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Case Report
Time:2006.1.23
Site:臨床病理科簡報室
Speaker:I2 楊秀謙
Brief History
• A 25 y/o nurse had recently returned to the United States
from a stay in Brazil(巴西), where she had worked at a
clinic treating rural patients.
• Symptoms: fever, anorexia, weight loss, shortness of
breath, myalgia.
• Visit her primary care doctor.
• P.E: a thin woman, a slightly enlarged liver and spleen,
lymphadenopathy (+), upper and lower eyelid edema in
R’t eye, along with conjunctivitis.
• EKG: abnormalities of the P, T waves and the QRS
complex, cardiomegaly(+)
Case Report
• Thick and thin blood smears were ordered and
were stained by the Giemsa method.
• Microscopic examination : a few flagellated
spindle-shaped protozoan parasites (some
assuming a C shape) with undulating membranes.
• Diagnosis: An infection with a blood parasite
Case Report
QUESTIONS
1. What is the name of this patient's illness? Which blood protozoan parasite is
causing the infection?
2. How is this infection transmitted?
3. Why is the vector for this protozoan known as the "kissing bug"?
4. Describe the life cycle of this parasite.
5. What is the name of the lesion that may develop at the site of inoculation of
the parasite? What is the name given to the unilateral edema of the eye in this
disease?
6. Which methods are available to diagnosis this infection?
7. How does this parasite differ from other parasites in the same genus?
8. How is this infection treated?
9. This infection may be acquired during blood transfusion. List other protozoan
parasitic infections that may be transmitted during blood transfusions.
10. Explain the cardiac abnormalities found in this patient. Which other
complication may occur?
LYMPHADENOPATHY
• Analysis of lymphadenopathy : > 2/3 p’ts →nonspecific
causes or URI (viral or bacterial), <1% : malignancy.
• 186 of 220 patients (84%) evaluation of lymphadenopathy
→ “benign” diagnosis.
• 34 patients (16%) : malignancy (lymphoma or metastatic
adenocarcinoma).
• 186 p’ts: 63% (112) : nonspecific or reactive etiology (no
causative agent found)
• The remainder: most commonly infectious mononucleosis,
toxoplasmosis, or tuberculosis.
Clinical Assessment
• Extent of lymphadenopathy:
localized or generalized, size, texture, nodal tenderness, signs of
inflammation over the node, skin lesions, splenomegaly.
• Adult, cervical adenopathy, Hx of smoke→ ENT exam.
• Localized, regional adenopathy: involvement of a single anatomic area.
• Generalized adenopathy : involvement > 3 noncontiguous
lymph node areas.
• Generalized lymphadenopathy : nonmalignant disorders
→ infectious mononucleosis(EBV, CMV), toxoplasmosis, AIDS,
viral infections, SLE, MCTD.
→ALL, CLL, malignant lymphomas →generalized in adults.
TABLE 54-1 Diseases Associated with Lymphadenopathy
Toxoplasmosis
• Toxoplasma gondii
• Found throughout the world(more than 60
million people in USA)
• Very few have symptoms→ keeps the
parasite from causing illness.
• Pregnant women and individuals with
compromised immune systems→serious
health problems.
Toxoplasmosis
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Fever
Sore throat
Sore muscles and tiredness
Swollen glands in the neck, armpits or groin
Temporary blurred vision or loss of vision
Most people who are infected do not show any signs of
the disease.
Persons who are pregnant or are experiencing a
suppressed immune system due to AIDS, cancer or
following organ transplants are at higher risk for illness.
Toxoplasmosis
• P.E:
• Toxoplasmosis cannot be diagnosed on
clinical grounds alone because it may
mimic a variety of other diseases.
• No clinical features are pathognomonic for
toxoplasmosis.
• Lymphadenopathy is the most common
finding.
Leishmaniasis
• Spread by the bite of infected sand flies.
• Cutaneous leishmaniasis →skin sores(one
or more cutaneous lesions →sandflies have
fed ) painless or painful.
• Visceral leishmaniasis →internal organs of
the body (spleen, liver, bone marrow)
Leishmaniasis
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Cutaneous leishmaniasis:
Skin sores
Raised edge sores - like a volcano with a central crater
Scabs
Swollen glands or underarm glands
Visceral leishmaniasis:
Fever
Weight loss
Enlarged spleen or liver(usually spleen > liver)
Swollen glands
Bone marrow symptoms
WBC, RBC, PLT ↓
Leishmaniasis
• Some patients develop post kala-azar
dermal leishmaniasis.
• Visceral leishmaniasis →opportunistic
infection →HIV(+)
• Laboratory Diagnosis:
Examination of Giemsa-stained slides of the
relevant tissue is still the technique most
commonly used to detect the parasite.
Trypanosomiasis
• Each individual may experience symptoms differently.
• Symptoms: within one to four weeks of infection
→initially nonspecific ( fever, skin lesions, rash, edema, or swollen
lymph nodes on the back of the neck) →meningoencephalitis
• personality change
• weight loss, loss of concentration
• irritability
• progressive confusion, slurred speech, seizures, difficulty walking and
talking
• sleeping for long periods of the day, insomnia at night
• Untreated→death (within several weeks to month)
Trypanosomiasis
• Acute stage: 1 percent of cases
The first sign: chagoma (swelling and thickening of the skin near the
site of infection), redness, enlarged lymph nodes nearby.
→Romaña's sign – a person's eye on one side of the face swells,
usually at the bite wound or where feces were deposited or
accidentally rubbed into the eye.
• Other symptoms: fatigue, fever, enlarged liver or spleen, swollen
lymph glands, rash, loss of appetite, diarrhea, and vomiting.
• In infants and in very young children →brain damage→ death.
• In general, a person's symptoms last from 4 to 8 weeks and then they
go away, even without treatment.
Trypanosomiasis
• Indeterminate stage: 8 to 10 wks after infection
→ last for many years → not have symptoms
• Chronic stage→ serious symptoms :
Enlarged heart, altered heart rate or rhythm,
heart failure, cardiac arrest
Enlargement or perforation of the esophagus or
large bowel →swallowing difficulties, severe
constipation.
Filariasis
• Not feel any symptoms until after the adult worms die.
• Not life threatening →permanently damage lymph system
and kidneys.
• Lymph system does not work right→fluid collects →
swelling in the arms, the vulva, breasts, legs, the genital
area
→ lymphedema (swell to several times its normal size)
• Difficult for your body to fight germs and infections.
• More bacterial infections in skin and lymph system →
hardening and thickening of the skin → elephantiasis
Filariasis
• Acquire early in childhood →take years to manifest itself.
• May be no clinical symptoms→ outwardly healthy(hidden lymphatic
pathology and kidney damage )
• The asymptomatic form of infection →the presence in the blood of
thousands or millions of larval parasites (microfilariae) and adult
worms located in the lymphatic system.
• The worst symptoms →appear in adults(M > F).
• M(10-50%) →genital damage: hydrocoele (fluid-filled balloon-like
enlargement of the sacs around the testes) and elephantiasis of the
penis and scrotum.
Chagas disease (American trypanosomiasis)
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A human tropical parasitic disease
Americas, particularly in South America. P
Pathogenic agent : flagellate protozoan: Trypanosoma cruzi
hematophagous insects of the subfamily Triatominae (Family Reduviidae).
Numerous common names varying by country: assassin bug, benchuca,
vinchuca, kissing bug, chipo, barbeiro, et cetera.
The most common insect species belong to the genera Triatoma, Rhodnius,
and Panstrongylus.
Other forms of transmission : ingestion of food contaminated with parasites,
blood transfusion, fetal transmission
Trypanosoma cruzi is a member of the same genus as the infectious agent of
African sleeping sickness, but its clinical manifestations, geographical
distribution, life cycle and insect vectors are quite different.
Infection cycle of Trypanosoma cruzi, the pathogen of Chagas disease
無鞭毛體
錐鞭毛體
側鞭毛體
CDC-DPD
Chagas disease
• Acute stage: 1 percent of cases
The first sign: chagoma (swelling and thickening of the skin near the
site of infection), redness, enlarged lymph nodes nearby.
→Romaña's sign – a person's eye on one side of the face swells,
usually at the bite wound or where feces were deposited or
accidentally rubbed into the eye.
• Other symptoms: fatigue, fever, enlarged liver or spleen, swollen
lymph glands, rash, loss of appetite, diarrhea, and vomiting.
• In infants and in very young children →brain damage→ death.
• In general, a person's symptoms last from 4 to 8 weeks and then they
go away, even without treatment.
Chagas disease
• Indeterminate stage: 8 to 10 wks after infection
→ last for many years → not have symptoms
• Chronic stage →
cardiomyopathy: the most serious manifestation
Enlarged heart, altered heart rate or rhythm,
heart failure, cardiac arrest
Enlargement or perforation of the esophagus or
large bowel →swallowing difficulties, severe
constipation.
Adult Rhodnius prolixus taking a blood meal
through human skin. The insect transmits the
parasites which cause Chagas disease in feces
that they deposit near the site of their bite.
Scratching or rubbing by the person bitten can
transfer the parasites into the body via the wound
or other sites such as the eye.
Trypanosoma cruzi in thin blood film (Leishmans
stain) showing developing tryptomastigotes that
have a free flagellum.
Photomicrograph of Trypanosoma cruzi parasites (Chagas disease pathogen).
US Federal Government public domain image (CDC).
Different stages of triatomine insects, the
vectors of Chagas disease.
Acute Chagas Disease in a young child. The eye
sign of Romana is present. This is frequently
seen in acute cases and is presumed to mark the
point of entry of the parasite.
Laboratory diagnosis
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Microscopic examination:
a) fresh anticoagulated blood, or its buffy coat, for motile parasites
b) thin and thick blood smears stained with Giemsa, for visualization of
parasites; it can be confused with the 50% longer Trypanosoma rangeli,
which has not shown any pathogenity in humans yet.
Isolation
a) inoculation into mice
b) culture in specialized media (e.g. NNN, LIT)
c) xenodiagnosis, where uninfected Reduviidae bugs are fed on the
patient's blood, and their gut contents examined for parasites 4 weeks later.
Immunodiagnostic tests:
Complement fixation, indirect hemagglutination, IFA, RIA, ELISA,
PCR(most promising)
Treatment
• Medication : only effective when given during the
acute stage
• The drugs of choice are azole or nitroderivatives
such as benznidazole or nifurtimox, but resistance
to these drugs has already been reported.
• These agents: very toxic many adverse effects
• Use of oxidosqualene cyclase inhibitors and
cysteine protease inhibitors : cure experimental
infections in animals.
Treatment
• Chronic stage→manage the clinical manifestations of the disease:
Drugs and heart pacemaker for chronic heart failure and arryhthmias
Surgery for megaintestine
• The disease per se is not curable in this phase.
Chronic heart disease caused now a common reason for heart
transplantation surgery.
→ After operation, survival rates can be significantly improved by
using lower dosages of the immunosuppressant drug cyclosporine.
• Direct stem cell therapy of the heart muscle using bone marrow cell
transplantation →dramatically reduce risks of heart failure in Chagas
patients.
• Patients have also been shown to benefit from the strict prevention of
reinfection, though the reason for this is not yet clearly understood.
Parasitic infections which may be transmitted
during blood transfusions
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Malaria
Babesiosis
Toxoplasmosis
Chagas’ Disease
THANKS FOR YOUR
ATTENTION!
Chagas disease
The Fight for Recognition: Chagas’ Disease Meets Controversy
Anna Moorhouse, Science Journalist
English and Cell and Molecular Biology, Simon Fraser University
Questions？