Parasitic Diseases Flashcards
Define parasite and parasitic diseases
Parasite = an organism that lives in another organism called a host.
-They thrive to the detriment of the host.
Parasitic disease = infectious diseases caused or transmitted by a parasite.
List the 3 main types of parasites that cause parasitic disease
- Protozoa
- Helminths
- Ectoparasites
List the ways parasites can infect humans
- Vector borne
- Ingestion
- Inhalation
- Penetration of skin
- Penetration of eyes
- Sexual contact
List the risk factors for parasitic infection
- Walking barefoot
- Inadequate disposal of feces
- Lack of hygiene
- Close contact with someone carrying a parasite
- Insect bites
- Eating undercooked foods
- Unwashed fruits and vegetables
List the 4 protozoans
- Amoebas
- Flagelletes
- Ciliates
- Sporozoa
Define protozoa
- Protozoa are single celled organisms that multiply by simple binary division.
- Protozoa can multiply in their human hosts and cause overwhelming infection.
What are the 2 morphological forms of protozoa?
- Trophozoite
- Cyst
Define trophozoite
- Feeding and reproducing stage that lives within the host
- Active, infective stage
Define cyst
Infective form that survives in the environment
Define amoebas
- Protozoa with no truly defined shape
- Move and acquire food through the use of pseudopodia
- Found in water sources throughout the world
- Few cause disease**
Name 2 amoeba
- Naegleria fowleri (primary amoebic meningoencephalitis)
2. Acanthamoeba spp. (contact lens contaminant)
Etiology of Acanthamoeba spp.
- Can cause infections in humans and animals.
- Commonly found in lakes, swimming pools, tap water and heating & air conditioning units.
How does infection with Acanthamoeba spp occur?
through cuts or scrapes, the conjunctiva, or through inhalation
What diseases does Acanthamoeba spp cause?
Can cause diseases such as amoebic keratitis and encephalitis.
List the 2 morphology of Acanthamoeba spp.
- Trophozoite (active and infective)
- Cyst (dormant and environmentally hardy; can survive for years under extreme temperatures and pH)
Life Cycle of Acanthamoeba spp.
- The trophozoites replicate through mitosis.
- Under less favorable circumstances, the trophozoites become cysts (for survival).
- The trophozoites then enter the body via ulcerated or broken skin or through the lower respiratory tract.
- They then invade the CNS via hematogenous dissemination.
What is Acanthamoeba Keratitis?
- A rare but serious infection of the eye that can result in permanent visual impairment or blindness.
- In the US, 85% cases occur in contact lens users.
Why are contact lens wearers at risk for Acanthamoeba Keratitis?
- Hold amoebas onto the eye
- Trapping water
- Using old solution
- Using tap water to clean lens
S/sx of Acanthamoeba Keratitis
-Pain and redness of the eye
-Foreign body sensation
-Photophobia
–Blurred vision
Excessive tearing
-Pain out of proportion to clinical findings is a classic feature ofAcanthamoebakeratitis; however, especially early in the disease, lack of pain does not preclude the diagnosis.
Acanthamoeba Keratitis on physical exam
- Conjunctival hyperemia
- Episcleritis
- Scleritis
- Loosening of the corneal epithelium
Diagnosis of Acanthamoeba Keratitis
- Refer to an ophthalmologist.
- Clinical picture and growth of the amoeba from scraping of the eye.
- They can see the amoeba on confocal microscopy.
Tx of Acanthamoeba Keratitis
- Topical cationic antiseptic agent such as polyhexamethylene biguanide (0.02%) or chlorhexidine (0.02%) with or without a diamidine such as propamidine (0.1%) or hexamidine (0.1%).
- The duration of therapy may last six months to a year. *
- Pain control can be helped by topical cyclopegic solutions (topical numbing) and oral nonsteroidal medications
Prevention of Acanthamoeba Keratitis
- Visit your eye care provider for regular eye examinations.
- Wear and replace contact lenses according to the schedule prescribed by your eye care provider.
- Remove contact lenses before any activity involving contact with water, including showering, using a hot tub, or swimming.
- Wash hands with soap and water and dry before handling contact lenses.
- Clean contact lenses according to instructions from your eye care provider and the manufacturer’s guidelines.
- Store reusable lenses in the proper storage case.
What is Granulomatous Amoebic Encephalitis (GAE)?
- GAE is a rare, usually fatal infection of the CNS caused by Acanthamoeba spp.
- Usually occurs in people with weakened immune systems.
- Usually enter through the skin or lungs and spread to the bloodstream.
S/sx of GAE
- Mental status changes
- Loss of coordination
- Double or blurred vision
- Sensitivity to light
- Skin sores
- Other neurologic problems
Diagnosis of GAE
- CT or MRI Brain
- Spinal tap
- Biopsy of brain or skin sores
Tx of GAE
- Usually combination therapy
- Multidrug therapy: Miltefosine with one or more antifungal and antibiotics.
Etiology of Naegleria fowleri
“Brain eating amoeba”
- Naegleria fowleriproduces an acute, and usually lethal infection of the brain called primary amebic meningoencephalitis (PAM).
- Commonly found in warm freshwater, i.e. lakes, rivers, and hot springs.
How does Naegleria fowleri infect people?
Infects people when water containing the amoeba enters the body through the nose.
Life cycle of Naegleria Fowleri
- Cyst
- Trophozoite- infective stage
- Flagellate (they infect humans or animals by penetrating the nasal tissue and migrating to the brain via the olfactory nerves)
S/sx of Naegleria Fowleri
- Symptoms start about 5 days after infection.
- Initial symptoms include: headache, fever, N/V.
- Later symptoms include: neck stiffness, confusion, lack of attention, loss of balance, seizures, hallucinations and coma.
- Disease progresses rapidly and usually causes death within about 5 days.
Diagnosis of Naegleria Fowleri
- CSF sample
- Biopsy
- Tissue specimens: immunofluorescence, PCR, amoeba culture.
- Due to rarity of the infection and difficulty in initial detection, about 75% of diagnoses are made postmortem.
Tx of Naegleria Fowleri
- Amphotericin B
- Miconazole/fluconazole/ketoconazole and/or rifampin
- Dexamathasone
- Recently an investigational breast cancer and anti-leishmania drug, Miltefosine, has shown some promise in combination with some of these other drugs
Define Flagellates
- Protozoa that possess at least one flagellum
- Number and arrangement of flagella important to determining the species
List the Flagellates
- Chagas disease
- African sleeping sickness
- Leishmaniasis
Which organism causes Chagas disease?
Trypanosoma cruzi
Where is Chagas disease endemic?
Central and South America
Transmission of Chagas disease
- Transmission occurs through bites by triatominebugs.
- After they bite and ingest blood, they defecate on the person.
- The person can become infected ifT. cruziparasites in the bug feces enter the body through mucous membranes or breaks in the skin.
- “Kissing bugs” feed preferentially from the faces/lips
What other ways is Chagas disease transmitted?
- Congenital transmission (from a pregnant woman to her baby);
- Blood transfusion;
- Organ transplantation;
- Consumption of uncooked food contaminated with feces from infected bugs; and
- Accidental laboratory exposure
S/sx of Chagas disease
-Acute stage
-Acute- when occurs in endemic areas usually in childhood and asymptomatic.
-1-2 weeks after exposure
Indurated, erythematous lesion “chagoma” appears at the site of parasite entry.
-“Romana sign” inoculation in the conjunctiva, unilateral periocular and palpebral edam with conjunctivitis and preauricular lymphadenopathy.
S/sx of Chagas disease
-Latent stage
- Have parasitological and/or serologic evidence of T. cruzi but have neither symptoms, abnormal physical findings, nor cardiac or GI involvement.
- Many are identified by screening enzyme-linked immunosorbent blood assay(ELISA) and confirmatory radiommunoprecipitation assay (RIPA) when they donate blood.
S/sx of Chagas disease
-Chronic stage
- Develops in 20-40% after a latent phase that may last years to decades.
- Main effects are cardiac and GI***
Diagnosis of Chagas disease
- Light microscopy of blood smears or tissues
- Screening serologic test confirmed by a second test- indirect fluorescent antibody (IFA), enzyme immunoassays (EIA)or ELISA and followed by RIPA
- PCR based tests
- Once diagnosed, should get screening EKG and CXR.
- With any cardiac abnormalities get ECHO and with GI symptoms get GI contrast studies or endoscopy.
Treatment of Chagas disease
- Antiparasitic treatment is indicated for all cases of acute or reactivated Chagas disease and for chronicTrypanosoma cruziinfection in children up to age 18.
- Congenital infections are considered acute disease.
- Treatment is strongly recommended for adults up to 50 years old with chronic infection who do not already have advanced Chagas cardiomyopathy.
Antiparasitic treatment for Chagas disease
- Benznidazole - approved by FDA for use in children 2–12 years of age but is not yet available in U.S. pharmacies.
- Nifurtimox - Nifurtimox is not currently FDA approved
- Both drugs are currently available under investigational protocols from CDC.
Prevention of Chagas disease
- Plastering walls and replacing thatched roofs, spraying of houses.
- Travelers – don’t sleep in adobe dwellings or use bed nets.
Which organism causes African Sleeping Sickness?
Trypanosoma brucei
Etiology of African Sleeping Sickness
- The insect vector is the tsetse fly*
- Humans usually infected when bitten by infected tsetse flies
What are the 3 stages of Trypanosomiasis?
- Cutaneous
- Hemolymphatic
- CNS
S/sx of African Trypanosomiasis
-Cutaneous
- Papule develops at the site of the tsetse fly bite with a few days to 2 weeks.
- Evolves into a dusky red, painful, indurated nodule (trympanosomal chancre)*
S/sx of African Trypanosomiasis
-Hemolymphatic
- Over several weeks or months with intermittent fever, headaches, rigors, muscle and joint pain and transient facial swelling develops.
- Generalized lymphadenopathy often occurs.
- “Winterbottom sign”- enlarged lymph nodes in the posterior cervical triangle.
S/sx of African Trypanosomiasis
-CNS
- Causes persistent headaches, inability to concentrate, personality changes, daytime somnolence, tremor, ataxia and terminal coma.
- Without treatment patients die in coma of undernutrition or secondary infections.
