Zoonoses Flashcards
Leptospira
Gram negative, obligate aerobe spirochete
Periplasmic flagella. Two internal flagella within periplasma
Secretes soluble haemolysin (bursts RBCs)
Leptospirosis/Weil’s disease
Caused by Leptospira interrogans
Serogroup icterohaemorrhagiae is main serovar causing disease
Contact with infected urine, soil, food (from carrier or infected animal)
Leptospirosis effects
Renal injuries (interstitial nephritis)
Hepatocellular disease due to vasculitis
Meningitis
Symmetric pretibial rash
Leptospire infection
Penetrate skin through breaches
Disseminate haematogenously and establish in target organ
Produce adhesins for binding to host cell components (ECM, cadherin)
Secrete proteases and haemolysins that degrade host membrane
Can survive within macrophages and induce apoptosis
Leptospira treatment/prevention
Antibiotics (penicillin, tetracycline)
Serovar-specific vaccine
Prophylaxis with short/long-term tetracycline
Borrelia burgdorferi
Helical cell shape
Periplasmic flagella
BBK32 protein forms catch bonds with endothelial cells of blood vessels to move along without being swept away
B. burgdorferi genome
One large linear chromosome
21 other linear and circular plasmids
Plasmid Ip25 necessary for Borrelia infection
Uses manganese to avoid scavenging for iron (no free iron in tissues/fluids as a defence mechanism)
B. burgdorferi life cycle
Unfed larval ticks acquire B. burgdorferi by feeding on infected rodent
Spirochetes multiply and persist in midguts of tick to nymph stage
When nymph feeds, spirochetes migrate to salivary glands and are transmitted to new mammal host
Lyme disease
Stage 1 3-30 days after bite Flu-like symptoms (fatigue, headache) Skin rashes in 80% of individuals Stage 2 weeks or months after Severe headache and neck pain Arthritis in 60% of patients Neurological symptoms
B. burgdorferi infection
Decreases expression of OspA lipoprotein (prevents injection) which allows detachment from the gut
Expresses OspC which aids flow to tick salivary glands
Tick protein Salp15 binds OspC in salivary glands
Protects against neutralising antibodies in the new host
Cryptosporidium
Coccidian protozoan parasite
Hosts are animals (livestock) and humans
Cryptosporidium parvum causes cryptosporidiosis
Pathogenic form is oocyst
Cryptosporidium infection
Sporozoites excyst from oocysts and invades epithelial cells of the gastrointestinal tract
Develops into trophozoite
Cell death results from invasion, multiplication and extrusion
T cell-mediated inflammation can produce microvilli death and crypt. growth
Cryptosporidiosis
Diarrhoea, pain, fever
Symptoms last longer in immunocompromised individuals
No effective treatment (eukaryotic cell within eukaryotic human)