Extraintestinal protozoa Flashcards
Prevalence of malaria (Plasmodium species)
In 2016, 216 million cases of malaria occurred worldwide. 445,000 people died, mostly children in the African Region. There are 1,700 cases of malaria in the United States/year, mainly travelers and immigrants
Plasmodium species (5)
- Plasmodium falciparum – most common, most deadly (cerebral)
- Plasmodium vivax – 2nd most problematic (splenic rupture)
- Plasmodium ovale
- Plasmodium malariae
- Plasmodium knowlesi – most commonly in macaques, rare
human infection
Malaria symptoms
Primary pathology is the result of RBC hemolysis. Symptoms: fever, sweats, chills, headache, fatigue, anemia, and splenomegaly. Paroxysm-intensification of the symptoms
Sporogony
The process of spore formation in parasitic sporozoans, which occurs in the intestinal tract of the mosquito. This is the mosquito portion of the plasmodium life cycle
Schizogony
Asexual phase of plasmodium, occurring in the human host
Infective stage of plasmodium
An infected mosquito inoculates the host with sporozoites when it takes a blood meal, and sporozoites infect hepatic cells (exoerythrocyte cycle). They mature into schizonts, which rupture and release merozoites. Merozoite invades RBC
Recrudescence
Treatment followed by parasite reappearance
Plasmodium falciparum
Most severe form; causes cerebral malaria, blocks capillaries, DIC, blackwater fever. RBCs lyse during malaria infection, causing the urine to turn black due to hemoglobin, which is what “blackwater fever” refers to. Infects any stage of RBC. 36-48 hour periodicity. Maurer’s dots are an identifying characteristic of P. falciparum. The number of merozoites in the shizont is 8-36
Maurer’s dots
A membrane-like vacuole or structure within the red blood cell. With P. falciporum, we see multiple rings within the RBC. The rings look purple within the RBCs during microscopy. The presence of the rings is an identifying characteristic of P. falciparum
Gametocyte
One and a half times the diameter of the erythrocyte, in length, seen with RBCs under a microscope. This is diagnostic for plasmodium falciparum
Plasmodium vivax
Only infects reticulocytes = low parasite burden. 48 hr periodicity. Trophozoites – amoeboid, Shuffner’s dots. Number of merozoites in schizonts 12-24
Plasmodium ovale
First identified 1922, similar to P. vivax. Only infected reticulocytes – low burden. 48 hour periodicity. Trophozoites with single chromatin dot
– Shuffner’s dots, fimbriation
* Number of merozoites in shizonts 4-12
– Smaller than P.vivax
– Elongated to oval shaped
Plasmodium malariae
Recrudescence for many years-symptoms from RBC forms. Infects mature RBC. 72 hour periodicity. Trophozoite is thicker than P. falciparum. Band formation during maturation. Zieman’s stippling. Number of merozoites in schizonts 6-12. Maybe arranged in rosette
2 hosts of plasmodium life cycle
- Intermediate- human
- Definitive- Anopheles mosquito
Plasmodium life cycle (9 steps)
- Female mosquito blood meal –
sporozoites= infective agent for
humans - Sporozoites infect hepatic cells = schizonts
- Schizonts to merogony to form merozoites, to circulation ending the exo-erythrocytic cycle
- Plasmodium vivax and ovale species- dormant stage in the liver, relapses infection in weeks to years
- Erythrocytic schizogony (asexual multiplication within erythrocytes).
- Merozoites infect red blood cells- responsible for disease
- Mature to trophozoites may undergo schizogony to form schizonts, then merogony to release merozoites, infect red
blood cells & continue the erythrocytic cycle. - Trophozoites can mature into gametocytes
- The male gamete makes microgametocytes, and
the female gamete makes macrogametocytes. Ingested by mosquito-infectious agent
Diagnosis of Plasmodium (5)
- Symptoms
- History
- Blood smear—finger stick or
anticoagulant - Giemsa or Wright’s stains
- Thick and thin smears
Babesia species
Causes Babesiosis, human infections are caused by B. microti, B. divergens, B. duncani, and a 4th un-named strain, but there are over 100 species. It can be confused with P. falciparum.
Babesia distribution
Little known in malaria endemic
countries. In Europe, B. divergens is found in splenectomized patients. B. microti is found in most (Northeast and
Midwest), nonsplenectomized. Babesia duncani - found in Washington and California. MO-1 isolated from patients in
Missouri
Babesia symptoms
Can be asymptomatic (serology positive). Symptoms include fever, chills, sweating, myalgias, fatigue, hepatosplenomegaly, and hemolytic anemia. Incubation period is 1 to 4 weeks or greater. Disease can be severe in immunosuppressed, splenectomized, elderly. B. divergens has more severe symptoms (frequently fatal if not appropriately treated). In B. microti, clinical recovery usually occurs.
Babesia diagnosis
Smear – merozoite stage = maltese cross = pathognomonic
Diagnosis - serology, thick and thin blood smears, PCR
Trypanosoma brucei
Hemoflagellate, causes African sleeping sickness. Trypanosoma brucei subspecies rhodesiense (acute, rapid onset),
subspecies gambiense (chronic infection). Transmitted by the Tsetse fly.
Trypomastigote
15 to 30um length
* Elongated body with posterior
flagellum
* central nucleus with
POSTERIOR kinetoplast
* Buffy coat smear best method
for diagnosis
Babesia life cycle
Trypanosoma life cycle
African sleeping sickness symptoms (4)
- Gambian – neurologic deterioration
- Rhodesian - Rapid onset, leading to possible death.
- Recurring fever, lymphadenopathy, cervical lymph nodes involvement producing lesion = Winterbottom’s sign. – suggest brain involvement
- Sleeping sickness stage – invasion of CNS – behavior changes, apathy, fatigue,
confusion, meningoencephalopathy, death
Trypanosoma cruzi
South American trypanosomiasis – Chaga’s Disease. Caused by the Triatomid (reduviid) bug or “Kissing Bug”- they are nocturnal and feed on sleeping victims. trypomastigotes similar to
other species (nucleus & posterior kinetoplast), but found in form of a “C”. Reservoirs include dogs, rodents,
cats, pigs, opossums and raccoons- not found in other species. Can not eradicate
Trypanosoma cruzi symptoms (5)
- Scratch at bite site, introduces feces into skin
- Acute infection – asymptomatic, unilateral periorbital swelling if feces rubbed into eye
- Chronic infection - amastigotes replicate in myocytes resulting in cardiomyopathy,
congestive heart failure. - Mega-syndromes – esophagus, colon
- End stage disease – heart transplant, surgery for organ removal (colon)
Leishmania species (2)
- Primary Cutaneous Leishmaniasis- Leishmania donovani complex
– donovani, infantum chagasi - Cutaneous tropical sores – Old world (tropica complex)
& New world (braziliensis & Mexicana complex)
* Leishmania tropica complex
* Leishmania mexicana complex
Leishmania infective stage
Introduced by sandfly. Promastigote- regurgitation of parasite into the subcutaneous tissue as fly takes a blood meal. Enters into macrophage which subsequently ruptures releasing
parasite to disseminate and infect. Amastigote taken up by blood meal will transform in midgut of fly
Leishmania symptoms
Visceral Kala-Azar - disseminated disease. Mild, self-limiting to sudden onset. Spiking fevers, anorexia, malaise. Chronic – abdominal pain, low-grade fever, hepato & splenomegaly,
anemia
Primary Cutaneous Leishmaniasis-old world symptoms
Rash at site of bite progressing
over months to ulceration- raised, red margin, crusting, benign and self-healing. May cause deep-subcut infection. Possible disseminated disease
Primary Cutaneous Leishmaniasis- new world symptoms
Aggressive, cutaneous ulcers with mucous membrane spread (oral, nasal, pharyngeal) = espundia
Leishmania life cycle
Leishmania diagnosis (4)
- Blood smear with:
– Amastigotes within
macrophage cells. Oval intracellular, 4-8um - ELISA, NAAT
- IHC – parasites stain
with H & E, Wright’s
stain, NOT GMS - Amastigotes have bar-like
kinetoplast adjacent to
nucleus. Helps to differentiate from Histoplasma capsulatum
Trypanosoma diagnosis (4)
- Blood smear– Trypomastigote, Amastigotes in somatic
cells (myocytes) - T. cruzi – circular
trypomastigotes on blood
smears, letter “C” - Detailed history to
differentiate from other
infections. - ELISA, NAAT, serology
Toxoplasma gondii
Coccidia, worldwide distribution- most common human infections. Has a high prevalence. In France, transmitted by eating raw or undercooked meat. In Central America, the frequency of stray cats and climate favoring survival of oocysts and soil exposure. United States 22.5%,-seroprevalence among
women of childbearing age
(15 to 44 years) of 15%
Toxoplasma gondii life cycle
Acquired Toxoplasma gondii symptoms
Asymptomatic infection, benign and self-limited. 10% to 20% of patients have cervical lymphadenopathy and/or a flu-like illness. The clinical course is; symptoms usually resolve within a few weeks to months. In rare cases, ocular infection with visual loss can occur. Immunocompromised patients may experience CNS disease
– retinochoroiditis, pneumonitis, or other systemic disease,
AIDS=toxoplasmic encephalitis
Congenital toxoplasmosis
An acute primary infection acquired by the mother during pregnancy. The incidence and severity of congenital toxoplasmosis vary with the
trimester during which infection was acquired. Immediate maternal treatment reduces the incidence of congenital
infection and reduce sequelae in the infant. Subclinical infection at birth will subsequently develop signs or symptoms of congenital toxoplasmosis.
Toxoplasma gondii diagnosis (3)
- Observation of parasites in patient specimens - lymph node
biopsy. - Detection of parasite genetic material by PCR, especially in
detecting congenital infections in utero. - Serologic testing is the routine method of diagnosis
Naegleria fowleri
Worldwide distribution, free-living amoeba. Found in soil and freshwater- ponds, streams, municipal tap- water, spas, air-humidifiers. Acute & lethal CNS disease– Primary amebic
meningoencephalitis (PAM). No cysts stage in human
Acanthamoeba
Worldwide distribution, free-living amoeba. Found in soil and freshwater- ponds, streams, municipal tap- water, spas, air-humidifiers. Opportunistic pathogen, may cause corneal infections. If immunocompromised- granulomatous amebic
encephalitis (GAE)
Acanthamoeba trophozoite
Infective stage – eye, nasal tissue, respiratory tract, broken skin. They are 10-25 μm, large prominent karyosome. Sluggish motility at 25°C, better at 37°C
Acanthamoeba cysts
Have 2 walls- a wrinkled fibrous outer wall (exocyst) and an inner wall (endocyst) that may be hexagonal, spherical, star-shaped or polygonal. Cysts may be found in the brain, eyes, skin, lungs and other organs.
Naegleria fowleri trophozoites
Infective stage – nasal tissue to brain. They are 8 to 15 um, large prominent karyosome. 1+ pseudopodia, active motility at 25 or 37°C. Ameboflagellate, only the former of which is found in humans. Trophozoites may get over 40 μm
Naegleria fowleri and Acanthamoeba diagnosis (4)
- Examination of CSF
- Giemsa-stained smear
- Stained smears - brain tissue, skin, cornea biopsy
or corneal scrapings trophozoites and cysts (Acanthamoeba only:
HIGHLY resistant to chlorine) - Real-Time PCR – CDC developed assay
Trichomonas vaginalis
Tissue protozoa, worldwide prevalence among persons
with multiple sexual partners
or other venereal diseases. Incubation period is 5 to 28 days
Trichomonas vaginalis symptoms- males
Asymptomatic infection most
common- occasionally, urethritis,
epididymitis, and prostatitis
Trichomonas vaginalis symptoms- females
Symptomatic infection- vaginitis, purulent discharge, vulvar and cervical lesions, abdominal pain, dysuria and dyspareunia
Trichomonas vaginalis life cycle
Trichomonas vaginalis trophozoites
Pear-shaped (pyriform), 7-30μm long. Has five flagella: four anteriorly, one posteriorly along the outer membrane of the undulating membrane. Large nucleus at the wider, anterior end, chromatin granules, small
karyosome. Cytoplasm - granules, often not seen in Giemsa-stained specimens.
Trichomonas vaginalis diagnosis
Wet prep of vaginal fluids - parasite motility, DFA, molecular
methods
