Parasitic Diseases
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Transcript Parasitic Diseases
Parasitic Diseases
Parasitic Diseases
PROTOZOAL DISEASES
HELMINTHIASE
Malaria
Malaria is caused by obligate intracellular protozoa
of the genus Plasmodium
Plasmodium including P. falciparum, P. malariae, P.
ovale, and P. vivax
Plasmodium has a complex life cycle
Asexual phase (schizogony) in humans
sexual phase (sporogony) in mosquitoes
Erythrocytic phase of Plasmodium:
Merozoites released from schizonts in the liver
penetrate erythrocytes
When inside the erythrocyte, the parasite transforms
into the ring form
Ring form which enlarges to become a trophozoite
Ring form and trophozoite can be identified with
Giemsa stain on blood smear
Transmission:
Anopheles mosquitoes female
Blood transfusion
Contaminated needle
transplacentally to a fetus
Epidemiology
Malaria is an important cause of fever and morbidity
in the tropical world
Infected foreign civilians from endemic areas who
travel
Citizens who travel to endemic areas without
appropriate chemoprophylaxis
Clinical Manifestations
The incubation period ranges from 6 to 30 days
depending on the Plasmodium species
The most characteristic clinical feature of malaria is
febrile paroxysms
The classic symptoms of the febrile paroxysms of malaria
include high fever, rigors, sweats) and headache
Paroxysms coincide with the rupture of schizonts that
occur:
Every 48 hours with P. vivax and P ovale (tertian periodicity)
Every 72 hours with P. malariae (quartan periodicity)
Short-term relapse→recurrence of symptoms after a
primary attack due to the survival of erythrocyte
forms in the bloodstream
Long-term relapse→renewal of symptoms long after
the primary attack due to release of merozoites from
an exoerythrocytic
Long-term relapse occurs with:
P vivax and P. ovale because of persistence in the liver
P malariae because of persistence in the erythrocyte
Distinctive physical signs may include:
splenomegaly (common)
Hepatomegaly
pallor due to anemia
Laborarcry and Imaging Studies
The diagnosis of malaria→stained smears of
peripheral blood
In nonimmune persons, symptoms typically occur 1
to 2 days before parasites are detectable on blood
smear
Obtaining smears several times each day over 3
successive days
Both thick and thin blood smears should be
examined
multiply infected erythrocyte containing
signet-ring P. falciparum trophozoites
,
Treatment
Oral chloroquine is the recommended treatment
except for chloroquine-resisranr P. falciparum
Quinine sulfate plus tetracycline, quinine plus
pyrimethamine-sulfadoxine, or mefloquine are used
for chloroquine-resistant malaria
Quinidine gluconate is used for parenteral treatment
Complications and Prognosis
Cerebral malaria is a complication of P. falciparum
infection:
Coma
Repeated seizures
Hypoglicemia
Other complications:
splenic ruprure, renal failure
severe hemolysis (blackwater fever)
pulmonary edema, hypoglycemia, thrombocytopenia
algid malaria (sepsis syndrome with vascular collapse
Death most frequent with complicated P. falciparum
malaria
Death is increased in children with measles
intestinal parasites, schistosomiasis, anemia, and
malnutrition
Prevention
There are two components of malaria prevention:
Reduction of exposure to infected mosquitoes
Chemoprophylaxis
Chemoprophylaxis:
All visitors to and residents of the tropics
Children of nonimmune women
started 1 to 2 weeks before a person enters the endemic area
except for doxycycline which can be started 1 to 2 days before
continue
for at least 4 weeks after the person leaves
Areas of the world that are free of chloroquine-
resistant malaria strains, chloroquine is given once
per week
In areas where chloroquine-resistant P. falciparum
exists, atovaquone-proguanil, mefloquine, or
doxycycline may be given as chemoprophylaxis
Atovaquone-proguanil is generally recommended for
shorter trips (up to 2 wk), since it must be taken
daily
Atovaqoune-proguanil is started 1-2 days before
travel, and mefloquine is started 2 wk before travel
Toxoplasmosis
Infection is acquired by:
infectious oocysts, such as those excreted by newly infected
cats
from ingesting cysts in contaminated, undercooked meat
Less commonly, transmission occurs transplacentally
during acute infection of pregnant women
Acquired toxoplasmosis:
usually asymptomatic
Symptomatic infection is typically a heterophile-negarive
mononucleosis syndrome
Disseminated infection is more common in
immunocompromised person
Congenital Toxoplasmosis
The later in pregnancy that infection occur but the
less severe the illness
Serologic diagnosis:
fourfold increase in antibody tirer or seroconversion
positive IgM antibody titer
positive polymerase chain reaction (PCR) for T. gondii
Treatment:
pyrimethamine and sulfadiazine
folinic acid
Spiramycin is used in therapy of pregnant women with
toxoplasmosis
Corticosteroids are reserved for patients with acute CNS or ocular
Ingesting only well-cooked meat
avoiding cats or soil in areas where cats defecate are
prudent measures for pregnant or
immunocompromised persons
Administration of spiramycin to infected pregnant
women→congenital infection↓
Amebiasis
E. histolytica
The 2 most common forms of disease:
amebic colitis
amebic liver abscess
Infection is acquired through the ingestion of parasite
Cysts can be killed by heating to 55°C
Food or drink contaminated with Entamoeba cysts and
direct fecal-oralcontact are the most common means of
infection.
Amebic Colitis:
occur within 2 wk of infection
Diarrhea is frequently associated with tenesmus
most patients do not present with grossly bloody
stools
fever documented in only one third of patients
High in children 1-5 yr of age
Amebic Liver Abscess:
Serious manifestation of disseminated infection, is
uncommon in children
Enlargement and tenderness of the liver
Changes at the base of the right lung, such as
elevation of the diaphragm and atelectasis or
effusion
examining 3 stools →Sensitivity can be increased to
85-95%
phagocytosed erythrocytes (specific for E.
histolytica)
The most sensitive serologic test, indirect
hemagglutination
Rapid antigen and antibody tests for bedside
diagnosis
Chronic amebiasis should be excluded before
initiating corticosteroid treatment for IBD
Giardiasis
The life cycle of Giardia is composed of 2 stages:
trophozoites and cysts
Giardia trophozoites contain 2 oval nuclei anteriorly
and 4 pairs of flagella
Outbreaks associated with drinking water
Asymptomatic carriage may persist for several
months
Transmission of Giardia is common in child-care
centers, consumers of contaminated water, travelers
to certain areas
Transmission of Giardia:
water contaminated with Giardia cysts
food-borne
The incubation period of Giardia infection usually is
1-2 wk but may be longer
Acute infectious diarrhea, or chronic diarrhea
Failure to thrive and abdominal pain or cramping
Most infections in both children and adults are
asymptomatic
Stools initially may be profuse and watery and later
become greasy
Giardia has been associated with iron deficiency
Stool enzyme immunoassay (EIA) or direct
fluorescent antibody tests for Giardia antigens
3 stool specimens
Aspiration or biopsy of the duodenum
HELMINTHIASE
Helminths are divided into three groups:
roundworms, or nematode
two groups of flatworms, the trematodes (flukes) and the
cestodes (tapeworms)
Hook Worms
Ankylostoma duodenale ,Necator americanus
The larvae are found in warm, damp soil and infect
humans by penetrating the skin
The worms mature and attach to the intestinal wall,
where they suck blood and shed eggs
Albendazole or mebendazole or pyrantel pamoate
Intense pruritus (ground itch)
Examination of fresh stool for hookworm eggs is
diagnostic
Cutaneous Larva Migrans
Cutaneous larva migrans (creeping eruption) is
caused by the larvae of several nematodes, primarily
hookworms
A. braziliense is the most common cause
After penetrating the skin, larvae localize at the
epidermal-dermal junction and migrate in this plane,
moving at a rate of 1-2 cm /day
erythematous, serpiginous tracks, which occasionally
form bullae
Intense localized pruritus, without any systemic
symptoms, may be associated with the lesions
If left untreated, the larvae die, and the syndrome
resolves within a few weeks to several months
Treatment with ivermectin
Ascariasis
After humans ingest the eggs, Iarvae are released
and penetrate the intestine migrate to the lungs,
ascend the trachea, and are swallowed
Manifestations may be the result of migration of the
larvae
Pulmonary ascariasis
Intestinal ascariasis
Examination of fresh stool for characteristic eggs is
diagnostic
The fertile ova are oval in shape with a thick
mammillated covering measuring
albendazole (400 mg PO once, for all ages
mebendazole (1 00 mg bid PO for 3 days or 500 mg
PO once forall ages)
pyrantel pamoate (11 mg/kg PO once, maximum
1g)
Piperazine citrate (75 mg/kg/day for 2 days
maximum 3.5 g/day)
neuromuscular paralysis of the parasite and rapid expulsion
of the worms
treatment of choice for intestinal or biliary obstruction
Visceral Larva Migrans
Toxocara canis, or, Iess commonly, the cat
tapeworm, Toxocara cati
These organisms also cause ocular larva migrans
Visceral larva migrans is most common in young
children with pica who have dogs or cars as pets
Ingesred eggs hatch into larvae that penetrate the
gastrointestinal tract and migrate to the liver,…
Symptoms of visceral larva migrans:
result of the number of migrating worms
Associated immune response
Eye examination may reveal granulomatous lesions
near the macula or disc
Eosinophilia and hypergammaglobulinemia
ELISA
This is usually a self limited illness
In severe disease, albendazole or mebendazole is
used
Entrobiasis
Humans ingest the eggs carried on hands, present in
house dust or on bedclothes
At night, the females migrate to the perianal area to
lay their eggs
The most common symptoms are nocturnal anal
pruritus (pruritus ani)
Vaginitis and salpingitis may develop secondary to
aberrant worm migration
The eggs are detected by microscopically examining
adhesive cellophane tape pressed against the anus
Treatment:
albendazole(400 mg), mebendazole (100 mg),
pyrantel pamoate(11 mg/kg, maximum 1g) each given as a
single oral dose
and repeated in 2 weeks
Echinococcosis
Hydatid or unilocular cyst disease caused by
Echinococcus granulosus
Alveolar cyst disease caused by Echinococcus m
ultilocularis
Humans acquire echinococcosis by ingesting eggs
and become an intermediate host
The eggs hatch in the intestinal tract, and the larva
(oncospheres) penetrare the mucosa and enter the
circulation to pass to the liver
Pulmonary cysts may cause hemoptysis, cough,
dyspnea, and respiratory distress
Brain cysts appear as tumors
liver cysts cause problems as they compress and
obstruct blood flow
Ultrasonography identifies cystic lesions, and the
diagnosis is confirmed by serologic testing
Treatment:Surgical resection plus albendazole
Neurocysticercosis
Taenia. solium, and is the most frequent helminthic infection
of the CNS
Humans are infected after consuming cysticerci in raw or
undercooked larva-containing pork→adult pork tapeworm
Infection with the invasive intermediate stage (cysticercus) is
called cysticercosis
Ingestion of food or water contaminated with the eggs of T.
solium.
Cysts typically enlarge slowly, causing no or minimal
symptoms
The cyst then begins to swell, and leakage of antigen incites an
inflammatory response
The CSF shows lymphocytic or eosinophilic pleocytosis
The diagnosis is confirmed by serologic testing
Neurocysticercosis is treated:
Albendazole or praziquantel
corticosteroids for concomitant cerebral inflammation from
cyst death
Anticonvulsant drugs
Life cycle of Taenia saginata and Taenia
solium
Taenia solium - The Pork Tapeworm