You are on page 1of 23

STUDENT PROJECT

CRYPTOSPORIDIUM INFECTION

SGD B5
Group Members:
JOHANES PRASETYO HARJANTO (1702511096)
JONATHAN YOSHUA PATUAN (1702511098)
PUTU NADIRA WIDYAKANIA (1702511100)
PUTU BAGUS BRAMANTHANA TIRTHA (1702511101)
I KETUT RAMA ARDIANA (1702511105)
NI MADE WINI JAYESTHIWI WANAMI PUTRI (1702511107)
MADE SABRINA PRATIVA PRASADITYA A. (1702511111)
GABRIELA QUEENSANYA LIENARDY (1702511113)
KRISTOFORUS WILLIAM (1702511114)
STEVEN VALENTINO HARTONO (1702511116)
YAALINI MURASOLI MARAN (1702511226)
DHARSNEE PERIMAISIVAM (1702511227)

PROGRAM STUDI PENDIDIKAN DOKTER


FAKULTAS KEDOKTERAN
UNIVERSITAS UDAYANA
2018
PREFACE

“Om Swastyastu”
First of all, we want to show our gratitude to God because only by God’s
graces and blessings we were able to finish our Student Project in the Biomedik II
block. We made this paper to fulfill the needs of our assignment marks in this block
and also to spread information to the readers about the related topic. This Student
Project mainly Cryptosporidium and the infection it causes in humans. By reading
this paper, we hope the readers may either know something about this topic deeper
or add some new information they have not known before.
We are very grateful that we still be able to finish this assignment properly
even though we met several obstacles. Of course, we need some help from others.
Therefore, we would like to thank:
1. dr. Ni Luh Ariwati, as our evaluator in this Student Project and lecturer who
guided us in making this assignment, evaluated it, and gave us some
feedbacks,
2. dr. I Wayan Gede Sutadarma, M.Gizi, as our facilitator and supervisor who
also gave us guidance through this whole block, especially in making this
Student Project,
3. All lecturers in the Biomedik II block for the valuable information they had
given us,
4. Our beloved friends, especially from Program Studi Pendidikan Dokter year
2017, who also participated in the making of this Student Project.
We realize that there are many weaknesses and faults we made in doing this
assignment, and thus we apologize for such things. In the end, we hope the readers
can give us advices and suggestions to help us become better writers.
”Om Shanti, Shanti, Shanti Om”

Denpasar, 12 January 2018


Writers

i
TABLE OF CONTENTS

COVER
PREFACE ..........................................................................................................i
TABLE OF CONTENTS ..................................................................................ii
LIST OF PICTURES ........................................................................................iii
LIST OF TABLE ..............................................................................................iv
CHAPTER I: INTRODUCTION
Background .............................................................................................1
Purposes ..................................................................................................2
Benefits....................................................................................................2
CHAPTER II: CONTENT
Epidemiology ..........................................................................................3
Characteristics of Cryptosporidium ........................................................4
Etiology ...................................................................................................6
Life Cycle ................................................................................................6
Transmission ...........................................................................................11
Pathology and Symptoms ........................................................................11
Diagnosis and Detection..........................................................................12
Treatment and Prevention .......................................................................14
CHAPTER III: CONCLUSION
Conclusion ...............................................................................................15
Advices and Suggestions ........................................................................15
REFERENCES

ii
LIST OF PICTURES

Picture 2.1 The Life Cycle of Cryptosporidium ................................................7

iii
LIST OF TABLE
Table 2.1 Spesies Cryptosporidium, Rute Infeksi Serta Gejala
Yang ditimbulkan ........................................................................ 4

iv
CHAPTER I
INTRODUCTION

1.1. Background
Indonesia is a tropical country that almost in every year are facing many kinds
of infectious or non-infectious disease. Most of the infectious disease caused by
bacteria, viruses, parasite and fungi. But, even though nowadays the technologies
and studies are improving well, there are still many disease that still not recognize
by the society. Some of the example are infection that caused by a parasite called
as Cryptosporidium sp.1
Cryptosporidium is can cause one of the emerging zoonotic disease in
worldwide. Cryptosporidiosis is a highly prevalent and extremely widespread
disease documented by over 1000 reports in humans in 95 countries on all
continents except Antarctica. Considering that cryptosporidiosis is primarily spread
by ingestion of contaminated water, was ranked fifth among the 24 most important
food-borne parasites in a global ranking by a joint Food and Agriculture
Organization (FAO)/World Health Organization (WHO) expert committee in
2012.2 Infectious agents transmitted from animals to humans usually called as
zoonotic disease. Cryptosporidiosis can be transmitted by domestic and wild
ruminants (sheep, goats, mouflon sheep, blesboks, nyalas, white-tailed deer, Père
David’s deer, sika deer, ibexes, buffalos, and yaks), rodents (squirrels, chipmunks,
woodchucks, beavers, porcupines, deer mice, house mice, and gerbils), carnivores
(raccoons), and primates (lemurs and humans).3
Of approximately 8 million worldwide annual deaths of children under 5 years
of age, diarrhea is associated with 10-5%. An epidemiological study of over 22.000
infants and children in Africa and Asia found that Cryptosporidium was one of the
four pathogens responsible for most of the severe diarrhea and was considered the
second greatest cause of diarrhea and death in children after rotavirus. In developing
countries cryptosporidiosis is reported to account for 20% of all cases of diarrhea
in children and, depending on location, at some point in life the percentage of
affected persons in a population was estimated to range from 20–90%.1

1
Cryptosporidiosis will become a serious problem in Indonesia if we are not
aware with the disease and the parasite. From this paper we would like to give some
explanation about Cryptosporidium and also the disease that can caused by
Cryptosporidium.

1.2. Purpose
1. To understand the definition, morphology, until the pathogenesis of
Cryptosporidium.

1.3. Benefits
1. For student, to add more information and knowledge about
Cryptosporidiosis.
2. For lecturer, lead to the importance of this disease, the lecturer can add this
material to the study goal of the medicine student.

2
CHAPTER II
CONTENT

2.1. Epidemiology
The distribution of the Cryptosporidium sp. is commonly very wide and it is
found in every each part of the world, therefore the prevention is quite hard because
it needs to involve the individual sanitation and hygiene. The distribution is
especially high in developing countries. What should be noted is that in many
developing or even developed countries, there are no constant surveillance to detect
Cryptosporidium. The distribution also varies geographically. In the United
Kingdom, it is found that the most common Cryptosporidium is C. parvum and C.
hominis. In other European countries, it is found that C. parvum dominated, but in
countries like America, China, Japan, and Australia is more dominated by C.
hominis. Also, within a single country the finding varies, like in the country like
United States, New Zealand, and Ireland the C. parvum is more common in rural
areas.4
Cryptosporidiosis occurs more frequently in children and infants than in
adults, regardless from developing or developed countries. It usually occurs to child
aging from 1 to 9 and also seems to peak during summer seasons due to public
swimming venues. Globally, there is 1 among 5 children who suffers diarrheal
result in death during the first 5 years of life and occurs mostly in sub-Saharan
Africa and South Asia. To be noted is that Cryptosporidium is dangerous regardless
of the HIV effects because it was the second most common pathogen in infants with
increased risk of death around toddlers’ age 12-23 months.4
Cryptosporidiosis is the most common main cause of diarrheal disease and
has an even worse effect on immune compromised people. Besides HIV-infected
people, those individuals that are also put at a high risk are those that suffer X-
linked hyper immunoglobulin M syndrome, children with leukaemia, and organ
transplant recipients. For the HIV-infected people, the severity and prolonged
chance of the disease is dependent on the CD4 count. The normal rate of CD4 count
in human body is around 500 to 1500, while in HIV-infected people the CD4 count
is only 200 or less. If the count is below 50 it can greatly increase the severity and

3
prolonged chance. The parasite can also colonize the extra intestinal sites like gall
bladder, biliary tract, pancreas, and lungs.4
We know that many people often travels from their home countries to other
cities or other countries, data states that around year 2011 about 980 million people
travelled internationally. TD (Traveller Diarrhoea) is mostly caused by Giardia and
Cryptosporidium. Travelling increases the risk factor for acquiring infection also
with spore-forming protozoa such as Cyclospora. Studies has shown that a great
portion of these travellers complained about having GI problems and harbor
intestinal pathogens. There is even a proof of a novel type of Cryptosporidiosis
found in the gastro-intestinal of a traveller returning UK from Indian subcontinent.
It is called Cryptosporidiosis viatorum which is a form of that has different
symptoms from C. parvum and C. hominis because the patient vomits less but the
duration disease lasts longer.4

2.2. Characteristics of Cryptosporidium


Cryptosporidium is a pathogen of the apicomplexan genus. These
intracellular parasites can be distributed to reptiles, fish, birds and mammals. Until
today, more than 20 Cryptosporidium species have been identified: C. parvum, C.
hominis, C. felis, C. canis, C. wrairi, C. saurophilum, C. suis, C. scophthalmi, C.
bovis, C. andersoni, C. muris, C. serpentis, C. molnari, C. galli, C. meleagridis, C.
baileyi, C. ubiquitum, C. meleagridis, C. scrofarum, C. cuniculus and C. fayeri.
Among the species that have been successfully identified, there are several species
that can infect humans such as C. parvum, C. muris, and C. hominis. The species is
distinguished by oocysts and their pathogenesis properties. C. parvum will be more
pathogenic than C. muris, whereas C. hominis are pathogenic especially to children.
In addition to the discovery of several species from Cryptosporidium, several
studies have suggested that Cryptosporidium has several subtypes, such as C.
parvum which have subtypes IIa, IIc and IId and C. hominis which have subtypes
Ia, Id, Ie. The subtype is capable of generating different symptoms of infected
patients.5-6, 8
In the human body, Cryptosporidium sp may be present in the small intestine,
esophagus, pharynx, jejunum, ilium, appendix, gallbladder, rectum and pancreatic

4
ducts. If the individual is immunocompetent, then the parasite will be found only in
the small intestine. In immunocompromised individuals parasites can be found in
the digestive and respiratory tract.7

Table 2.1 Spesies Cryptosporidium, Rute Infeksi Serta Gejala Yang


ditimbulkan.22

The infective form of Cryptosporidium is oocyst. Oocyst is excreted through


stools of individuals infected with Cryptosporidium. Cryptosporidium can be
transmitted through the air, drinks, food, hands and impurities of an infected
individual through an anal sex relationship contaminated with Cryptosporidium.9
The disease that can be caused by Cryptosporidium is cryptosporidiosis, which is

5
an opportunistic infection found in humans and animals. Cryptosporidiosis causes
diarrhea in children. The diarrhea experienced may be acute diarrhea and chronic
diarrhea. In immunocompromised people, diarrhea can heal on its own but in
immunocompromised individuals it may continue to be chronic and may lead to
death.6
The reason of why Cryptosporidium parvum cause the most severe symptoms
of diarrhea are Cryptosporidium parvum has more pathogenic properties than
Cryptosporidium muris, other than that, Cryptosporidium parvum also more
resistant to disinfectant.23

2.3. Etiology
Cryptosporidium mostly found in contaminated drinking water, eating
uncooked food that contains of Cryptosporidium, soil or surfaces that has been
contaminated with feces from infected humans or animals and possibly from
developing country which is still lack for sanitation.9-11 An impact from climate and
weather transmission also could infect from Cryptosporidium, for example, the rain
peaks, increased pollution from farm waste, or calving and lambing activities.
Cryptosporidium is transmitted from person-to-person contacts and it is not spread
by contact with blood.9,12 Cryptosporidium can be spread by putting something into
the mouth or swallowing something that has a contact with a person or animal that
has been infected, touching surfaces, or changing diapers for baby.9

2.4. Life Cycle


Cryptosporidium has a monoxenous life cycle. This means this parasite lives
in only one kind of host throughout its whole life cycle. Cryptosporidium life cycle
is completed in the gastrointestinal tract of human body. The only exogenous stage
of Cryptosporidium life cycle is the oocyst form. The oocyst is characterized by
distinct inner and outer layers with four mature and infectious sporozoites. It is
about 4 – 6 m in diameter. This is the infective form of Cryptosporidium.13
First, the oocysts which contain four sporozoites are excreted by the infected
host through several ways. The oocysts are excreted mostly through feces. Besides,
they may also be excreted through respiratory secretions. These oocysts are

6
transmitted mainly through contacts with contaminated water, such as drinking
water and recreational water, like swimming pools or waterparks. In the United
States, there are many outbreaks have happened in these recreational places and
also in day care centers. Several food sources can also become Cryptosporidium
transmission agents, for example chicken salad.14
After the oocysts enter host body through ingestion or possible inhalation,
excystation occurs, influenced by the exposure to gastric acid, bile salts, and/or
proteolytic enzymes in host upper gastrointestinal tract. Excystation is when the
sporozoites are released from the oocysts. The sporozoites escape the oocysts
through small sutures in the end of the oocysts wall (one suture for each oocyst).
The sporozoites are motile, they then attach their apical membrane selectively to
the enterocytes’ (simple columnar epithelium in small intestine, known as intestinal
absorptive cells) apical membrane luminal surface. They may also parasitize the
epithelial cells of the other gastrointestinal tract parts and other tissues, such as the
biliary tract, pancreatic duct, sinuses, and respiratory tract. The apical complex of
sporozoites then release membrane-lysing molecules causing the epithelial cells
membranes and microvilli to indent and fold around the sporozoites. The
sporozoites will be located in parasitophorous vacuoles (PVs). It is intracellular, but
in extracytoplasmic compartment, below the cells’ outer membrane. The PVs are
structures made by the parasites in order to protect themselves from
phagolysosomes inside the cells, and also to allow parasites development. The
parasites also form feeder organelles which are located at the base of the PVs (one
feeder organelle for each PV). The feeder organelles are distinctive electron-dense
structures that allow exchange of molecules between the developing intracellular
parasites and the host cells. Next, after invasion, the sporozoites differentiate into
rounded trophozoites. Then, the parasites undergo asexual multiplication,
merogony or schizogony. Firstly, the trophozoites become type I meronts or
schizonts, containing six to eight merozoites. The merozoites are quite similar to
sporozoites, they are curved and have double inner membranes, apical complex of
rings, and micronemes (protein that supports the cellular processes, like invasion,
migration, etc.).15

7
Picture 2.1 The Life Cycle of Cryptosporidium.2

The rupture of type I meronts release mature merozoites. These mature


merozoites then invade the adjacent epithelial cells and become either type I or type
II meronts. The cycling of this type I meronts shows how this parasite persists in
human body (Cryptosporidium parvum). The type II meronts invade the host cells
and then undergo sexual cycle (gametogony). The type II meronts firstly become
microgamonts (male) and macrogamonts (female), it can be seen as early as 36
hours after infection. The gamonts then attach and fuse together. The fertilization
of the macrogamonts by the microgametes (produced by the microgamonts) results
in zygotes forming. The zygotes later develop into sporulated oocysts in the infected
host, containing four fully developed and infectious sporozoites. There are two
types of oocysts, thick-walled and the thin-walled oocysts. The thick-walled
oocysts are excreted from the host to the environment. They are capable to survive
for long periods outside. They are also in infective forms. Therefore, the parasites
may be transmitted to another host and infect the new host through fecal-oral
transmission. Usually, for humans, the time counted from infectious oocysts
ingestion to its excretion (prepatent period) is 4 – 22 days. Otherwise, the thin-

8
walled oocysts are primarily involved in autoinfection of the intestine, providing a
second mechanism. The parasites can auto-infect the host, and result in similar
infection.13
2.4.1 Extra Intestinal Infection
Not only in intestine, the Cryptosporidiosis can be happen as
well in another organ such as lung, and hepar (biliary tree). The
infection happen due to patient immune system, in
immunocompromised patients the possibility to get any extra
intestinal infection are even more than the immunocompetent patient.
We give a case of extra intestinal Cryptosporidiosis to give a clear
understanding about the pathogenesis of Cryptosporidium.
A 35‑year‑old non‑alcoholic rural male presented with 5‑days
history of intermittent fever with chills, cough with expectoration and
breathlessness. After admission patient had history of four episodes of
profuse watery diarrhea associated with nausea and one episode of
watery vomiting. There was no history of hemoptysis, blood in stool,
and weight loss. He had a history of farming before hospitalization.
He was not suffering from any chronic illness and had no addiction to
any drugs.24
Sputum samples were examined for the presence of bacteria,
fungus, mycobacterium and nocardia with Grams staining,
Ziehl‑Neelsen (ZN) staining, and modified acid‑fast stains (kinyon
stain). Sputum culture was done for these organisms according to their
specific culture media. Microscopic examination of sputum smear
stained with ZN and modified ZN staining showed of 4‑6 μ, circular
and acid‑fast structures. These structures were identified as oocysts of
Cryptosporidium parvum. Modified ZN staining of stool smear also
showed a lot of Cryptosporidium oocysts. The presence of acid‑fast
structures of Cryptosporidium oocysts were confirmed on repeat
modified ZN staining of sputum and stool sample after 2 days. No
pathogenic bacteria including mycobacterium tuberculosis were
grown in culture. Blood and urine culture were sterile for any

9
pathogenic bacteria. Chest X‑ray PA view revealed right lower zone
consolidation. After conformation of Cryptosporidium infection, he
was treated with nitazoxanide for 3 days. He became asymptomatic
with complete resolution of opacities on chest X‑ray after treatment.
Oocysts were no longer detected in stool and sputum.24
From one of the case above, that is a case of extra intestinal
infection from Cryptosporidium in lung. Ingestion can occur via
person‑to‑person, zoonotic, waterborne, food‑borne and airborne
contact. Cryptosporidium usually infect small gastrointestinal tract
epithelium, multiplies within the macrophages and causes diarrheal
diseases. Theses spores can migrate to the whole gastrointestinal tract,
respiratory epithelium, and biliary tract. Severity of diseases depends
on the immunity of the patients. In immunocompetent individuals
rapid clearance of the organism is responsible for asymptomatic and
self‑limiting disease.25 Pulmonary cryptosporidiosis rarely reported
and commonly associated with diarrhea. The pathogenesis of lung
disease is not fully understood. The lung diseases can occur due to the
inhalation of spores or migration of oocysts from gastrointestinal tract
through circulating phagocytes. The common presenting symptoms of
pulmonary cryptosporidiosis are non‑specific and typically include
chronic cough, fever, and dyspnea. Radiological changes may or may
not occur.26
In patients with AIDS or other immunocompromised state,
including immunodeficiency syndrome and solid organ
transplantation, the organism has been known to infect the biliary tree,
producing a syndrome similar to PSC. The incidence of biliary tree
Cryptosporidiosis is particularly high in patients with X-linked hiper-
IgM syndrome; these patients lack the CD40 receptors CD40L
interaction in the immune response to Cryptosporidium. Sign and
symptom include right upper quadrant abdominal pain, nausea,
vomiting, fever and biochemical evidence of anicteric cholestasis.27

10
2.4.2 Auto Infection
Cryptosporidium completed the life cycle in the host by producing two
types of oocyst, which is thick-walled oocyst are shed in the feces and
waiting the indigestion of another host, while thin-walled oocyst continued
in the infected host and causing the autoinfection.28 The autoinfection itself
could be worse in the infected host by infected extraintestinal site of human
body, like the conjunctiva of the eye, respiratory tract, gall bladder, lymph
nodes, testicle, ovary, uterus and vagina.29

2.5 Transmission
Parasites of Cryptosporidium are usually transmitted by infected human or
animal stool. Cryptosporidium can be found in many places like in soil, food, water,
or even every surfaces that have ever been in contact and contaminated by feces of
infected human or animal. Fortunately Cryptosporidium cannot spread by contact
with blood. Water that is categorized as contaminated include water that is not
boiled or filtered. Cryptosporidium are also found throughout the world. That’s
why travellers in developing countries usually has a higher risk to get infected by
Cryptosporidium parasites. Also, immunocompromised people are at risk for severe
disease.9
There are many ways Cryptosporidium can be spread, for example:
swallowing something that has been in direct contact with contaminated feces of
infected person or animal, drinking contaminated water or beverages, and eating
uncooked food that has been contaminated by Cryptosporidium parasites.9

2.6. Pathology and Symptoms


Cryptosporidium infection in healthy individuals causes gastrointestinal illness.
Watery diarrhea is a characteristic of this infection, and it may be profuse and
prolonged. Other common symptoms are low-grade fever, nausea, vomiting and
abdominal pain. Nonspecific symptoms such as myalgia, malaise, headache,
weakness, and anorexia may also occur. Symptoms in immunocompromised
patients, HIV/AIDS patients for example, may be more severe, prolonged, and even
life-threatening.16-18 They experience a transient self-limiting illness.16 There are
some cases of asymptomatic infections.17 Cryptosporidium can also cause reactive

11
arthropathy.17,18 Cryptosporidiosis causes profuse watery diarrhea due to
malabsorption. Most cases report that the diarrhea spontaneously resolves itself
within 7 to 14 days. Immunocompromised patients, particularly HIV/AIDS
patients, can experience chronic diarrhea that may last for months to years without
proper treatment. Biliary and pulmonary complications can also happen in
immunocompromised patients. Said complications include malnutrition, cognitive
impairment, and hindrance to growth. Cryptosporidiosis appears to be related with
more chronic symptoms and higher rate of mortality than other causes of diarrhea
in children. Mortality can happen in the early infection stages particularly in
immunocompromised patients.21

2.7. Diagnosis and Detection


2.7.1 Detection of Cryptosporidium with microscopic method

Histological studies were conducted with fecal specimens of


Cryptosporidium oocysts, organisms that often cause fatal watery diarrhea
in AIDS patients, to better distinguish them from yeasts. The specimens
were from 3 patients with AIDS or suspected AIDS. The method used were
bright field and Nomarski interference contrast microscopy of wet-mounted
stools preserved in 10% formalin and stained by Giemsa and by the Neelsen
modified acid-fast technique. Electron microscope sections were postfixed
in osmium tetroxide. Ultra-thin sections were stained with and lead citrate
before microscopic examination. Oocysts appeared under bright field
microscopy as 3 x 4 mcm ellipsoidal bodies with a central large round
granule, known as the residuum, and 1-4 granules. Interference contrast
microscopy revealed banana-shaped sporozoites surrounding the residuum,
clearly differentiating them from yeasts. Acid-fast stain turned the crescent-
shaped sporozoites red and the residuum deep red, while yeasts stained blue.
Cryptosporidium could easily by distinguished from yeast ultrastructurally
by their double cell wall. Thus, interference microscopy and acid-fast
staining are helpful to separate Cryptosporidium from similar sized yeasts,
an alternative to intestinal biopsy which has formerly been required to
diagnose this parasite in immune-compromised patients. 30

12
2.7.2 Detection of Cryptosporidium with ELISA method

ELISA method in detection of cryptosporidium using stool specimen


and screen the helminthic egg using saline and iodine wet mount. Modified
acid-fast staining was performed on the direct stool smears and screening
was done for Cryptosporidium oocyst, which were spherical to elliptical and
stained bright pink against a blue background. Cryptosporidium antigen
detection by ELISA in a study from Department of Biochemistry and
Microbiology, University of Forth Hare, showed a sensitivity as high as
92.3% in HIV-positive subjects, however this technique does not tell if an
infection is active, passive or the antigen presence is as a result of a previous
infection. Remarkably, control subjects were all negative to
Cryptosporidium antigen. The pattern of result shown by ELISA confirm
that fluorescent monoclonal methods increase the sensitivity and specificity
of Cryptosporidium oocyst detection and hence provide excellent screening
techniques and offer useful data for epidemiological studies, and
consequently, control of the parasite.31

2.7.3 Detection of Cryptosporidium with PCR method

PCR diagnosis of Cryptosporidium studies that conducted at Murdoch


University, Fecal samples were diluted 1 in 4 in phosphate-buffered saline,
and 20 μl of this suspension was used for DNA extraction. A modification
of a previously described fecal extraction procedure was employed. Briefly,
20 μl of the fecal suspension was added to 80 μl of 10%
polyvinylpolypyrrolidone (PVPP) in distilled water and boiled for 10 min.
This solution was spun for 30 second, and the supernatant was added to a
tube containing 200 μl of Al buffer and 10 μl of glassmilk. The sample was
vortexed, incubated at 72°C for 5 min, and spun for 1 min, and the pellet
was washed twice with 700 μl of AW wash buffer. The pellet was then
vacuum dried, and the DNA was eluted by adding 50 μl of AE elution buffer
incubating the solution at 72°C for 10 min, spinning for 1 min, and
transferring the supernatant to a fresh tube. A 2,5-μl aliquot of the eluate

13
was used for PCR analysis. The primers used in this study had previously
been extensively tested for specificity and sensitivity. PCR amplification
conditions were as previously described. Duplicate reactions were run for
each sample, one consisting of the test sample and a second reaction mixture
containing the test DNA which was spiked with Cryptosporidium DNA in
order to rule out PCR inhibition.32

2.8. Treatment and Prevention


Ways to treat cryptosporidiosis are still limited; there is no fully effective drug
treatment or a vaccine. Among HIV-infected patients, highly active antiretroviral
therapy (HAART) has been a tremendous help against cryptosporidiosis.
Unfortunately, utilization of HAART requires great cost, which in turn makes it not
readily available in poor regions that needs help the most. Currently, the thiazole
compound, nitazoxanide (NTZ) is the only approved drug by the US Food and Drug
Administration for use against cryptosporidiosis in immunocompetent patients, but
it is not yet licensed in Europe.18 It has been shown that nitazoxanide increased both
clinical and microbiological cure rates and reduced the severity and duration of
symptoms in immunocompetent patients. On the other hand, patients with HIV are
unaffected by nitazoxanide, even with high doses and prolonged treatment.20
Immunocompromised patient needs to undergo a specific chemotheraphy.
There are three cases for patient with AIDS, First one is Intestinal
Cryptosporidiosis. They need to use a paramomycin and azithromycin for a month,
and those treatment need to be accompanied with HAART to increase the patient’s
immunity. The second is pulmonary Cryptosporidiasis. For this case, the same
treatment as the first one can improve the condition of the patient. A massive
healing can be seen from the patient’s lungs and feses. The third is Billiary
Cryptosporidiosis. In this case, The patient will suffer an abdominal pain with a
papillary Stenosis. Other than medicine treatment only, the patient must be given a
sphincterotomy measure that can improve the life of the patient.9

14
CHAPTER III
CONCLUSION

3.1. Conclusion
1. Cryptosporidiosis is a highly prevalent and extremely widespread disease
documented by over 1000 reports in humans in 95 countries on all
continents except Antarctica.
2. The infective form of Cryptosporidium is oocyst. Oocyst is excreted through
stools of individuals infected with Cryptosporidium.
3. Cryptosporidium infection in healthy individuals causes gastrointestinal
illness.
4. Diagnosis of cryptosporidiosis uses stool sample. Microscopy, striptest,
ELISA and real-time PCR is often used for examine Cryptosporidium.
5. Ways to treat cryptosporidiosis are still limited; there is no fully effective
drug treatment or a vaccine.

3.2. Advice and Suggestions


1. For Students
We suggest the students to learn more about Cryptosporidium in order to
widen their knowledge about existing parasites that attack humans.
2. For Lecturers
We suggest lecturers to include the material of Cryptosporidium in the
future lectures to allow future medical students to be better equipped in the
field.

15
REFERENCES

1. Ryan U, Fayer R, Xiao L. Cryptosporidium species in humans and


animals: current understanding and research needs. Parasitology. 2014;
141:1667-8.
2. Li N et al. Subtyping Cryptosporidium ubiquitous, a zoonotic pathogen
emerging in humans. 2014.
3. Han BA, Schmidt JP, Bowden SE, Drake JM. Rodent reservoirs of future
zoonotic diseases. Cross Mark. 2015;112(22): 7039-7044.
4. Cacciò SM, Putignani L. Epidemiology of human cryptosporidiosis.
Cryptosporidium: parasite and disease. 2014: 43-79. doi 10.1007/978-3-
7091-1562-6
5. Li W, Li Y, M Song, Lu Y, Yang J, Tao W, et al. Prevalence and genetic
characteristics of Cryptosporidium, Enterocytozoon bieneusi and Giardia
duodenalis in cats and dogs in Heilongjiang province, China. Veterinary
Parasitology. 2015;208(3-4): 125-134.
6. Parsons M, Travis D, Lonsdorf E, Lipende I, Roellig D, Kamenya S et al.
Epidemiology and molecular characterization of Cryptosporidium spp. in
humans, wild primates, and domesticated animals in the greater gombe
ecosystem, Tanzania. PLOS Neglected Tropical Diseases. 2015;9(2).
7. Maryanti E. Epidemiology of cryptosporidiosis. JIK. 2011;5: 1-6.
8. Iqbal J, Khalid N, Hira P. Cryptosporidiosis in Kuwaiti children:
association of clinical characteristics with Cryptosporidium species and
subtypes. 2018.
9. CDC. Parasites – Cryptosporidium (also known as “Crypto”). 2017.
Available from: https://www.cdc.gov/parasites/crypto/infection-
sources.html
10. Leitch GJ, He Q. Cryptosporidiosis-an overview. Journal of Biomedical
Research. 2011;25(1): 1-16
11. Sow SO, Muhsen K, Nasrin D, Blackwelder WC, Wu Y, Farag TH, et al.
The burden of cryptosporidium diarrheal disease among children < 24
months of age in moderate/high mortality regions of sub-Saharan Africa
and South Asia, utilizing data from the Global Enteric Multicenter Study
(GEMS). PLoS Negl Trop Dis. 2016;10(5).
12. Putignani L, Menichella D. Global Distribution, Public Health and Clinical
Impact of the Protozoan Pathogen Cryptosporidium. Hindawi. 2010;
13. Sears CL, Kirkpatrick BD. Cryptosporidiosis and isosporiasis. In:
Gillespie SH, Pearson RD, editors. Principles and practice of clinical
parasitology. Chichester: John Wiley & Sons Ltd; 2001: 141-2.
14. Centers for Disease Control and Prevention. Cryptosporidiosis. 2017 Nov
8 [accessed on January 13th 2018]. Available at:
https://www.cdc.gov/dpdx/cryptosporidiosis/index.html
15. Carruthers VB, Tomley FM. Microneme proteins in apicomplexans.
Subcell Biochem. 2008;47: 33-45.
16. Bouzid M, Hunter PR, Chalmers RM, Tyler KM. Cryptosporidium
pathogenicity and virulence. Clinical Microbiology Reviews. 2013;26(1):
115-134. doi: 10.1128/CMR.00076-12
17. Rehn M, Wallensten A, Widerström M, Lilja M, Grunewald M, Stenmark
S, et al. Post-infection symptoms following two large waterborne outbreaks
of Cryptosporidium hominis in Northern Sweden, 2010-2011. BMC Public
Health. 2015;15: 529. doi:10.1186/s12889-015-1871-6.
18. Cacciò SM, Chalmers RM. Human cryptosporidiosis in europe. Clin
Microbiol Infect. 2016;22(6): 471-80. doi:10.1016/j.cmi.2016.04.021.
19. Koop DV, Brinkman M, Wilke H, Mulder B. Laboratory diagnosis of
Cryptosporidium using microscopy, striptest, ELISA and real-time PCR.
2014;1:2.
20. Shirley D-AT, Moonah SN, Kotloff KL. Burden of disease from
Cryptosporidiosis. Current Opinion in Infectious Diseases. 2012;25(5):
555-563. doi:10.1097/QCO.0b013e328357e569
21. Janssen B, Snowden J. Cryptosporidiosis. [Updated 2017 Oct 9]. In:
StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2017 Jun.
Available from: https://www.ncbi.nlm.nih.gov/books/NBK448085/
22. G Certad, E Viscogliosi, M Chabe, SM Caccio. Pathogenic mechanisms of
cryptosporidium and giardia. Cell Press. 2017; 20: 4-5.
23.
24. H Kumar, VB Singh, BL Meena, J Agrawal, S Beniwal, T Swami.
Pulmonary cryptosporidiosis in an immunocompetent host treated
successfully with nitazoxanide. Lung India 2016; 33: 69-70.
25. Wolska‑Kusnierz B, Bajer A, Caccio S, Heropolitanska‑Pliszka E,
Bernatowska E, Socha P, et al. Cryptosporidium infection in patients with
primary immunodeficiencies. J Pediatr Gastroenterol Nutr 2007; 45:
458‑64.
26. Corti M, Villafañe MF, Muzzio E, Bava J, Abuín JC, Palmieri OJ.
Pulmonary cryptosporidiosis in AIDS patients. Rev Argent Microbiol
2008;40:106‑8
27. RL Kradin. Diagnostic pathology of infectious disease. 2nd rev. China:
Elsevier, 2018. 310-1 p.
28. Shirley D, Moonah S, Kotloff K. Burden of disease from Cryptosporidiosis. HHS
Public Access. 2012;25(5):555-563
29. Fayer R, Xiao L. Cryptosporidium and Cryptosporidiosis. 2008:560.
30. Vanathy K, Parija SC, Mandal J, Hamide A, Krishnamurthy S. Detection of
Cryptosporidium in stool samples of immunocompromised
patients;1(1):p(41-46)
31. Elgun G, Koltas IS. Investigation of Cryptosporidium spp. antigen by
ELISA method in stool specimens obtained from patients with
diarrhea.2010:108;p(395-97)
32. Kuzehkanan AB, Rezaeian M, Zeraati H, et al. A Sensitive and Specific
PCR Based Method for Identification of Cryptosporidium Sp. Using New
Primers from 18S Ribosomal RNA;6(4):p(1-7)

You might also like