Transcript IMMUNOLOGY IN PARASITIC INFECTIONS

IMMUNOLOGY IN
PARASITIC INFECTIONS
YL6
ASMPH
WINIFREDA U. DE LEON
PARASITES
UNICELLULAR - PROTOZOA
MALARIA
AMEBIASIS
TRYPANOSOMIASIS
MULTICELLULAR – HELMINTHS
SCHISTOSOMIASIS
FILARIASIS
HOOKWORM DSE
STRONGYLOIDOSIS
WHY INFECTED INDIVIDUALS
RESPOND DIFFERENTLY TO
THE SAME PARASITE?
HOST- PARASITE INTERACTION
HOST – WANTS TO PROTECT
HIMSELF FROM
THE PARASITE
PARASITE – WANTS TO
EVADE HUMAN DEFENSES
HOST FACTORS
GENETICS – GENERAL MAKE-UP
MAJOR HISTOCOMPATIBILITY COMPLEX (MHC)
HUMAN LEUCOCYTE ANTIGEN (HLA)
e.g. SICKLE CELL TRAIT – PROTECTS VS PLAS
FALCIPARUM MALARIA
DUFFY BLOOD FACTOR – SUSCEPTIBLE TO
PLAS VIVAX MALARIA
NUTRITIONAL STATUS
HIGH PROTEIN – NOT GOOD FOR INTESTINAL PROTOZOAN
HIGH CARBOHYDRATE – GOOD FOR TAPEWORMS
LOW IRON – RISK FOR DEVELOPMENT OF ANEMIA
HORMONAL BALANCE
AGE
NON-SPECIFIC DEFENSES
HOST
PHYSICAL AND CHEMICAL BARRIER
SKIN
SPHINCTERS
SECRETIONS/ EXCRETIONS
MEMBERS OF NORMAL FLORA
ACID pH :
gastric
vagina
HUMAN REFLEXES
SKIN LAYERS
INTACT SKIN
PARASITE
HOST
HOOKWORMS FILARIFORM
STRONGYLOIDES FILARIFORM
HYALURONIDASE – AIDS IN SKIN
PENETRATION
SCHISTOSOMA CERCARIAE
PENETRATION GLANDS
ACIDIC pH
HOST
VAGINAL CANAL
TRICHOMONAS VAGINALIS - AFFECTED
GASTRO INTESTINAL TRACT
ENTAMEBA HISTOLYTICA CYST
GIARDIA LAMBLIA CYST
ASCARIS EGG )
TRICHURIS EGG ) THICK EGG SHELL
TAENIA EGGS )
MUCUS MEMBRANE
MUCUS MEMBRANE
MUCUS SECRETION
HOST
CAN ENVELOP PARASITE – MOTILITY
OF GIARDIA LAMBLIA TROPHOZOITES
W/C CAN DIMINISH PATHOLOGY
HUMAN REFLEXES
COUGHING
EXPULSION OF LUNG FLUKE EGGS
EXPULSION OF ADULT ASCARIS
URINATION
FLUSH OUT TRICHOMONAS
VAGINALIS
INFLAMMATORY RESPONSES
PHAGOCYTES
COMPLEMENT
HUMORAL MEDIATORS
BRADYKININS
FIBRINOLYTIC SYSTEMS
PHAGOCYTES
CELLULAR COMPONENTS
EOSINOPHILS/ NEUTROPHILS
INCREASE IN NUMBER
EXHIBIT KILLING ACTION
MACROPHAGES
PHAGOCYTOSIS
NEUTROPHIL EXTRACELLULAR TRAPS
LYMPHOID COMPONENTS
SKIN ASSOCIATED LYMPHOID TISSUES
(SALT)
LANGERHANS CELLS
DENDRITIC CELLS
MAST CELLS
GUT ASSOCIATED LYMPHOID TISSUES
(GALT)
LYMPH NODES
HOST
STATUS
OUTCOME
IMMUNOCOMPETENT -
RESISTANCE
IMMUNE-COMPROMISED
SUSCEPTIBILITY
PATHOLOGY
INFECTION
PATIENT - EXPOSURE TO PARASITE
ANTIGEN
ACQUIRED IMMUNE DEFENSE
-RECOGNITION OF NON SELF
-HAS MEMORY
-SPECIFIC
PURPOSE
DISTINGUISHES SELF FROM NONSELF
ELIMINATES THE NON SELF
SPECIFIC/ ADAPTIVE
DEFENSES
IMMUNE RESPONSES
HUMORAL
B- LYMPHOCYTES AND
ANTIBODIES
CELL MEDIATED
T-LYMPHOCYTES AND THEIR
SOLUBLE PRODUCTS
ANTIGEN
MAY BE PRESENT ONLY IN ONE STAGE OF
PARASITE DEVELOPMENT
OR MAY BE PRESENT IN ALL STAGES
ANTIGEN
ANTIGEN PRESENTING CELLS
T- HELPER LYMPHOCYTES
T- HELPER LYMPHOCYTES
SUBSETS
TH1
INTERLEUKIN 2
GAMMA INTERFERON
CYTOTOXIC LYMPHOCYTES
CMIR
Th2
ILN 4,5 & 6
B- LYMPHOCYTES
PLASMA CELLS
(ANTIBODIES)
HIR
CLASSES OF
IMMUNOGLOBULINS
ANTIBODIES
IMMUNOGLOBULINS
IgE, IgG, IgM AND IgA
NON SPECIFIC + HIR + CMIR CAN WORK AT THE
SAME TIME
IgE + MAST CELLS, EOSINOPHILS & GOBLET
CELLS = EXPULSION OF GIT HELMINTHS
IgE + INFLAMMATORY CELLS = CYTOCIDAL
ACTION ON SCHISTOSOMA spp
ANTIBODY DEPENDENT CELL
MEDIATED CYTOTOXICITY (ADDC)
IgE
+ EOSINOPHILS
EOSINOPHIL ACTIVATING FACTOR
INTERLEUKIN 5
GRANULOCYTE –MONOCYTE COLONY
STIMULATING FACTOR
DESTRUCTION OF MICROFILARIAE
SCHISTOSOME
ADCC
ANAPHYLAXIS
IgE
+ HOMOCYTOTROPHIC IgG1
= DEGRANULATION OF MAST
CELLS AND BASOPHILS
= TYPE 1 HYPERSENSITIVITY
HYDATID CYST
ARTHROPOD BITES
MAST CELL DEGRANULATION
HYDATID CYST
ECHINOCOCCUS GRANULOSUS
IgM AND IgG
NOT EFFECTIVE AGAINST GIT HELMINTHS
OPSONIZATION (PHAGOCYTOSIS) OF
TRYPANOSOMES
PREVENT PENETRATION OF HOST CELLS: RBC
(PLASMODIA, BABESIA)
IgM AND IgG + COMPLEMENT
= LYSIS OF TRYPANOSOMES
IgA
IgA + IgM = MEDIATE ADCC IN
GIARDIA INFECTION
IgA + IgG + CMI = SEPARATION OF
CRYPTOSPORIDIUM FROM
ENTEROCYTES
IgA + GALT = PROTECTIVE vs
INTESTINAL HELMINTHS (TAPEWORM)
MACROPHAGES
ANTIGEN PRESENTING CELLS
PRODUCED BY LYMPHOKINE
ACTIVATION :
INTRACELLULAR DESTRUCTION
-OF PLASMODIUM/ BABESIA IN RBC
-OF LEISHMANIA IN MACROPHAGES
T LYMPHOCYTES
Th (HELPER) – ANTIBODY PRODUCTION
Tdth (DELAYED TYPE OF HYPERSENSITIVITY)
– PRODUCTION OF LYMPHOKINES
- RECRUITMENT OF CELLS INTO
GRANULOMA FORMATION
e.g. SCHISTOSOMA
Tc (CYTOTOXIC)- CANNOT KILL HELMINTHS
BUT CAN DESTROY PARASITIZED CELLS
Ts (SUPPRESSOR) + MACROPHAGES =
REGULATION/ MODULATION OF
IMMUNE RESPONSE
Th1 RESPONSE
Th1 + GAMMA INTERFERON
MINIMIZES ILN 13 CAN PROTECT
vs FIBROSIS IN SCHISTOSOMA
INFECTION
PARASITE EVASION
MECHANISMS vs HOST
PARASITE GLYCAN
IMMUNE SUPPRESSION
ANTIGENIC VARIATION
HOST MIMICRY
SEQUESTRATION
PARASITE GLYCAN
IMMUNE SUPPRESSION
PLASMODIA – REDUCES THE IMMUNE FUNCTION OF
MACROPHAGES
- LESSEN PHAGOCYTOSIS
- DEFECTIVE PROCESSING OF ANTIGEN
AFRICAN TRYPANOSOMES – PRODUCTION OF
LARGE AMOUNT OF VARIABLE SURFACE
GLYCOPROTEINS (VSG’s)
- DEFECTIVE ANTIGEN PROCESSING
- IMPAIR T & B CELL ACTIVITIES
HOOKWORM ADULTS IN THE
INTESTINES
Produces glycoprotein ( Neutrophil inhibitory factor
(NIF) that can resist acute inflammatory response
1. Blocks the adhesion of activated human
neutrophils to vascular endothelial cells
2. Blocks the release of H2O2 from activated
neutrophils
3. Blocks the ingestion of serum opsonized
particles by inhibiting neutrophil binding to the
integrin receptor CD11, CD13 and CD18
HOOKWORM ADULTS
Excretory-Secretory Products Stimulates fibrinolysis
Glutathione S transferase
Anti IgG enzyme
Acetylcholinesterase
Prevents expulsion of the parasite
IMMUNE SUPPRESSION
ENTAMEBA HISTOLYTICA
SUPPRESSOR FACTOR vs MONOCYTES
FASCIOLA spp – DOWN REGULATION OF Th1
ACTIVITY
FILARIAL WORMS/ PLASMODIA
POLYCLONAL HYPER- GAMMA
GLOBULINEMIA
NO SPECIFICITY
IMMUNE SUPPRESSION
BLOCKING ANTIBODIES
FILARIAL WORMS
HOOKWORM (NECATOR)
IMMUNE RESPONSE OF MAN IS
DIRECTED TO DEEP LAYERS OF THE
HOOKWORM CUTICLE
IMMUNE SUPPRESSION
IMMUNE COMPLEXES
PLASMODIUM spp
TRYPANOSOMA CRUZI
CYSTICERCUS CELLULOSAE
SCHISTOSOMA
SUPPRESS INFLAMMATORY REACTION THROUGH
INHIBITION OF COMPLEMENT
NO DESTRUCTION OF PARASITE
ANTIGENIC VARIATION
CHANGE IN ANTIGENIC PROFILE
TRYPANOSOMA GAMBIENSE
GIARDIA LAMBLIA
VARIATION IN THE AMINO ACID SEQUENCE IN
PLASMODIUM FALCIPARUM
MEROZOITE SURFACE ANTIGEN (MSA)
RING INFECTED ERYTHROCYTE SURFACE
ANTIGEN (RESA)
TRYPANOSOMA GAMBIENSE
Pf VARIATION
Pf VARIATION
P. FALCIPARUM – GENETIC
REGULATION
HOST MIMICRY
MIMICS ANTIGEN OF HOST
ECHINOCOCCUS GRANULOSUS
BLOOD GROUP ANTIGEN
ACQUIRES ANTIGENIC MOLECULES OF
HOST
SCHISTOSOMA spp
SEQUESTRATION
ESCAPE THE HOST IMMUNE RESPONSE
HIDE INSIDE MACROPHAGES
TRYPANOSOMA CRUZI
LEISHMANIA spp
TOXOPLASMA GONDII
HIDE IN THE DEEP VASCULATURE
PLAS FALCIPARUM (KNOBS FOR
ATTACHMENT TO TINY CAPILLARIES
PARASITES – EVADE
PHAGOCYTOSIS
CEREBRAL MALARIA
ARE THESE IMMUNE
RESPONSES PROTECTIVE ?
FILARIASIS
TROPICAL PULMONARY EOSINOPHILIA
HYPERGAMMAGLOBULINEMIA
OVER PRODUCTION OF IgM
DEVELOPMENT OF IMMUNE
COMPLEXES
TPE
IMMUNE COMPLEXES
MALARIA (PLASMODIUM)
HYPERACTIVE MALARIUS SPLEEN
(HMS)
DISTURBANCE IN HIR
SPLENOMEGALY AND ANEMIA
PLAS MALARIAE – DEPOSITED IN
GLOMERULI CAUSING KIDNEY
FAILURE/ NEPHROTIC SYNDROME
IMMUNE COMPLEXES
OTHER ADVERSE EFFECTS
SEQUESTRATION
PLAS FALCIPARUM
CAUSES CEREBRAL INVOLVEMENT
LEISHMANIA
DESTRUCTION OF MACROPHAGES
GRANULOMA FORMATION
SCHISTOSOMA
MAIN CAUSE OF PATHOLOGY
OTHER ADVERSE EFFECTS
LOSS OF HIR
IMMUNE-DEFICIENCY
AT RISK OF OPPORTUNISTIC
PARASITIC INFECTIONS
LOSS OF CMIR
STRONGYLOIDOSIS
TRIGGERS EXTRAINTESTINAL
DISSEMINATION
AREAS OF INTEREST
IMMUNOREGULATION
CHRONIC INFECTION – DAMPENS
T- CELL RESPONSIVENESS
EFFECT OF NITRIC OXIDES + ILN 10
ON PATHOLOGY
AREAS OF INTEREST
INTERACTION BETWEEN ENDOCRINE
SYSTEM AND IL 6
PREMUNITION OR CONCOMITANT
IMMUNITY
IMMUNE RESPONSE TO COINFECTION
POSSIBILITY OF IMMUNOLOGICAL
DISORDER LIKE AUTO-IMMUNITY
HOW TO APPLY IN
MEDICAL SCIENCE
IMMUNODIAGNOSIS
Ab DETECTION
Ag DETECTION
VACCINE DEVELOPMENT
DRUG DEVELOPMENT
THANK YOU AND
GOOD DAY