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Features of lung involvement depend on localization of the cyst. If it is close
to pleura, pain syndrome is the early manifectation. If it localizes close to
pulmonary trunk, patient can have cough, haemoptysis, dyspnoea.
Other presentations are due to the involvement of bone (invasion of the
medullary cavity with slow bone erosion producing pathologic fractures), the CNS
(space-occupying lesions with intracranial hypertension and epilepsy), the heart
(conduction defects, pericarditis), and the pelvis (pelvic mass).
ECHINOCOCUSS
Complications. One of the most severe complications is rupture of
echinococcus cyst, which can occur spontaneously or at surgery and may lead to
multifocal dissemination of protoscolices, which can form additional cysts.
Rupture of the cyst may also lead to allergic manifestations such as pruritus,
oedema, dyspnoea, anaphylactic shock and appearance of peritonitis, pleuritis,
meningitis or other inflammatory reactions.
Specific diagnostics. A number of serological tests have been developed for
detection of antibody to specific echinococcal antigens, for example, an immune-
enzyme analysis, a Western blot assay. Cysts in the liver elicit positive antibody
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responses in 90% of cases, whereas up to 50% of individuals with cysts in the
lungs are seronegative. That’s why a negative test does not exclude the diagnosis
of echinococcosis. Another drawback in serological diagnostics is cross-reactivity
with sera of patients with Taenia solium.
Radiographic and related imaging studies are important in detecting and
evaluating echinococcal cysts. Plain x-rays will define pulmonary cysts of E.
granulosus – usually as rounded masses of uniform density – but may miss cysts in
other organs unless there is cyst wall calcification (as occurs in the liver). MRI,
CT, and ultrasound reveal well-defined cysts with thick or thin walls. However, the
most pathognomonic finding, if demonstrable, is that of daughter cysts within the
larger cyst. This finding, like eggshell or mural calcification on CT, is indicative of
E. granulosus infection and helps to distinguish the cyst from carcinomas, bacterial
or amebic liver abscesses, or hemangiomas. In contrast, ultrasound or CT of
alveolar hydatid cysts reveals indistinct solid masses with central necrosis and
plaquelike calcifications.
Examination of sputum, duodenal juice, faeces can be done to find
protoscolices in case of rupture of the cyst into hollow organs.
In general blood analysis can be seen nonpermanent eosinophilia to 15 %
and increased ESR.
Treatment. Therapy for cystic echinococcosis is based on considerations of
the size, location, and manifestations of cysts and the overall health of the patient.
Surgical removal of hydatid cysts remains the treatment of choice in many
countries. In some countries PAIR (percutaneous aspiration, infusion of scolicidal
agents, and reaspiration) is now recommended instead of surgery. PAIR is
contraindicated for superficially located cysts (because of the risk of rupture), for
cysts with multiple thick internal septal divisions, and for cysts communicating
with the biliary tree. For prophylaxis of secondary peritoneal echinococcosis due to
inadvertent spillage of fluid during PAIR, the administration of albendazole (15
mg/kg daily in two divided doses) should be initiated at least 4 days before the
procedure and continued for at least 4 weeks afterward. PAIR, when implemented
by a skilled practitioner, yields rates of cure and relapse equivalent to those
following surgery, with less perioperative morbidity and shorter hospitalization.
Surgery is the treatment of choice for complicated E. granulosus cysts (e.g.,
those communicating with the biliary tract) or for areas where PAIR is not
possible. For E. granulosus, the preferred surgical approach is pericystectomy, in
which the entire cyst and the surrounding fibrous tissue are removed. Albendazole
should be administered adjunctively, beginning several days before resection and
continuing for several weeks after it.
Chemotherapy. Benzimidazole compounds have been shown to be effective
against hydatid disease. The administration of 3-4 courses of albendazole in a dose
of 10 to 15 mg/kg body weight per day (divided in two doses) for 28 days with
drug-free periods of 2 weeks is used. This regime cures approximately one-third of
cases of liver hydatid disease and causes partial regression of cysts in another third
of patients. Small liver or lung hydatid cysts may be treated with albendazole.
Albendazole is also indicated, when surgery is contraindicated. Mebendazole may
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also be used, although it is less effective than albendazole. Albendazole,
mebendazole, and other benzimidazole compounds should not be used in pregnant
women because of their potentially teratogenic effects. Since benzimidazoles are
potentially hepatotoxic, liver enzymes should be monitored before and during
treatment.
Regular medical check-up of patient with Echinococcosis after operation
lasts not less than 8 years. Patients should be examined by different doctors
(gastroenterologist, pulmonologist, neuropathologist and others, dependently on
prior localization of cyst) not less than 1 time in two years. Instrumental and
serological examination should be done to them.
HYMENOLEPIASIS NANA Infection with H. nana, the dwarf tapeworm,
is the most common of all the cestode infections. H. nana is endemic in both
temperate and tropical regions of the world. Infection is spread by fecal/oral
contamination and is common among institutionalized children.
Etiology and Pathogenesis. H. nana is the only cestode of humans that does
not require an intermediate host. Both the larval and adult phases of the life cycle
take place in the human. The adult—the smallest tapeworm parasitizing humans—
is 2 cm long and dwells in the proximal ileum. Proglottids, which are quite small
and are rarely seen in the stool, release spherical eggs 30–44
m in diameter,
each of which contains an oncosphere with six hooklets. The eggs are immediately
infective and are unable to survive for >10 days in the external environment. When
the egg is ingested by a new host, the oncosphere is freed and penetrates the
intestinal villi, becoming a cysticercoid larva. Larvae migrate back into the
intestinal lumen, attach to the mucosa, and mature into adult worms over 10–12
days. Eggs may also hatch before passing into the stool, causing internal
autoinfection with increasing numbers of intestinal worms. Although the life span
of adult H. nana worms is only 4–10 weeks, the autoinfection cycle perpetuates the
infection.
The life cycle of Hymenolepis nana starts, when microscopic eggs are
passed with the stool of an infected human. They then get ingested either by
rodents, humans (definite hosts) or insects (intermediate hosts). If a person ingests
eggs (from contaminated fingers, water, food or soil), oncospheres (hexacanth
larvae) hatch in the small intestine.
A larva penetrates an intestinal villus and develops into a cysticercoid. A
cysticercoid develops to look more like an adult having a scolex (head) and a neck.
It bursts out of the villus, attaches to the intestinal mucosa and matures into an
adult in the last part of the small intestine, ileum. Its long neck starts producing
segments, proglottids, which make up the body.
A proglottid absorbs nutrients from the surroundings and grows bigger
before it detaches from the tail. Each proglottid has both male and female
reproductive organs. It copulates with itself or with other proglottids of the same
individual or nearby tapeworms. A gravid proglottid releases thousands of eggs