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OBAT

PENYAKIT PARASIT
Moch Aris Widodo
PPD UNISMA

The major parasitic diseases, including::


protozoan diseases (amebiasis, malaria),
helminthic infections (ascariasis, enterobiasis),
ectoparasitic infestations (head and body lice).

Initial Presentation
Nonspecific fever, chills, rigors, diaphoresis, malaise, vomiting Orthostatic
hypotension,Electrolyte abnormalities
Erythrocytic Phase
Prodrome: Headache, anorexia, malaise, fatigue, myalgias Nonspecific complaints
such as abdominal pain, diarrhea, chest pain, and arthralgias
Paroxysm: High fever, chills, and rigor. Cold phase: Severe pallor, cyanosis of the
lips and nail bed, and cutis, anserina (goose flesh)
Hot phase: Fever between 40.5C (104.9F) and 41C (105.8F).
Sweating phase:Follows hot phase by 26 hours. Fever resolves
Marked fatigue and drowsiness, warm, dry skin, tachycardia, cough, severe
headache, nausea, vomiting, abdominal pain, diarrhea, and delirium
Lactic acidosis and hypoglycemia (with falciparum malaria) Anemia Splenomegaly
P. falciparum Infections
Hypoglycemia, acute renal failure, pulmonary edema, severe anemia,
thrombocytopenia, high-output heart failure, cerebral congestion, seizures and coma,
and adult respiratory syndrome

ECTOPARASITES
A parasite that lives on the outside the body of the host is called an
ectoparasite. Approximately 6 to 12 million people become infested
with pediculosis yearly in the United States.108 Pediculosis usually is
associated with poor personal hygiene, and infections are passed from
person to person through social and sexual contact. The three types of
human lice belong to two genera: Pediculus, including the head and
body lice, and Phthirus, with only one species, the crab louse.9,100105
The human louse is detectable to the human naked eye and measures
approximately 2 to 3 mm in length.

LICE
The two species that belong to this group include Pediculus humanus
capitis (head louse) and P. humanus corporis (body louse). Female
lice deposit eggs on the hair. The eggs (or nits) remain firmly attached
to the hair, and in about 10 days, the lice hatch to form nymphs,
which mature in 2 weeks. Using both their piercing mouth parts and
a pumping device, the larvae and adults feed on the blood of the host.
The body louse and head louse are essentially identical, although they
live on different parts of the body. Unlike the head louse, which lives
on the hair, the body louse is more frequently found on clothing of
the infected host.
Pubic or crab lice are found on the hairs around the genitals, although
they can occur in other areas of the body (e.g., eyelashes,
beards, and axillae). Patients usually complain of severe pruritus
from papular lesions produced by the bite of the louse. Hypersensitivity
to foreign material injected by the lice can produce macular
swellings and occasionally can lead to secondary bacterial
Infections.

NEMATODES
HOOKWORM DISEASE
This is an infection of the small intestine caused by either Ancylostoma
duodenale or Necator americanus. N. americanus is found
in the southeastern United States, where the temperature and humidity
provide the proper environment. Ancylostoma is seen rarely in the
United States.
The life cycles of both species of hookworm are similar. The
adult worms live in the small intestine attached to the mucosa. The
females liberate eggs, which are eliminated in the feces and develop
into larvae. Infective larva enter the host in contaminated food or
water or penetrate the skin, where a papular eruption with localized
edema and erythema can result.
In the small intestine, where the adult worm lives attached
to the mucosa, injury is usually caused by mechanical and lytic
destruction of tissue. The loss of blood can lead to anemia and
hypoproteinemia.8991
Stool should be examined for eggs and the rhabditiform larvae.
Eosinophilia (30% to 60%) is present in patients with chronic infection.

TREATMENT: Hookworm Disease


Mebendazole (Vermox), an oral synthetic benzimidazole, is the
agent of first choice. It is also effective against ascariasis, enterobiasis,
and trichuriasis. The adult dose for treatment of hookworm infestation is 100
mg twice daily for 3 days. Pediatric patients older than 2 years of age should
receive the same dose as adults.
ASCARIASIS
Ascariasis is caused by the giant roundworm Ascaris lumbricoides.
Female worms range from 20 to 35 cm in length. The worm is found
worldwide but more commonly in areas where sanitation is poor.
Approximately 4 million people in the United States have ascariasis.
Clinical Manifestations
During migration of the larvae through the lungs, patients can present with
pneumonitis, fever, cough, eosinophilia, and pulmonary infiltrates. Other
symptoms of ascariasis include abdominal discomfort abdominal obstruction,
vomiting, and appendicitis.Diagnosis is made by demonstrating the characteristic
egg in the stool
TREATMENT: Ascariasis
In both adults and pediatric patients older than 2 years of age, the
treatment for ascariasis is mebendazole (Vermox) 100 mg twice daily
for 3 days. An alternative drug for ascariasis is pyrantel pamoate
(Antiminth)..

AMEBIASIS
EPIDEMIOLOGY AND ETIOLOGY
Because of its worldwide distribution and serious gastrointestinal
manifestations, amebiasis is one of the most important parasitic diseases
of humans.
The major causative organism in amebiasis is Entamoeba histolytica, which
inhabits the colon and must be differentiated from the E. dispar, which is
associated with an asymptomatic carrier state and is considered nonpathogenic.
Although E. histolytica and E. dispar are indistinguishable morphologically, recent
researchusing monoclonal antibodies has been able to separate the two
Invasive amebiasis is almost exclusively the result of E. histolytica
infection. Approximately 50 million cases of invasive disease result
each year worldwide, leading to an excess of 100,000 deaths.
The incidence of amebiasis is estimated at about 4% in the general population.45
The highest incidence is found in institutionalized mentally retarded patients,
sexually active homosexuals, patients with acquired immune deficiency syndrome
(AIDS)

TREATMENT: Amebiasis
DESIRED OUTCOME
In amebiasis, the goals of therapy are initially to eradicate the parasite
by use of specific amebicides and then to render supportive therapy.
TREATMENT REGIMENS
Anumber of different regimens have been suggested depending on the
category of amebiasis:
asymptomatic cyst passers,
intestinal amebiasis,
amebic liver abscess.
Electrolyte replacement and nutritional support are essential adjunctive treatment
modalities. Large hepatic abscess or amebic pericarditis may require needle
aspiration, percutaneous catheter drainage, or rarely, surgery before drug
therapy.
Most regimens require a combination of drugs administered concurrently or
sequentially.
A careful history should be taken when one of the differential diagnoses
is ulcerative colitis because corticosteroid administration has the potential to
unmask amebiasis and produce toxic megacolon. All patients diagnosed as
having inflammatory bowel disease should have their stools examined carefully
and serologic testing done for amebiasis to avoid the serious consequence that
results from the administration of corticosteroids.

PHARMACOLOGIC THERAPY
Metronidazole (Flagyl), tetracycline, dehydroemetine, and chloroquine
(Aralen) are tissue-acting agents,(are absorbed well)
whereas iodoquinol (Yodoxin), diloxanide furoate (Furamide), and paromomycin
(Humatin) are luminal amebicides (POOR ABSORBED)
In the asymptomatic cyst passer, it is necessary to eradicate the causative agent
from the lumen to prevent intestinal amebiasis or the development of amebic liver
abscess.
Drug effectiveness must be monitored by stool examination,
i.e., from one to three negative specimens from 1 to 3 months after
treatment.
Asymptomatic cyst passers and patients with mild intestinal
amebiasis should receive one of the following luminal agents:
paromomycin2530 mg/kg per day three times daily for 7 days,
iodoquinol 650 mg three times daily for 20 days,
diloxanide furoate 500 mg three times daily for 10 days.
These regimens have cure rates of between 84% and 96%.
The pediatric dose for paromomycin is the same as in adults, whereas the dose of
iodoquinol is 3040 mg/kg per day in three doses for 20 days, and the dose of
diloxanide furoate is 20 mg/kg per day in three doses for 10

Patients with severe intestinal disease or liver abscess


should receive metronidazole 750 mg three times daily for
10 days, followed by a course of one of the luminal
agents indicated earlier.
An alternative regimen of metronidazole 2.4 g/day for 2
days has been suggested to treat intestinal amebiasis.45
In the pediatric patient, the dose of oral metronidazole is
50 mg/kg per day in divided doses to be followed by a
luminal agent.
Patients who are too ill to take oral metronidazole should
receive the drug in equivalent doses by the intravenous
route.

GIARDIASIS
EPIDEMIOLOGY AND ETIOLOGY
Giardia lamblia (also known as G. intestinalis or G. duodenalis), an
enteric protozoan, is the most common intestinal parasite responsible
for diarrheal syndromes throughout the world. The most frequently identified
intestinal parasite in the United States, with a prevalence rate of 16% in some
areas.
G. lamblia has been identified as the first enteric pathogen seen in children in
developing countries, with prevalence rates between 15% and 30%.57
There are two stages in the life cycle of G. lamblia: the trophozoite and the cyst.
G. lamblia, which is found in the small intestine, the gallbladder, and biliary
drainage, is a pear-shaped trophozoite with four pairs of flagella. Two nuclei lie in
the area of the sucking disk, giving the protozoan a characteristic facelike image.
The distribution of giardiasis is worldwide. Children seem to be affected more
frequently than adults. Children in day-care centers may infect parents and other
family members. In less developed countries, fecal contamination of the
environment and lack of potable water, education, and housing continue to be risk
factors for giardiasis among children.

PATHOLOGY
Giardiasis results from ingestion of G. lamblia cysts in fecally contaminated
water or food. The protozoan excysts under the stimulus of lowgastric pH to
release the trophozoite. Colonization and multiplication of the trophozoite lead to
mucosal invasion, localized edema, and flattening of the villi, resulting in
malabsorption states in the host.
Lactose intolerance precipitated by giardiasis can persist even after eradication
of the protozoan. Achlorhydria, hypogammaglobu- Steatorrhea, vitamin B12 and
fat-soluble vitamin deficiencies anemia, or deficiency in secretory mmunoglobulin
A (IgA) are predispositions for giardiasis
Clinical Presentation of Giardiasis
Acute Onset
Diarrhea, cramplike abdominal pain, bloating, and flatulence Malaise, anorexia,
nausea, and belching
Chronic
Diarrhea: Foul-smelling, copious, light-colored, fatty stools; weight
Loss Periods of diarrhea alternating with constipation Steatorrhea, vitamin B12
and fat-soluble vitamin deficiencies

PHARMACOLOGIC THERAPY
All symptomatic adults and children older than 8 years of age should be
treated with metronidazole 250 mg three times daily for 7 days. The
alternative drugs include furazolidone 100 mg four times or paromomycin
2530 mg/kg per day in divided doses daily for 1 week.
Paromomycin 2530 mg/kg per day in three dosesfor 7 days or bacitracin or
bacitracin zinc may be safe agents in pregnancy.
The pediatric dose for metronidazole is 15 mg/kg per day three times daily for
5 to 7 days.
Furazolidone suspension 6 mg/kg per day in four doses for 7 to 10 days and
nitazoxanide (Alinia) suspension (a recently approved agent) 100200 mg
every 12 hours for 3 days are alternative drugs for children.
Albendazole 400 mg daily for 5 days has been cited to produce cure rates of
97% and as being equivalent to metronidazole in children.

LEISHMANIASIS
EPIDEMIOLOGY AND ETIOLOGY
This disease is caused by a protozoan belonging to the genus Leishmania.
The three variations of the disease are visceral leishmaniasis
(kala-azar, black fever, or Assam fever), cutaneous leishmaniasis,
and mucocutaneous leishmaniasis. The visceral form is caused
predominantly by L. donovani, whereas the other two forms are caused
by other species.
Leishmania exist in two forms: as a flagellated extracellular parasite
in the sandfly vector (Phlebotomus in the Indian subcontinent and
Lutzomyia and Psychodopygus in North and South America, Africa,
or the Middle East) and an aflagellar amastigote (intracellular form)
in the host.
The major reservoirs for Leishmania, depending on geographic location, are
dogs, foxes, squirrels, and rodents. The sandflies ingest the parasite when they
feed on the reservoir animals. After metamorphosis in the gut of the sandfly, the
parasite is transferred to the human host when the infected sandfly takes a
blood meal. Cutaneous leishmaniasis seen most frequently in the United States
is caused by either L. braziliensis or L. mexicana, which are endemic to
south Mexico and Central America.

Clinical Manifestation of Leishmaniasis


Visceral: Early
Papule that may ulcerate, Asymptomatic period (dissemination of the amastigote
to organs: spleen, liver, bone marrow, and lymphatic tissue)
Visceral: Late (38 Months)
Fever, chills, malaise, weight loss, abdominal distension, and
Hepatosplenomegaly Persisting raised ulcer
Cutaneous and Mucocutaneous
Mutilation of nose, soft palate, and trachea (L. braziliensis) quired from
transfusion of contaminated blood and accidental needle stick injuries. Patients
with advanced-stage acquired immunodeficiency syndrome (AIDS) are reported
to be highly susceptible to leishmaniasis.
TREATMENT: Leishmaniasis
DESIRED OUTCOME
The major goal is to eradicate the amastigote in the tissue and to
minimize the ensuing complications of leishmaniasis.
PHARMACOLOGIC THERAPY
All three forms of leishmaniasis are treated with stibogluconate
sodium (antimony sodium gluconate-pentavalent antimony,Pentostam), which

Giardiasis
Nama : Albendazole 200 mg tablet (zentel)
Indikasi :Giardiasis Ascariasis Neurocysticercosis
Efek samping GI: Abdominal pain, nausea, diarrhea, increase in liver function
enzymes
Haqti hati : Not recommended in children <2 years old
Quinacrine 100 mg
GI: Nausea, anorexia, vomiting Headache, toxic psychosis, hepatitis, and aplastic
anemia
Avoid in pregnancy, psychosis and psoriasis
Nitazoxanide (Alinia)100 mg/5 mL suspension
Abdominal pain, diarrhea, vomiting, and headache
Rarely may produce yellow sclerae
Metronidazole (Flagyl) Oral: 250-mg, 500-mg tablets
GI: Nausea, anorexia, vomiting, diarrhea, abdominal cramping, glossitis, metallic
taste CNS: Dizziness, vertigo, headache, paresthesias
Avoid alcohol; alcohol ingestion will cause the disulfiram reaction: abdominal
distress, vomiting, hypotension
Contraindication: First trimester of pregnancy

MALARIA
Atovaquone 250 mg plus Proguanil 100 mg Proguanil 100 mg (Malarone) Prevention and
treatment of P. falciparum malaria
Abdominal pain, nausea, vomiting and headache
Chloroquine phosphate (Aralen, Nivaquine) 250- and 500-mg tablets; 50 mg/mL (as
HCl); 5-mL ampule
Malaria
GI: Nausea, vomiting, diarrhea CNS: Dizziness, headache, blurring of vision, confusion,
fatigue Derm.: Pruritus
Administer oral dose after meals
IV route: Recommend ECG monitoring
Contraindication: Patients with psoriasis or porphyria
Pyrimethamine (Daraprim) 25-mg tabletMalaria ES GI: Abdominal pain, vomiting,
Glossitis,Hemat.: Megaloblastic anemia, hemolytic anemia
Recommended that folinic acid 15 mg/day be concurrently administered; can cause
hemolysis in patients with G6PDc deficiency
Pyrimethamine 25 mg plus sulfadoxime 500 mg (Fansidar) P. falcipariumresistant
Malaria ES GI: Nausea, abdominal pain, stomatitis. Hemat.: Agranulocytosis,
aplastic anemia, leukopenia
Combination has been reported recently to cause the Stevens-Johnson syndrome;
patients should be advised to call their physician/ pharmacist if a skin rash or other
reactions are seen

Malaria
Quinidine gluconate 500 mg base/mL; 10 mL
Acute malaria \
GI: Nausea, vomiting, diarrhea
Card.: Hypotension, widening of QRS and QT on ECG, heart block
Administration of IV quinidine requires close monitoring; should normally monitor
ECG and all vital signs
Quinine sulfate 325-mg and 650-mg tablets Acute malaria Cinchonism: Flushing,
dizziness, nausea, vomiting, diarrhea (levels over 10 mcg/mL)
Card.: Hypotension, widening of QRS complex
Hemat.: Hemolysis, leukopenia, thrombocytopenia
When drug is administered IV, it should be administered by slow infusion (600 mg
over 8 h); close monitoring of
vitals and ECG
Avoid use: IM administration

Amebiasis
Diloxanide furoateb (Furamide) 500-mg tablet
GI: Nausea, flatulence ES: Derm.: Pruritus
Iodoquinol (Yodoxin) 210-mg tablet
GI: Abdominal pain, diarrhea
Derm.: Rash May interfere with thyroid function test
Contraindication: Patients with iodine intolerance
Metronidazole (Flagyl) Oral: 250-mg, 500-mg tablets
GI: Nausea, anorexia, vomiting, diarrhea, abdominal cramping, glossitis, metallic
taste CNS: Dizziness, vertigo, headache, paresthesias
Avoid alcohol; alcohol ingestion will cause the disulfiram reaction: abdominal
distress, vomiting, hypotension
Contraindication: First trimester of pregnancy

Obat cacing
Ivermectin (Stromectal) 6-mg tablet
Strongyloidiasis Pediculosis
Dizziness, somnolence, tremor, vertigo, pruritus, abdominal pain
Should be taken with a full glass of water
Mebendazole (Vermox) 100-mg chewable tablet
Ascariasis, trichuriasis, hookworm, pinworm,
GI: Abdominal pain, diarrhea CNS: Headache, dizziness Other: Pyrexia,
neutropenia
Drug should be taken with meals
Contraindication: Pregnancy
Drug interaction: Can increase serum levels of theophylline
Pyrantel pamoate (Antiminth) 50-mg/mL suspension
Pinworm Hookworm
GI: Anorexia, nausea, abdominal cramps, diarrhea
CNS: Headache, dizziness

Sodium stibogluconate(Pentostam)f
Leishmaniasis
GI: Nausea, vomiting, abdominal pain, pancreatitis, increase LFTs
Musculoskel: Myalgia, fatigue Card.: T-wave inversion, bradycardia
Hemat.: Leukopenia, thrombocytopenia
pancreatitis
Highly toxic, requires careful monitoring of vitals and ECG; caution in patients with
liver or cardiac problems
Nifurtimoxd (Lampit, Bayer 2502)
South American trypanosomiasis
GI: Anorexia, nausea
CNS: Peripheral neuritis, psychosis
Hemat: Hemolysis in G6PDc deficiency patients
Monitor pulmonary function and hematologic parameters

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