bio123 Flashcards
(152 cards)
1
Q
local inflammatory response
A
IL-8 release from damaged endothelial cells
TNF released rom macrophages to help recruit neutrophils and allow migration from blood .
histamine release from mast cells - vasodilation and inc blood vessel permeability .
activation of clotting and complement cascades
neutrophils secrete cehmokines to recruit monocytes from blood
phagocytosis of phatogens
macrophages migrate into tissue and secrete IL-1 and TNF-a recruit lymphocytes , monocytes and neutrophils
2
Q
complement
A
-initiators bind pathogens
-enzymes
-opsonins promote phagocytosis
- anaphylatoxins cause inflammation
- membrane attack proteins lyse pathogens
-complement receptors on pathogen or neutrophils
-regulatory proteins - limit complement activation
3
Q
Infectious agents
A
Viruses, bacteria, fungi, and parasites (including protozoa and helminths).
4
Q
Acute infections
A
Infections typically caused by viruses and bacteria.
5
Q
Chronic infections
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Infections often caused by parasites.
6
Q
Parasitism
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A parasitic relationship benefits one species and harms the other.
7
Q
Mutualism
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A symbiotic relationship where both species benefit.
8
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Commensalism
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A symbiotic relationship where one species benefits and the other is unaffected.
9
Q
Stages of infectious disease
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Incubation, Prodromal, Illness, Convalescence.
10
Q
Incubation
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The stage from infection to first symptoms.
11
Q
Prodromal
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The stage with mild, general symptoms.
12
Q
Convalescence
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The recovery phase of infectious disease.
13
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Biological Response Gradient
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Not all infected individuals experience the same disease severity.
14
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Factors influencing disease severity
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Infecting dose, age, sex, genetics, nutrition, co-infections.
15
Q
EBV in children
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~1% symptomatic.
16
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Stages of infectious disease progression
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Invasion, Multiplication, Spread, Pathogenesis.
17
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Invasion
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Entry into host (e.g. skin, oral, sexual, inhalation).
18
Q
Pathogenesis
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Development of disease symptoms.
19
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Transmission routes
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Different routes influence how diseases are prevented and managed.
20
Q
Plasmodium transmission
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Via mosquito bite.
21
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HIV transmission
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Via blood or sex.
22
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Influenza transmission
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Via droplets.
23
Q
Incidence
A
New cases in a time period.
24
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Prevalence
A
Total current cases at a point in time.
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Mortality
Deaths due to disease in a defined population and time.
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High-income country deaths
75% of deaths in 70+ age group; main causes: non-communicable diseases.
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Low-income country deaths
40% of deaths in children under 15; main causes: communicable diseases.
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DALY
Disability-Adjusted Life Year = Years of Life Lost (YLL) + Years Lived with Disability (YLD).
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Importance of DALY
Measures total health burden (not just deaths) and allows comparison across diseases and regions.
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Limitations of DALY
Does not include economic impacts, such as loss of income or productivity, health system burden, social stigma, tourism loss, or community disruption.
31
Origin of the term 'immunity'
From Latin 'immunis', meaning exempt.
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Historical observations of immunity
Thucydides (430 BC): Recovered plague victims could nurse the sick. 15th-century China/Aztecs: Inhaled smallpox crusts for protection. Jenner (18th century): Cowpox vaccination protects against smallpox.
33
Three main lines of defence in the immune system
Stop entry (barriers). Flush out or kill invaders if entry occurs. Remember the invader (adaptive immunity) to prevent reinfection.
34
Key mechanical barriers of the innate immune system
Skin: Dry, acidic (pH 3-5), with dead cells and resident bacteria. Tight junctions: Block antigen passage. Mucosal surfaces: Respiratory tract mucus traps pathogens.
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Physiological barriers involved in innate immunity
Antimicrobial peptides (e.g., defensins). Lysozyme in tears and saliva. Low stomach pH kills microbes. Commensal microbiota outcompete pathogens. Complement proteins, cytokines, and interferons activate defences.
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Main innate immune cell types and their roles
Phagocytes: Neutrophils, macrophages, dendritic cells (ingest and kill pathogens). Granulocytes: Neutrophils, eosinophils, mast cells, basophils (contain toxic granules). Lymphocytes: NK cells and innate lymphoid cells (target infected cells and secrete cytokines).
37
Four classical signs of inflammation
Heat (Calor), Redness (Rubor), Swelling (Tumor), Pain (Dolor) → First described by Cornelius Celsus in the 1st century BC.
38
Main steps of the local inflammatory response
Chemokines (e.g., IL-8) and TNF-α recruit neutrophils. Histamine from mast cells increases permeability. Complement and clotting cascades are activated. Neutrophils recruit monocytes. Macrophages secrete IL-1 and TNF-α to attract more immune cells.
39
Systemic acute-phase response
Triggered by inflammation → systemic effects: Fever (speeds up immune reactions). Leukocytosis (increased white blood cells). Acute-phase protein production (e.g., CRP from liver) → enhances complement activation and phagocytosis.
40
Complement system and its roles
Composed of >35 serum proteins, mainly from the liver. Functions: Opsonization (tagging microbes for phagocytosis). Membrane attack complex (MAC) formation → cell lysis. Inflammation promotion via anaphylatoxins. Cross-talk with adaptive immunity (e.g., antibody recruitment).
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How the innate immune system detects pathogens
Pathogens carry PAMPs (e.g., LPS in E. coli). Recognized by host PRRs (e.g., TLR4). Phagocytosis process: Attachment via pseudopodia. Engulfment into a phagosome. Fusion with lysosome → degradation. Pathogen destroyed by oxygen-dependent (oxidative burst) or oxygen-independent (e.g., lysozyme, defensins) methods.
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What pathogen causes plague?
Plague is caused by Yersinia pestis, a gram-negative, facultative anaerobic bacterium from the Enterobacteriaceae family.
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How does Yersinia pestis adapt to flea and mammal hosts?
Survives at ambient temperature in fleas (digestive tract). Survives at body temperature in mammals (bloodstream).
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What is the natural reservoir and primary vector for Y. pestis?
Natural hosts: wild rodents (marmots, gerbils, squirrels, prairie dogs). Vector: Oriental rat flea (Xenopsylla cheopis).
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Describe the flea-borne transmission cycle of Y. pestis.
Forms biofilms in the flea's proventricular valve, blocking feeding. Flea regurgitates bacteria into new host when feeding attempt fails.
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What are the three major forms of plague?
Bubonic plague: swollen lymph nodes (buboes). Septicaemic plague: bloodstream infection, gangrene. Pneumonic plague: lung infection, aerosol transmission.
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What are the symptoms and outcomes of bubonic plague?
Swollen lymph nodes, fever, chills, nausea. 50-60% mortality untreated; <5% mortality if treated early.
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What happens in septicaemic plague?
Dissemination through bloodstream. Disseminated intravascular coagulation (DIC), tissue necrosis, blackened extremities ("Black Death"). Nearly 100% fatal untreated.
49
Describe pneumonic plague symptoms and transmission.
Primary: inhalation of infectious droplets. Secondary: spread from bubonic form to lungs. Causes severe pneumonia, cyanosis, circulatory collapse. 100% fatal untreated within 24 hours.
50
Outline the three historical plague pandemics.
Justinianic Plague (541 AD): ~25 million deaths. Black Death (1347-1351): ~30-50% of European population died. Modern Plague (1894): Originated in China, ~10 million deaths globally.
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How is plague transmitted to humans?
Flea bites (bubonic, septicaemic). Contact with infected tissues. Inhalation of respiratory droplets (pneumonic).
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How is plague diagnosed?
Microscopy of samples from lymph nodes, blood, sputum, bronchial washings. Gram-negative rods with bipolar staining. PCR and antigen tests if cultures are negative.
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What treatments are available for plague?
Antibiotics: streptomycin, tetracycline, chloramphenicol. Early diagnosis critical; pneumonic plague requires treatment within 18-24 hours.
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How did Y. pestis evolve from Y. pseudotuberculosis?
Diverged ~10,000 years ago. Acquired ymt gene for flea survival. Lost rcsA, enhancing biofilm formation for flea blockage.
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Why is Y. pestis considered a potential bioweapon?
High fatality rates, fast spread via aerosols. Historical use: corpses launched into besieged cities. WHO (1970) estimate: 150,000 people infected from release over a large city.
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What are the current risks of drug-resistant plague?
Emergence of multidrug-resistant strains (e.g., Madagascar). Potential for rapid transmission and high mortality if resistant to standard antibiotics.
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Pathogen causing malaria
Malaria is caused by protozoa of the genus Plasmodium.
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Species of Plasmodium that infect humans
Five species infect humans: P. falciparum, P. vivax, P. ovale, P. malariae, P. knowlesi.
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Global burden of malaria as of 2023
An estimated 263 million cases and 597,000 deaths, mainly in Africa, especially affecting children under 5 years old.
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Transmission of malaria
By the bite of an infected female Anopheles mosquito.
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Environmental range of malaria transmission
Limited to areas between 60°N and 40°S, at elevations under 2000m, with temperatures that allow parasite development inside mosquitoes.
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Human stages of the Plasmodium life cycle
Mosquito injects sporozoites into blood. Sporozoites infect liver → merozoites released. Merozoites invade RBCs → trophozoites → schizonts → merozoites. Some merozoites develop into gametocytes for mosquito uptake.
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Hypnozoites
Hypnozoites are dormant liver forms produced by P. vivax and P. ovale, enabling relapses years after initial infection.
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Erythrocytic cycle
Merozoites infect RBCs → grow into trophozoites, replicate into schizonts, and rupture RBCs releasing more merozoites, causing cyclic fevers and anaemia.
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Symptoms and complications of malaria
Fever, chills, sweating. Anaemia, jaundice, organ dysfunction. Cerebral malaria (especially P. falciparum). Severe forms include Blackwater fever and respiratory distress.
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Sequestration in P. falciparum infections
Infected RBCs stick to blood vessel walls via PfEMP1, blocking circulation and leading to cerebral malaria and organ failure.
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Diagnosis of malaria
Giemsa-stained blood films. Rapid diagnostic tests (RDTs) detecting Plasmodium antigens. Molecular methods (PCR) for low-level parasitaemia.
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Treatment of malaria with quinine and chloroquine
Both prevent haem detoxification inside the parasite's food vacuole, causing toxic haem buildup and killing the parasite.
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Chloroquine resistance
Through mutations in the PfCRT transporter which expels chloroquine from the parasite's food vacuole, allowing survival despite drug treatment.
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Mosquito stages of the malaria parasite
Mosquito ingests gametocytes. Gametes form and fertilise to form zygote → ookinete → oocyst. Oocyst releases sporozoites which migrate to salivary glands.
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Insecticide-treated bed nets
They reduce child mortality by up to 31%, preventing mosquito bites and reducing mosquito populations in the community.
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Recommended malaria vaccines by WHO
RTS,S/AS01 (2021) and R21/Matrix-M (2023). Both significantly reduce severe malaria in young children when combined with nets and chemoprophylaxis.
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Why are nematodes considered successful parasites?
Highly preadapted physiology. Can survive extreme osmotic, temperature, and pH conditions. Tough outer cuticle resists host immune responses. High reproductive output (e.g., Ascaris 200,000 eggs/day).
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What is the basic body plan of nematodes?
"Tube within a tube" structure: alimentary canal from mouth to anus. Wide size range: e.g., Dioctophyme renale (1 m) vs Enterobius vermicularis (10 mm).
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Do nematodes reproduce asexually?
No asexual reproduction. Rare parthenogenesis reported but not common in animal-parasitic nematodes.
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What is the life cycle pattern of nematodes?
All nematodes undergo 4 larval stages and 4 moults. Parasitism evolved independently at least 9 times in nematodes.
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What is the global burden of nematode infections?
Over 20% of the world's population infected with GI nematodes. Ascaris lumbricoides: ~1200 million cases globally. Wuchereria bancrofti: ~120 million cases of lymphatic filariasis.
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What does overdispersion mean in nematode infections?
Few hosts harbour most worms: >70% of worms in <15% of hosts. Major source of infective stages; heavily infected individuals are at highest morbidity risk.
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Describe the life cycle of Ascaris lumbricoides.
Direct life cycle (soil-transmitted). Ingested eggs hatch → larvae migrate to lungs → re-enter gut → mature into adults.
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What are key features of Ascaris lumbricoides eggs?
Female lays 200,000/day. Thick-shelled, survive harsh conditions. Embryonate in moist, warm soil in 18 days to weeks.
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What are the symptoms of ascariasis due to larval migration?
Lung inflammation → haemorrhagic pneumonia, fever, eosinophilia. Allergic hypersensitivity (e.g., asthma-like symptoms).
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What are the intestinal symptoms of heavy Ascaris infection?
Malnutrition, nausea, intestinal blockage (can be fatal). 85% of blockages occur in children aged 1-5 years.
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What happens when adult Ascaris worms "wander"?
Migrate to bile duct (jaundice), appendix (peritonitis), nasal cavity, trachea (can cause suffocation).
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How is ascariasis diagnosed?
Coprological: eggs in faeces. Serological: antibody/antigen detection (no point-of-care test). Molecular (PCR): detects DNA from eggs. Imaging: radiology or ultrasound.
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Describe the life cycle of Wuchereria bancrofti.
Transmitted by mosquito. Larvae enter human skin → migrate to lymphatics → mature into adults → release microfilariae → taken up by mosquito.
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What are the symptoms of lymphatic filariasis (elephantiasis)?
Lymphoedema, hydrocele (scrotal swelling), thickening of skin, bacterial infections, tropical pulmonary eosinophilia.
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How is lymphatic filariasis prevented and treated?
No vaccine. Prevent mosquito bites (nets, repellents). Mass drug administration: ivermectin, diethylcarbamazine, albendazole to reduce microfilariae and transmission.
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Cestodes
Also called tapeworms; dorsoventrally flattened, ribbon-like bodies. Can reach extreme lengths (e.g. T. saginata up to 12 m). Lack gut and locomotory systems; nutrients absorbed via tegument.
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Body structure of a cestode
Scolex: head with suckers and sometimes hooks. Strobila: body made of proglottids. Proglottids mature from neck: immature → mature → gravid (release eggs).
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Scolex differences between T. solium and T. saginata
T. solium (pork tapeworm): 4 suckers + rostellum with hooks. T. saginata (beef tapeworm): 4 suckers, no hooks or rostellum.
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Proglottids in reproduction
Each proglottid is monoecious (both male and female organs). After fertilisation, gravid proglottids detach and pass in faeces.
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Distinguishing T. saginata and T. solium proglottids
T. saginata: 15-20 uterine branches. T. solium: 7-13 uterine branches. Eggs of both species are morphologically identical.
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Nutrient absorption in cestodes
Via the metabolically active tegument. Surface area increased by microtriches (microvilli-like projections).
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Cestode excretory system
Based on protonephridia or flame cells. Beating cilia create a current to expel waste and conserve water.
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Life cycle of T. saginata and T. solium
Humans are the definitive host. Eggs ingested by intermediate host (cow/pig) → oncospheres encyst as cysticerci in tissue. Humans ingest infected meat → cysticerci evaginate and develop into adult tapeworms.
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Infective form of T. saginata and T. solium
Cysticerci in undercooked beef (T. saginata) or pork (T. solium). Become infective after 7-10 weeks and survive for several months.
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Geographical distributions of T. saginata and T. solium
T. saginata: Worldwide; common in Africa, Eastern Europe, Philippines, Latin America. Rare in India. T. solium: Worldwide; more common where humans and pigs co-exist. Rare in Muslim countries.
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Symptoms of adult tapeworm infection
Usually mild: abdominal pain, nausea, weight loss. Psychological distress from passing motile segments. T. saginata causes more symptoms due to its larger size.
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Human cysticercosis
Caused by ingestion of T. solium eggs, not undercooked pork. Humans act as accidental intermediate hosts. Cysts form in tissues, especially brain (neurocysticercosis).
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Symptoms and risks of cysticercosis
Muscles: often asymptomatic. Eyes: visual disturbance, detached retina. Brain: seizures, headaches, balance issues, and potential sudden death.
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Echinococcus granulosus
Dog tapeworm; dogs = definitive host, humans = accidental intermediate host. Forms large hydatid cysts (1-20 cm) mostly in liver and lungs. Can lead to severe complications if untreated.
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Diagnosis and treatment of hydatid disease
Diagnosed via ultrasound, CT, or MRI. Treatment options: PAIR technique (puncture, aspiration, injection, re-aspiration). Surgery (if lesion is localised). Albendazole (inhibits tubulin polymerisation). "Watch and wait" in select cases.
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Schistosomiasis
Caused by parasitic trematodes (schistosomes). Affects over 200 million people, with 600 million at risk. Second most devastating parasitic disease after malaria.
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Major species of schistosomes infecting humans
S. mansoni (Africa), S. haematobium (Africa, Middle East), S. japonicum (SE Asia, China). Minor species: S. intercalatum, S. mekongi.
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Main factors maintaining schistosome transmission
Contaminated water with eggs. Suitable snail intermediate host. Human contact with infected water.
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Advantages of using an intermediate host
Asexual reproduction increases numbers. Extends survival by infecting multiple species. Channels parasite to definitive host.
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Cercarial stage of schistosomes
Shed from snail host, highly motile. Survive 12-48 hours in water. Use forked tail and enzymes to penetrate human skin.
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What happens when cercariae enter the human host
Become schistosomula, shedding tail and glycocalyx. Migrate via bloodstream and lymphatics to liver. Only 30-50% of penetrated cercariae mature.
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Adult schistosomes
Dioecious (separate sexes), female lives in male's gynaecophoric canal. Mate for life; live up to 5 years. Reside in venous system of bladder (S. haematobium) or intestines (other species).
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Schistosome egg production and characteristics
Eggs produced 25-30 days after infection. 300-3000 eggs/day per female. Eggs have a characteristic spine used for diagnosis.
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Snail stage of the schistosome life cycle
Miracidia hatch from eggs in water. Infect snails → transform into primary and secondary sporocysts. Release thousands of cercariae to restart cycle.
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Clinical phases of schistosomiasis
Cercarial dermatitis (swimmer's itch). Acute schistosomiasis (Katayama syndrome): fever, urticaria, cough. Established infection: organ-specific symptoms. Late-stage disease: chronic organ damage.
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Symptoms associated with S. haematobium infection
Haematuria, painful urination, bladder inflammation. Long-term: bladder cancer, infertility, ectopic pregnancy.
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Granuloma formation in schistosomiasis
Immune cells surround trapped eggs to prevent toxin damage. Granulomas lead to fibrosis, causing obstruction and tissue damage.
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Hepatosplenic disease caused by S. mansoni
Portal hypertension, ascites, enlarged liver/spleen. Fibrosis around portal veins ("pipe-stem fibrosis").
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Diagnosis and treatment of schistosomiasis
Diagnosis: eggs in urine/stool, ultrasound, serology. Treatment: Praziquantel, which damages the parasite tegument and causes muscle paralysis.
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Challenges to eliminating schistosomiasis
Reinfection common due to snail presence. Praziquantel less effective on immature worms. Integrated approach needed: chemotherapy, snail control, sanitation, education.
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Central Nervous System (CNS)
brain and spinal cord.
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Peripheral Nervous System (PNS)
cranial and peripheral nerves.
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Sensory Function
detect internal/external changes.
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Integrative Function
analyse and decide responses.
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Motor Function
initiate movement or glandular secretion.
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Sagittal Plane
divides left and right.
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Coronal Plane
divides front and back.
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Transverse Plane
divides top and bottom.
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Superior
above.
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Inferior
below.
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Anterior/Ventral
front.
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Posterior/Dorsal
back.
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Medial
toward midline.
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Lateral
away from midline.
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Cerebrum
largest part; cortex + subcortical areas.
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Cerebellum
balance and coordination.
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Brainstem
involuntary control (e.g., breathing, heart rate).
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Frontal Lobe
decision making, voluntary movement.
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Parietal Lobe
integrates sensory information, motor coordination.
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Temporal Lobe
hearing, speech, object recognition, emotion.
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Occipital Lobe
visual processing.
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Subcortical Structures
Hypothalamus, amygdala, hippocampus, thalamus, basal ganglia involved in memory, emotion, motor control, and sensory processing.
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Midbrain Structure
Colliculi: direct eye movement; Tegmentum: movement coordination, alertness; Cerebral peduncle: control of ocular muscles.
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Spinal Cord Sections
Cervical, thoracic, lumbar, sacral, coccygeal; critical link between CNS and PNS; innervates body regions.
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Somatic Division of PNS
voluntary control of skeletal muscle.
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Autonomic Division of PNS
involuntary control (sympathetic = fight or flight, parasympathetic = rest and digest).
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Enteric Division of PNS
controls gut movement and secretion.
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Afferent Pathways
sensory input to CNS ('Arriving').
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Efferent Pathways
motor output from CNS ('Exiting').
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Reflex Arc of Knee-Jerk Response
Sensory afferents → spinal cord dorsal column → interneurons → efferent motor neurons → muscle contraction; occurs without brain input.
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Major Cell Types of CNS
Neurons: conduct electrical signals; Microglia: immune surveillance and response; Astrocytes: structural and metabolic support; form glial scars; Oligodendrocytes: form myelin sheaths (PNS = Schwann cells).
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White Matter
myelinated axon bundles; fast conduction (up to 150 m/s).
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Grey Matter
unmyelinated cell bodies.
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Cerebrospinal Fluid (CSF) Functions
provides brain buoyancy, cushions, waste removal (produced by choroid plexus).
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Blood-Brain Barrier
endothelial tight junctions selectively protect the brain from harmful blood substances.
