Case Report

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Case Report

• Time2006.1.23
• Site????????
• SpeakerI2 ???

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Brief History

• A 25 y/o nurse had recently returned to the
  United States from a stay in Brazil(??), 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 Rt eye, along with
  conjunctivitis.
• EKG abnormalities of the P, T waves and the QRS
  complex, cardiomegaly()

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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

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Case Report
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QUESTIONS

• What is the name of this patient's illness? Which
  blood protozoan parasite iscausing the
  infection?
• How is this infection transmitted?
• Why is the vector for this protozoan known as the
  "kissing bug"?
• Describe the life cycle of this parasite.
• What is the name of the lesion that may develop
  at the site of inoculation ofthe parasite? What
  is the name given to the unilateral edema of the
  eye in this disease?
• Which methods are available to diagnosis this
  infection?
• How does this parasite differ from other
  parasites in the same genus?
• How is this infection treated?
• This infection may be acquired during blood
  transfusion. List other protozoanparasitic
  infections that may be transmitted during blood
  transfusions.
• Explain the cardiac abnormalities found in this
  patient. Which othercomplication may occur?

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LYMPHADENOPATHY

• Analysis of lymphadenopathy gt 2/3 pts
  ?nonspecific causes or URI (viral or bacterial),
  lt1 malignancy.
• 186 of 220 patients (84) evaluation of
  lymphadenopathy ? benign diagnosis.
• 34 patients (16) malignancy (lymphoma or
  metastatic adenocarcinoma).
• 186 pts 63 (112) nonspecific or reactive
  etiology (no causative agent found)
• The remainder most commonly infectious
  mononucleosis, toxoplasmosis, or tuberculosis.

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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 gt 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.

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TABLE 54-1 Diseases Associated with
Lymphadenopathy
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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.

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Toxoplasmosis

• 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.

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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.

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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)

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Leishmaniasis

• 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 gt liver)
• Swollen glands
• Bone marrow symptoms
• WBC, RBC, PLT ?

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Leishmaniasis

• Some patients develop post kala-azar dermal
  leishmaniasis. 
• Visceral leishmaniasis ?opportunistic infection
  ?HIV()
• Laboratory DiagnosisExamination of
  Giemsa-stained slides of the relevant tissue is
  still the technique most commonly used to detect
  the parasite.

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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)

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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.

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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.

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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

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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 gt 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.

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Chagas disease (American trypanosomiasis)

• 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.

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Infection cycle of Trypanosoma cruzi, the
pathogen of Chagas disease
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CDC-DPD
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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.

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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.

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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.
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Photomicrograph of Trypanosoma cruzi parasites
(Chagas disease pathogen).
US Federal Government public domain image (CDC).
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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.
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Laboratory diagnosis

• 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)

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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.

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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.

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Parasitic infections which may be transmitted
during blood transfusions

• Malaria
• Babesiosis
• Toxoplasmosis
• Chagas Disease

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THANKS FOR YOUR ATTENTION!
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Chagas disease
                                               
The Fight for Recognition Chagas Disease
Meets Controversy Anna Moorhouse, Science
JournalistEnglish and Cell and Molecular
Biology, Simon Fraser University
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Questions?