MicrobiologyTier 1Medical Sciences concept

Infection-associated diseases and malignancies (viral and bacterial associations)

Core concept

Chronic infection can drive malignancy or immune-mediated disease via oncogenic viral proteins, chronic inflammation, or immune dysregulation -- pairing organism to consequence is the exam task
EBV: Burkitt lymphoma (esp. endemic African form, associated with co-infection/immune modulation by malaria), nasopharyngeal carcinoma, Hodgkin lymphoma, post-transplant lymphoproliferative disease (PTLD), and AIDS-associated Burkitt lymphoma
HHV8: Kaposi sarcoma and primary effusion lymphoma -- both strongly linked to immunosuppression (HIV/AIDS, transplant)

Organism	Associated condition
EBV	Burkitt lymphoma, nasopharyngeal carcinoma, Hodgkin lymphoma, PTLD
HTLV-1	Adult T-cell leukaemia/lymphoma (ATL)
HHV8	Kaposi sarcoma, primary effusion lymphoma
H. pylori	Gastric MALT lymphoma, gastric adenocarcinoma
HBV/HCV	Hepatocellular carcinoma
HPV	Cervical, anal, oropharyngeal squamous cell carcinoma
Schistosoma haematobium	Bladder squamous cell carcinoma
Influenza	Secondary bacterial pneumonia (S. pneumoniae, S. aureus) -- damaged respiratory epithelium/impaired mucociliary clearance, not itself malignant but a key superinfection pairing

Malaria (esp. P. falciparum) co-infection is specifically linked to endemic Burkitt lymphoma via chronic B-cell stimulation and impaired EBV-specific T-cell immunity, allowing unchecked EBV-driven B-cell proliferation

Trap: attributing all Burkitt lymphoma to EBV alone -- the endemic (African) form's strong EBV association is potentiated by chronic malaria; sporadic and immunodeficiency-associated (AIDS) Burkitt forms have variable EBV association
H. pylori eradication can induce regression of early-stage gastric MALT lymphoma -- a rare example of antimicrobial therapy treating a malignancy directly, reflecting the antigen-driven nature of the lymphoma
Recognising the influenza -> secondary bacterial pneumonia pattern matters clinically: a patient improving from influenza then deteriorating with new fever/purulent sputum suggests superinfection, not a normal viral course

HHV8/EBV-driven malignancies cluster in immunosuppressed patients (HIV, transplant) -- same underlying principle as PTLD risk post-transplant (loss of immune surveillance over a latent oncogenic virus)
HPV vaccination strategy is built directly on this causal link -- prevention of the causative infection prevents the downstream malignancy
Chronic inflammation-driven carcinogenesis (H. pylori, HBV/HCV, Schistosoma) shares the common theme of prolonged tissue injury/regeneration promoting malignant transformation, distinct from the direct oncogene-driven mechanism of EBV/HHV8/HPV

3 more sections, plus exam facts

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