ]
The following groups have an elevated risk of being exposed to Cryptosporidium:[ ]








Child care workers
Parents of infected children
People who take care of other people with cryptosporidiosis
International travelers
Backpackers, hikers, and campers who drink unfiltered, untreated water
People, including swimmers, who swallow water from contaminated sources
People who handle infected cattle
People exposed to human feces through sexual contact
Cases of cryptosporidiosis can occur in a city that does not have a contaminated water supply. In a
city with clean water, it may be that cases of cryptosporidiosis have different origins. Testing of
water, as well as epidemiological study, are necessary to determine the sources of specific
infections. Note that Cryptosporidium typically does not cause serious illness in healthy people. It
may chronically sicken some children, as well as adults who are exposed and immunocompromised.
A subset of the immunocompromised population is people with AIDS. Some sexual behaviours can
transmit the parasite directly.
Life cycle[ ]
Cryptosporidium spp. exist as multiple cell types which correspond to different stages in an
infection (e.g., a sexual and asexual stage).[ ] As an oocyst – a type of hardy, thick-walled spore – it
can survive in the environment for months and is resistant to many common disinfectants,
particularly chlorine-based disinfectants. After being ingested, the oocysts excyst in the small
intestine. They release sporozoites that attach to the microvilli of the epithelial cells of the small
intestine. From there they become trophozoites that reproduce asexually by multiple fission, a
14
process known as schizogony. The trophozoites develop into Type 1 meronts [ ] that contain 8
daughter cells.[ ]
These daughter cells are Type 1 merozoites, which get released by the meronts. Some of these
merozoites can cause autoinfection by attaching to epithelial cells. Others of these merozoites
become Type II meronts,[18] which contain 4 Type II merozoites.[ ] These merozoites get released
and they attach to the epithelial cells. From there they become either macrogamonts or
microgamonts.[ ] These are the female and male sexual forms, respectively.[ ] This stage, when
sexual forms arise, is called gametogony.[ ]
Zygotes are formed by microgametes from the microgamont penetrating the macrogamonts. The
zygotes develop into oocysts of two types.[ ] 20% of oocysts have thin walls and so can reinfect the
host by rupturing and releasing sporozoites that start the process over again. ] The thick-walled
oocysts are excreted into the environment.[18] The oocysts are mature and infective upon being
excreted.[ ]
Pathogenesis[ ]
The oocysts are ovoid or spherical and measure 5 to 6 micrometers across. When in flotation
preparations they appear highly refractile. The oocysts contains up to 4 sporozoites that are bowshaped.[ ]
As few as 2 to 10 oocysts can initiate an infection.[ ] The parasite is located in the brush border of the
epithelial cells of the small intestine.[ ] They are mainly located in the jejunum. When the
sporozoites attach the epithelial cells’ membrane envelops them. Thus, they are “intracellular but
extracytoplasmic”.[ ] The parasite can cause damage to the microvilli where it attaches.[ ] The
infected human excretes the most oocysts during the first week.[ ] Oocysts can be excreted for weeks
after the diarrhea subsides from infections by C. parvum or C. hominis;[ ] however,
immunocompetent individuals with C. muris infections have been observed excreting oocysts for
seven months
The immune system reduces the formation of Type 1 merozoites as well as the number of thinwalled oocysts.[ ] This helps prevent autoinfection. B cells do not help with the initial response or the
fight to eliminate the parasite.[ ]
Diagnosis[ ]
There are many diagnostic tests for Cryptosporidium. They include microscopy, staining, and
detection of antibodies. Microscopy ] can help identify oocysts in fecal matter.[ ] To increase the
chance of finding the oocysts, the diagnostician should inspect at least 3 stool samples.[ ] There are
several techniques to concentrate either the stool sample or the oocysts. The modified formalin-ethyl
acetate (FEA) concentration method concentrates the stool.[20] Both the modified zinc sulfate
centrifugal flotation technique and the Sheather’s sugar flotation procedure can concentrate the
15
oocysts by causing them to float.[ ] Another form of microscopy is fluorescent microscopy done by
staining withauramine.[ ]
Other staining techniques include acid-fast staining,[ ] which will stain the oocysts red. ] One type of
acid-fast stain is the Kinyoun stain.[ ] Giemsa staining can also be performed. ] Part of the small
intestine can be stained with hematoxylin and eosin (H & E), which will show oocysts attached to
the epithelial cells.[ ]
Detecting antigens is yet another way to diagnose the disease. This can be done with direct
fluorescent antibody (DFA) techniques.[ ] It can also be achieved through indirect
immunofluorescence assay.[ ] Enzyme-linked immunosorbent assay (ELISA) also detects antigens.[ ]
Polymerase chain reaction (PCR) is another way to diagnose cryptosporidiosis. It can even identify
the specific species of Cryptosporidium.[ ] If the patient is thought to have biliary cryptosporidiosis,
then an appropriate diagnostic technique is ultrasonography. If that returns normal results, the next
step would be to perform endoscopic retrograde cholangiopancreatography.[ ]
Prevention[ ]
Many treatment plants that take raw water from rivers, lakes, and reservoirs for public drinking
water production use conventional filtration technologies. This involves a series of processes,
including coagulation, flocculation, sedimentation, and filtration. Direct filtration, which is typically
used to treat water with low particulate levels, includes coagulation and filtration, but not
sedimentation. Other common filtration processes, including slow sand filters, diatomaceous earth
filters and membranes will remove 99% ofCryptosporidium.[ ] Membranes and bag and cartridge
filters remove Cryptosporidium product-specifically.
While Cryptosporidium is highly resistant to chlorine disinfection,[ ] with high enough
concentrations and contact time, Cryptosporidium will be inactivated by chlorine dioxide and ozone
treatment. The required levels of chlorine generally preclude the use of chlorine disinfection as a
reliable method to control Cryptosporidium in drinking water. Ultraviolet light treatment at
relatively low doses will inactivate Cryptosporidium. Water Research Foundation-funded research
originally discovered UV's efficacy in inactivatingCryptosporidium.
One of the largest challenges in identifying outbreaks is the ability to identify Cryptosporidium in
the laboratory. Real-time monitoring technology is now able to detectCryptosporidium with online
systems, unlike the spot and batch testing methods used in the past.
The most reliable way to decontaminate drinking water that may be contaminated
by Cryptosporidium is to boil it.
In the US the law requires doctors and labs to report cases of cryptosporidiosis to local or state
health departments. These departments then report to the Center for Disease Control and
Prevention.[ ] The best way to prevent getting and spreading cryptosporidiosis is to have good
hygiene and sanitation.[ ] An example would be hand-washing.[ ]Prevention is through washing
16
hands carefully after going to the bathroom or contacting stool, and before eating. People should
avoid contact with animal feces.[ ] They should also avoid possibly contaminated food and water.[
]
In addition, people should refrain from engaging in sexual activities that can expose them to feces.[
Standard water filtration may not be enough to eliminate Cryptosporidium; boiling for at least 1
minute (3 minutes above 6,500 feet (2,000 m) of altitude) will decontaminate it. Heating milk at
71.7 °C (161 °F) for 15 seconds pasteurizes it and can destroy the oocysts' ability to infect. [ ] Water
can also be made safe by filtering with a filter with pore size not greater than 1 micrometre, or by
filters that have been approved for “cyst removal” by NSF International National Sanitation
Foundation.[ ] Bottled drinking water is less likely to contain Cryptosporidium, especially if the
water is from an underground source.[ ]
People with cryptosporidiosis should not swim in communal areas because the pathogen can reside
in the anal and genital areas and be washed off. They should wait until at least two weeks after
diarrhea stops before entering public water sources, since oocysts can still be shed for a while. Also,
they should stay away from immunosuppressed people. ] Immunocompromised people should take
care to protect themselves from water in lakes and streams.[21] They should also stay away from
animal stools and wash their hands after touching animals. To be safe, they should boil or filter their
water. They should also wash and cook their vegetables.[
The US CDC notes the recommendation of many public health departments to soak contaminated
surfaces for 20 minutes with a 3% hydrogen peroxide (99% kill rate) and then rinse them
thoroughly, with the caveat that no disinfectant is guaranteed to be completely effective against
Cryptosporidium. However, hydrogen peroxide is more effective than standard bleach solutions.[ ]
Treatment[ ]
Symptomatic treatment primarily involves fluid rehydration, electrolyte replacement (sodium,
potassium, bicarbonate, and glucose), and antimotility agents (e.g.,loperamide). Supplemental zinc
may improve symptoms,[ ] particularly in recurrent or persistent infections or in others at risk
for zinc deficiency.
Giardiasis
Giardiasis (popularly known as beaver fever) ] is a zoonotic parasitic disease caused by
the flagellate protozoan Giardia lamblia(also sometimes called Giardia intestinalis and Giardia
duodenalis). ] The giardia organism inhabits the digestive tract of a wide variety of domestic and
wild animal species, as well as humans. It is one of the most common pathogenic parasitic infections
in humans worldwide; in 2013, there were about 280 million people worldwide with symptomatic
giardiasis.[ ]
17
Signs and symptoms[ ]
Symptoms vary from none to severe diarrhea with poor absorption of nutrients.[ ] It can result in
weakness, loss of appetite, stomach cramps, vomiting (uncommon), bloating, excessive gas, and
burping. Symptoms typically develop 9–15 days after exposure,[ ] but may occur as early as one
day.[ ]
Symptoms are caused by Giardia organisms infecting the cells of the duodenum and jejunum of
the small intestine[ ] and blocking nutrient absorption. Most people are asymptomatic; only about a
third of infected people exhibit symptoms. If the infection is not treated, these symptoms may last
for six weeks or more.
Symptomatic infections are well recognized as causing lactose intolerance, ] which, while usually
temporary, may become permanent. Although hydrogen breath testsindicate poorer rates of
carbohydrate absorption in those asymptomatically infected, such tests are not diagnostic of
infection.[ ] It has been suggested that these observations are explained by symptomatic giardia
infection allowing for the overgrowth of other bacteria.
Some studies have shown giardiasis should be considered as a cause of vitamin B12 deficiency as a
result of the problems caused within the intestinal absorption system.[ ]
Cause[ ]
Giardiasis is caused by the protozoan Giardia lamblia.[ ] The infection occurs in many animals
including beavers hence its nickname, cows, rodents, and sheep.[ ] Animals are believed to play a
role in keeping infections present in an environment.[ ]
Risk factors[ ]
Those at greatest risk are travelers to countries where giardiasis is common, people in child care
settings, those who are in close contact with someone who has the disease, people who swallow
contaminated drinking water, backpackers or campers who drink untreated water from lakes or
rivers, people who have contact with animals who have the disease, and men who have sex with
men."[ ]
It occurs more often during the summer in the United States.[ ] This is believed to be due to a greater
amount of time spent on outdoor activities.[ ]
Wilderness travel within the United States is believed to be a risk factor with poorly treated or
untreated water playing a role.[ ]
Transmission[ ]
Giardiasis is transmitted via the fecal-oral route with the ingestion of cysts.[ ] Primary routes are
personal contact and contaminated water and food.[ ] The cysts can stay infectious for up to three
months in cold water.[ ]
18
Not all Giardia infections are symptomatic, and many people can unknowingly serve as carriers of
the parasite.[ ]
Pathophysiology[ ]
Giardia are flagellated protozoans that cause decreased expression of brush border enzymes,
morphological
changes
to
the microvillus,
and programmed
cell
death of
small
intestinal epithelial cells. There is no invasion of giardia trophozoites, and small intestinal
morphology may appear normal in light microscopy.
The attachment of trophozoites causes villus flattening and inhibition of enzymes that break down
disaccharide sugars in the intestines. Ultimately, the community of microorganisms that lives in the
intestine may overgrow and may be the cause of further symptoms, though this idea has not been
fully investigated. The alteration of the villi leads to an inability of nutrient and water absorption
from the intestine, resulting in diarrhea, one of the predominant symptoms. In the case of
asymptomatic giardiasis, there can be malabsorption with or without histological changes to the
small intestine. The degree to which malabsorption occurs in symptomatic and asymptomatic cases
is highly varied.
The species Giardia intestinalis uses enzymes that break down proteins to attack the villi of the
brush border and appears to increase crypt cell proliferation and crypt length of crypt cells existing
on the sides of the villi. On an immunological level, activated host T lymphocytes attack endothelial
cells that have been injured in order to remove the cell. This occurs after the disruption of proteins
that connect brush border endothelial cells to one another. The result is heavily increased intestinal
permeability.
There appears to be a further increase in programmed cell death by Giardia intestinalis, which
further damages the intestinal barrier and increases permeability. There is significant upregulation of
the programmed cell death cascade by the parasite, and, furthermore, substantial downregulation of
the anti-apoptotic protein Bcl-2 and upregulation of the proapoptotic protein Bax. These connections
suggest a role of caspase-dependent apoptosis in the pathogenesis of giardiasis.
Giardia protects its own growth by reducing the formation of the gas nitric oxide by consuming all
local arginine, which is the amino acid necessary to make nitric oxide. Arginine starvation is known
to be a cause of programmed cell death, and local removal is a strong apoptotic agent.[ ]
Diagnosis[ ]


According to the CDC, detection of antigens on the surface of organisms in stool specimens is
the current test of choice for diagnosis of giardiasis and provides increased sensitivity over more
common microscopy techniques.[ ]
A trichrome stain of preserved stool is another method used to detect giardia.[ ]
19




Microscopic examination of the stool for motile trophozoites or for the distinctive
oval G.lamblia cysts can be performed.
The entero-test uses a gelatin capsule with an attached thread. One end is attached to the inner
aspect of the patient's cheek, and the capsule is swallowed. Later, the thread is withdrawn and
shaken in saline to release trophozoites which can be detected with a microscope.
Immunologic enzyme-linked immunosorbent assay (ELISA) testing is now available. These
tests are capable of a 90% detection rate or more.[ ]
Because Giardia lamblia is difficult to detect, this often leads to a delay in diagnosis or
misdiagnosis; several tests should be conducted over a one-week period.[ ]
Prevention[ ]
The CDC recommends hand-washing and avoiding potentially contaminated food and untreated
water.[ ]
Boiling suspect water for one minute is the surest method to make water safe to drink and kill
disease-causing microorganisms such as Giardia lamblia if in doubt about whether water is
infected.[20] Chemical disinfectants or filters may be used.
According to a review of the literature from 2000, there is little evidence linking the drinking of
water in the N. American wilderness and Giardia.[ ] The researcher notes that treatment of drinking
water for Giardia may not be as important as recommended hand-washing in wilderness regions in
North America.[ ] CDC surveillance data (for 2005 and 2006) reports one outbreak (6 cases) of
waterborne giardiasis contracted from drinking wilderness river water in Colorado. However, less
than 1% of reported giardiasis cases are associated with outbreaks.[ ]
Treatment[ ]
Treatment is not always necessary as the infection usually resolves on its own. However, if the
illness is acute or symptoms persist and medications are needed to treat it,
anitroimidazole medication is used such as metronidazole, tinidazole, secnidazole or ornidazole.[ ]
The World Health Organization and Infectious Disease Society of America recommend
metronidazole as first line therapy. The US CDC lists metronidazole, tinidazole, andnitazoxanide as
effective first-line therapies;[ ] of these three, only nitazoxanide and tinidazole are approved for the
treatment of giardiasis by the US FDA. A meta-analysis done by the Cochrane Collaboration found
that compared to the standard of metronidazole, albendazole had equivalent efficacy while having
fewer side effects, such as gastrointestinal or neurologic issues. ] Other meta-analyses have reached
similar conclusions.[ ] Both medications need a five to 10 day long course; albendazole is taken once
a day, while metronidazole needs to be taken three times a day. The evidence for comparing
metronidazole to other alternatives such as mebendazole, tinidazole or nitazoxanide was felt to be of
very low quality.[ ] While tinidazole has similar side effects and efficacy to metronidazole, it is
administered with a single dose.[ ]
20
Resistance has been seen clinically to both nitroimidazoles and albendazole, but not nitazoxanide,
though nitazoxanide resistance has been induced in research laboratories so is theoretically possible.[
]
The exact mechanism of resistance to all of these medications are not well understood.[ ] In the case
of nitroimidazole-resistant strains of Giardia, other drugs are available which have showed efficacy
in treatment including quinacrine, nitazoxanide, bacitracin zinc, furazolidone and paromomycin.[ ]
During pregnancy, paromomycin is the preferred treatment drug because of its poor intestinal
absorption, and thus less exposure to the fetus.[ ] Alternatively, metronidazole can be used after the
first trimester as there has been wide experience in its use for trichomonas in pregnancy.
Sarcocystis
Sarcocystis is a genus of protozoa. Species in this
infecting mammals, and some infectingreptiles and birds.
genus
are parasites,
the
majority
The life-cycle of a typical member of this genus involves two host species, a definitive host and an
intermediate host. Often the definitive host is a predator and the intermediate host is its prey. The
parasite reproduces sexually in the gut of the definitive host, is passed with the feces and ingested by
the intermediate host. There it eventually enters muscle tissue. When the intermediate host is eaten
by the definitive host, the cycle is completed. The definitive host usually does not show any
symptoms of infection, but the intermediate host does.
There are about 130 recognized species in this genus. Revision of the taxonomy of the genus is
ongoing, and it is possible that all the currently recognised species may in fact be a much smaller
number of species that can infect multiple hosts.
The name Sarcocystis is dervived from Greek: sarx = flesh and kystis = bladder.
History[ ]
The organism was first recognised in a mouse by Miescher in 1843.[ ] His findings were not
recognised as a protist initially and the literature referred to the structures he described as
"Miescher's Tubules". Incidentally Miescher's son — Johann Friedrich Miescher —
discovered DNA. Similar structures were found in pig muscle in 1865 but these remained unnamed
until 1899 when the name Sarcocystis meischeriana was proposed to identify them.
Initially it was unclear whether these organisms were fungi or protozoa. This uncertainty was
resolved in 1967 when electron microscopic studies showed that these organism were protozoa,
related to Toxoplasma and Eimeria. The life cycle remained unknown until 1970 when bradyzoites
from sarcocysts in bird muscles were inoculated into cultured mammalian cells and underwent
development into sexual stages and oocysts. Transmission studies with the three morphotypes found
in cattle then considered a single species - Sarcoplasma fusiformis - in dogs, cats and humans
revealed that these were three different species now named Sarcoplasma bovicanis, Sarcoplasma
bovifelis and Sarcoplasma bovihominis.
21
Life cycle[ ]
The heteroxenous (more than one obligatory host in its life cycle) life cycle of
these apicomplexan parasites remained obscure until 1972 when the prey-predator relationship of its
definitive and intermediate hosts was recognised. The life cycles of about 60 of these species is now
known.
In outline gametogony and sporogony occur in the intestine of the definitive host while
both schizogony which
occurs
in
various
tissues
and
the
formation
of sarcocysts (containing bradyzoites and metrocytes) occurs principally in the muscles of the
intermediate host. In some cases a single species may act as both the definitive and intermediate
host.
Oocysts are passed in the feces of an infected definitive host. The oocyst undergoes sporogony
creating two sporocysts. Once this is complete the oocyst itself undergoes lysis releasing the
sporocysts into the environment. Sporocysts typically contain 4 sporozoites and measure 15-19 by
8-10 micrometres.
An intermediate host such as a cow or pig then ingests a sporocyst. Sporozoites are then released in
the body and migrate to vessels where they undergo the first two generation of asexual reproduction.
These rounds result in the development ofmeronts. This stage lasts about 15 to 16 days after
ingestion of sporocysts. Merozoites emerge from the second generation meronts and enter the
mononucleate cells where they develop by endodyogeny. Subsequent generations of merozoites
develop downstream in the direction of blood flow to arterioles, capillaries, venules, and veins
throughout the body subsequently developing into the final asexual generation in muscles.
Merozoites entering muscle cells round up to form metrocytes and initiate sarcocyst formation.
Sarcocysts begin as unicellular bodies containing a single metrocyte and through asexual
multiplication numerous metrocytes accumulate and the sarcocyst increases in size. As the sarcocyst
matures, the small, rounded, noninfectious metrocytes give rise to crescent-shaped bodies
called bradyzoites that are infections for the definitive host. Time required for maturation varies
with the species and may take 2 months or more.
In species in which symptoms develop these typically occur 20–40 days after ingestion of
sporocysts and during the subsequent migration of sporozoites through the body vessels. Acute
lesions (oedema, hemorrhages and necrosis) develop in the affected tissues. The parasite has a
predilection for skeletal muscle (myositis), cardiac muscle (petechial hemorrhages of cardiac muscle
and serosae), and lymph nodes (oedema, necrosis and hemorrhage). These lesions are associated
with maturation of second generation of meronts within the endothelial and subendothelials cells.
Occasionally mononuclear infiltration or hyperemia has been observed in the lamina propria of the
small intestine. After the acute phase cysts may be found in various muscular tissues, generally
without pathology.
22
Once the intermediate host is eaten by the definitive host such as a dog or human, the parasite
undergoes sexual reproduction within the gut to create macrogamonts and microgamonts. Most
definitive hosts do not show any clinical sign or symptoms. Fusion of a macrogamont and a
microgamont creates a zygote which develops into an oocyst. The oocyst is passed through the
faeces completing the life cycle.
A second life cycle has more recently been described whereby carnivores and omnivores pass the
infectious stages in their faeces. Ingestion of this material may lead to successful infection of the
ingesting animal.
Birds[ ]
Although sarcocysts were first reported in the muscles of birds by Kuhn in 1865 not until 1977 was
the first life cycle involving a bird (Gallus gallus) and a carnivore (Canis familiaris) described by
Munday et al. In 1986 the first life cycle involving birds as both the definitive (Northern goshawk Accipiter gentilis) and intermediate (Atlantic canary - Serinus canaria) hosts was described by Cern
and Kvasnovsk.[ ]
Taxonomy[ ]
The taxonomy of this genus and its relationship to other protozoal genera is currently under
investigation.
Related
genera
include: Besnoitia, Caryospora, Cystoisospora, Frenkelia, Isospora, Hammondia, Hyaloklossia, Lan
kesterella,Neospora and Toxoplasma.
Sarcocystis is the largest genus within the family Sarcocystidae and consists of species which
infecting a range of animals including mammals, birds and reptiles. Frenkelia, another genus within
this family, consists of parasites that use rodents as intermediate hosts and birds of prey as definitive
hosts.
It appears that Besnoitia, Hammondia, Neospora and Toxoplasma form a single clade. Within this
clade Toxoplasma andNeospora appear to be sister clades. Isospora also appear to belong to this
clade and this clade is a sister to Sarcocystis.Frenkelia appears to be very closely related
to Sarcocystis.
Several molecular studies have suggested that Frenkelia is actually a species of Sarcocystis. This
genus was distinguished from Sarcocystis on the basis of its tendency to encyst within
the brain rather than within muscle. This distinction may not be taxonomically valid.
Within the genus a number of clades have been identified. These include one that contains S.
dispersa, S. lacertae, S. mucosa, S. muris, S. neurona and S. rodentifelis.[4] Frenkelia also groups
with this clade.
23
Evolution[ ]
These protozoa are mostly found in mammals. They do not appear to infect mammals of the
superorder Afrotheria and infect only two species of the Xenarthra. Because of this pattern the genus
may have evolved in the Northern hemisphere from a preexisting protozoan species that infected
mammals.
Alternatively because a number of Australian marsupials are also infected by this genus, marsupials
may have been the original hosts of this genus and the parasites were spread to the Northern
hemisphere by birds.
A third possibility is that the genus originally infected birds and was spread world wide by these
hosts.
A final possibility because of the existence of life cycles where both the intermediate and final hosts
are reptiles, the genus may have originated in reptiles and spread from there to other genera.
The resolution of this question awaits the outcome of further molecular studies.
Clinical: Human[ ]
Infection with this parasite is known as sarcosporidiosis. Because of initial confusion over the
taxonomy of this parasite it was originally referred to as Isospora hominis. The older literature may
refer to this organism.
Epidemiology[ ]
Human infection is considered rare with less than one hundred published cases of invasive disease
(approximately 46 cases reported by 1990). These figures represent a gross underestimate of the
human burden of disease.
The extremes of age reported to date are a 26-day-old infant and a 75-year-old man. Infectons have
been reported fromAfrica, Europe (Germany, Spain and Poland), the United States (California),
Central and South America, China, India, Tibet,Malaysia and Southeast Asia.
Stool examinations in Thai laborers showed that sarcocystis infection had a prevalence of ~23%.
Virtually all cases appeared to be asymptomatic which probably explains the lack of recognition. A
study of 100 human tongues obtained at post mortum in Malaya revealed an infection rate of 21%.
There was no sex difference and the age range was 16 to 57 years (mean 37.7 years).[ ]
Route of infection[ ]
Infection occurs when undercooked meat is ingested. The incubation period is 9–39 days. Human
outbreaks have occurred in Europe. Rats are a known carrier.
It has been suggested that contaminated water may be able to cause infection but this presently
remains a theoretical possibility.
24
Pathology[ ]
The pathology is of two types: a rare invasive form with vasculitis and myositis and an intestinal
form that presents withnausea, abdominal pain, and diarrhea. While normally mild and lasting under
48 hours, the intestinal form may occasionally be severe or even life-threatening. The invasive form
may involve a wide variety of tissues including lymph nodes, muscles and the larynx.
Clinical features[ ]
In volunteer studies with infected beef symptoms appeared 3–6 hours after eating. These included
anorexia, nausea, abdominal pain, distension, diarrhea, vomiting, dyspnoea and tachycardia. All
symptoms were transient and lasted about 36 hours. In a second series symptoms - abdominal pain,
distension, watery diarrhea and eosinophilia - appeared at 1 week and resolved after 3 weeks.
Clinical cases have been associated with acute fever, myalgias, bronchospasm, pruritic rashes,
lymphadenopathy, subcutaneous nodules associated with eosinophilia, elevated erythrocyte
sedimentation rate and elevated creatinine kinase levels. Symptoms may last as long as five years.
Segmental necrotizing enteritis has been reported on one occasion.
Diagnosis[ ]
Definitive diagnosis by biopsy of an infected muscle. Sarcocysts are identifiable
with hematoxylin and eosin. The PAS stain may be helpful but variable uptake of stain is common.
Along with the sarcocysts inflammatory cells may be found. Other findings include myositis,
myonecrosis, perivascular and interstitial inflammation, vasculitis and eosinophilic myositis.
Treatment[ ]
Because infection is rarely symptomatic, treatment is rarely required. There have been no published
trials
so
treatment
remains
empirical.
Agents
that
have
been
used
includealbendazole, metronidazole and cotrimoxazole for myositis. Corticosteroids have also been
used for symptomatic relief.
Amprolium and salinomycin was effective in preventing severe illness and death in experimentally
infected calves and lambs. These agents have not been tried in humans to date.
Prevention[ ]
Infection can be prevented by cooking the meat before eating. Alternatively freezing the meat at -5C
for several days before ingestion will kill the sporocysts.
Fasciolosis
Fasciolosis (also known as fascioliasis, distomatosis and liver rot) is a parasitic worm infection
caused by the common liver fluke Fasciola hepatica as well as by Fasciola gigantica. The disease is
a plant-borne trematode zoonosis, and is classified as a Neglected Tropical Disease (NTD). It
affects humans, but its main host is ruminants such as cattle and sheep. The disease progresses
25
through four distinct phases; an initial incubation phase of between a few days up to three months
with little or no symptoms; an invasive or acute phase which may manifest with: fever, malaise,
abdominal pain, gastrointestinal symptoms, urticaria, anemia, jaundice, and respiratory
symptoms. The disease later progresses to a latent phase with less symptoms and ultimately into a
chronic or obstructive phase months to years later. In the chronic state the disease causes
inflammation of the bile ducts, gall bladder and may cause gall stones as well as fibrosis. While
chronic inflammation is connected to increased cancer rates it is unclear whether fasciolosis is
associated with increased cancer risk.
Up to half of those infected display no symptoms, and diagnosis is difficult because eggs are often
missed in fecal examination. The methods of detection are through fecal examination, parasitespecific antibody detection, radiological diagnosis as well as laparotomy. In case of a suspected
outbreak it may be useful to keep track of dietary history, which is also useful for exclusion of
differential diagnoses. Fecal examination is generally not helpful because eggs can seldom be
detected in the chronic phase of the infection. Eggs appear in the feces first between 9–11 weeks
post-infection. The cause of this is unknown, and it is also difficult to distinguish between the
different species of fasciola as well distinguishing them from Echinostomes and Fasciolopsis. Most
immunodiagnostic tests detect infection with very high sensitivity and as concentration drops after
treatment it is a very good diagnostic method. Clinically it is not possible to differentiate from
other liver and bile diseases. Radiological methods can detect lesions in both acute and chronic
infection, while laparotomy will detect lesions and also occasionally eggs and live worms.
Because of the size of the parasite (adult F. hepatica: 20–30 × 13 mm, adult F. gigantica: 25–75×12
mm) fasciolosis is a big concern. The amount of symptoms depend on how many worms and what
stage the infection is in. The death rate is significant in both sheep and cattle, but generally low
among humans. Treatment with triclabendazole is highly effective against the adult worms as well
as various developing stages. Praziquantel is not effective, and older drugs such as bithionol are
moderately effective but also cause more side effects. Secondary bacterial infection
causing cholangitis is also a concern and can be treated with antibiotics, and toxaemia may be
treated with prednisolone.
Humans are infected by eating water grown plants. Infection may also occur by drinking
contaminated water with floating young fasciola. Human infection is rare even if the infection rate
is high among animals. Especially high rates of human infection have been found in Bolivia, Peru
and Egypt, and this may be due to consumption of certain foods. No vaccine is available to protect
people against Fasciola infection. Preventative measures are primarily treating and immunization
the livestock. Other methods include using molluscicides to decrease the amount of snails that act
as vectors, but it is not practical. Educational methods to decrease consumption of wild watercress
and other waterplants has been shown to work in areas with a high disease burden. Fascioliasis
occurs in Europe, Africa, the Americas.
26
Signs and symptoms
The course of fasciolosis in humans has 4 main phases:




Incubation phase: from the ingestion of metacercariae to the appearance of the first symptoms;
time period: few days to 3 months; depends on number of ingested metacercariae and immune
status of host
Invasive or acute phase: fluke migration up to the bile ducts. This phase is a result of
mechanical destruction of the hepatic tissue and the peritoneum by migrating juvenile flukes
causing localized and or generalized toxic and allergic reactions. The major symptoms of this
phase are:
 Fever, Abdominal pain, loss of appetite, flatulence, nausea, diarrhoea, Urticaria,
cough, dyspnoea, chest pain, hemoptysis, Hepatomegaly and splenomegaly, Ascites,
Anaemia, Jaundice.
Latent phase: This phase can last for months or years. The proportion of asymptomatic subjects
in this phase is unknown. They are often discovered during family screening after a patient is
diagnosed.
Chronic or obstructive phase:
This phase may develop months or years after initial infection. Adult flukes in the bile ducts cause
inflammation and hyperplasia of the epithelium. The resulting cholangitis and cholecystitis,
combined with the large body of the flukes, are sufficient to cause mechanical obstruction of the
biliary duct. In this phase, biliary colic, epigastric pain, fatty food intolerance, nausea,
jaundice, pruritus, right upper-quadrant abdominal tenderness, etc., are clinical manifestations
indistinguishable from cholangitis, cholecystitis and cholelithiasis of other origins. Hepatic
enlargement may be associated with an enlarged spleen or ascites. In case of obstruction, the gall
bladder is usually enlarged and edematous with thickening of the wall. Fibrous adhesions of the gall
bladder to adjacent organs are common. Lithiasis of the bile duct or gall bladder is frequent and the
stones are usually small and multiple.
Other animals
Clinical signs of fasciolosis are always closely associated with infectious dose (amount of ingested
metacercariae). In sheep, as the most common definitive host, clinical presentation is divided into 4
types:


Acute Type I Fasciolosis: infectious dose is more than 5000 ingested metacercariae. Sheep
suddenly
die
without
any
previous
clinical
signs. Ascites, abdominal
haemorrhage, icterus, pallor of membranes, weakness may be observed in sheep.
Acute Type II Fasciolosis: infectious dose is 1000-5000 ingested metacercariae. As above,
sheep die but briefly show pallor, loss of condition and ascites.
27


Subacute Fasciolosis: infectious dose is 800-1000 ingested metacercariae. Sheep are lethargic,
anemic and may die. Weight loss is dominant feature.
Chronic Fasciolosis: infectious dose is 200-800 ingested metacercariae. Asymptomatic or
gradual development of bottle jaw and ascites (ventral edema), emaciation, weight loss.
In blood, anemia, hypoalbuminemia, and eosinophilia may be observed in all types of fasciolosis.
Economical effect of fasciolosis in sheep consists in sudden deaths of animals as well as in
reduction of weight gain and wool production. In goats and cattle, the clinical manifestation is
similar to sheep. However, acquired resistance to F. hepatica infection is well known in adult
cattle. Calves are susceptible to disease but in excess of 1000 metacercariae are usually required to
cause clinical fasciolosis. In this case the disease is similar to sheep and is characterized by weight
loss, anemia, hypoalbuminemia and (after infection with 10,000 metacercariae) death. Importance
of cattle fasciolosis consist in economic losses caused by condemnation of livers at slaughter and
production losses especially due to reduced weight gain.
In sheep and sometimes cattle, the damaged liver tissue may become infected by
the Clostridium bacteria C. novyi type B. The bacteria will release toxins into the bloodstream
resulting in what is known as black disease. There is no cure and death follows quickly. As C.
novyi is common in the environment, black disease is found wherever populations of liver flukes
and sheep overlap.
Intermediate hosts
Intermediate hosts of F. hepatica are freshwater snails from family Lymnaeidae. Snails from
family Planorbidaeact as an intermediate host of F. hepatica very occasionally.
Mechanism
The development of infection in definitive host is divided into two phases: the parenchymal
(migratory) phase and the biliary phase. The parenchymal phase begins when excysted juvenile
flukes penetrate the intestinal wall. After the penetration of the intestine, flukes migrate within the
abdominal cavity and penetrate the liver or other organs. F. hepatica has a strong predilection for
the tissues of the liver. Occasionally, ectopic locations of flukes such as the lungs, diaphragm,
intestinal wall, kidneys, and subcutaneous tissue can occur. During the migration of flukes, tissues
are mechanically destroyed and inflammation appears around migratory tracks of flukes. The second
phase (the biliary phase) begins when parasites enter the biliary ducts of the liver. In biliary ducts,
flukes mature, feed on blood, and produce eggs. Hypertrophy of biliar ducts associated with
obstruction of the lumen occurs as a result of tissue damage.
Diagnosis
Most immunodiagnostic tests will detect infection and have a sensitivity above 90% during all
stages of the diseases. In addition antibody concentration quickly drops post treatment and no
28
antibodies are present one year after treatment, which makes it a very good diagnostic method. In
humans, diagnosis of fasciolosis is usually achieved parasitologically by findings the fluke eggs in
stool, and immunologically by ELISA . Coprological examinations of stool alone are generally not
adequate because infected humans have important clinical presentations long before eggs are found
in the stools. Moreover, in many human infections, the fluke eggs are often not found in the faeces,
even after multiple faecal examinations.
Furthermore, eggs of F. hepatica, F.
gigantica and Fasciolopsis
buski are
morphologically
indistinguishable.
Therefore,
immunonological methods such ELISA and enzyme-linked immunoelectrotransfer blot, also called
Western blot, are the most important methods in diagnosis of F. hepatica infection. These
immunological tests are based on detection of species-specific antibodies from sera.
The antigenic preparations used have been primarily derived from extracts of excretory/secretory
products from adult worms, or with partially purified fractions. In addition, biochemical and
haematological examinations of human sera support the exact diagnosis (eosinophilia, elevation of
liver enzymes). Ultrasonography and xray of the abdominal cavity, biopsy of liver, and gallbladder
punctuate can also be used. False fasciolosis (pseudofasciolosis) refers to the presence of eggs in the
stool resulting not from an actual infection but from recent ingestion of infected livers containing
eggs. This situation (with its potential for misdiagnosis) can be avoided by having the patient follow
a liver-free diet several days before a repeat stool examination.
Treatment and prevention
Several drugs are effective for fascioliasis, both in humans and in domestic animals. The drug of
choice in the treatment of fasciolosis is triclabendazole, a member of thebenzimidazole family
of anthelmintics. The drug works by preventing the polymerization of the molecule tubulin into
the cytoskeletal structures, microtubules.
Nitazoxanide has been found effective in trails, but is currently not recommended. The life
cycle includes freshwater snails as an intermediate host of the parasite.
29
Babesiosis
Babesiosis is
a malaria-like parasitic
disease caused
by
infection
with Babesia,
[ ]
a genus of Apicomplexa. Human babesiosis is an uncommon but emerging disease in the
Northeastern and Midwestern United States and parts of Europe, and sporadic throughout the rest of
the world. It occurs in warm months. ] Ticks transmit the human strain of babesiosis, so it often
presents with other tick-borne illnesses such as Lyme disease.[ ] After trypanosomes, Babesia is
thought to be the second-most common blood parasite of mammals, and they can have a major
impact on health of domestic animals in areas without severe winters. In cattle, a major host, the
disease is known as Texas cattle fever, redwater, or piroplasmosis
Classification
Babesia species are in the phylum Apicomplexa, which also has the protozoan parasites that
cause malaria, toxoplasmosis, and cryptosporidiosis.[3] Four clades of Babesiaspecies infect humans.
The main species in each clade are:
1. B. microti (<3 µm)
2. B. duncani, related to babesia of dogs
3. B. divergens (cattle parasite seen mostly in Europe) and B. venatorum (roe deer parasite,
formerly called EU1), most closely related to the large babesia clade
4. Large Babesia (>3 µm) mostly infects ungulates, but also includes K01 strain (an isolated
case observed in South Korea, see isolated cases)
Signs and symptoms
Half of all children and a quarter of previously healthy adults are asymptomatic
with Babesia infection. For those who develop symptoms, they are similar to malaria, because both
cause fever and hemolytic anemia. People with symptoms usually become ill 1 to 4 weeks after the
bite, or 1 to 9 weeks after transfusion of contaminated blood products. A person infected with
babesiosis gradually develops malaise and fatigue, followed by a fever. Hemolytic anemia, in which
red blood cells are destroyed and removed, also develops. Chills, sweats, and thrombocytopenia (a
low number of platelets in the blood) are also common symptoms.
Less common symptoms and physical exam findings of mild-to-moderate babesiosis:[ ]

Headache

Muscle pain
Anorexia
Nonproductive cough (mucus is not coughed up)
Arthralgias (noninflammatory joint pain, unlike arthritis, which is inflammatory)
Nausea
Vomiting





30

Sore throat

Abdominal pain
Pink eye
Photophobia
Weight loss
Emotional lability
Depression
Hyperesthesia (more sensitive to stimuli)
Enlarged spleen
Pharyngeal erythema
Enlarged liver













Jaundice (yellowing of the skin and of the sclera)
Retinopathy with splinter hemorrhages
Retinal infarcts
Neutropenia]
In more severe cases, symptoms similar to malaria occur, with fevers up to 40.5 °C (105 °F),
shaking chills, and severe anemia (hemolytic anemia). Organ failure may follow, including adult
respiratory distress syndrome. Severe cases occur mostly in people who have had a splenectomy.
Severe cases are also more likely to occur in the very young, very old, and persons
with immunodeficiency, such as HIV/AIDS patients.
A reported increase in human babesiosis diagnoses in the 2000s is thought to be caused by more
widespread testing and higher numbers of people with immunodeficiencies coming in contact with
ticks, the disease vector.[ ] Little is known about the occurrence of Babesia species in malariaendemic areas, where Babesia can easily be misdiagnosed as Plasmodium.
Human patients with babesiosis may exhibit premunity
Pathophysiology
Babesia parasites reproduce in red blood cells, where they can be seen as cross-shaped inclusions
(four merozoites asexually budding, but attached together forming a structure looking like a
"Maltese cross")[ ] and cause hemolytic anemia, quite similar to malaria.
Unlike the Plasmodium parasites that cause malaria, Babesia species lack an exoerythrocytic phase,
so the liver is usually not affected.
In nonhuman animals, Babesia canis rossi, Babesia bigemina, and Babesia bovis cause particularly
severe forms of the disease, including a severe haemolytic anaemia, with positive erythrocyte-insaline-agglutination test indicating an immune-mediated component to the haemolysis. Common
sequelae include haemoglobinuria "red-water", disseminated intravascular coagulation, and
"cerebral babesiosis" caused by sludging of erythrocytes in cerebral capillaries.
31
In bovine species, the organism causes hemolytic anemia, so an infected animal shows pale mucous
membranes initially. As the levels of bilirubin (a byproduct of red blood cell lysis) continue to
increase, the visible mucous membranes become yellow in color (icterus) due to the failure of the
liver to metabolise the excess bilirubin. Hemoglobinuria is seen due to excretion of red-blood-cell
lysis byproducts via the kidneys. Fever of 40.5 °C (105 °F) develops due to release of inflammatory
byproducts.
Diagnosis
Only specialized laboratories can adequately diagnose Babesia infection in humans, and as a
result,Babesia infections are considered highly under-reported. It develops in patients who live in or
travel to an endemic area or receive a contaminated blood transfusion within the preceding 9 weeks,
so this aspect of the medical history is vital.[8] Babesiosis may be suspected when a person with such
an exposure history develops persistent fevers and hemolytic anemia. The definitive diagnostic test
is the identification of parasites on a Giemsa-stained thin blood smear.[ ]
So-called "Maltese cross formations" on the blood film are essentially diagnostic of babesiosis, since
they are not seen in malaria, the primary differential diagnosis.[7] Careful examination of
multiple smears may be necessary, since Babesia may infect less than 1% of circulating red blood
cells, thus be easily overlooked.[ ]
Serologic testing for antibodies against Babesia (both IgG and IgM) can detect low-level infection
in cases with a high clinical suspicion, but negative blood film examinations. Serology is also useful
for differentiating babesiosis from malaria in cases where people are at risk for both infections.
Since detectable antibody responses require about a week after infection to develop, serologic
testing may be falsely negative early in the disease course.[ ]
A polymerase chain reaction (PCR) test has been developed for the detection of Babesia from the
peripheral blood.[ ] PCR may be at least as sensitive and specific as blood film examination in
diagnosing babesiosis, though it is also significantly more expensive.[ ] Most often, PCR testing is
used in conjunction with blood film examination and possiblyserologic testing.[ ]
Other laboratory findings include decreased numbers of red blood cells and platelets on complete
blood count.
In animals, babesiosis is suspected by observation of clinical signs (haemoglobinuria and anaemia)
in animals in endemic areas. Diagnosis is confirmed by observation of merozoites on thin film blood
smear examined at maximum magnification under oil using Romonovski stains (methylene blue and
eosin). This is a routine part of the veterinary examination of dogs and ruminants in regions where
babesiosis is endemic.
Babesia canis and B. bigemina are "large Babesias" that form paired merozoites in the erythrocytes,
commonly described as resembling "two pears hanging together", rather than the "Maltese cross" of
the "small Babesias". Their merozoites are around twice the size of small Babesias.
32
Cerebral babesiosis is suspected in vivo when neurological signs (often severe) are seen in cattle that
are positive for B. bovis on blood smear, but this has yet to be proven scientifically. Outspoken red
discolouration of the grey matter post mortem further strengthens suspicion of cerebral babesiosis.
Diagnosis is confirmed post mortem by observation of Babesia-infected erythrocytes sludged in the
cerebral cortical capillaries in a brain smear.
Treatment[ ]
In
mild-to-moderate
babesiosis,
the
treatment
of
choice
is
a
combination
of atovaquone and azithromycin. This regimen is preferred to clindamycin and quinine because side
effects are fewer. The standard course is 7 to 10 days, but this is extended to at least 6 weeks in
people with relapsing disease. It is recommended that even mild cases are treated to decrease the
chance of inadvertently transmitting the infection by donating blood.[ ] In life-threatening
cases, exchange transfusion is performed.[ ] In this procedure, the infected red blood cells are
removed and replaced with uninfected ones. Imizol is a drug used for treatment of babesiosis in
dogs.[ ] Extracts of the poisonous, bulbous plantBoophone disticha are used in the folk
medicine of South Africa to treat equine babesiosis. B. disticha is a member of the daffodil
family Amaryllidaceae and has also been used in preparations employed as arrow
poisons, hallucinogens, and in embalming. The plant is rich in alkaloids, some of which display an
action similar to that of scopolamine.[ ]
Epidemiology[ ]
Babesiosis is a vector-borne illness usually transmitted by Ixodes scapularis ticks. Babesia
microti uses the same tick vector as Lyme disease and ehrlichiosis, and may occur in conjunction
with these other diseases.[ ] The organism can also be transmitted by blood transfusion. Ticks of
domestic animals, especially Rhipicephalus (Boophilus) microplus and R. (B.) decoloratus transmit
several species of Babesia to livestock, causing considerable economic losses to farmers in tropical
and subtropical regions.
In the United States, the majority of babesiosis cases are caused by B. microti, and occur in the
Northeast and northern Midwest from May through October.[ ] Areas with especially high rates
include eastern Long Island, Fire Island, Nantucket Island, and Martha's Vineyard.
In Europe, B. divergens is the primary cause of infectious babesiosis and is transmitted by I. ricinus.
Babesiosis has emerged in Lower Hudson Valley, New York since 2001.[ ]
In Australia, babesiosis of types B. duncani and B. microti has recently been found in symptomatic
patients along the eastern coastline of the continent.[ ] A similar disease in cattle, commonly known
as tick fever, is spread by Babesia bovis and B. bigemina in the introduced cattle tick Rhipicephalus
microplus. This disease is found in eastern and northern Australia.[
33
Balantidiasis
Balantidiasis is a protozoan infection caused by infection with Balantidium coli.[
Symptoms[ ]
Symptoms can be local due to involvement of the intestinal mucosa, or systemic in nature and
include either diarrhea or constipation.
Transmission[ ]
Balantidium is the only ciliated protozoan known to infect humans. Balantidiasis is a zoonotic
disease and is acquired by humans via the feco-oral route from the normal host, the pig, where it is
asymptomatic. Contaminated water is the most common mechanism of transmission.[ ]
Treatment[ ]
Balantidiasis can be treated with tetracycline,[ ] carbarsone, metronidazole, or diiodohydroxyquin.
History and epidemiology
The first study to generate Balantidiasis in humans was undertaken by Cassagrandi and Barnagallo
in 1896. ] However, this experiment was not successful in creating an infection and it was unclear
whether Balantidium coli was the actual parasite used.[ ] The first case of Balantidiasis in the
Philippines, where it is the most common, was reported in 1904. Currently, Balantidium coli is
distributed worldwide but less than 1% of the human population is infected. Pigs are a major
reservoir of the parasite, and infection of humans occurs more frequently in areas where pigs
comingle with people.[ ] This includes places like the Philippines, as previously mentioned, but also
includes countries such as Bolivia and Papua New Guinea. But pigs are not the only animal where
the parasite is found. In a Japanese study that analyzed the fecal samples in 56 mammalian
species, Balantidium coli was found to be present not just in all the wild boars tested (with wild
boars and pigs being considered the same species), it was also found in five species of non human
primate: Chimpanzee (Pan troglodytes), White-handed gibbon (Hylobates lar), Squirrelmonkey
(Saimiri sciurea), Sacred baboon (Comopithecus hamadryas), and Japanese macaque (Macaca
fuscata).[ ] In other studies, Balantidium coli was also found in species from the
orders Rodentia and Carnivora.[ ]
Morphology
Balantidium coli exists in either of two developmental stages: Trophozoites and Cysts.[ ] In the
trophozoite form, they can be oblong or spherical, and are typically 30 to 150 µm in length and 25 to
120 µm in width.[ ] It is its size at this stage that allows Balantidium coli to be characterized as the
largest protozoan parasite of humans.[ ] Trophozoites possess both a macronucleus and a
34
micronucleus, and both are usually visible. The macronucleus is large and sausage-shaped while the
micronucleus is less prominent. At this stage, the organism is not infective but it can replicate
by transverse binary fission.
In its cyst stage, the parasite takes on a smaller, more spherical shape, with a diameter of around 40
to 60 µm.[ ] Unlike the trophozoite, whose surface is covered only with cilia, the cyst form has a
tough wall made of one or more layers.[ ] The cyst form also differs from the trophozoite form
because it is non-motile and does not undergo reproduction. ] Instead, the cyst is the form that the
parasite takes when it causes infection.[ ]
Disease diagnosis
The diagnosis of Balantidiasis can be an intricate process, partly because the related symptoms may
or may not be present. However, the diagnosis of Balantidiasis can be considered when a patient has
diarrhea combined with a probable history of current exposure to amebiasis through travel, contact
with infected persons, or anal intercourse.]In addition, the diagnosis of Balantidiasis can be made by
microscopic examination of stool or tissue samples.[ ]
Prevention[
Preventative measures require effective personal and community hygiene. Some specific safeguards
include the following:

Purification of drinking water.

Proper handling of food.
Careful disposal of human feces.
Monitoring the contacts of balantidiasis patients.


Leishmaniasis
Leishmaniasis, also spelled leishmaniosis, is a disease caused by protozoan parasites of the
genus Leishmania and spread by the bite of certain types of sandflies.[ ] The disease can present in
three main ways: cutaneous, mucocutaneous, or visceral leishmaniasis.[ ] The cutaneous form
presents with skin ulcers, while the mucocutaneous form presents with ulcers of the skin, mouth,
and nose, and the visceral form starts with skin ulcers and then later presents with fever, low red
blood cells, and enlarged spleen and liver.
Infections in humans are caused by more than 20 species of Leishmania. Risk factors include
poverty, malnutrition, deforestation, and urbanization. All three types can be diagnosed by seeing
the parasites under the microscope. Additionally, visceral disease can be diagnosed by blood tests.
35
Leishmaniasis can be partly prevented by sleeping under nets treated with insecticide. Other
measures include spraying insecticides to kill sandflies and treating people with the disease early to
prevent further spread.[ ] The treatment needed is determined by where the disease is acquired, the
species of Leishmania, and the type of infection.[ ] Some possible medications used for visceral
]
disease
include liposomal
amphotericin
B,
a
combination
of pentavalent
[
]
[
]
antimonials and paromomycin,
andmiltefosine.
For
cutaneous
disease,
[]
paromomycin, fluconazole, or pentamidine may be effective.
About 12 million people are currently infected[ ] in some 98 countries.[ ] About 2 million new cases[
]
and between 20 and 50 thousand deaths occur each year. About 200 million people in Asia, Africa,
South and Central America, and southern Europe live in areas where the disease is
common. The World Health Organization has obtained discounts on some medications to treat the
disease.[ ] The disease may occur in a number of other animals, including dogs and rodents.[ ]
Signs and symptoms
The symptoms of leishmaniasis are skin sores which erupt weeks to months after the person is bitten
by infected sand flies.
Leishmaniasis may be divided into the following types:[ ]



Cutaneous leishmaniasis is the most common form, which causes an open sore at the bite sites,
which heals in a few months to a year and half, leaving an unpleasant-looking scar. Diffuse
cutaneous leishmaniasis produces widespread skin lesions which resembleleprosy, and may not
heal on its own.[ ]
Mucocutaneous leishmaniasis causes both skin and mucosal ulcers with damage primarily of the
nose and mouth.
Visceral leishmaniasis or kala-azar ('black fever') is the most serious form, and is potentially
fatal if untreated.[ ] Other consequences, which can occur a few months to years after infection,
include fever, damage to the spleen and liver, and anemia.[ ]
Leishmaniasis is considered one of the classic causes of a markedly enlarged (and therefore
palpable) spleen; the organ, which is not normally felt during examination of the abdomen, may
even become larger than the liver in severe cases.
Cause[
Leishmaniasis is transmitted by the bite of infected female phlebotomine sandflies[ ] which can
transmit
the
protozoa Leishmania.[ ] The
sandflies
inject
the
infective
stage,
metacyclicpromastigotes, during blood meals (). Metacyclic promastigotes that reach the puncture
wound are phagocytized by macrophages () and transform into amastigotes (). Amastigotes multiply
in infected cells and affect different tissues, depending in part on whichLeishmania species is
involved (. These differing tissue specificities cause the differing clinical manifestations of the
36
various forms of leishmaniasis. Sandflies become infected during blood meals on infected hosts
when they ingest macrophages infected with amastigotes ). In the sandfly's midgut, the parasites
differentiate into promastigotes (), which multiply, differentiate into metacyclic promastigotes, and
migrate to the proboscis ().
The genomes of three Leishmania species (L. major, L. infantum, and L. braziliensis) have been
sequenced, and this has provided much information about the biology of the parasite. For example,
in Leishmania, protein-coding genes are understood to be organized as largepolycistronic units in a
head-to-head or tail-to-tail manner; RNA polymerase II transcribes long polycistronic messages in
the absence of defined RNA pol II promoters, and Leishmania has unique features with respect to
the regulation of gene expression in response to changes in the environment. The new knowledge
from these studies may help identify new targets for urgently needed drugs and aid the development
of vaccines.[ ]
Vector[ ]
Although most of the literature mentions only one genus transmitting Leishmania to humans
(Lutzomyia) in the New World, a 2003 study by Galati suggested a new classification for New
World sand flies, elevating several subgenera to the genus level. Elsewhere in the world, the
genus Phlebotomus is considered the vector of leishmaniasis.[ ]
Organisms[ ]
Visceral disease is usually caused by Leishmania donovani, L. infantum, or L. chagasi,[ ] but
occasionally these species may cause other forms of disease.[ ] The cutaneous form of the disease is
caused by more than 15 species of Leishmania.
Risk factors[ ]
Risk factors include poverty, malnutrition, deforestation,lack of sanitation and urbanization.
Diagnosis[ ]
Leishmaniasis is diagnosed in the hematology laboratory by direct visualization of
the amastigotes (Leishman-Donovan bodies). Buffy-coat preparations of peripheral blood or
aspirates from marrow, spleen, lymph nodes, or skin lesions should be spread on a slide to make a
thin smear and stained with Leishman stain or Giemsa stain (pH 7.2) for 20 minutes. Amastigotes
are seen within blood and spleen monocytes or, less commonly, in circulating neutrophils and in
aspirated tissue macrophages. They are small, round bodies 2–4 μm in diameter with indistinct
cytoplasm, a nucleus, and a small, rod-shaped kinetoplast. Occasionally, amastigotes may be seen
lying free between cells.[ ] However, the retrieval of tissue samples is often painful for the patient
and identification of the infected cells can be difficult. So, other indirect immunological methods of
diagnosis are developed, including enzyme-linked immunosorbent assay, antigen-coated dipsticks,
and direct agglutination test. Although these tests are readily available, they are not the standard
diagnostic tests due to their insufficient sensitivity and specificity.
37
Several different polymerase chain reaction tests are available for the detection
of Leishmania DNA. With this assay, a specific and sensitive diagnostic procedure is finally
possible.
Prevention

Leishmaniasis can be partly prevented by using nets treated with insecticide while sleeping.

Stray dog removal
Treatment[edit]
The treatment is determined by where the disease is acquired, the species of Leishmania, and the
type of infection. For visceral leishmaniasis in India, South America, and the
Mediterranean, liposomal amphotericin B is the recommended treatment and is often used as a
single dose. Rates of cure with a single dose of amphotericin have been reported as 95%. In India,
almost all infections are resistant to pentavalent antimonials. In Africa, a combination of pentavalent
antimonials and paromomycin is recommended. These, however, can have significant side
effects. Miltefosine, an oral medication, is effective against both visceral and cutaneous
leishmaniasis. Side effects are generally mild, though it can cause birth defects if taken within 3
months of getting pregnant. It does not appear to work for L. major or L. braziliensis.
The evidence around the treatment of cutaneous leishmaniasis is poor. A number of topical
treatments may be used for cutaneous leishmaniasis. Which treatments are effective depends on the
strain, with topical paromomycin effective for L. major, L. tropica, L. mexicana, L. panamensis,
and L.
braziliensis.
Pentamidine
is
effective
for L.
guyanensis.
Oral fluconazole or itraconazole appears effective in L. major and L. tropica.
Epidemiology
Leishmaniasis occurs in 88 tropical and subtropical countries. About 350 million people live in these
areas. The settings in which leishmaniasis is found range from rainforests in Central and South
America to deserts in western Asia and the Middle East. It affects as many as 12 million people
worldwide, with 1.5–2.0 million new cases each year. The visceral form of leishmaniasis has an
estimated incidence of 500,000 new cases. More than 90% of the world's cases of visceral
leishmaniasis are in India, Bangladesh, Nepal, Sudan, and Brazil.[16]As of 2010, it caused about
52,000 deaths, down from 87,000 in 1990. Different types of the disease occur in different regions
of the world.[2] Cutaneous disease is most common in Afghanistan, Algeria, Brazil, Colombia, and
Iran, while mucocutaneous disease is most common in Bolivia, Brazil, and Peru, and visceral
disease is most common in Bangladesh, Brazil, Ethiopia, India, and Sudan.
Leishmaniasis is found through much of the Americas from northern Argentina to South Texas,
though not in Uruguay or Chile, and has recently been shown to be spreading to North
Texas.[17] Leishmaniasis is also known as papalomoyo, papa lo moyo, ulcero de los chicleros,
38
and chiclera in Latin America.[18] During 2004, an estimated 3,400 troops from
the Colombian army, operating in the jungles near the south of the country (in particular around the
Meta and Guaviare departments), were infected with leishmaniasis. Allegedly, a contributing factor
was that many of the affected soldiers did not use the officially provided insect repellent because of
its disturbing odor. Nearly 13,000 cases of the disease were recorded in all of Colombia throughout
2004, and about 360 new instances of the disease among soldiers had been reported in February
2005.
The disease is found across much of Asia, and in the Middle East. Within Afghanistan,
leishmaniasis occurs commonly in Kabul, partly due to bad sanitation and waste left uncollected in
streets, allowing parasite-spreading sand flies an environment they find favorable. In Kabul, the
number of people infected was estimated to be at least 200,000, and in three other towns
(Herat, Kandahar, and Mazar-i-Sharif) about 70,000 more occurred, according to WHO figures from
2002.[][verification needed] Kabul is estimated as the largest center of cutaneous leishmaniasis in the
world, with around 67,500 cases as of 2004. Africa, in particular the East and North, is also home to
cases of leishmaniasis.
Leishmaniasis is mostly a disease of the developing world, and is rarely known in the developed
world outside a small number of cases, mostly in instances where troops are stationed away from
their home countries. Leishmaniasis has been reported by U.S. troops stationed in Saudi
Arabia and Iraq since the Gulf War of 1990, including visceral leishmaniasis. In September 2005,
the disease was contracted by at least four Dutch marines who were stationed in Mazari Sharif,
Afghanistan, and subsequently repatriated for treatment.[citation needed]
Trypanosomiasis
Trypanosomiasis or trypanosomosis is the name of several
by parasitic protozoan trypanosomesof the genus Trypanosoma.
diseases
in vertebrates caused
In humans this includes African trypanosomiasis and Chagas disease. A number of other diseases
occur in other animals.
Approximately 30,000 people in 36 countries of sub-Saharan Africa have African trypanosomiasis,
which is caused by eitherTrypanosoma brucei gambiense or Trypanosoma brucei
rhodesiense. Chagas disease causes 21,000 deaths per year mainly inLatin America
Signs and symptoms
The tsetse fly bite erupts into a red chancre sore and within a few weeks, the person can experience
fever, swollen lymph glands, blood in urine, aching muscles and joints, headaches and irritability. In
the first phase, the patient has only intermittent bouts of fever with lymphadenopathy together with
39
other non-specific signs and symptoms. The second stage of the disease is marked by involvement
of the central nervous system with extensive neurological effects like changes in personality,
alteration of the biological clock (the circadian rhythm), confusion, slurred speech, seizures and
difficulty in walking and talking. These problems can develop over many years and if not treated,
the person dies. It is common to the African continent.
Treatment
Diagnosis is often missed in the first phase of the disease due to non-specific nature of
symptoms. Pentamidine and Suramin are
used
for
treatment
in
the
first
phase.Melarsoprol, nifurtimox and eflornithine are drugs used in second phase of the disease.
However none of the therapies available are optimal in terms of adverse events and ease of
administration.
Other animals

Nagana, or animal African trypanosomiasis, also called 'Souma' or 'Soumaya' in Sudan.

Surra
Mal de caderas (of central South America)
Murrina de caderas (of Panama; Derrengadera de caderas)
Dourine
Cachexial fevers (various)










Gambian horse sickness (of central Africa)
Baleri (of Sudan)
Kaodzera (Rhodesian trypanosomiasis)
Tahaga (a disease of camels in Algeria)
Galziekte, galzietzke (bilious fever of cattle; gall sickness of South Africa)
Peste-boba (of Venezuela; Derrengadera)
Some species of cattle such as the African buffalo, N'dama, and Keteku appear trypanotolerant and
do not develop symptoms. Calves are more resistant than adults.
Clinical signs and diagnosis[edit]
Cattle may show enlarged lymph nodes and internal organs. Haemolytic anaemia is a characteristic
sign. Systemic disease and reproductie are common, and cattle appear to waste away.
Horses with dourine show signs of ventral and genital edema and urticaria.
Infected dogs and cats may show severe systemic signs.
Diagnosis relies on recognition of the flagellate on a blood smear. Motile organisms may be visible
in the buffy coat when a blood sample is spun down. Serological testing is also common.
40
Prevention.
Diminazene, homidium, isometadium, suramin, and melarsomine can all be used to treat infections.
Resistance is increasing in endemic areas and recurrent treatments may be necessary.
The use of trypanotolerant breeds for livestock farming should be considered if the disease is
widespread.
Fly control is another option but is difficult to implement.
[[The main approaches to controlling African trypanosomiasis are to reduce the reservoirs of
infection and the presence of the tsetse fly. Screening of people at risk helps identify patients at an
early stage. Diagnosis should be made as early as possible and before the advanced stage to avoid
complicated, difficult and risky treatment procedures.
Coenurosis in humans
Coenurosis is a parasitic infection that results
dog tapeworm species Taenia multiceps, T. serialis.
when
humans
ingest
the
eggs
of
It is important to distinguish that there is a very significant difference between intestinal
human tapeworm infection and human coenurosis. Humans are the definitive hosts for some
tapeworm species, the most common being T. saginata and T. solium (pork and beef tapeworms).
This means that these species can develop into full grown, reproductively capable adult worms
within the human body. People infected with these species have a tapeworm infection. In contrast,
the four species that cause human coenurosis can only grow into mature, reproductively capable
worms inside their definitive hosts, canids such as dogs, wolves, foxes and coyotes. Humans who
ingest eggs from any of these four species of Taenia become intermediate hosts, or places where the
eggs can mature into larvae but not into adult worms. When humans ingest these eggs, the eggs
develop into tapeworm larvae that group within cysts known as coenuri, which can be seen in
the central nervous system, muscles, and subcutaneous tissues of infected humans. People with
coenurosis do not develop a tapeworm infection because the larvae of coenurosis-causing parasites
cannot develop into worms inside of humans.
Clinical signs in Humans
In humans, this parasitic infection causes a variety of symptoms, depending on where the cyst
occurs. The tapeworm larvae group together to form fluid filled cysts in various body tissues. These
cysts start out small, but as the larvae grow, the cyst can reach the size of an egg. The cysts of T.
multiceps are usually between 2 and 6 cm in diameter and are most commonly found in the CNS and
can contain anywhere from a few to over a hundred worm larvae within them. T serialis and T.
glomerata cysts present in the CNS, muscles, or subcutaneous tissue, and T. brauni cysts occupy
these same areas but occur in the eye more frequently than the other three species.
41
When the cyst occurs in the brain, as it often does, the infected individual may experience
headaches, seizures, vomiting, paralysis affecting one side of the body (hemiplegia), paralysis
involving one limb (monoplegia), and loss of ability to coordinate muscles and muscle movements.
Many of these symptoms are due to the buildup of inter-cranial pressure from the growing cyst or
from the cyst pressing on other parts of brain.
When the cyst occurs in the spinal cord, it can cause severe pain and inflammation, and loss of
feeling in some nerves.
When the cyst occurs in the eyes, it causes decreased vision and headaches.
In the muscular and subcutaneous tissues, the cyst causes disfiguring nodules that can protrude out
of the body. These nodules can be painful, uncomfortable, and can cause loss of muscle function.
Transmission
The definitive hosts for these Taenia species are canids. The adult tapeworms live in the intestines
of animals like dogs, foxes, and coyotes. Intermediate hosts such as rabbits, goats, sheep, horses,
cattle and sometimes humans get the disease by inadvertently ingesting tapeworm eggs (gravid
proglottids) that have been passed in the feces of an infected canid. This can happen from ingesting
food, water or soil that has been contaminated by dog feces. The disease cannot be transmitted from
one intermediate host to another, but it is still not a good idea to eat meat that presents with cystic
nodules from coenurosis.
Taeniasis
Taeniasis is a parasitic disease due to infection with tapeworms belonging to the genus Taenia. The
two most important humanpathogens in the genus are Taenia solium (the pork tapeworm)
and Taenia saginata (the beef tapeworm). Taeniasis is generally asymptomatic, but severe infection
causes weight loss, dizziness,abdominal pain, diarrhea, headaches, nausea, constipation, chronic
indigestion, and loss of appetite.
A type of taeniasis called cysticercosis is caused by accidental infection with the eggs of T.
solium from contaminated food and water. It is known as the most pathogenic form caused by
tapeworms. A specific form of cysticercosis called neurocysticercosis is said to be the most common
infection of the central nervous system.
Signs and symptoms
Taeniasis is generally asymptomatic and is diagnosed when a portion of the worm is passed in the
stool. It is not fatal, although cysticercosis can cause epilepsy and neurocystocercosis can be fatal.
42
Taenia solium
Infection by T. solium is normally asymptomatic. Heavy infection is indicated by intestinal
irritation, anaemia, and indigestion.
Cysticercosis
There are accidental consumptions of eggs of T. solium from contaminated vegetables or water. The
eggs enter the intestine where they develop into larvae. The larvae enterbloodstream and invade host
tissues. This clinical condition, called cysticercosis, is the most frequent and severe disease caused
by
any
tapeworm.
It
can
lead
to
severe
headaches,
dizziness,
occasional seizures, dementia, hypertension, lesions in the brain, blindness, tumor-like growths, and
low eosinophil levels. It is the cause of major neurological problems, such
as hydrocephalus, paraplegy, meningitis, convulsions, and even death.
Taenia saginata
Taenia saginata infection is asymptomatic, but heavy infection causes weight
loss, dizziness, abdominal pain, diarrhea, headaches, nausea, constipation, chronic indigestion, and
loss of appetite. It can cause antigen reaction that induce allergic reaction. It is an also rare cause
of pancreatitis, cholecystitis, and cholangitis.
Transmission
Taeniasis is contracted after eating undercooked or raw pork and beef that contain the larvae.
Cysticercosis occurs after ingestion of contaminated food, water, or soil that contain T. solium
eggs. Infection is acquired by eating undercooked beef and pork that contain the fluidfilled cysticerci of the tapeworms. The adult worms live in the lumen of the intestine where they
cause the symptoms. They acquire nutrients from the intestine, leading to malnutrition of the host.
The gravid proglottids, body segments containing fertilised eggs, are released in the faeces of the
host. Then they are consumed by an intermediate host such as a cow or pig, where they hatch within
the duodenum to become larvae, penetrate through the intestinal wall into nearby blood vessels, and
enter the bloodstream. Once they reach organs such as the skeletal muscles, liver or lungs, the larvae
then develop into a cyst, which then becomes a fluid-filled cysticercus. These contaminated tissues
are then consumed through raw or undercooked meat.
Diagnosis
Diagnosis of taeniasis is mainly using stool sample, particularly by identifying the eggs. However,
this has limitation at the species level because tapeworms basically have similar eggs. Examination
of the scolex or the gravid proglottids can resolve the exact species. But body segments are not often
available, therefore, laborious histological observation of the uterine branches.
43
Prevention
The fundamental prevention strategy is hygiene and sanitation. Secondary measures include
stricter meat-inspection standards, livestock confinement, health education, safe meat preparation,
mass drug therapy, and identifying and treating human and pig carriers. Moreover, a high level of
sanitation and prevention of human faecal contamination of pig feeds also plays a major role in
prevention. Infection can be prevented with proper disposal of human faeces around pigs, cooking
meat thoroughly and/or freezing the meat at −10 °C for 5 days. For human cysticercosis, dirty hands
are attributed to be the primary cause. Proper cooking of meat is an effective prevention
Treatment
Oral anti-parasitic drugs such as praziquantel are the treatment of choice. (5–10 mg/kg, singleadministration) or niclosamide (adults and children over 6 years: 2 g, single-administration after a
light breakfast, Albendazole is also highly effective.
Echinococcus
The genus Echinococcus includes six parasite species of cyclophyllid tapeworms to date, of the
family Taeniidae. Infection with Echinococcus results in hydatid disease, also known as
echinococcosis.
Echinococcus is triploblastic - it has three layers- outermost ectoderm, middle mesoderm, and inner
endoderm. An anus is absent, and it has no digestive system. Its body is covered by tegument and
the worm is divided into a scolex, a short neck, and three to six proglottids. Its body shape is ribbonlike.
In humans, this causes a disease called echinococcosis. The three types of echinococcosis are cystic
echinococcosis caused by E. granulosus, alveolar echinococcosis caused by E. multilocularis, and
polycystic echinococcosis caused by E. vogeli or E. oligarthrus. A worm's incubation period is
usually long and can be up to 50 years. Cystic echinococcosis is mostly found in South and Central
America,Africa, the Middle East, China, Italy, Spain, Greece, Russia, and the western United
States (Arizona, New Mexico, and California).
Echinococcosis
is
a zoonosis;
humans
are
dead-end
hosts.
The definitive
hosts are carnivorous predators - dogs, wolves, foxes, and lions. The adult tapeworm lives in their
small intestines and delivers eggs to be excreted with the stool. The intermediate hosts are infected
by ingesting eggs. Sheep, goats, cattle, camels, pigs, wild herbivores, and rodents are the usual
intermediate hosts, but humans can also be infected.
The egg hatches in the digestive system of the intermediate host, producing an onchospher. It
penetrates the intestinal wall and is carried by bloodstream to liver, lung, brain, or another organ. It
settles there and turns into a bladder-like structure called hydatid cyst. From the inner lining of its
44
wall, protoscoleces (i.e. scoleces with invaginated tissue layers) bud and protrude into the fluid
filling the cyst.
After the death of the normal intermediate host, its body can be eaten by carnivores suitable as
definitive hosts. In their small intestines, protoscoleces turn inside out, attach, and give rise to adult
tapeworms, completing the lifecycle. In humans, the cysts persist and grow for years. They are
regularly found in the liver (and every possible organ: spleen, kidney, bone, brain, tongue and skin)
and are asymptomatic until their growing size produces symptoms or are accidentally discovered.
Cysts are detected with ultrasound, X-ray computed tomography, or other imaging techniques.
Antiechinococcus antibodies can be detected with serodiagnostic tests - indirect fluorescent
antibody, complement fixation, ELISA.
Diphyllobothriasis
Diphyllobothriasis is the infection caused by tapeworms of the Diphyllobothrium genus,
commonly Diphyllobothrium latum.
Geographic distribution
Diphyllobothriasis occurs in areas where lakes and rivers coexist with human consumption of raw or
undercooked freshwater fish. Such areas are found in Europe, newly independent states of the
former Soviet Union, North America, Asia, Uganda, Peru and Chile. It is particularly common
in Japan, because of sushi.
Around the middle of the 20th century in Japan, before advancements in refrigeration, many
sushi/sashimi connoisseurs suffered great morbidity and mortality from Diphyllobothrium after
eating unrefrigerated sashimi. Through research in parasitology, scientists came to realize that the
primary cause was the relatively favorable parasite-breeding conditions that raw fish offered.
The disease is rare in the United States. It was, however, once more common and was referred to as
"Jewish housewife's disease" because Jewish housewives preparing the traditional "gefilte fish"
frequently tasted the fish before it was cooked.
Clinical features
Diphyllobothriasis can last for decades if untreated. Most infections are asymptomatic.
Manifestations may include abdominal discomfort, diarrhea, vomiting and weight loss. Vitamin B12
deficiency with subsequent megaloblastic anemia may occur, but has not for several decades in D.
latum infections, possibly because of improved nutrition. In one test, nearly half of the ingested
vitamin was absorbed by D. latum in otherwise healthy patients, while 80-100% was absorbed by
45
the worm in patients with anemia. It is not known why anemia occurs in some cases but not others.
Massive infections may result in intestinal obstruction. Migration of proglottids can
cause cholecystitis or cholangitis.
Females cases are disproportionately reported, most likely due to the higher likelihood for them to
be involved in meal preparation, rather than any morphological differences.
Diagnosis
Microscopic identification of eggs in the stool is the basis of specific diagnosis. Eggs are usually
numerous and can be demonstrated without concentration techniques. Examination of proglottids
passed in the stool is also of diagnostic value.
Though it is difficult to identify the eggs or proglottids to the species level, the distinction is of little
medical importance because, like most adult tapeworms in the intestine, all members of this genus
respond to the same drugs.
Treatment
Upon diagnosis, treatment is quite simple and effective. The standard treatment for
diphyllobothriasis, as well as many other tapeworm infections is a single dose of praziquantel, 5–10
mg/kg orally once for both adults and children. An alternative treatment is niclosamide, 2 g orally
once for adults or 50 mg/kg (max 2 g) for children. Albendazole can also be effective.
Prevention
Avoid ingestion of raw freshwater fish. Adequate cooking or freezing of freshwater fish will kill the
encysted fish tapeworm larvae. Also, because human feces is an important mechanism for spreading
eggs, proper disposal of sewage can cut down on infection of fish and thus of humans.
46