Protozoan and Helminth Infections Flashcards
Normal Blood Cell Counts/ Functions
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)
Malaria transmission
Transmitted by female Anopheles
mosquito
malaria incubation
Merozoite incubates and multiplies
in liver for 8-10 days
malaria RBC recepturs
RBC receptors: glycophorin A for
P. falciparum and Duffy antigen
for P. vivax
malaria pathogenesis
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
malaria complications
Cerebral malaria complication:
convulsion, coma, death
Invasion of red blood cells by merozoites
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
schizont multicellular stage
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,
clinical features of malaria
Clinical Features Fever Chills Rigors Myalagia Diarrhea
complications of malaria
Cerebral malaria -progressive headache, neck
stiffness, convulsions
(seizures), coma
(unconsciousness) Severe anemia Hypoglycemia Lactic acidosis Splenomegaly Glomerulonephritis
malaria pathogenesis
nephrotic syndrome in P. malariae
Deposition of malaria
antigens on
glomerular membrane
surface
Damage to the
endothelial surface of
glomeruli
High protein
excretion
Low serum albumin
cerebral malaria
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
malaria, diagnosis
Dx: microscopic demonstration of merozoites and trophozoites
on Giemsa-stained thick/thin blood smars DNA-based
techniques
malaria, treatment
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
malaria control
Control: vaccine development, vector control, bednets
impregnated with mosquito repellents
malaria, new treatment approaches
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
other malaria complications
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
capillary blockages in SCD and cerebral malaria
normal blood flow and sickled RBCs
adhesion of malaria -parasitized red cells to capillary endothelium in cerebral capillaries resulting in cerebral malaria
shared characteristics of cerebral malaria and SCD
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
Burkitt’s lymphoma and malaria
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
pneumocystitis jirovecii infection of lung in immunocompromised
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
occlusion of alveli by pneumocystis jiroveii infection
Occlusion of
alveoli by cell
debris from dead
macrophages, dead
lymphocytes and
dead P. jirovecii
cells, resulting in
apoxia and
interstitial
pneumonia
replication/rupture of toxoplasma gondii in macrophage
Organism has
predilection
for cells of
the: Lung Heart Lymphoid
organs Eye
