Transcript of THE ROLE OF INFECTIONS IN THE EMERGENCE OF NON – COMMUNICABLE DISEASES (NCDs): Compelling needs...
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- THE ROLE OF INFECTIONS IN THE EMERGENCE OF NON COMMUNICABLE
DISEASES (NCDs): Compelling needs for novel strategies. By PROF. G.
C. ONYEMELUKWE (MON) FORMER CHAIRMAN FEDERAL MINISTRY OF HEALTH
EXPERT COMMITTEE ON NCDs
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- NON COMMUNICABLE DISEASES AND RISK FACTORS
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- INTRAUTERINE INFECTIONS AND FOETAL IMPRINTING BAKERS HYPOTHESIS
I.Foetal malnutrition and stress(infection) II.Foetal programming,
Immune programming III.Intrauterine growth retardation(low birth
weight) A.INSULIN RESISTANCE, NIDDM, HYPERTENSION, STROKE, CORONARY
HEART DISEASE IN ADULT LIFE. UTI, TOXOPLASMA, RUBELLA, CMV, HERPES.
FORRESTAL T. HISTORIC EARLY LIFE ORIGINS OF HYPERTENSION IN AFRICA.
J. Nutr.2004:134:211-6. B.PSYCHOLOGICAL; SCHIZOPHRENIA - CYTOKINE
INDUCED PROBLEM DURING FOETAL NEURODEVELOPMENT BY RUBELLA,
INFLUENZA, TOXOPLASMOSIS BROWN. A. PRENATAL INFECTIONS AS RISK FOR
SCHIZOPHRENIA. SCHIZOPHRENIA BULL 2006;32(2); 200- 202.DOGRA S. V.
INTRAUTERINE GROWTH. C.MALARIA SCHISTOMIASIS IN MOTHER MAKES TH 2
RESPONSE TH 1 RESPONSE IN CHILDHOOD.
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- CLASSIFICATIONS OF INFECTIONS INTRACELLULAR AND EXTRACELLULAR
1.BACTERIA 2.VIRUSES 3.CHLAMYDIA 4.PARASITES 5.PRIONS
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- Cell mediated INNATE SYSTEM WORKS WITH ADAPTIVE IMMUNE
SYSTEM
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- MECHANISMS TOXINS ENDOTOXIN MIMICRY Rheumatic fever/ Rheumatic
disease INDUCE AUTOIMMUNE TYPE I - IV PRION/CALCIFICATION
HOST/IMMUNE PARASITE/INFECTION INTERACTION AGGRESSINS IMMUNO
SUPPRESSION ONCOGENE CO-CARCINOGEN SUPPRESSION OF AUTOIMMUNITY
(Plasmodium knowelsi on NZB mice) CELLULAR DIFFERENTIATION (Ad 36
virus Adipocyte) PERSISTENCE/ TRANSFORMATION CHRONIC INFLAMMATION
MODULATION OF TH1/TH2/T(REG) BALANCE CYTOKINE CHEMOKINES GENE
PRESSURE (MALARIA) 1.Sickle gene 2.Thalasemia 3.G6PD
HYPERSENSITIVITY (TYPE I V)
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- STRESS INFECTIONS CRIME/VIOLENCE CHRONIC STRESS ANXIETY
DEPRESSION PSYCHONEUROIMMUNOLOGY NEUROENDOCRINEIMMUNE AXIS STRESS
INDUCED MEMORY DYSFUNCTION IL-6 HEART DISEASE ARTHRITIS INFECTIONS
AND STRESS
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- OBESITY OF INFECTIOUS ORIGIN Nikhil V. Dhurandhar, PhD; Richard
L. Atkinson,MD; Aftab Ahmed,PhD. GGH JOURNAL.COM 2004:20(3) A
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- FAT CELL IN ENERGY HOMEOSTASIS, INFLAMATION, IMMUNITY
1.RESISTIN 2.LEPTIN 3.ADIPONECTIN INSULIN RESISTANCE 4.VISFATIN
5.APELIN 6.TUMOUR NECROSIS FACTOR (TNF) 7.RETINOL BINDING PROTEIN
8.MONOCYTE CHEMOTACTIC PROTEIN1 (MCP-1) 9.PLASMINOGEN ACTIVATOR
INHIBITOR 1 (PAI-1) 10.INTERLEUKIN 6 ABDOMINAL FAT CELL IS
ACTIVE
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- PATHOGENS RESPONSIBLE FOR OBESITY PATHOGEN (REFERENCE) ANIMAL
MODEL POSSIBLE MECHANISM(S) *Human adenovirus (11,15,16) Chickens,
mice, nonhuman primates Up-regulation of preadipocyte
differentiation Human adenovirus(33)ChickensUnknown SMAM-1
adenovirus (8,9)ChickensUnknown Borna-disease virus
(10,50,51)RatsHypothalamic damage Chlamydia pneumoniae(68) No
animal model, associated with weight gain in humans Unknown Scrapie
agent (76-79)Mice Hypothalamic-pituitaryadrenal axis damage Canine
Distemper virus (5)Mice Hypothalamic damage, reduced hypothalamic
leptin receptor expression Rous-Associated virus-7
(6,7)ChickensReduced thyroid hormone levels * Human pathogens,
and/or associated with human obesity.
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- Adenovirus Ad-36: Up-regulation of fat cell differentiation,
reduced leptin secretion. Borna-disease virus (BDV) Hypothalamic
damage Hypothalamus Scrapie agent Hypothalamic- pituitaryadrenal
axis damage GLUT-1 Alterations Rous virus-7 RAV-7: Reduced thyroid
hormone levels Adipose tissue Chlamydia pneumonia Immunomodulators
(?) ADIPOGENIC PATHOGENS AND THE POTENTIAL MECHANISMS LEADING TO
OBESITY Canine distemper virus (CDV) 1. Reduced catecholamine
Levels 2. Hypothalamic damage 3. Reduced expression of hypothalamic
leptin receptor 4. Down-regulation of Melanin- concentrating
hormone precursor mRNA
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- METABOLIC SYNDROME AND ALTERED GUT MICROBIOTA IN MICE LACKING
TOLL-LIKE RECEPTORS Matam Vijay- Kumar, Jesse D. Aitken, Frederic
A. Carvalho, Tyler C. Cullender, Simon Mwangi, Shanthi Srinivasan,
Shanthi V. Sitaraman, Rob Knight, Ruth E. Ley, Andrew T. Gewirtz.
Sci 2010, Apr;328 (9): 5975,228- 231 DOI: 10.1126/sci.1179721 TLR-5
DEFICIENT MICE cannot recognize PAMP(pathogen associated molecular
pattern of bacteria
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- Metabolic adaptation of C57Bl/6J and SWR/J mice to infection
with H. polygyrus. A) Body weights of nave mice compared to those
infected with H. polygyrus for 21 days, Mean SEM, N=58 in each
group; B) Average food intake per 24 hours in nave vs. 21 day H.
polygyrus infected mice, Mean SEM, N=58 mice per group, *p=0.001;
C) A comparison of energy expenditure in nave vs. H. polygyrus
infected SWR/J mice over 24 hours measured by indirect calorimetry,
arrows indicate dark cycle period, N=4 mice per group; D) Total
ambulatory activity in nave vs. H. polygyrus infected SWR/J mice
over 24 hours, arrows indicate dark cycle period, N=4 mice per
group.
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- CANCER AND INFECTIONS TOTAL INFECTION-ATTRIBUTABLE CANCERS
WORLDWIDE AgentCancer# cases% all Ca. H. PyloriStomach592,0005.5
Lymphoma11,500 HPVCervix492,8005.2 Anogenital53,880
Oropharynx14,500 HBV, HCVLiver535,0004.9 EBVNasopharynx78,1001.0
Hodgkin L.28,600 Burkitt L.6,700 HIV/HHV8Kaposi sarcoma66,2000.9
Non-Hod. L.36,100 Schistosomes Bladder 10,6000.1 HTLV-1ATL3,3000.03
Liver flukesBile duct2,5000.02 Total1,932,80017.8 B
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- I-A Ca in Developing and Developed Countries Developed
CountriesDeveloping Countries SiteAgent# cases% all Ca# cases% all
Ca. LiverHBV,HCV48,0001.0475,0008.2 Flukes02,500
CervixHPV83,4001.7409,4007.0 StomachH. pylori192,0003.8400,0006.9
KaposiHHV83,7000.162,5001.1 NHLHIV/EBV9,3000.226,8000.7 EBV
(BL)1006,600 H.pylori5,6005,900 HTLV-15502,790
AnogenitalHPV22,4500.431,4300.5 Nasopharyn x EBV6,5000.171,6001.2
OropharynxHPV5,6000.18,8000.2 Hodgkin L.EBV11,5000.217,1000.3
BladderSchistos00.010,6000.2 Total389,0007.71,527,00026.3
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- COULD INFECTIONS CAUSE PROSTRATE CANCER? IS A VIRUS INVOLVED?
1.Robert Schlaberg in 2006 found a virus called Xenotropic
murine-like retrovirus, or XMRV, in the cell samples from prostate
cancer patients. RNaseL gene, XMRV is one of the retroviruses. IS A
PARASITE INVOLVED? 1.Parasites called Trichomonas vaginalis (T.
vaginalis) Casey, G et al.(2002),32 (4), 581-583
doi:10.1038/ng1021; Urisman, A et al.(2006) RNASEL Variant PLoS;
Pathogens, 2 (3) doi:10.1371 Stark, J. et
al.(2009),JNCI.doi:10.1093.
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- PRINCIPLES OF ONCOLOGY Uncontrolled proliferation induces
apoptosis Noxa, Puma p53 Bak,Bax BclxL,Mc1 Noxa, Puma BclxL, Mcl1
Cyt C caspases Mule Bak/Bax
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- NATURAL HISTORY OF CERVICAL HPV INFECTIONS Atypia/ASCUS/
CIN1-2/LSIL CIN2-3/CIS/HSIL
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- STRATEGIES FOR HPV VACCINATION Prevent Infection Mediate
Regression Eliminate Residual Disease
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- HBV and HCV in the etiology of Hepatocellular Carcinoma
Prevalence of HCC is correlated with endemic chronic infection with
HBV and HCV Chronic HBV and HCV infections result in cirrhosis in ~
15% of subjects in 25-30 years, with HCC arising in ~1% of subjects
with cirrhosis. Non-viral cirrhosis is also a risk factor for HCC.
HCC only arises in the context of cirrhosis.
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- Hepatitis viruses are very diverse Hepatitis C virus (HCV) is a
positive strand RNA Flavivirus. HCV core induces signalling
pathways E2 interferes with interferon signalling
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- EBV is associated with multiple cancers Burkitts lymphoma Post
transplant lymphomas Hodgkins lymphoma Nasopharyngeal carcinoma
Gastric cancer
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- EBV is associated with multiple cancers EBV infection occurs in
> 90% of the population; cancer is very rare. Most EBV
associated cancers are associated with immunosuppression -
transplantation (drugs); HIV; malaria; EBV causes cancer in both B
cells, where the virus is latent and productive, and in epithelial
cells that do not support viral latency.
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- EBV associated cancers PTLD EBNAs1-3, LMPs1-2b Hodgkins EBNA1,
LMP1,2A Burkitts EBNA1 only Other B cells Nave B cell Germinal
Center Memory B cell
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- EBV associated cancers Epithelial cell Nasopharyngeal Carcinoma
EBNA1, LMP1, 2a Plasma cells Memory B cell
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- HHV-8 (KSHV) and Cancer Kaposis sarcoma - spindle cell
(endothelial origin) Pulmonary Effusion Lymphoma Multicentric
Castlemans Disease - B cell (non- cancer) Viral genome encodes
homologues for cellular genes that block innate and adaptive
immunity, block apoptosis, induce proliferation.
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- STAGES IN DEVELOPMENT OF CANCER 1.Protooncogenes (c-onc genes)
are the cellular counterparts of v-onc genes. Their functions are
cellular growth and development. The activation of c-onc genes with
mutation leads to uncontrolled cell growth. a. Growth factors b.
Growth factor receptors c. Signal transducers d. Transcription
factors 2. Antioncogenes (tumor suppressor genes). When these genes
lose their suppressive effects, unpreventable growth occurs. a.
Retinoblastoma gene (Rb) b. p53 c. Wilms tumor gene (WTI) d. VHL
gene in Von-Hippel Lindau syndrome e. NF1 and NF2 genes in neurofi
bromatosis f. APC and DCC genes in familial adenomatous
polyposis
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- HUMAN ONCOGENIC DNA VIRUSES TAXONOMIC GROUPINGEXAMPLESTUMOR
TYPES AdenoviridaeAdenovirus types 9, 12, 18, 31Various solid
tumors in rodents HepadnaviridaeHBVHepatocellular carcinoma
HerpesviridaeEBVBurkitts lymphoma Nasopharyngeal carcinoma B-cell
lymphoma Hodgkins lymphoma KSHV (HHV-8)Kaposis sarcoma Primary eff
usion lymphoma Multicentric Castlemans disease PapillomaviridaeHPV
types 6, 11, 16, 18, 31, 45Oral, cervical, and anal cancer Merkel
cell polyomavirusMerkel cell carcinoma PolyomaviridaeBK virus, JC
virusSolid tumors in rodents PoxviridaeMCVVarious solid tumors HBV:
Hepatitis B virus, EBV: Epstein-Barr virus, KSHV: Kaposis
sarcoma-associated herpesvirus, HHV: Human herpes virus, HPV:Human
papillomavirus, MCV: Molluscum contagiosum virus
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- HUMAN ONCOGENIC RNA VIRUSES. Taxonomic grouping ExamplesTumor
types RetroviridaeHTLV type 1 Adult T-cell leukemia
FlaviviridaeHepatitis C virusHepatocellular carcinoma HTLV: Human
T-cell leukemia virus.
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- NUTRITION AND INFECTION SPIRAL OF MALNUTRITION AND INFECTION
INADEQUATE DIETARY INTAKE APPETITE LOSS NUTRIENT LOSS MALABSORPTION
ALTERED METABOLISM WEIGHT LOSS GROWTH FATTERING LOWERED IMMUNITY
MUCOSAL DAMAGE DISEASE: INCIDENCE DURATION SEVERITY Onyemelukwe GC,
Ogoina D, Ibiam G E, GH Ogbadu. Aflatoxins in body fluids and food
of Nigerian children with protein- energy malnutrition. Afri. J. of
Food, Agriculture, Nutrition and development, 12: (5 )2012, ISSN
1684 5374 (KWASHIOKOR,MARASMUS,STUNTING.) AFLATOXINS FROM FUNGI
ASPERGILLUS FLAVUS HYPERMETABOLISM IL-1,IL-6,TNF, FEVER PROTEIN
LOOSING ENTEROPATHY C
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- UNDERNUTRITION INFECTION DECREASED IMMUNE FUNCTION -INNATE
-ACQUIRED IMPAIRED ABSORPTION. ALTERED GUT LUMEN. MUCOSAL
INJURY
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- CARDIOVASCULAR - ATHEROSCLEROSIS D
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- ATHEROSCLEROSIS IS ASSOCIATED WITH MULTIPLE PATHOGENIC
MECHANISMS IN HIV-INFECTED ANTIRETROVIRAL-NAVE OR TREATED
INDIVIDUALS. Piconi, Stefania;Parisotto, Serena; Rizzardini,
Guiliano; Passerini, Simone; Meraviglia, Paola; Schiavini, Monica;
Niero, Fosca; Biasin, Mara; Bonfanti, Paolo; Ricci, Elena Delfina;
Trabattoni, Daria; Clerici, Mario. AIDS 2013,27:381-389. 1.HIV-
infected patients have a greater burden of sub-clinical and
clinical atherosclerotic disease compared to the general
population. 2.A complex pathogenesis drives atherogenesis in HIV
infection. Thus, whereas inflammation could be responsible for this
process in ART- nave individuals. 3.ABCA-1, an ATP-binding
transporter cassette protein involved in cholesterol efflux, which
is inhibited by Nef, is up-regulated in ART- treated
individuals.
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- 1. CHRONIC HEPATITIS C VIRUS INFECTION IS ASSOCIATED WITH EARLY
ATHEROSCLEROSIS. Mostafa et al Gut June 28, 2010. 2. Bacterial
persistence in phagocyte cells by Dr. Emil Kozarov in Columbia
University: J. Atherosclerosis Thrombosis Bacillus Enterobacter
hormaechei chronic infection. Periodontal bacteria in carotid
artery. 3. Autoimmunity to heat shock proteins(HSP 60) from
bacteria with autoantibodies in the lesion. Zhu et al 2001.
Am.Coll.Cardiol.Florida 850. 4. Individual pathogens CMV, Hepatitis
A, Herpes simplex 1 (HSV1), Herpes simplex 2 (HSV2), C.pneumoniae,
Helicobacter pylori. 5. Pathogen burden. Zhu J. et al; Am. J.
Cardiol.2000, 85: 140-146 of multiple infections with intracellular
organisms in (4 )above asociated with elevated C-reactive
proteins.
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- INFLUENZA AND CARDIOVASCULAR DISEASE Mohammad Madjid, MD;
Ibrahim Aboshady, MD; Imran Awan, MD; Silvio Litovsky, MD; S.Ward
Casscells, MD. Tex Heart Inst J 2004; 31:4-13 We appraise the
relationship between influenza and coronary heart disease, on the
basis of Bradford Hills criteria of causality. We show that our
proposed relationship meets the following criteria: strength of
association, consistency, temporal sequence, coherence, biologic
plausibility, experimental evidence, and analogy.
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- INFECTIOUS AGENTS IMPLICATED IN ATHEROSCLEROSIS Chlamydia
pneumoniae Cytomegalovirus Herpes simplex viruses 1 and 2 (HSV-1,
HSV-2) Helicobacter pylori Mycoplasma pneumoniae Porphyromonas
gingivalis Enterovirus species Salmonella typhi Streptococcus
sanguis Coxsackie B virus Adenovirus species Mycoplasma
gallisepticum Mareks disease virus Measles virus Epstein-Barr virus
Human immunodeficiency virus Mycoplasma fermentans Coxiella
burnetti Actinobacillus actinomycetemcomitans Bacteroides forsythus
Hepatitis A virus Prevotella intermedia Influenza virus
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- EFFECTS OF INFLUENZA ON THE COAGULATION SYSTEM
TargetEffectStudy Platelet aggregation50-53IncreasedIn vivo human
and animal Platelet count50,54,55DiminishedIn vivo and in vitro
human AT III56DiminishedIn vivo human Clotting time57IncreasedIn
vivo human DIC prevalence58IncreasedIn vivo human PT61ProlongedIn
vivo human PTT61ProlongedIn vivo human Fibrinogen62DecreasedIn
vitro human Factor V61DiminishedIn vivo human Factor
VIII61DiminishedIn vivo human FDPs56,61,63Markedly IncreasedIn vivo
and in vitro human Fibrin monomers63PositiveIn vitro human Soluble
fibrin61IncreasedIn vivo human Staphylococcal clumping test61
AbnormalIn vivo human
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- PlasminogenDecreasedIn vivo human 1-Antitrypsin ReducedIn vivo
human 2-Macroglobulin5 ReducedIn vivo human Plasmin inhibitor
complexes Produced, then consumed In vivo human Secondary
fibrinolysis56InitiationIn vivo human Tissue factor64,65IncreasedIn
vivo human Factor VII64ActivationIn vivo human Factor
X64ActivationIn vivo human TFPI66 Exhausts the inhibitory effect In
vivo human MonocytesActivate the procoagulantIn vivo human
Endothelial cell damage57 A. Release of phosphatidyl serine B.
Lysis a. Exposure of the prothrombotic extracellular matrix to the
vascular lumen b. Alteration of the procoagulant-anticoagulant
balance
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- HILLS CRITERIA FOR CAUSALITY Strength of association
Consistency Temporal sequence Coherence Biologic plausibility
Biologic gradient (dose-response relationship) Specificity
Experimental evidence Analogy
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- RECOMMENDATIONS FOR IMPROVING INFLUENZA CONTROL IN
CARDIOVASCULAR PATIENTS Motivate doctors and patients by increasing
recognition of the heart-protective effect of flu shots Update
cardiology practice guidelines to include flu shots Examine the
feasibility of financial incentives to doctors and patients to
improve adherence to existing guidelines Determine which virus
strains trigger cardiovascular events Strengthen educational
efforts to persuade pediatricians, internists, gynecologists, and
family practitioners to improve vaccination rate of household
contacts of patients with heart disease Intensify research on the
mechanism of the effect of the virus on the vascular system Design
new clinical trials to determine high-risk groups that may benefit
from influenza prevention in terms of cardiovascular
prevention
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- PRION DISEASES E Kajander E (2006). "Nanobacteria--propagating
calcifying nanoparticles". Lett Appl Microbiol 42 (6): 549-52.
www.nanobac.org Nanobacteria cause kidney stones and arterial
classifications
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- F AUTOIMMUNE DISEASES AND ALLERGIES
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- STRACHAN DV BMJ, 1989 HYGIENE HYPOTHESIS
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- HYGIENE HYPOTHESIS I.Worm Therapy. Worm therapy has been or is
being studied in humans as a treatment for several immunological
diseases including Crohn's disease, Ulcerative Colitis, Multiple
Sclerosis, Eczema or atopic dermatitis and allergies. Autoimmune
liver disease has also been demonstrated to be modulated by active
helminth infections. II.The Hygiene Hypothesis & Worm therapy.
a. Extra-cellular antigens primarily trigger the TH2 response, as
observed with allergies, while intracellular antigens trigger a TH1
response. The Hygiene Hypothesis states that there is a regulatory
action between the two types of response. b. The Old Friends
Hypothesis modifies the Hygiene Hypothesis, proposing that T
regulator cells (T regs) only become mature and completely
effective if they are stimulated by repeated exposure to
microorganisms and parasites that are relatively benign and which
have coexisted with humans throughout our evolutionary history.
III.Which worms are used in therapy? Only Necator Americanus meet
all these requirements, although Trichuris Suis Ova only, so it is
more expensive at therapeutic doses. The main difference between N.
americanus and T. suis is residency time, because T. suis has a
lifespan of only 2-3 weeks in humans, while N. americanus has an
average life span of 5 years.
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- DC= DENDRITIC CELLS; APC=ANTIGEN PRESENTING CELLS;
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- DENDRITIC CELLS PRESENTATION OF ANTIGENS LEAD TO FORMATION OF
Treg and TISSUE GROWTH FACTOR (TGF-b)
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- CHILDREN IN WESTERN COUNTRIES VERSUS CHILDREN IN AFRICAN
COUNTRIES
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- IL-25 elicits a multi-potent progenitor cell population that
promotes Th2 cytokine responses Steven A. Saenz1, Mark C.
Siracusa1, Jacqueline G. Perrigoue1, Sean P. Spencer1, Joseph F.
Urban Jr.2, Joel E. Tocker3, Alison L. Budelsky3, Melanie A.
Kleinschek4, Robert A. Kastelein4, Taku Kambayashi5, Avinash
Bhandoola5, and David Artis. Nature. 2010 April 29; 464(7293):
13621366. doi:10.1038/nature08901.
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- PARASITES AND ALLERGIC DISEASES
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- VACCINATION with Human Hookworm Vaccine "Necator americanus
Aspartic Protease-1 M74 Generates Neutralizing Antibodies and a
Potent Immune Response in BALB/c Mice. Amar R. Jariwala, George
Washington University; Xi Chen, George Washington University; Mark
S. Pearson, James Cook University; Brian Keegan, Baylor College of
Medicine; Jill B. Brelsford, George Washington University; Medical
Immunology Commons; 4-22-2013
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- INFANT GUT MICROBIOTA AND THE HYGIENE HYPOTHESIS OF ALLERGIC
DISEASE: IMPACT OF HOUSEHOLD PETS AND SIBLINGS ON MICROBIOTA
COMPOSITION AND DIVERSITY Meghan B Azad 1, Theodore Konya 2,
Heather Maughan 3, David S Guttman 3, Catherine J Field 4, Malcolm
R Sears 5, Allan B Becker 67, James A Scott 2, Anita L Kozyrskyj
17* and CHILD Study Investigators 7. Allergy, Asthma & Clinical
Immunology 2013, 9:15 doi:10.1186/1710-1492-9-15 1 2 3 4 5 67 2 17
7
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- Model for the possible influence of pets and siblings on infant
gut microbiota and subsequent development of atopic disease.
Household pets (D, dogs; C, cats) and siblings increase infant
exposure to environmental microbes, promoting enrichment for
distinct combinations of organisms within the gut microbiota;
overall richness and diversity are also impacted. Despite favoring
different microbiota profiles, the net effect of both pets and
siblings is to promote healthy immune system development and
protect against atopic disease. Further research is required to
characterize the underlying biological mechanisms. Azad et al.
Allergy, Asthma & Clinical Immunology 2013 9:15
doi:10.1186/1710- 1492-9-15
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- G. MENTAL DISEASES- DEPRESSION AND VIRAL INFECTIONS Shalini,
Malhotra; Nirmaljit, Kaur; P. Kumar; M.S. Bhatia; Charu, Hans.
Delhi psychiatry journal vol. 15 no.1 1.Human immunodeficiency
virus 2.Hepatitis C virus 3.Epstein-Barr Virus 4.Herpes simplex
virus 5.Influenza virus 6.Hepatitis B virus 7.Hepatitis A virus
8.BORNA DISEASE VIRUS 9.Human T-cell Lymphotropic virus (HTLV).
markers of inflammation (C-reactive protein, interleukin 1 and 6)
were positively correlated with depression.43. Cytokines seem to
trigger a quick onset of what is called sickness behavior-meaning
malaise and fatigue, as well as a delayed onset of depressed.
etanercept (a TNFtumor necrosis factor-blocker) reduced depressive
symptoms in people with psoriasis.
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- MECHANISM OF ACTION OF MICROBIAL PATHOGENS IN DEPRESSION A.
Chronic infection with any of these viruses can lead to raised
interferon-alpha levels (interferon-alpha is secreted by cells of
the immune system as it tries to control the virus), and it is now
known that interferon-alpha can significantly affect the serotonin
system. B Coxsackie virus B, which have a particular affinity for,
and disruptive action on, the hypothalamus. C. Raising glutamate
and quinolinic acid levels in the brain (high glutamate levels are
linked to depression). The excess glutamate/quinolinic acid in this
case comes from the activated microglia cells (microglia are
specialized macrophages permanently resident in the brain). D.
Depression can sometimes be caused by low levels of the adrenal
hormone cortisol. Viruses like enterovirus often chronically infect
the adrenal glands. E. Chronic fatigue syndrome, the working memory
and long-term recall is often severely disrupted.
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- LIST OF NON COMMUNICABLE DISEASES (NCDs) AND THEIR KNOWN OR
PROBABLE INECTIOUS RISK FACTORS CARDIOVASCULAR H
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- RESEARCHES IN CARDIOVASCULAR DISEASES 1.RHEUMATIC FEVER/
RHEUMATIC HEART DISEASE- Grp A, B, C streptococcal pharynigitis and
skin infections Ogunbi et al (lagos) J. Epid. Comm. Health 1978
march 3(1) 68-71 2. Endomyocardial fibrosis(EMF) and loa loa
induced eosinophilia. Others trichinella spiralis,ascaris,
hookworm, toxoplasmosis Andy JJ et al (Calabar, Ife) Acta tropica
1998; 69 127-140 Urhogide A, Falase A (Ibadan) Afri J Med Med Sci
1987, 16 133
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- 3. PERIPARTUM CARDIAC FAILURE (PPCF) Zaria syndrome- salt lake,
Hot bath, volume overload,pre HT, ? Viral myocarditis Davidson N,
Parry E Q J Med N S 1976, 47 431-461, Adesanya c et al Trop. Geog
Med 1989, 41 (3) 190-196, Ford l, Abdullahi et al Q J Med 1998 91
93-103 Danbauchi SS Trop Doc 2002,32 24-27 4. OTHERS DUE TO
MYOCARDITIS from toxoplasmosis, coxsackie B virus and chlamydia.
Falase A (Ibadan) Heart vessels Supp 1985 1, 232-35, Cenac A et
al(Niger) Med Trop(Mars) 2000,60,2, 137-40 5.ECLAMPSIA AND
INFECTION Ekwempu CC(Zaria) Tropical doctor 1980 174-78 Ekwempu CC
Int J Gynae Obstect 1980, 18 4, 300-2
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- NEUROLOGY/ PSYCHIATRY
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- 1. Tropical spastic paraparesis and HTLV1 Roman GC et al
Neurology 1985,35, 1158 2. Epidemic seasonal ataxia and viral
(arbovirus) encephalitis Adamolekun B et al Met Brain Dis 1997, 12,
251 3. Post malaria cerebellar ataxia Osuntokun BO Afr J Med Med
Sci 1983, sept 3-4, 165-172 4. Typhoid and Fregoli syndrome(rare
persecutory delusion) Stanley et al (Jos), Nig J Med 2002,4, no
1,jan-march 33-34 5. Typhoid and neuropsychiatric manifestation
Osuntokun et al Arch 1972 Neurol 27 July 7-13 RESEARCHES IN
NEUROLOGICAL IN AFRICA
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- AUTOIMMUNE/ ENDOCRINE NOTE: EFFECT OF MALARIA PLASMODIUM
BERGHEI IN REDUCED INCIDENCE OF AUTOIMMUNE DISEASES. B. M.
GREENWOOD; VOLLER. A. SUPPRESSION OF AUTOIMMUNE DISEASE IN NEW
ZEALAND MICE ASSOCIATED WITH INFECTION IN MALARIA II. NZB MICE.
CLIN.EXP. 1970; IMMUNOL. 71(6) 805-815
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- GASTROINTESTINAL DISEASES
- Slide 73
- 1. LIVER CIRRHOSIS, HBV AND SCHISTOSOMIASIS FAKUNLE Y, ET AL
(ZARIA) 2. HBV, HCV,HDV(DELTA VIRUS) OJO S ET AL EAST AFRI MED
J,1995,72,II,719-21 3. HELICOBACTER PYLORI AND PEPTIC ULCER
HOLCOMBE C ET AL (MAIDUGURI) TRANS R SOC TROP MED HYG 1994 88,569
4. MALARIA AND TROPICAL SPLENOMEGALY SYNDROME Fakunle Y, Greenwood
B, 1976 Trans R Soc Trop Med Hyg 70 346-51 Fakunle Y, Greenwood
B,1977 Clin exp Immunol 28, 153- 6 RESEARCHES IN GIT DISEASES
- Slide 74
- RENAL DISEASES
- Slide 75
- SOME RESEARCHES ON RENAL DISEASES 1. QUARTAN MALARIAL
NEPHROPATHY Hendricks RG, Adeniyi A (Ibadan) Kidney Int 1979, 16,64
2. SCABIES AND NEPHRITIS INCLUDING NEPHROTIC SYNDROME Whittle HC et
al Trans R Soc Trop Med Hyg 1973 67, 349-363 Abdulrahman m,b 1984 J
Inf Mar 8, 100-9 Aikionbare H et al 1984 Nig J Paed 11,2,59-62 3.
VIRAL HEPATITIS AND IMMUNE COMPLEX GLOMERULONEPHRITIS, LEPROSY,
YERSINIA ENTEROCOLITICA(BY RENNER.A) ETC.
- Slide 76
- RESPIRATORY DISEASES
- Slide 77
- RESEARCHES IN RESPIRATORY DISEASES 1. Asthma and air borne
fungi (Aspergillus fumigatus), house dust mite (dermatophagoides
farinae/pterysinnus) Lawande R, Onyemelukwe GC (Zaria) Ann allergy
1984 52(1) 47 Onyemelukwe GC (Zaria) et al Ann Allergy 1986 Feb
56(2), 167-70 2. Asthma and hookworm Salako LA N.Eng J Med
1970,283,264 3. Asthma and strongyloides Nwokolo CU, BMJ,1973, 1,
153
- Slide 78
- VICIOUS CYCLE HYPOTHESIS IN COPD
- Slide 79
- CANCERS AND OTHER DISEASES
- Slide 80
- 1.Mutation of tumor suppressor gene in codon 249 by aflatoxin
in PLCC. Ndububa et al Afri J Med Sci 2001 30, 125- 127 2.
Schistosomiasis and bladder cancers Bedwani R et al(Egypt) Bri J
Cancer 1998, 77,1186-9 3. Aflatoxin B1B2 G1 G2(Aspergillus flavus)
and PLCC Ndububa et al Afri J.Med Sci 2001 30, 125- 127 Onyemelukwe
et al Toxicol Letters,1982,56,2, 167-70 RESEARCHES IN CANCER