Mechanism of Parasitic Infections

Question 1

Describe the pathogenesis of Chaga’s Disease
(phases: acute, indeterminate, chronic), pathology: what symptoms can be experienced?

Answer 1

• doobie bugs? (idk man) vector blood meal and defecation => scratching accelerates infection (or feed on mucosal cells eyes)
• protozoa disease w/ complex life cycle
• amastigotes invade host cells which reproduce and form tryptomastagotes which can be fed on from the doobie bug again.
• Acute: 1-12 days nest of amastigotes w/ trypanosomes present in blood, mild/localised infection fever, swelling, lymphadenopathy max up to 3 months
• instigation of pro inflammatory cytokines via TH-1
  fatal contraction in children with damage to heart and brain tissue
• Chronic/ Indeterminate?? : lifelong infection w/ no apparent disease will be positive for parasite DNA
  feeding on nerve cells in gut ENS (peristalsis affected) digestive system damage megacolon/megarectum etc.
  undetected in x-rays (asymptomatic
• cardiomyopathy from parasitic damage = unable to contract efficiently
  arrhythmia / ventricular tachycardia
  heart valve insufficiency / increased risk of thrombosis

Question 2

Describe the pathology of leishmania
(life cycle, phases, pathology)

Answer 2

new world cutaneous leishmaniasis
- endemic in South America, north Africa &Middle East
- vector: sandfly blood meals transfers promastigotes, binds to macrophage surface receptors engulfed by histiocyte [asexual production] cell bursts which release and reuptake other host cells

• scraping around ulcer/symmetric lesions edge and visible in plaque under microscopy [invaded macrophages]
  suboptimal immune response may cause reactivation of symptoms from old scarring. [leishmainia recividens]
  poor immune response forming widespread nodular infiltrations packed with parasites.

Acute: host inflammatory response - cytotoxic CD8+ cells = killing parasite = tissue damage / macrophage killing, and TH-1 pro-inflammatory response

Clinical Latency: sterile immunity not achieved small numbers of parasite present on old scars

rare Relapse: local immunosuppression , inadequate inflammatory response = accelerated parasite reproduction

Question 3

Understand how parasitic infections are controlled

Answer 3

PROTOZOA:
- tinidazole
- metronidazole
- nitazoxanide
- benzndiazole
- meglumine antimoniate

HELMINTHS:
- albendenzole
- diethylcarbamazine
- pyrantel

ECTOPARASITES:
- malathion lotions (kill adults)
- ivermectin

PREVENTION:
- building regulation
- education on sanitation
- swamp removals
- pesticides to reduce vector survival
- periodic treatment for endemic areas
- mass injections
- reduce reservoir infections
- improve water sanitation

Question 4

Describe the onset and pathology of schistosomiasis
3 MAIN SPECIES:
- mansoni [hepato]
- haematobium [urinary]
- japonicium [hepato]

Answer 4

• cercariae exposure from bird schistosomes
• adult parasites lay eggs in circulation which are organised in granuloma in mucosal/luminal cells in liver/urinary tract
  granulation of TH-2 cells - tissue insults => repair => fibrosis
  epithelium pushed into = granuloma formation in small intestine
• mucosal residence triggers inflammatory response => could cause severe urinary damage => papilloma => nodular carcinoma/ heamatauria / calcified attenuated bladder and ⬆️ risk of secondary UTI

CHRONIC = PIPE STEM SCHISTOSOMIASIS
liver/spleen enlargement and cirrhosis => increased fatality

Question 5

Describe the onset and pathology of onchocerciasis

• what is it?
• parasite vectors
• symptoms and chronic effects
• how does blindness occur?

Answer 5

river blindness
- worm: onchocercea volvulus
- adult female worm transmitted via black flies
- inflammatory episodes via boring holes into blood feeding pool
- permanent scarring caused from microfilaraie => skin & eyes
- immunosuppressive effect on host
- uticarial type rash
- females reside in subcutaneous nodules
- premature ageing from elastin degradation
- punctuate opacities caused by cornea immune response (punctuate keratitis) => chronic onset causes fibrosis
=> eventual causing sclerosing keratitis
-microfilaraie migration into pigment epithelium / killing nerve cells/ retina spots lateral to macula => site of microfilaraie death