Clinical Pathology · MU Sofia

130. Insect vector transmitted infections – lime disease, malaria, hemorrhagic fevers. Etiology & pathogenesis. Organ site pathomorphology.

Covers Lyme disease from Borrelia burgdorferi through its three stages, including the histology of late chronic synovitis. Then describes malaria across the four Plasmodium species, the liver-to-red-cell life cycle, the fever pattern, brown hematin discolouration and cerebral malaria, with a Giemsa smear figure of P. falciparum. Ends with the main viral haemorrhagic fevers, their common symptoms and mechanisms such as liver damage, DIC and bone marrow dysfunction.

Inside: 1 section · 1 labelled picture · 15 flashcards · 2 min

Topic 130 of 138 in the MU Sofia syllabus for Clinical Pathology (Medicine, Year 4). The free AceMed note covers it in 1 section, about 352 words (2 min of reading), with 15 flashcards.

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  1. Insect vector transmitted infections - lyme disease, malaria, hemorrhagic fevers. Etiology & pathogenesis. Organ site pathomorphology

Insect vector transmitted infections - lyme disease, malaria, hemorrhagic fevers. Etiology & pathogenesis. Organ site pathomorphology

Lyme disease

Lyme disease is caused by infection with spirochete Borrelia burgdorferi, transmitted by deer ticks. It involves multiple organ systems and has three stages:

  • Stage 1 - Borrelia spirochetes multiply at site of entry, causing ‘bullseye skin lesion’ aka erythema chronicum migrans, along with a systemic fever, IgM and IgG AB are present in skin
  • Stage 2 - early disseminated stage where spirochetes spread causing lymphadenopathy, joint and muscle pain, cardiac arrhythmias, meningitis and sometimes CN involvement
  • Stage 3 - late disseminated stage where spirochetes cause chronic arthritis and encephalitis
  • Here, histology shows chronic papillary synovitis with synoviocyte hyperplasia, fibrin deposition and mononuclear cell infiltrates around joints

Malaria

Endemic in Asia and Africa, caused by one of four types of protozoa, Plasmodium falciparum, which causes tertian malaria is the most important (others are P. malariae, P. vivax and P. ovale).

Parasites are injected via mosquitos and multiply forming schizonts in liver cells, from here merozoites are release which affect RBCs, where asexual reproduction occurs, and trophozoites develop.

Giemsa thin smear, P. falciparum: delicate ring-form trophozoite in a red cell (lower arrow) and a banana-shaped gametocyte (upper arrow), typical of falciparum.

Image: “P. falciparum thin smear ring forms and gametocyte” by Jenkayaks, CC BY-SA 3.0, via Wikimedia Commons.

Clinical features show:

  • Fever and chills every 48-72 hours due to release of merozoites from RBCs
  • Hemolytic anemia
  • Release of brown hematin causes discolouration of spleen, liver, lymph nodes and bone marrow
  • Falciparum malaria often involves the brain and causes cerebral malaria

Remember: the four classic species:

  • P. vivax and P. ovale - tertian (every 48 h); dormant liver hypnozoites cause relapses
  • P. malariae - quartan (every 72 h)
  • P. falciparum - irregular ("malignant tertian"), high parasitaemia; infected red cells stick to brain capillaries, causing cerebral malaria

Haemorrhagic fever

Viral hemorrhagic fevers include:

  • Ebola
  • Marburg
  • Lassa fever
  • Yellow fever

All are characterised by bleeding and fever and can progress to high fever, shock and death. Petechiae, bleeding, edema, hypotension, malaise, muscle pain, diarrhea and shock are all common symptoms. Different pathogenesis for different fevers, but mechanisms include liver damage, DIC and bone marrow dysfunction.

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