Module 3 Flashcards
1
Q
Blood and tissue parasites
A
- protozoa: amoebas, nematodes and cestodes
- sporozoa
- free-living amoeba
- hemoflagellates
2
Q
Blood and tissue parasites (general characteristics)
A
- arthropod vector (blood parasites)
- mammals serve as definitive or intermediate host (tissue parasites)
- transmitted via ingestion
3
Q
Sporozoa
A
- Plasmodium species, Babesia species
- malaria life cycle includes schizogony (asexual cycle) and sporogony (sexual cycle) which take place in Anopheles mosquito
- babesia life cycle includes ticks (intermediate host) which are infected by taking blood of infected mammals or transovarial (females transmit infective forms to progeny)
4
Q
Schizogony (Plasmodium)
A
- asexual cycle which takes place in human or animal host
- sporozoites are injected into skin during mosquito bite
- enter bloodstream and invade liver cells
- replicates into multiple cryptic merozoites which are released into bloodstream as merozoites that invade RBC’s
- ring forms (trophozoites) develop within RBC’s
- trophozoites develop into schizonts (multi-nucleated forms)
- upon rupture of RBC, merozoites are released to invade other RBC’s
- some merozoites develop into micro (male) and macro (female) gametocytes
- gametocytes initiate sexual phase in mosquito stomach
- micro fertilizes macro to a zygote, which becomes an oocyst
- sporozoites develop in the oocyst and can be injected into next mammal
5
Q
Plasmodium life cycle stages
A
Gametocyte –> exflagellation –> sporocyst –> sporozoite –> proboscis –> cryptozoites –> merozoites –> rings –> trophozoites –> Schizont
6
Q
Identification of Plasmodium species
A
observe differences in size and distribution of the ring forms, size and shape of the gametocytes, and appearance or the infected erythrocytes
7
Q
ID of Plasmodium falciparum
A
- ring forms are small (< 1/4 of cell)
- RBC’s are not enlarged
- Schuffner’s dots do not appear
- multiple ring forms may be seen
- no schizonts seen
- presence of banana-shaped gametocytes
- high percentage of infected RBC’s
8
Q
Plasmodium falciparum (pathology)
A
- congestion of parenchyma and hypertrophy of cells in spleen and liver
- desposition of brown-black malarial pigment in Kupffer cells
- Hemoglobin casts in renal tubule cells (seen by dark red-black urine)
- vascular congestion of brain and capillary plugging by infected RBC’s
- febrile paroxysms every other day
- malignant tertian
- splenomegaly and anemia
- cerebral malaria (seizures, coma, etc.)
- progress of symptoms may be rapid
9
Q
ID of Plasmodium vivax
A
- infected RBC’s are enlarged and pale
- Schuffner’s dots are present
- Schizonts have > 13 segments
- rings forms are small
- trophozoite cytoplasm is flowing and ameboid
- malarial pigment is finely granular
- gametocytes have a single large nucleus with compact chromatin
10
Q
Plasmodium vivax (pathology)
A
- splenomegaly
- phagocytes have finely divided brown-black malarial pigment (hemozoin) - may be seen in Kupffer cells during cryptozoic stage
- malarial pigment must be distinguished from Hb deposits seen in hemochromatosis (stain blue with Prussian blue)
- fever spikes 48 hours apart
- benign tertian
11
Q
ID of Plasmodium malariae
A
- infected RBC’s are not enlarged and normochromogenic with no granules
- Schizonts have < 13 granules (8-9)
- cytoplasm in trophozoites is compact
- segments arrant in a rosette and clumps of brown malarial pigment is seen in the “hoff”
12
Q
Plasmodium malariae (pathology)
A
- mild splenomegaly
- malarial pigment is coarse and granular
- older kids have tendency to develop nephrotic syndrome
- fever spikes occur every 3rd day
- less anemia than with other species
13
Q
ID of Plasmodium ovale
A
- infected RBC’s are enlarged, pale and contain Schuffner’s dots
- oval shape of RBC’s**
- < 13 segments that are finely granular
- brown-staining malarial pigment present
14
Q
Plasmodium ovale (pathology)
A
- splenomegaly is often seen
- phagocytosis of malarial pigment by macrophages
- malarial pigment in cytoplasm in cryptozoic stage
- fever spikes every other day (tertian malaria)
- symptoms are usually mild
15
Q
Preparation of specimen for malarial examination
A
- thin and thick Giemsa-stained blood smears
- level of parisitemia can be determined
- ID based on background morphological changes in the infected RBC, and in appearance of trophozoites, schizonts and gametocytes
16
Q
Specific assays for malarial confirmation
A
- indirect fluorescent antibody (IFA)
- enzymes immunoassays
- species-specific PCR
17
Q
ID of Babesia
A
- ring forms are tiny
- four segments are formed during schizogony
- segments align across from each other in shape of a Maltese cross
18
Q
Babesia (pathology)
A
- fatal pathology is related to hypoxia and shock
- acute renal tubular necrosis
- jaundice
- hemorrhagic manifestations (DIC)
- symptoms often mimic the flu
- symptoms usually subside in one week
19
Q
ID of Toxoplasma gondii
A
- tachyzoites measure 2-4 x 6-8 microns and are bow-shaped
- have red-blue nucleus and pale blue-gray cytoplasm
- cysts measure 5-25 microns in diameter and are engorged with tiny bradyzoites
- no kinetoplast (differentiates it from amistigotes)
- intermediate host: birds, mice, humans
- final host: cat
20
Q
Toxoplasma gondii life cycle
A
oocysts in cat feces –> tachyzoites –> invasive tachyzoites –> tissue cyst –> bradyzoite –> cat reinfection
21
Q
Toxoplasma gondii (pathology)
A
- proliferating tachyzoites cause cell death, necrosis and intense PMN response to all involved organs (CNS, lungs, heart)
- meningoencephalitis, interstitial pneumonitis and focal myocarditis
- hydrocephalus is common
- cysts containing bradyzoites may be seen in brain and other organs following and immune response
- severe febrile illness with pneumonia, liver dysfunction and myocarditis in infants and kids
22
Q
Diagnosis (Toxoplasma)
A
- diagnosis made by demonstrating parasitic forms in blood, body fluids and/or tissue biopsies
- molecular assays and serology
23
Q
ID of Pneumocystis carinii
A
- cysts measuring up to 7 microns demonstrated in silver-stained preparations
- up to 8 nuclei may be seen with Giemsa or methylene blue stains
- opportunistic pathogen
24
Q
Pneumocystis carinii (pathology)
A
- causes pneumonia in ICP’s
- aveolar spaces fill with foamy, vacuolated, amorphous exudate
- interstitial plasma cell pneumonia
- difficulty breathing, dyspnea, nonproductive cough, fever
- progressive respiratory compromise often leads to death
25
Q
Hemoflagellates
A
Trypanosoma
Leishmania
26
Q
Hemoflagellates (general characteristics)
A
- vectors include flies
- reproduce via binary fission (no sexual forms)
- 4 stage life cycle
27
Q
Hemoflagellates life cycle
A
- motile, circulating trypoastigotes
- aflagellar amastigotes characteristic
- promastigote
- epimastigote
28
Q
Trypanosomes
A
- most commonly infect humans
- African trypanosomiasis = sleeping sickness is caused by Trypanosoma brucei with vector tse tse fly
- Chaga’s disease (South American) is caused by Trypanosoma cruzi with vector reduviid bug
- long and fishlike, rounded on one end, pointed on the other
- has posterior kinetoplast (dark-staining dot) and flagellum
- has a centrally located nucleus
29
Q
Trypanosomes (diagnosis)
A
- African: only seen in trypanosomal form in blood and lymph nodes early in infection and in CNS in chronic infection
- South American: circulating trypanosomal form and intracellular form seen
30
Q
Trypanosoma brucei gambiense
A
- diagnostic forms are spindle-shaped flagellates with posterior kinetoplast and undulating membrane and anterior flagellum
- circulating forms are few in number
- only trypomastigote stage occurs in humans
31
Q
Trypanosoma brucei rhodesiense
A
- diagnostic forms are spindle-shaped flagellates that are indistinguishable from T. gambiense
- difference is large number of circulating forms
32
Q
Trypanosoma brucei (pathology)
A
- intense subcutaneous inflammation
- lymphadenopathy and splenomegaly with infiltrate of lymphs, plasma cells and macrophages
- presence of Mott cells
- invade CNS causing leptomeningitis extending into the perivascular Virchow Robbins spaces
- intermittent long cycles of fever in stage 1
- slowly-progressive neurologic manifestations in stage 2
33
Q
Trypanosoma cruzi
A
- diagnostic forms are spindle-shaped and are shorter than T. brucei
- have distinctive “C” form
- intracellular amastigotes occur in tissues
34
Q
Trypanosoma cruzi (pathology)
A
- erythematous subcutaneous swelling (chagoma) develops at site of bug bite
- trypomastigotes invade host cells and assume an amastigote
- formation of cysts packed with amastigotes
- varying degrees of muscle fiber degeneration with surrounding acute and chronic myocarditis
- swelling of tissue around one eye at site of entry
- fever, malaise, anorexia and edema
- cardiac arythmias and cardiac failure in chronic infections
35
Q
ID of Leishmania
A
- dissemiated disease (kala azar) or remain in skin/mucous membrane (tropical sore)
- intermediate host: sandflies (Phelotomus and Lutzomyia)
- mammalian hosts: rodents, canines
- humans are accidental hosts
- organisms are small and oval
- have rod-shaped kinetoplasts perpendicular to nucleus and an anterior parabasal body giving rise to an inactive flagellum
- invade visceral organs
36
Q
Leishmania donovani (pathology)
A
- hepatomegaly, splenomegaly and lymphadenopathy
- phagocytic cells in these organs are full of leishmania
- immune complexes, mesangial proliferation and amyloid deposit in kidneys and can lead to renal failure
- spiking fever, chills and malarial symptoms in acute cases
- abdominal discomfort in chronic cases
- normo, normo anemia and leukopenia
- hypergammagglobulinemia, circulating immune complexes and rheumatoid factors lead to secondary complications
- gray pigmentation of skin
37
Q
Lieshmania (cutaneous) pathology
A
- identical to L. donovani
- lesions are confined to the skin
- diagnosis is made by finding amastigotes in stained smears from base of ulcers
