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Haemotology > Protozoan and Helminth Infections > Flashcards

Protozoan and Helminth Infections Flashcards

1
Q

Normal Blood Cell Counts/ Functions

A

Neutrophils: 50-70% WBCs, bacterial infections
 Eosinophils: 1-4% WBCs, parasitic infections, allergy
 Basophils: < 1% WBCs, allergic, type 1 reactions
 Lymphocytes: 30-40% WBCs, T&B cells, NK cells - T cells (CD4 and CD8 cells) - CD4 TH1 for intracellular infections/IFN-γ production, inflammatory/DTH responses - CD4 TH2 for antibody production by B cells - CD8 TC kills virus infected cells, organ transplants, tumor cells - Natural Killer (NK) Cells

 Monocytes: (phagocytic, 3-5%) macrophages, alveolar macro, dendritic cells, Kupfer cells (liver), histiocytes (connective tissue), microglial cells (brain)

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2
Q

Malaria transmission

A

Transmitted by female Anopheles
mosquito

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3
Q

malaria incubation

A

Merozoite incubates and multiplies
in liver for 8-10 days

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4
Q

malaria RBC recepturs

A

RBC receptors: glycophorin A for
P. falciparum and Duffy antigen
for P. vivax

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5
Q

malaria pathogenesis

A

Invades rbcs in blood circulation,
develops into schizont in 48 hrs;
ruptures, releases glycolipid toxin
that initiates malaria cascade with
cyclic fever, chills, anemia,
diarrhea, respiratory difficulty

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6
Q

malaria complications

A

Cerebral malaria complication:
convulsion, coma, death

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7
Q

Invasion of red blood cells by merozoites

A

Merozoites transform into ring
stage in 6-12 hrs
 Rings transform into trophozoites
in 12 hrs
 Trophozoites transform into
schizonts in 24 hrs
 Schizonts rupture to release
daughter merozoites into blood
circulation to infect new rbcs
 More than one ring in singe rbc
indicates P. falciparum infection

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8
Q

schizont multicellular stage

A

Schizont ruptures to
release merozoites, glycolipid toxin, soluble antigens and cellular metabolic products
 Each daughter
merozoite reinvades red blood cells
 Toxin (LPS-like) and
above products induce fever, chills,

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9
Q

clinical features of malaria

A

Clinical Features  Fever  Chills  Rigors  Myalagia  Diarrhea

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10
Q

complications of malaria

A

Cerebral malaria -progressive headache, neck
stiffness, convulsions
(seizures), coma
(unconsciousness)  Severe anemia  Hypoglycemia  Lactic acidosis  Splenomegaly  Glomerulonephritis

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11
Q

malaria pathogenesis

A
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12
Q

nephrotic syndrome in P. malariae

A

Deposition of malaria
antigens on
glomerular membrane
surface
 Damage to the
endothelial surface of
glomeruli
 High protein
excretion
 Low serum albumin

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13
Q

cerebral malaria

A

Caused by Plasmodium falciparum  Parasite-infected rbcs migrate to cerebral capillaries  Adhere to each other and to capillary endothelium by
cysteine-rich knobs  Occlusion of cerebral capillaries  progressive headache; neck stiffness  convulsions (seizures)  coma (unconsciousness)  Death if untreated
Cerebral occlusion by parasite- infected rbcs, stiff neck, convulsion, coma, death

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14
Q

malaria, diagnosis

A

Dx: microscopic demonstration of merozoites and trophozoites
on Giemsa-stained thick/thin blood smars DNA-based
techniques

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15
Q

malaria, treatment

A

Wide-spread resistance to chloroquine
 Primaquine to prevent dormant liver hypnozoites of P. vivax and elimination of gametocytes
 Fansidar (pyrimethamine-sulfadoxine), larium (mefloquine) and
doxycyline for prophylaxis and treatment
 Resistance to fansidar due to gene mutation for dihydrofolate
reductase
 Halofantrine, quinine and artemisinin for treatment of
chloroquine resistant malaria

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16
Q

malaria control

A

Control: vaccine development, vector control, bednets
impregnated with mosquito repellents

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17
Q

malaria, new treatment approaches

A

Combination Drug Therapy  Artemisinin-based combination therapy (ACT)  Artemether-lumenfantrine (Coartem)  Dihydroartemisinin-piperaquine (Artekin)  Artemisinin mefloquine  ACTs reduce drug resistance, but are 10 to 20
times more expensive than single drugs

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18
Q

other malaria complications

A

Explanations:  Sickle cell disease -double recessive Hb gene, vaso-occlusion,
ischemia, bone pain crisis, acute chest pain,
spleen atrophy, leg ulcers, jaundice, infections
(pneumonia, cholecystitis/gallstone disease,
osteomyelitis)

 Burkitt’s lymphoma (tumor of the jaw),
associated with EBV and malaria

19
Q

capillary blockages in SCD and cerebral malaria

A

normal blood flow and sickled RBCs

adhesion of malaria -parasitized red cells to capillary endothelium in cerebral capillaries resulting in cerebral malaria

20
Q

shared characteristics of cerebral malaria and SCD

A

Fever (cyclic, non-cyclic)  Anemia, hypoferremia, hypoxia  Vasocclusion (convulsion, ischemia)  Splenic dysfunction  Sepsis, inflammation (acute, chronic) underlie
complications of the two diseases  High mortality in malaria-endemic regions

21
Q

Burkitt’s lymphoma and malaria

A

Tumor of immature B cells
 Prevalent in Central/East Africa, Papua New
Guinea in 6-14 year olds, particularly boys
 Lymphoma associated with EBV and malaria
infections
 EBV antigens are mitogenic for B cells
 EBV nuclear antigen is prevalent in sera and
infected cells
 EBV DNA is integrated into DNA of host B cell;
present in tumor cells
 Malaria infection is also mitogenic for
B cells
 IL-10 analogue made by EBV prevents TH1
response
 Cellular oncogene (c-myc) is translocated from
chromosome 8 to chromosome 14, where it is
expressed
 Malaria mitogens; EBV mitogens and oncogens
lead to B cell proliferation and development of B
cell lymphoma of the jaw and face
 EBV also causes i) leukemia, Hodgin lymphoma ii)
nasophryngeal carcinoma in China and southeast
Asia; hairy oral leukoplakia, lesions of tongue/ mouth
in AIDS

22
Q

pneumocystitis jirovecii infection of lung in immunocompromised

A

Dormant, endogenous fungal
/protozoan? asymptomatic
cyst infections in lungs of
immunocompetent hosts
 Reactivated in cellular
immunocompromised
individuals (AIDS, leukemia),
immunosuppressive drugs)  Multiplies in large numbers  Occludes the alveoli
 Causes interstitial pneumonia  Treatment: Trimethoprim
sulfamethoxazole

23
Q

occlusion of alveli by pneumocystis jiroveii infection

A

Occlusion of
alveoli by cell
debris from dead
macrophages, dead
lymphocytes and
dead P. jirovecii
cells, resulting in
apoxia and
interstitial
pneumonia

24
Q

replication/rupture of toxoplasma gondii in macrophage

A

Organism has
predilection
for cells of
the:  Lung  Heart  Lymphoid
organs  Eye

25
Q

toxoplasma clinical phases

A

Asymptomatic
 Congenital – transplacental infection -spontaneous abortion, stillbirth, encephalitis, mental retardation, chorioretinitis, blindness
 Recrudescent – reactivated infection in immunocompromised, transplants, immunosuppressive therapy - mostly neurologic complications - encephalitis, cerebral mass lesions, chorioretinitis - endocarditis - seizures, confusion, lethargy

26
Q

Diagnosis and treatment of toxoplasma gondii

A

Diagnosis
- ELISA for specific IgM - tissue biopsy of lymph nodes, CSF, bone marrow, amniotic fluid

 Treatment - pyrimethamine sulfadiazine - pyrimethamine + clindamycin

27
Q

Leishmania parasites

A

Leishmania tropica (cutaneous )  L. aethiopica
(cutaneous
disseminated)  L. braziliensis
(mucocutaneous)  L. donovani (visceral)  All transmitted by
Phlebotomus sandfly  Macrophage

toxin destruction of epithelial layer

28
Q

Leishmaniasis clinical ; aethopica

A

Localized cutaneous lesions cutaneous lesions, in Leishmania tropica

L. aethopica disseminated cutaneous lesions an indication of cellular immunosuppression

29
Q

Leishmania braziliensis

A

Parasites also
transmitted by
Phlebotomus sandfly  Multiplication of
protozoan parasites in
macrophages
 Rupture of parasites
out of macrophages
 Dissemination of
infection in
mucocutaneous layer

30
Q

Visceral, systemic leishmaniasis L. donovani (kala-azar)

A

Initiated by insect bite  Multiplication and rupture in
macrophages  Dissemination by
macrophages to blood,
spleen, liver, lymph nodes  Slow disease with fever,
weight loss, splenomegaly,
hepatomegaly  Untreated die of liver failure

31
Q

Leishmania diagnosis and treatment

A

Diagnosis: microscopic demonstration of
Leishmania species
amastigotes in Giemsa stained skin scrapings or lymph node, spleen or bone marrow biopsies
 Disseminated cutaneous and visceral
leishmaniasis are complications of HIV infection in endemic countries
 Treatment: sodium stibogluconate for all four

32
Q

African and American Trypanosomiasi

A

African trypanosomiasis -Trypanosoma gambiense in West Africa -Trypanosoma brucei in East Africa, much more virulent  American trypanosomiasis (Chagas disease) -Trypanosoma cruzi in Central and South America; destruction of Purkinje fibers and
cardiomegaly  Antigenic variation in all trypanosome infections, with
consequent immune evasion and treatment

33
Q

Trypanosomes in lymph node

A

Trypanosoma gambiense in blood
after insect inoculation
 Trypanosomes migrate to the
lymph nodes, causing lymph node
enlargement/Winterbottom’s sign
and eventually to the brain
 Fever, splenomegaly, severe
headache, weight loss and coma
(sleeping sickness)
 Diagnosis by microscopic demo of
parasites in blood smears and CSF;
high serum parasite IgM
 Treatment: pentamidine,
melarsoprol

34
Q

triatoma vectors for what diseases

A

Triatoma (reduvid) vectors for Trypanosoma cruzi/Chaga’s Disease

35
Q

Chagoma in Chaga’s disease

A

Chagoma/ chancres
/swellings at sites of insect
bites
 Parasites introduced into
blood circulation; invade
macrophages and cardiac
muscle cells
 Parasite causes myocarditis
and enlargement of
ventricles (cardiomegaly) by
destruction of Purkinje
fibers; mega-esophagus and
megacolon by destruction of
afferent nerves

36
Q

Cardiomegaly by T. cruzi due to destruction of Purkinje fibers

A

Ventricular enlargement
to compensate for loss of
nerve conduction
 Parasite also invades
mesenteric nerves of the
esophagus and colon
 Lack of peritalsis leads to
esophagus and colon
enlargement

37
Q

Diagnosis and Treatment : T Cruzi

A

Diagnosis:
- based on clinical presentations -microscopic demonstration of trypanosomes in
Giemsa stained bood smears or lymph node
biopsies; serum parasite specific IgM
 Treatment: - suramin, pentamidine for acute and
melarsoprol for chronic trypanosomiasis - nifurtimox, benznidazole and allopurinol for
Chaga’s disease

38
Q

Onchocerca volvulus/River blindness

A

Transmitted by Simulium black flies  Adult worms live in subcutaneous nodules  Eye disease (chorioretinitis) due to damage of eye tissues by
microfilarial migration and intense inflammatory reactions from
antigen/antibody complex depositions  Migration thr’ eye tissues cause inflammation of sclera, retina
and choroid, leading to blindness  Wolbachia bacteria endosymbiont also contributes to
inflammatory reactions from antigen/antibody complex
depositions  Cause pruritis, hyperkeratosis, skin depigmentation, hanging
groin due to loss of skin elasticity and thickening  Called river blindness- vectors live near rivers  Treatable with ivermectin and doxycycline (Wolbachia bacteria)  Control by reduced exposure to streams that serve as breeding
sites for black flies

39
Q

Onchocerca in skin nodules

A
40
Q

Inflammatory damages in eye tissue

A

Sclerosing keratitis  Chorioretinis  Optic atrophy  All leading to river
blindness  Treatment:
Ivermectin plus and
surgical removal of
encapsulated nodules
of adult worms

41
Q

Lymphatic Filariasis

A

Caused by Wuchereria bancrofti and Brugia
malayi  Transmitted by mosquitoes  Adults live in lymph nodes and lymphatics of
the lower limbs  Inflammatory reactions and subsequent
calcification lead to occlusion of lymphatics,
hydrocoele and enlargement of scrotum and
limbs

42
Q

Diagnosis and Treatment : lymphatic filariasis

A

Diagnosis by demonstration of larval
microfilariae in blood smears  Treatment is effective with ivermectin  Vector control seems promising

43
Q

Life cycle of Dracunculus medinensis

A

Also known as guinea worm
 Mentioned in biblical accounts
 Larval stages live in fresh waters
and ingested by copepods (water
fleas)
 Reservoir hosts include dogs and
fur-bearing animals
 Humans infected by drinking water
with infected copepods
 Adults migrate, mate in
retroperitoneum
 Gravid females ulcerate in
subcutaneous tissues of the lower
extremities to expel larvae into
water
 Worldwide eradication by Carter
Foundation since 1976 almost
complete

44
Q

D. medinensis (contd)

A

No drugs and vaccine for guinea worm  Village doctors extract worms with a rolling twig  Worm breakage can lead to severe anaphylactic reactions  Drug of choice is niridazole or metronidazole for wond
treatment  Control by elimination of copepods in drinking water  Provision of safe drinking water

Haemotology (15 decks)

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