Named Animal Diseases

Spec Mapping — OCR H420 Module 4.1.1 — Communicable diseases, content statement on named animal diseases caused by bacteria, viruses, protoctista and fungi, with their causative pathogens and effects on the host (refer to the official OCR H420 specification document for exact wording). This lesson covers the seven OCR named animal diseases (tuberculosis, bacterial meningitis, HIV/AIDS, influenza, malaria, ringworm and athlete's foot) and links each cellular mechanism to clinical symptom and treatment.

Communicable disease is the single greatest killer in human history. The Black Death, smallpox, the 1918 influenza pandemic, malaria and HIV/AIDS between them have killed many hundreds of millions of people across two thousand years of recorded history. Even today, despite vaccines, antibiotics and improved public health, infectious diseases account for around a quarter of global deaths, falling disproportionately on the global south. OCR specification 4.1.1 requires you to know the named animal diseases below, in each case linking the pathogen type (bacterium / virus / protoctist / fungus), the named pathogen species, the tissue or cell type damaged, the clinical symptoms, and the available treatment. The lesson is content-dense by design — examiners reliably set 4-mark short-answer questions of the form "Name a named animal disease caused by a virus and describe how the virus damages the host." This lesson is your reference for those answers, and an opportunity to revisit cell biology, immunology and pharmacology through the lens of disease.

Key Definitions:

• Infection — the colonisation of a host by a pathogen, with or without overt symptoms.
• Incubation period — the time between infection and the appearance of symptoms; ranges from hours (cholera) to years (HIV → AIDS, leprosy).
• Reservoir host — an organism (often non-human) in which a pathogen is maintained, from which it can spread to other species.
• Zoonosis — a disease transmitted from animals to humans (TB from cattle, influenza from birds and pigs, HIV originally from chimpanzees, SARS-CoV-1/2 from bats via intermediate hosts).
• Opportunistic infection — an infection caused by a normally harmless or weakly pathogenic organism that exploits a weakened host immune system (e.g. Pneumocystis jirovecii pneumonia in HIV/AIDS).

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Overview Map of the Seven Named Diseases

Disease	Pathogen type	Named pathogen	Tissue / cell damaged	Key symptom	Treatment
Tuberculosis	Bacterium (acid-fast)	Mycobacterium tuberculosis (and M. bovis)	Alveolar macrophages, lung tissue	Chronic cough with blood, weight loss, night sweats	Combination antibiotics (isoniazid, rifampicin, pyrazinamide, ethambutol) for 6 months
Bacterial meningitis	Gram-negative bacterium	Neisseria meningitidis (also Strep. pneumoniae, Hib)	Meninges, cerebrospinal fluid	Severe headache, stiff neck, fever, photophobia, non-blanching rash	IV ceftriaxone or benzylpenicillin
HIV/AIDS	Retrovirus (RNA → DNA)	Human immunodeficiency virus	CD4⁺ T helper cells	Progressive immunodeficiency; opportunistic infections	Combination antiretroviral therapy (ART)
Influenza	(−)-ssRNA virus	Influenza A/B/C	Ciliated respiratory epithelium	Fever, cough, myalgia, malaise	Supportive; oseltamivir; annual vaccine
Malaria	Protoctistan parasite	Plasmodium falciparum (and vivax, malariae, ovale, knowlesi)	Liver cells then red blood cells	Cyclical fever, anaemia, possible cerebral malaria	Artemisinin-combination therapies (ACTs); chloroquine for sensitive strains
Ringworm	Dermatophyte fungus	Trichophyton, Microsporum, Epidermophyton	Keratinised skin, hair, nails	Circular itchy red lesion with raised edge	Topical clotrimazole/terbinafine; oral griseofulvin for severe
Athlete's foot	Dermatophyte fungus	Trichophyton rubrum	Skin between toes	Cracked, itchy, peeling skin	Topical antifungals; keep feet dry

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1. Tuberculosis (TB) — Mycobacterium tuberculosis

TB is a bacterial disease caused primarily by Mycobacterium tuberculosis (and M. bovis in cattle, which can also infect humans via unpasteurised milk — a classical zoonosis). Mycobacterium is unusual among bacteria: it has an exceptionally thick, waxy, mycolic-acid-rich cell wall that makes it acid-fast (retaining Ziehl–Neelsen carbolfuchsin stain after acid washing), profoundly resistant to drying and to lysozyme, and slow-growing (doubling time ~16–20 hours rather than 20 minutes for E. coli). Robert Koch isolated M. tuberculosis in 1882 and won the Nobel Prize in 1905 for his work on TB; the bacterium is sometimes still called "Koch's bacillus".

How it causes damage

• Inhaled droplets (1–5 µm aerosols generated by coughing) carry the bacilli into the alveoli.
• Alveolar macrophages engulf the bacteria but cannot destroy them — the waxy mycolic-acid coat blocks lysozyme, and M. tuberculosis secretes proteins that prevent phagosome–lysosome fusion, so the bacterium replicates inside the very cell that engulfed it.
• The infected macrophage recruits more macrophages and T cells, which together form a granuloma (tubercle) — a walled-off nodule of immune cells surrounding a necrotic, caseous (cheese-like) centre.
• Inside the granuloma, M. tuberculosis survives in a dormant state for years; reactivation occurs when the host's immune competence falls (HIV co-infection is the classic example, and is why TB is now the leading cause of death among HIV-positive people worldwide).
• Active disease destroys lung tissue, producing fibrotic scars and cavitations that reduce gas exchange surface area and predispose to haemoptysis (coughing blood) when the cavities erode into pulmonary blood vessels.
• Classic clinical symptoms: chronic cough lasting more than three weeks, blood in the sputum, weight loss ("consumption"), night sweats, low-grade fever, fatigue. Extrapulmonary TB can affect lymph nodes, bone (Pott's disease of the spine), kidneys, gut and the central nervous system.

Treatment

Treatment of active TB requires a long, multi-drug course because the slow growth and intracellular sanctuary of M. tuberculosis make single-drug regimens prone to resistance. The standard six-month regimen comprises:

• Isoniazid — inhibits mycolic-acid synthesis (cell-wall target).
• Rifampicin — inhibits bacterial RNA polymerase.
• Pyrazinamide — disrupts membrane transport at acidic intracellular pH.
• Ethambutol — inhibits arabinogalactan synthesis (cell-wall target).

Patients take all four for the initial two months, then isoniazid + rifampicin for a further four months. Non-completion of the full course is the single greatest driver of multidrug-resistant TB (MDR-TB), defined as resistance to at least isoniazid and rifampicin; extensively drug-resistant TB (XDR-TB) is resistant to even more.

The BCG vaccine (Bacillus Calmette–Guérin, a live attenuated M. bovis developed by Calmette and Guérin in 1908–1921) provides partial, age-dependent protection — strong against childhood miliary and meningeal TB, weak against adult pulmonary TB. Because of waning efficacy and high local prevalence of non-tuberculous mycobacteria, the UK ended universal schoolchild BCG vaccination in 2005, retaining it only for high-risk groups.

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2. Bacterial Meningitis

Bacterial meningitis is inflammation of the meninges (membranes covering the brain and spinal cord). It is caused by several bacteria, most commonly:

• Neisseria meningitidis (meningococcus)
• Streptococcus pneumoniae (pneumococcus)
• Haemophilus influenzae type b (Hib)

How it causes damage

• Bacteria colonise the nasopharynx asymptomatically in around 10 % of healthy adolescents and young adults — the typical reservoir.
• In susceptible individuals (post-viral upper-respiratory infection, complement deficiency, asplenia), the bacteria translocate into the bloodstream and circulate as meningococcaemia.
• They penetrate the blood–brain barrier at the choroid plexus and the post-capillary venules of the meninges, and replicate in the protected environment of the cerebrospinal fluid (CSF).
• The host innate immune response in CSF — a normally cell-poor compartment — releases massive amounts of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6). The resulting massive meningeal inflammation raises intracranial pressure, damages neurones, and disrupts cerebral blood flow.
• Lipopolysaccharide (LPS, endotoxin) released by lysed gram-negative bacteria drives disseminated intravascular coagulation in the systemic circulation, producing the characteristic non-blanching petechial rash of meningococcal septicaemia (the classical glass-tumbler test exploits this: petechiae remain visible under pressure where blanching rashes disappear).
• Untreated bacterial meningitis can be fatal within hours; case-fatality rates remain around 10 % even with optimal treatment, and 10–20 % of survivors have long-term sequelae (deafness, cognitive impairment, limb amputations following purpura fulminans).

Treatment

• Immediate intravenous antibiotics — empirical regimens are ceftriaxone or benzylpenicillin (or both) given the moment the diagnosis is suspected, ahead of laboratory confirmation. UK pre-hospital guidance authorises non-specialists to give benzylpenicillin on suspicion.
• Adjunctive corticosteroids (dexamethasone) reduce inflammatory sequelae in some forms of meningitis.
• Conjugate vaccines: MenC (1999), MenACWY (since 2015 for teenagers and university entrants — the dormitory settings of student halls are recognised transmission hotspots), MenB (Bexsero, since 2015 in the UK infant schedule), pneumococcal conjugate vaccine (PCV), Hib conjugate (since 1992). The UK MenC programme caused near-complete elimination of group-C disease within a decade and is a textbook example of conjugate-vaccine herd immunity.

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3. HIV/AIDS

Human immunodeficiency virus (HIV) is a retrovirus that causes acquired immune deficiency syndrome (AIDS).

Structure

• Two copies of single-stranded (+)-sense RNA genome (~9,200 nucleotides each).
• Inner conical capsid of p24 protein.
• An outer lipid envelope (acquired from the host plasma membrane on budding) studded with the surface glycoprotein gp120 and the transmembrane glycoprotein gp41.
• Inside the virion: reverse transcriptase (RNA-dependent DNA polymerase), integrase, and protease — all viral enzymes that are drug targets.

How it causes damage — the HIV replication cycle

flowchart TD
    A[gp120 binds CD4 + CCR5/CXCR4 co-receptor] --> B[gp41 mediates membrane fusion]
    B --> C[Capsid enters cytoplasm; uncoating]
    C --> D[Reverse transcriptase: RNA --> dsDNA]
    D --> E[dsDNA enters nucleus]
    E --> F[Integrase inserts proviral DNA into host genome]
    F --> G[Host RNA polymerase transcribes viral mRNAs]
    G --> H[Translation; Gag-Pol polyprotein produced]
    H --> I[Assembly at plasma membrane]
    I --> J[Budding; envelope acquired from host membrane]
    J --> K[Protease cleaves polyprotein; virion matures]

1. HIV's gp120 binds to CD4 receptors on T helper cells (and, less importantly, on macrophages and dendritic cells), then to a CCR5 (early infection) or CXCR4 (late infection) chemokine co-receptor.
2. Conformational changes in gp41 fuse the viral envelope with the host plasma membrane, releasing the capsid into the cytoplasm.
3. Reverse transcriptase copies the (+)-sense RNA into single-stranded then double-stranded DNA — this is the central oddity of retroviruses, running RNA → DNA against the conventional "central dogma" flow.
4. Integrase inserts the viral dsDNA into the host chromosome, producing a permanent provirus that the immune system cannot remove. From this point the infection is incurable with current therapy.
5. Host RNA polymerase II transcribes viral mRNAs; translation produces a Gag-Pol polyprotein; assembly at the plasma membrane and budding yield immature virions; viral protease cleaves the polyprotein into mature structural and enzymatic components.
6. Each productively-infected T helper cell releases hundreds of progeny virions and dies, either by direct cytopathic effect or by cytotoxic-T-cell killing recognising MHC-I-presented viral peptides.
7. CD4⁺ T helper counts fall over years (normal ~1,000 cells/µL). When they drop below ~200 cells/µL the immune system can no longer control normally harmless microbes, and the patient develops opportunistic infections that define AIDS: Pneumocystis jirovecii pneumonia, oesophageal candidiasis, cryptococcal meningitis, cytomegalovirus retinitis, Kaposi's sarcoma (driven by HHV-8) and TB reactivation.

Treatment

Combination antiretroviral therapy (cART or ART) — typically a triple-drug regimen combining two nucleoside reverse-transcriptase inhibitors (NRTIs, e.g. tenofovir + emtricitabine) with one third-class agent (an integrase inhibitor such as dolutegravir, or a non-nucleoside reverse-transcriptase inhibitor, or a protease inhibitor). Modern regimens reliably suppress viral replication to undetectable levels, restoring CD4 counts and allowing near-normal life expectancy, and "undetectable equals untransmissible" (U=U) is now the established public-health message: people on suppressive ART cannot transmit HIV sexually. Pre-exposure prophylaxis (PrEP) — daily tenofovir + emtricitabine taken by HIV-negative people at risk — is highly effective at preventing acquisition.

There is still no licensed HIV vaccine despite decades of research; the extreme variability of gp120 and the rapid integration of the provirus make conventional vaccine strategies fail.

Exam Tip: HIV is transmitted by exchange of bodily fluids — blood (sharing needles, transfusion before screening), semen, vaginal secretions and breast milk. It is not transmitted by casual contact, saliva, tears, mosquitoes or air. Vertical transmission from mother to child (during pregnancy, birth or breastfeeding) is now largely preventable with maternal ART.

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4. Influenza — Orthomyxoviridae

Influenza ("flu") is caused by influenza viruses A, B and C (type A is the most pathogenic).

Structure

• An enveloped virus with a segmented single-stranded (−)-sense RNA genome — eight segments in influenza A and B, seven in influenza C.
• The envelope is studded with two viral surface glycoproteins: haemagglutinin (HA) binds sialic-acid receptors on host cell surfaces and mediates membrane fusion; neuraminidase (NA) cleaves sialic acid to release progeny virions from infected cells.
• Eighteen H subtypes (H1–H18) and eleven N subtypes (N1–N11) are recognised; strain names such as H1N1 (1918 Spanish flu, 2009 swine flu pandemic) and H5N1 (avian flu) refer to the HA/NA combination.

Antigenic drift and antigenic shift

The segmented genome allows two distinct mechanisms of antigenic change:

• Antigenic drift — gradual point mutations in HA and NA accumulate because the viral RNA polymerase has no proofreading. Drift produces the seasonal flu strains that require an annual vaccine update.
• Antigenic shift — sudden major change when two different influenza strains infect the same host (often a pig or duck acting as a "mixing vessel") and reassort their segments, producing a novel HA/NA combination against which the human population has no immunity. Shift is the basis of pandemic influenza: 1918 H1N1, 1957 H2N2, 1968 H3N2, 2009 H1N1.

How it causes damage

• HA binds sialic acid (N-acetylneuraminic acid) receptors on the surface of ciliated respiratory epithelial cells. Avian influenza HAs prefer α2,3-linked sialic acid (predominant in the lower bird gut and lower human lung); human-adapted HAs prefer α2,6 (upper human respiratory tract).
• The virus is endocytosed; acidification of the endosome triggers HA-mediated membrane fusion and release of the viral ribonucleoprotein into the cytoplasm.
• Replication occurs in the nucleus (unusual for an RNA virus); progeny virions bud from the apical membrane and neuraminidase cleaves sialic acid to release them.
• Lytic infection destroys the ciliated epithelium lining the airways, eliminating the mucociliary escalator that normally clears mucus and microbes upwards to the throat.
• Loss of ciliated epithelium predisposes to secondary bacterial pneumonia, most often by Staphylococcus aureus and Streptococcus pneumoniae — historically the major cause of death in influenza outbreaks, including most fatalities in the 1918 pandemic.
• Systemic symptoms (high fever, myalgia, headache, fatigue) are driven by interferons and pro-inflammatory cytokines released by infected cells and recruited leucocytes, not by direct viral cytopathy at distant sites.

Treatment

• Supportive care is the basis of management for most cases — rest, fluids, paracetamol for fever.
• Neuraminidase inhibitors (oseltamivir/Tamiflu, zanamivir/Relenza) block release of progeny virions from infected cells and shorten symptom duration if given within 48 hours; they are reserved for severe cases and at-risk groups.
• Annual vaccines based on WHO predictions of circulating strains (trivalent or quadrivalent, covering two A subtypes and one or two B lineages). Efficacy varies year-to-year (typically 40–60 %) depending on how well the predicted strains match circulating drift variants.

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5. Malaria — Plasmodium

Malaria is a protoctistan disease caused by several species of Plasmodium, most dangerously Plasmodium falciparum. It kills approximately 600,000 people annually, mostly children under 5 in sub-Saharan Africa.

Life cycle

flowchart LR
    A[Infected female Anopheles mosquito] --> B[Sporozoites injected into blood]
    B --> C[Liver cells: replication]
    C --> D[Merozoites released into blood]
    D --> E[Invade red blood cells]
    E --> F[RBCs burst: fever, anaemia]
    F --> G[New mosquito feeds and takes up gametocytes]
    G --> A

How it causes damage