Toxoplasmosis

What is toxoplasmosis?
• Toxoplasmosis is a parasitic disease caused by the
protozoan Toxoplasma gondii.
• The organism was first described in 1908 in Tunis by
Nicolle and Manceaux within the tissues of the gundi.
In the same year it was also described in Brazil by
Splendore within the tissues of a rabbit.
• The parasite infects most warm-blooded animals,
including humans, but the primary host are cats.
• Animals are infected by eating infected meat, by
ingestion of faeces of a cat that has itself recently
been infected, or by transmission from mother to
fetus.
• Cats have been shown as a major reservoir of this
infection.
 Toxoplasmosis in the US

• Toxoplasmosis is considered the 3rd leading cause of

death attributed to food borne illness in the United
States.

• More than 60 million men, women, and children in the

U.S. carry the Toxoplasma parasite.

• Very few human carriers have symptoms because the

immune system usually keeps the parasite from causing
illness.
 Toxoplasmosis in the World

• In various places throughout the world, it has been shown

that up to 95% of some populations have been infected
with Toxoplasma. Infection is often highest in areas of the
world that have hot, humid climates and lower altitudes.

• High recorded rates of infection (93%) were found in Parisian

women who prefer undercooked or raw meat; at least 50% of their
children are likewise infected
• High prevalence in Central/South America has been related to the
frequency of stray cats in a climate favoring survival of oocysts and
soil exposure.
 People typically become infected by three
principal routes of transmission:
• Food borne
• Animal-to-human (zoonotic)
• Mother-to-child (congenital, acquired during
pregnancy, main case of human-to-human
transmission).
Transmission • Rare instances
• Organ transplant recipients can become
infected by receiving an organ from a
Toxoplasma-positive donor.
• Rarely, people can also become infected by
receiving infected blood via transfusion.
• Laboratory workers who handle infected blood
can also acquire infection through accidental
inoculation.
 Symptoms
Acute toxoplasmosis
• During acute toxoplasmosis, symptoms are often influenza-like:
• Swollen lymph nodes, or muscle aches and pains that last for a month or more.
• Severe toxoplasmosis: young children, immunocompromised patients
(individuals living with HIV/AIDS, under chemotherapy, or that recently
received an organ transplant)
• Can cause damage to the brain or the eyes
• Up to 80% of congenitally-infected newborn babies have retinochoroidal lesions/scars
vs. 2.5-20% in postnatal T. gondii infection

Latent toxoplasmosis
• In most immunocompetent patients, the infection enters a latent phase,
during which only bradyzoites are present, forming cysts in nervous and
muscle tissue.
• Most infants who are infected while in the womb have no symptoms at
birth but may develop symptoms later in life.
 Taxonomic classification
• Kingdom: Protista
Phylum: Apicomplexa
Class: Conoidasida
Subclass: Coccidiasina
Order: Eucoccidiorida
Family: Sarcocystidae
Genus: Toxoplasma
Specie: gondii
 The life cycle of T. gondii has two phases:
• Sexual part of the life cycle (coccidia like): only in
members of the Felidae family (domestic and wild
cats), the parasite's primary host.

• Asexual part of the life cycle: warm-blooded animals

(other mammals, including felines, and birds).
Life Cycle of Toxoplasma gondii

Life cycle
Enteroepithelial cycle:
only in the cat

Extraintestinal cycle: in
cat and other
mammals
 Life forms
• This parasite is polymorphic, and its life forms
are:

• Tissue Cyst or zoitocyst

• Oocysts
• Tachyzoite
• Bradyzoite
 Enteroepithelial cycle
1. only in the cat

• Tissue cysts are ingested by a cat (e.g., by feeding on an infected mouse).

• The cysts survive passage through the stomach of the cat and the parasites
infect epithelial cells of the small intestine where they undergo sexual
reproduction and oocyst formation.

Tomasina & Francia et al., 2020

 Enteroepithelial cycle - Continue
a.Cat ingests oocyst or zoitocyst  sporozoites released  invade gut
epithelial cells
b.Merogony  merozoites  rupture, release, infect
c.Gametogony (3-15 days after infection with infective oocysts)  macro- &
microgametocytes  oocyst with sporont (immature)
d.Oocyst out with host’s feces  sporogony  sporozoites

Tomasina & Francia et al., 2020

A-C occurs in jejunum, ileum and D-E in jejunum, ileum and colon.
 Oocysts
• Oocysts of Toxoplasma gondii are shed only in the feces
of domestic and wild felids, the definitive hosts.

• Oocysts are shed unsporulated in the feces and take

48-72 hours to sporulate and become infective.

• Sporulation is temperature and oxygen dependent

(optimally efficient at temperatures closer to 25°C).

• Mature oocysts measure 10-12 µm in diameter and

contain two sporocysts with four sporozoites each.

• This stage is equipped with a multilayer wall that protects

it from adverse environmental conditions, the only stage
of the whole cycle of the parasite that develops outside
the host cell!
 Extraintestinal stage
 Other warm blood animals
 host ingests oocyst or zoitocyst  sporozoites released 
penetrate gut; invade tissues (muscles; brain; lymph nodes;
tachyzoites
macrophages)
 Period of rapid merogony  merozoites = tachyzoites  rupture,
release, infect
Extraintestinal stage - Continue
Tachyzoites localize in neural and muscle tissue and develop into
tissue cyst bradyzoites

Rate of merogony slows

merozoites = bradyzoites accumulate in zoitocysts or cyst

 Tachyzoites
•Motile, asexually reproducing form of the parasite.
•These trophic forms are called tachyzoites (tachy means rapid) in reference to their high
level of replication.
• 4-8 µm long by 2-3 µm wide, with a tapered anterior end, a blunt posterior end and a
large nucleus.
•They may be found in various sites throughout the body of the host.

Dubey et al., 1998

 Tachyzoites

• In the intermediate hosts (as well the definitive

host, felines), the parasite invades cells, forming
intracellular so-called parasitophorous vacuoles.

•T. gondii propagates by a series of binary fissions

until the infected cell eventually bursts and
tachyzoites are released.

• Free tachyzoites are usually efficiently cleared by

the host's immune response, although some
manage to infect cells and form bradyzoites, thus
maintaining the infection.

Dubey et al., 1998

Tachyzoites

Scanning electron
micrograph of a
tachyzoite of
Toxoplasma gondii
(purple) adhered to a
lymphocyte (beige).
From: MacLaren et al.
(2004) Veterinary
Parasitology 125:301–
312

Attias et al., 2020

Tachyzoites

Scanning electron
micrograph of a
tachyzoite of
Toxoplasma gondii
(purple) invading a
macrophage (beige).
The cell body of the
parasite is constricted
at the point of contact
with the host cell.

Attias et al., 2020

Tachyzoites

Scanning electron
micrograph of a host
cell (beige) from which
the plasma membrane
was scrapped,
showing the
parasitophorous
vacuole with a rosette
of tachyzoites of
Toxoplasma gondii
(purple) linked to each
other by a filamentous
network (pink).

Attias et al., 2020

 Bradyzoite
• Bradyzoite is the antonym of tachyzoite; these are slow growing
forms.
• Vacuoles form tissue cysts mainly within the muscles and brain.
• Cysts are very difficult to eradicate entirely, the parasites can evade
the host’s immune system by being inside cells;

Dubey et al., 1998

 Bradyzoite
• Bradyzoite is the antonym of tachyzoite, which is a stage of rapid
growth.
• Vacuoles form tissue cysts mainly within the muscles and brain.
• Cysts are very difficult to eradicate entirely, the parasites can evade
the host’s immune system by being inside cells;
• In chronic (latent) toxoplasmosis, bradyzoite microscopically presents
as clusters enclosed by an irregular crescent-shaped wall (a
pseudocyst), in infected muscle and brain tissues.

Dubey et al., 1998

The three infective stages of Toxoplasma gondii

(a) Tachyzoite, (b) Bradyzoite, and (c) Sporozoite. The nucleus (blue) is surrounded by the rough
endoplasmic reticulum (Yelow). Above it, The Golgi complex (green) and the apicoplast (blue-green).
The single mitochondrion spreads through the cytosol (red). Dense granules (magenta) and amylopectin
granules (white) are dispersed in the cytosol. The apical complex is composed by the cilindrical conoid.
Below, the secretory organelles: micronemes (Orange) and rhoptries (pink). The cell body is limited by
three membrane units (the pellicle) and below it a set of subpelicular microtubules.

Attias et al., 2020

 Tissue Cysts or zoitocyts Dubey et al., 1998

• Usually range in size from 5-50 µm in

diameter. Cysts are usually spherical
in the brain but more elongated in
cardiac and skeletal muscles.

Unstained cyst of T. gondii.

• They may be found in various sites
throughout the body of the host but
are most common in the brain and
skeletal and cardiac muscles.

stained cyst of T. gondii.

 Tissue Cysts or zoitocyts

Sequence of cystogenesis. (1) invasion of a host cell. (2) formation of the parasitophorous vacuole. (3) Division os
parasites without formation of a residual body. (4) Thickening of the vacuolar membrane by deposition of
molecules secreted by the bradyzoites. (5) and (6) The cyst wall thickens and the bradyzoites continue to divide
slowly. (7) The fully formed cyst can fill most of the cytoplasm of the host cell.

Attias et al., 2020

Tissue Cysts or zoitocyts

Scheme of a tissue cyst of

Toxoplasma gondii. The cyst wall is
thick and filamentous. Each cyst may
contain hundreds of bradyzoites

Attias et al., 2020

Tissue Cysts or zoitocyts

Dubey et al., 1998

 Symptoms/Clinical presentation
Acute toxoplasmosis
• During acute toxoplasmosis, symptoms are often influenza-like:
• Swollen lymph nodes, or muscle aches and pains that last for a month or more.
• Severe toxoplasmosis: young children, immunocompromised patients
(individuals living with HIV/AIDS, under chemotherapy, or that recently
received an organ transplant)
• Can cause damage to the brain or the eyes
• Up to 80% of congenitally-infected newborn babies have retinochoroidal lesions/scars
vs. 2.5-20% in postnatal T. gondii infection

Latent toxoplasmosis
• In most immunocompetent patients, the infection enters a latent phase,
during which only bradyzoites are present, forming cysts in nervous and
muscle tissue.
• Most infants who are infected while in the womb have no symptoms at
birth but may develop symptoms later in life.
 Clinical presentation in adults
Latent/chronic toxoplasmosis
• Maculopapular rash;
• Hepatitis, encephalomyelitis, myocarditis;
• Retinochoroiditis (may evolve to blindness).

Recently acquired ocular

Toxoplasmosis. Retinochoroiditis with
necrosis.

Attias et al., 2020

 Clinical presentation in congenital infections
• Most infections contracted during this period are severe;

• Retinochoroiditis, encephalomyelitis, and hydrocephalus or

microcephaly are common sequelae of infection at this stage
(suggestive of toxoplasmosis when seen in young children).

• Retinochoroiditis presentations later after birth (only 20%

symptomatic);

• In newborns: fever, pneumonitis, hepatosplenomegaly,

convulsions, severe visual impairment an arrested mental
development
 Clinical presentation in congenital infections

• Toxoplasma encephalomyelitis may result in cerebral

calcifications
Clinical presentation in congenital infections

Bilateral macular scar in classical congenital toxoplasmosis. Courtesy: Prof. Rubens Belfort Jr.

Attias et al., 2020

 Cerebral Toxoplasmosis

Necrotic foci in
patient with
cerebral
toxoplasmosis
(immunocompro
mised patients)

Expansive necrosis, leading to compression of the ventricular space and deviation of the septum pellucidum.

Attias et al., 2020

 Biological modifications of the host
• Reproductive changes
• A recent study has indicated Toxoplasmosis correlates
strongly with an increase in boy births in humans.

• According to the researchers, depending on the

antibody concentration, the probability of the birth of a
boy can increase up to a value of 0.72 ... which means
that for every 260 boys born, 100 girls are born.
 Biological modifications of the host
Behavioral changes

• The parasite has the ability to change the behavior of its host: infected rats and
mice are less fearful of cats — in fact, some of the infected rats seek out cat-urine-
marked areas. This effect is advantageous to the parasite, which will be able to
sexually reproduce if its host is eaten by a cat. The mechanism for this change is
not completely understood, but there is evidence that toxoplasmosis infection
raises dopamine levels and concentrates in the amygdala in infected mice.

• The findings of behavioral alteration in rats and mice have led some scientists to
speculate that toxoplasma may have similar effects in humans, even in the latent
phase that had previously been considered asymptomatic.

• Toxoplasma is one of a number of parasites that may alter their host's behaviour as
a part of their life cycle. The behaviors observed, if caused by the parasite, are
likely due to infection and low-grade encephalitis, which is marked by the presence
of cysts in the brain.

• Cysts may produce or induce production of a neurotransmitter, possibly dopamine,

therefore acting similarly to dopamine reuptake inhibitor type antidepressants and
stimulants.
 Biological modifications of the host -
continuation

Correlations have been found between latent Toxoplasma

infections and various characteristics:

• Decreased novelty-seeking behavior

• Slower reactions
• Lower rule-consciousness and jealousy (in men)
• More warmth and conscientiousness (in women)
 Biological modifications of the host
Toxoplasma's role in schizophrenia

• The possibility that toxoplasmosis is one cause of schizophrenia has been studied
by scientists since at least 1953.

• These studies had attracted little attention from U.S. researchers until they were
publicized through the work of prominent psychiatrist and advocate E. Fuller
Torrey. In 2003, Torrey published a review of this literature, reporting that almost
all the studies had found that schizophrenics have elevated rates of Toxoplasma
infection.

• A 2006 paper has even suggested that prevalence of toxoplasmosis has large-
scale effects on national culture. These types of studies are suggestive but
cannot confirm a causal relationship (hard to establish a causal relationship).
 Biological modifications of the host
• Toxoplasma's role in schizophrenia

• Acute Toxoplasma infection sometimes leads to psychotic symptoms not unlike

schizophrenia.

• Some anti-psychotic medications that are used to treat schizophrenia, such as

Haloperidol, also stop the growth of Toxoplasma in cell cultures.

• Several studies have found significantly higher levels of Toxoplasma antibodies

in schizophrenia patients compared to the general population.

• Toxoplasma infection causes damage to astrocytes in the brain, and such

damage is also seen in schizophrenia
 Diagnosis

• Clinical
• Ocular disease is diagnosed based on the appearance of the lesions in the
eye, symptoms, course of disease, and often serologic testing.

Attias et al., 2020

 Diagnosis
• Parasitologic
• Diagnosis can be made by direct observation of the parasite in stained tissue
sections, cerebrospinal fluid (CSF), or other biopsy material. These techniques
are used less frequently because of the difficulty of obtaining these specimens.

• Parasites can also be isolated from blood or other body fluids (for example, CSF)
but this process can be difficult and requires considerable time.

• Observation of parasites in patient specimens, such as bronchoalveolar lavage

material from immunocompromised patients, or lymph node biopsy.

• Isolation of parasites from blood or other body fluids, by intraperitoneal

inoculation into mice or tissue culture. The mice should be tested for the
presence of Toxoplasma organisms in the peritoneal fluid 6 to 10 days post
inoculation; if no organisms are found, serology can be performed on the
animals 4 to 6 weeks post inoculation.
 Diagnosis
• Serology

• Serologic testing is the routine method of diagnosis, because the techniques

described above are technically complex and generally not rewarding.

• A test that measures immunoglobulin G (IgG) is used to determine if a person has

been infected.

• If it is necessary to try to estimate the time of infection, which is of particular

importance for pregnant women, a test which measures immunoglobulin M (IgM) is
also used along with other tests such as an avidity test.
 ELISA
(Enzyme-linked immuabsorbent assay)
Direct method (detect antibodies)

Chromofor

Enzyme
(peroxidase or phosphatase)
Antibody
anti-human

Antibody
(patient)

Antigen
(parasite) Support
Indirect Imunoflurescence

Objetive
lens Light
Ab2 linked to
Ab1 fluorochrome
Ag
(microorg.) slide

UV
Light
A: Formalin-fixed T. gondii
B: Negative IFA for
tachyzoites, stained by
antibodies to T. C: Negative IFA for
immunofluorescence (IFA). This is antibodies to T. gondii,
a positive reaction (tachyzoites + gondii.
polar stain reaction.
human antibodies to Toxoplasma
+ FITC-labelled antihuman IgG =
fluorescence.)
 Diagnosis

• Molecular
• The parasite's DNA can be detected by PCR in the amniotic fluid; it can be
useful in cases of possible mother-to-child (congenital) transmission.
 Polymerase Chain Reaction (PCR)

3’ 5’

heat DNA Heat and

DNA
polymerase
polymerase

5’ 3’ Primers hybridise Primers grow to

single strands become
DNA complementary
strands

heat

DNA
polymerase

Exponential Primers hybrideze

with new and old
Amplification
strands
 Treatment
• Treatment is often only recommended for people with
serious health problems, with impaired immune responses.

• Medications that are prescribed for acute Toxoplasmosis are:

• Pyrimethamine — an antimalarial medication.

• Sulfadiazine — an antibiotic used in combination with pyrimethamine to treat
toxoplasmosis.
• Clindamycin — an antibiotic. This is used most often for people with HIV/AIDS.
• Spiramycin — another antibiotic. This is used most often for pregnant women to
prevent the infection of their child.
 Treatment

• In people with latent toxoplasmosis, the cysts are immune to

these treatments, as the antibiotics do not reach the
bradyzoites in sufficient concentration.

• Medications that are prescribed for latent Toxoplasmosis are:

• atovaquone — an antibiotic that has been used to kill Toxoplasma cysts inside
AIDS patients.

• clindamycin — an antibiotic which, in combination with atovaquone, seemed to

optimally kill cysts in mice

• However, in latent infections successful treatment is not

guaranteed, and some subspecies exhibit resistance.
 Prophylaxis
People who are healthy should follow the guidelines below to reduce risk of
toxoplasmosis. If you have a weakened immune system, it is recommended to see
guidelines for Immunocompromised Persons.

Reduce Risk of Toxoplasmosis from Food

• To prevent risk of toxoplasmosis and other infections from food:
• Cook food to safe temperatures. A food thermometer should be used to measure
the internal temperature of cooked meat. Do not sample meat until it is cooked.
• Beef, lamb, and veal roasts and steaks should be cooked to at least 145°F throughout.
• Pork, ground meat, and wild game should be cooked to 160°F.
• Whole poultry should be cooked to 180°F in the thigh.

• Peel or wash fruits and vegetables thoroughly before eating.

 Prophylaxis
Reduce Risk of Toxoplasmosis from Food

• Wash cutting boards, dishes, counters, utensils, and hands with hot soapy water
after contact with raw meat, poultry, seafood, or unwashed fruits or vegetables.

• Freeze meat for several days before cooking to greatly reduce chance of infection
(-21°C for 28 days for oocysts, though the muscle cysts are killed by freezing at -6
°C for 1 day or immediately at –21°C).

• The U.S. Government and the meat industry continue their efforts to reduce T.
gondii in meat.
 Prophylaxis
How to reduce Risk of Toxoplasmosis from the Environment

• Avoid drinking untreated drinking water, particularly when traveling in less

developed countries.

• Wear gloves when gardening and during any contact with soil or sand because it
might be contaminated with cat feces that contain Toxoplasma. Wash hands
thoroughly after gardening or contact with soil or sand.

• Keep outdoor sandboxes covered.

• Feed cats only canned or dried commercial food or well-cooked table food, not
raw or undercooked meats.

• Change the litter box daily if you own a cat. The Toxoplasma parasite does not
become infectious until 1 to 5 days after it is shed in a cat's feces.
 Prophylaxis
How to reduce Risk of Toxoplasmosis from the Environment

• If you are pregnant or immunocompromised:

• Avoid changing cat litter if possible. If no one else can

perform the task, wear disposable gloves and wash your
hands thoroughly with soap and water afterwards.

• Keep cats indoors.

• Do not adopt or handle stray cats, especially kittens. Do not get

a new cat while you are pregnant.
• Cats eliminate oocysts for about 2 weeks following a primary infection; however,
on reinfection, because of developing immunity cats shed fewer oocysts, or none
at all, and for a shorter time.
Cryptosporidiosis
Dr. Rosa A. Maldonado
What is Cryptosporidiosis?
• It is a diarrheal disease caused by microscopic parasites of
the genus Cryptosporidium

• Many species of Cryptosporidium exist that infect humans

and a wide range of animals.

• The parasite is protected by an outer shell that allows it to

survive outside the body for long periods of time and makes
it very resistant to chlorine disinfection.

• This parasite can be transmitted in several different ways,

however water is a common method of transmission.

• Cryptosporidium is one of the most frequent causes of

waterborne disease (drinking water and recreational water)
among humans in the United States.
• Cryptosporidium parvum and Cryptosporidium hominis are the most
prevalent species causing disease in humans

• infections by C. felis, C. meleagridis, C. canis, and C. muris have also

been reported.
• Sporulated oocysts, containing 4 sporozoites, are excreted by
the infected host through feces and possibly other routes such
as respiratory secretions.

• Transmission of Cryptosporidium parvum and C. hominis occurs

mainly through contact with contaminated water (e.g., drinking
or recreational water). Occasionally food sources, such as
chicken salad, may serve as vehicles for transmission.
• Many outbreaks in the United States have occurred in
waterparks, community swimming pools, and day care centers.

• Zoonotic and anthroponotic transmission of C. parvum and

anthroponotic transmission of C. hominis occur through
exposure to infected animals or exposure to water
contaminated by feces of infected animals.
• Following ingestion (and possibly inhalation) by a suitable host, excystation occurs.

• The sporozoites are released and parasitize epithelial cells of the gastrointestinal tract or
other tissues such as the respiratory tract.

• In these cells, the parasites undergo asexual multiplication (schizogony or merogony) and
then sexual multiplication (gametogony) producing microgamonts (male) and
macrogamonts (female)

• Upon fertilization of the macrogamonts by the microgametes, oocysts develop that

sporulate in the infected host.

• Two different types of oocysts are produced, the thick-walled, which is commonly excreted
from the host and the thin-walled oocyst, which is primarily involved in autoinfection.

• Oocysts are infective upon excretion, thus permitting direct and immediate fecal-oral
transmission.

• Note that oocysts of Cyclospora cayetanensis, another important coccidian parasite, are
unsporulated at the time of excretion and do not become infective until sporulation is
completed.
Cryptosporidium pathogenesis

Glucose-coupled Na+
absorption is decreased and
Cl- secretion is increased.
Diarrhea is due to osmotic
disequilibrium

Many factors may be involved in the diarrhea associated with cryptosporidiosis. (Modifie
from Clark and Sears, Parasitology Today 12:221, 1996.)
 Cryptosporidium pathogenesis
• The watery nature of the diarrhea associated with Cryptosporidium
infections has suggested the presence of an enterotoxin.

• However, there is no evidence for a toxin-mediated secretory diarrhea

despite efforts to identify such a toxin.

• Associated with this disruption of enterocyte (i.e., intestinal epithelial

cells) function is a blunting of the villi and crypt cell hyperplasia.

• A possible mechanism of pathogenesis is that the infection of

intestinal epithelial cells with Cryptosporidium damages the
enterocytes and eventually leads to their death. This triggers cell
division in the crypt region (i.e., hyperplasia) to replace the damaged
cells. The combination of destruction of absorptive cells at the tips of
the villi and the increase in the Cl--secreting crypt leads to an overall
enhanced secretion.

• increased intercellular permeability and inflammation in the

submucosal layer could also contribute to the secretory process via
cytokines and neurohormones
Epidemiology
• Since the first reports of human cases in 1976

• Cryptosporidium has been found worldwide.

• Outbreaks of cryptosporidiosis have been reported in

several countries, the most remarkable being a waterborne
outbreak in Milwaukee (Wisconsin) in 1993, that affected
more than 400,000 people.
 Disease
• Infection with Cryptosporidium sp. results in a wide range of manifestations, from
asymptomatic infections to severe, life-threatening illness.

• Incubation period is an average of 7 days (but can range from 2 to 10 days).

• Watery diarrhea is the most frequent symptom, and can be accompanied by

dehydration, weight loss, abdominal pain, fever, nausea and vomiting.

• In immunocompetent persons, symptoms are usually short lived (1 to 2 weeks); they

can be chronic and more severe in immunocompromised patients, especially those with
CD4 counts <200/µl.

• While the small intestine is the site most commonly affected, symptomatic
Cryptosporidium infections have also been found in other organs including other
digestive tract organs, the lungs, and possibly conjunctiva.
 Diagnosis

• Acid-fast staining methods, with or without stool concentration,

are most frequently used in clinical laboratories.

• For greatest sensitivity and specificity, immunofluorescence

microscopy is the method of choice (followed closely by enzyme
immunoassays).

• Molecular methods are mainly a research tool.

• Antibody detection: There are currently no commercially available
serologic assays for the detection of Cryptosporidium-specific
antibodies.

• However, immunoblots for detecting the 17 and 27 kDa sporozoite

antigens associated with recent infection may be useful for
epidemiologic investigations.
 Treatment

• There's no reliable treatment for cryptosporidiosis, and

recovery usually depends on the health of your immune
system. Most healthy people recover within 10 days to two
weeks without medical attention.

• If you have a compromised immune system, the illness can

endure and lead to significant malnutrition and wasting.
The goal of treatment is to alleviate symptoms and
improve your immune response.
 Treatment
• Cryptosporidium treatment options include:

• Anti-parasitic drugs. These medications can help alleviate diarrhea by attacking the
metabolic processes of the cryptosporidium organisms. These drugs include nitazoxanide
(Alinia), paromomycin (Humatin) and azithromycin (Zithromax).

• Anti-motility agents. These medications slow down the movements of your intestines and
increase fluid absorption to relieve diarrhea and restore normal stools. These medications
include loperamide and its derivatives (Anti-Diarrheal Formula, Imodium).

• Fluid replacement. You'll need replacement of fluids and electrolytes — minerals such as
sodium, potassium and calcium that maintain the balance of fluids in your body — lost to
persistent diarrhea, either orally or intravenously. These precautions will help keep your
body hydrated and functioning properly.

• Anti-retroviral therapies . If you have HIV/AIDS, highly active anti-retroviral therapy

(HAART) can reduce the viral load in your body and boost your immune response. Restoring
your immune system to a certain level may completely resolve symptoms of
cryptosporidiosis.
 Prophylaxis
• Cryptosporidium infection is contagious, so take precautions to avoid spreading
the parasite to others.

• All preventive methods aim to reduce or prevent the transmission of the

cryptosporidium germs that are shed in human and animal feces. Precautions are
especially important for people with compromised immune systems.

• Follow these suggestions:

• Practice good hygiene. Wash your hands with soap and water after using the toilet,
changing diapers and before and after eating.
• Thoroughly wash all fruits and vegetables that you will eat raw.
• Purify drinking water if you have a weakened immune system or are traveling in an area
with a high risk of infection. Methods include filtering and boiling (at least one minute at a
rolling boil).
• Limit swimming activities in lakes, streams and public swimming pools, especially if the
water is likely to be contaminated or if you have a compromised immune system.
• Avoid fecal exposure during sexual activity.
• Handle newborn farm and domestic animals with care. Be sure to wash your hands after
handling the animal