Shigella dysenteriae causes bacillary dysentery characterized by frequent bloody and mucoid stools, abdominal cramps and fever. It is an invasive enteric pathogen causing mucosal ulceration.
Exo-erythrocytic schizogony (pre-erythrocytic stage) occurs in hepatocytes of the liver where sporozoites multiply into merozoites before they invade RBCs.
In the mosquito midgut, zygotes develop into oocysts on the gut wall; each oocyst produces many sporozoites that migrate to the salivary glands.
Amphetamines stimulate the central nervous system; barbiturates are central nervous system depressants producing sedation and respiratory depression.
Amphetamines are central nervous system stimulants. LSD is a hallucinogen (not a narcotic); heroin is an opioid narcotic; benzodiazepines are anxiolytics/sedatives (not primary pain killers).
Athlete's foot (tinea pedis) is a superficial fungal infection of the skin caused by dermatophytes (fungi).
Chronic excessive alcohol consumption leads to liver injury, fibrosis and ultimately cirrhosis. Other substances may damage the liver but alcohol is the classic cause.
Sporozoites migrate to the salivary glands of the infected female Anopheles mosquito and are injected into humans during a bite. In the human they then invade hepatocytes.
Correct associations: Leishmania donovani → Kala-azar (visceral leishmaniasis); Wuchereria bancrofti → Filariasis; Trypanosoma gambiense → Sleeping sickness; Entamoeba histolytica → Amoebiasis.
Paratope is the antigen-binding site located on the variable region of an antibody (formed by variable domains of heavy and light chains) that specifically recognizes the epitope.
Type I hypersensitivity (allergic reactions) involves IgE antibodies bound to mast cells and basophils; on re-exposure crosslinking of IgE triggers histamine release.
Metastasis is the process by which cancer cells invade, enter circulation or lymphatics and establish secondary tumors at distant sites.
HIV is a retrovirus that carries two copies of single-stranded positive-sense RNA and uses reverse transcriptase to make DNA.
Activated B cells differentiate into plasma cells which are antibody-secreting factories producing large quantities of immunoglobulin.
Primary lymphoid organ — Thymus: site of T-lymphocyte maturation and differentiation (selection of self-tolerant T cells). Secondary lymphoid organ — Tonsils: lymphoid tissue in the pharynx that traps inhaled/ingested pathogens, contains B and T cells, initiates adaptive immune responses and produces antibodies locally.
Primary: Thymus. Secondary: Tonsils.
Macrophages are part of the internal innate immune barriers (cellular barriers). They perform phagocytosis of pathogens, secrete cytokines (e.g., IL-1, TNF) to recruit other immune cells, present antigen via MHC II to helper T cells (linking innate and adaptive immunity), and kill microbes using reactive oxygen/nitrogen species and lysosomal enzymes.
Cellular (phagocytic) innate barriers — macrophage-mediated defence.
Interferons (IFNs) are signaling proteins: Type I (IFN-α, IFN-β) are produced by virus-infected cells and induce an antiviral state in neighboring cells, upregulate MHC I expression and activate NK cells; Type II (IFN-γ) is produced by T cells and NK cells and activates macrophages, enhances antigen presentation and shapes adaptive immunity.
Interferons are cytokines produced by virus-infected and immune cells with antiviral and immunomodulatory roles.
Key chemical mediators released during inflammation include: histamine (from mast cells; increases vascular permeability), bradykinin (pain, vasodilation), prostaglandins and leukotrienes (derived from arachidonic acid; vasodilation, chemotaxis), cytokines such as IL-1 and TNF-α (fever, leukocyte activation), chemokines (leukocyte recruitment), complement fragments C3a/C5a (anaphylatoxins, chemotaxis) and nitric oxide (vasodilation, antimicrobial).
Histamine, bradykinin, prostaglandins, leukotrienes, cytokines (IL-1, TNF-α), chemokines, complement fragments (C3a, C5a), nitric oxide.
After entry, retrovirus (e.g., HIV) binds receptors (CD4 plus coreceptor), fuses with the host cell and releases RNA. Reverse transcriptase converts single-stranded viral RNA into double-stranded viral DNA. Integrase inserts this viral DNA (provirus) into the host genome. Host RNA polymerase II transcribes viral mRNA and genomic RNA. Viral proteins are translated; structural proteins and genomic RNA assemble at the plasma membrane. Virions bud off acquiring an envelope; viral protease cleaves polyproteins to produce mature infectious particles.
Retroviral replication: attachment & fusion → reverse transcription of ssRNA to dsDNA → integration into host genome (provirus) → transcription/translation of viral proteins → assembly and budding → maturation by viral protease.
Structure features to label/textually depict: two heavy (H) chains and two light (L) chains linked by disulfide bonds; each chain has variable (V) and constant (C) regions (VH, VL, CH, CL). The two antigen-binding sites are at the N-terminal variable regions (Fab regions) — contain paratopes that bind epitopes. The stem is the Fc region (constant heavy-chain domains) responsible for complement activation and binding to Fc receptors. A hinge region provides flexibility. Approximate molecular mass ~150 kDa. (If drawing, show Y-shaped molecule, label VH, VL at tips, CH/CL in arms and Fc in stem, indicate disulfide bonds and antigen-binding sites.)
Immunoglobulin (Ig) is a Y-shaped molecule of two identical heavy chains and two identical light chains with variable and constant regions forming Fab (antigen-binding) and Fc regions (effector functions).
Key cells of the innate immune system: neutrophils (rapid phagocytosis of microbes), macrophages/monocytes (phagocytosis, antigen presentation), dendritic cells (antigen capture and presentation to adaptive system), natural killer (NK) cells (kill virus-infected and tumor cells), mast cells and basophils (release histamine, mediate inflammation), eosinophils (combat helminths), and barrier epithelial cells (produce antimicrobial peptides). These act non–specifically and provide the first line of defence.
Neutrophils, macrophages (monocytes), dendritic cells, natural killer (NK) cells, mast cells, eosinophils, basophils and epithelial cells.
Definition: A vaccine contains whole organisms or parts (or genetic material) that elicit an immune response and immunological memory without causing full disease. Major types: 1) Live attenuated vaccines (weakened pathogen; e.g., measles vaccine) — strong, long-lasting immunity. 2) Killed/inactivated vaccines (e.g., killed polio) — safer but may need boosters. 3) Subunit vaccines (protein or polysaccharide antigens) and conjugate vaccines (polysaccharide linked to protein; e.g., Hib) — focus on specific antigens. 4) Toxoid vaccines (inactivated toxins; e.g., tetanus, diphtheria). 5) Recombinant protein vaccines (antigen produced by genetic engineering). 6) Viral vector vaccines (gene for antigen delivered by harmless virus). 7) DNA and mRNA vaccines (deliver genetic instructions for antigen production). Choice depends on pathogen, safety and type of immune response required.
A vaccine is a preparation that stimulates protective immunity against a specific disease. Types: live attenuated, killed/inactivated, subunit (including toxoid and conjugate), recombinant, toxoid, DNA/mRNA, and viral vector vaccines.
Diagnosis pathway: 1) Initial screening: HIV antibody/antigen tests (rapid assays, ELISA detecting anti-HIV antibodies and p24 antigen). 2) Confirmatory test: Western blot or nucleic acid test (HIV RNA PCR) to detect virus. 3) Staging and AIDS diagnosis: measure CD4+ T lymphocyte count and viral load. Clinical diagnosis of AIDS is made when CD4 count <200 cells/µl (or <14% CD4) or when the patient develops AIDS-defining opportunistic infections (e.g., Pneumocystis pneumonia, Kaposi's sarcoma).
Screen with HIV antibody/antigen tests (rapid test or ELISA), confirm by Western blot or HIV RNA PCR; diagnose AIDS when CD4+ T cell count falls below 200 cells/µl (or <14% CD4) or when specific opportunistic infections/clinical criteria are present.
Justification: The immune system normally distinguishes self from non‑self by central and peripheral tolerance mechanisms. Failure of tolerance (due to genetic predisposition, molecular mimicry, infection, or breakdown of regulatory T cell function) leads to immune recognition of self-antigens. This generates autoantibodies and autoreactive T cells that attack host tissues, causing chronic inflammation and organ damage. Clinical examples include rheumatoid arthritis (autoantibodies against joint components), type I diabetes (destruction of pancreatic β-cells) and systemic lupus erythematosus (wide spectrum of autoantibodies). Hence autoimmunity is a misdirected immune response against self.
Autoimmunity occurs when self-tolerance fails and the immune system mounts responses against self-antigens, producing autoantibodies and autoreactive T cells that damage tissues (examples: rheumatoid arthritis, type I diabetes, systemic lupus erythematosus).
Diphtheria: causative agent Corynebacterium diphtheriae. Spread by respiratory droplets and close contact. Characteristic signs include sore throat, low-grade fever, formation of a greyish pseudomembrane over tonsils/pharynx that can obstruct airways, cervical lymphadenopathy (‘‘bull neck’’), and complications like myocarditis and peripheral neuropathies from diphtheria toxin. Typhoid: causative agent Salmonella enterica serovar Typhi (Salmonella typhi). Transmitted by faecal–oral route (contaminated food and water). Presents with sustained high fever, headache, malaise, abdominal pain, constipation or diarrhoea, ‘rose spots’ on the trunk, hepatosplenomegaly; severe cases may develop intestinal bleeding or perforation.
Diphtheria — Agent: Corynebacterium diphtheriae; Transmission: respiratory droplets; Symptoms: sore throat, fever, formation of pseudomembrane in throat, lymphadenopathy, possible myocarditis and nerve palsies. Typhoid — Agent: Salmonella typhi; Transmission: faecal–oral via contaminated food/water; Symptoms: prolonged high fever, headache, abdominal pain, constipation or diarrhoea, rose spots, hepatosplenomegaly, possible intestinal haemorrhage/perforation.
The presence of merozoites (intraerythrocytic forms released from schizonts) in peripheral blood indicates malaria caused by Plasmodium spp. Diagnosis: blood smear microscopy showing Plasmodium trophozoites/merozoites or rapid antigen tests. Clinical features include fever with chills, periodicity depending on species.
Malaria (infection by Plasmodium species).
(i) Principal causative species: Wuchereria bancrofti (others include Brugia malayi, Brugia timori). (ii) Clinical features: acute episodes of fever and lymphangitis; chronic lymphatic obstruction leading to lymphedema and massive enlargement of limbs or genitalia (elephantiasis), scrotal hydrocele, and secondary infections. (iii) Mode of transmission: vector-borne — female mosquitoes (species vary by region: Culex, Anopheles, Aedes) transmit infective larvae; microfilariae show nocturnal periodicity and are taken up by mosquitoes and later transmitted as infective larvae during subsequent bites.
(i) Wuchereria bancrofti (also Brugia malayi and Brugia timori in some regions). (ii) Symptoms: lymphatic obstruction causing swelling (elephantiasis) of limbs and genitalia, recurrent fever, lymphangitis, hydrocele. (iii) Transmission: by infected mosquitoes (e.g., Culex, Anopheles, Aedes) that transmit microfilariae during blood meal.
Abrupt cessation of alcohol or drugs in dependent individuals produces a constellation of withdrawal symptoms. Mild-to-moderate symptoms include anxiety, restlessness, irritability, tremors, sweating, nausea, vomiting, headache, insomnia, muscle cramps, and strong drug/alcohol craving. Severe withdrawal (particularly alcohol, benzodiazepines, or barbiturates) can produce autonomic hyperactivity, hallucinations, delirium tremens (confusion, severe agitation, visual/tactile hallucinations), and seizures — medical emergency.
Common withdrawal symptoms: anxiety, irritability, tremors, sweating, nausea and vomiting, headache, insomnia, muscle aches, increased heart rate and blood pressure, hallucinations or delirium (severe alcohol withdrawal/delirium tremens), seizures, intense cravings, and depression.
The term ‘common cold’ covers illnesses caused by numerous viral pathogens (numerous rhinovirus serotypes, multiple coronaviruses, adenoviruses, etc.). High antigenic diversity and frequent antigenic variation across many serotypes mean a vaccine would need to target a very large number of distinct antigens. In addition, the protective mucosal (IgA) immunity is often short-lived and sterilising immunity is difficult to achieve. Because disease is usually mild and self‑limiting, the cost–benefit of developing a universal vaccine is low. These factors make a single effective vaccine against all causes of the common cold impractical.
Because the common cold is caused by many different viruses (especially over 100 rhinovirus serotypes plus coronaviruses, adenoviruses, enteroviruses) with high antigenic diversity and frequent variation; plus mucosal immunity is short‑lived, making a broad effective vaccine impractical.