3.2 Zoonotic bacterial pathogens

Zoonose

Zoonotic diseases - spread among animals and between animals and humans

Zoonotic disease overview

Able to be transmitted (by a vector) from other animals, wild/domestic to humans. diseases that normally exist in other animals but also infects humans. 75% emerging infectious diseases in humans are zoonotic, commonly transmitted via bites and scratches

Borrelia burgdorferi organism

not gram +/-, spirochete, endoflagella, extracellular pathogen, aerobic and microaerobic

Borrelia habitat

lyme disease infection transmitted by bite of infected ticks of the Ixodes ricinus complex, caused primarily by B. burgdorferi in the US and primarily B. afzelli, B. burgdorferi and B. garinii in Europe and Asia

B. burgdorferi source

Nymphal stage of I. scapularis is the primary vector, in northeastern US, rodents such as the white-footed mouse are the primary reservoir

Borrelia epidemiology

Lyme diseases caused by multiple Borrelia spe. Emergence of lyme disease driven by: climate change, organism has a very virulent strain called OspC type A

Borrelia clinical disease

early: fever, chills, headache, fatigue. later: facial palsy, irregular heartbeat, dizziness, bull’s eye. If a tick is attached for less than 24hrs, risk of lyme disease is sig. reduced

Early lyme disease

erythema migrans - mild manifestation red oval rash, hematogenous (can spread to secondary lesions). Constitutional symptoms: fatigue, myalgia, fever. meningeal irritation: headache. GI symptoms: hepatitis, pharyngitis

Acute disseminated lyme infection

Cutaneous - multiple target-shaped lesions (early). neurological manifestations - meningoencephalitis, cranial neuropathy (bell’s palsy), radiculopathy. Cardiac - occurs 3-5 weeks from erythema migrans, AV block

late lyme disease

neuro - fatigue, chronic encephalopathy, memory impairment, hypersomnolence, psychiatric issues. arthritis - knee, chronic lyme arthritis

Borrelia endoflagella V factors

corkscrew motion burrows soft tissues and organs

Borrelia biphasic mode of dissemination in ticks V factors

replicating spirochetes in gut form networks of nonmotile organisms that advance toward the basolateral surface of epithelial cells. become motile and penetrate the basement membrane and enter the hemocoel (body cavity) before reaching and entering salivary glands

Borrelia antigenic changes V factors

allows movement from tick to vertebrate. alters outer surface lipoproteins - OpsA/B expressed in tick gut, OspC expressed in saliva (essential for human infection)

fraction of spirochetes changing tick → vertebrate

OspA 100%→30%

Decorin-binding proteins

critical for virulence, adhere to human decorin (connective tissues)

Lyme disease treatment

Antibiotics - short-term effects, Vaccine LYMErix - based on OspA and elicits antibodies

Bacillus anthracis organism

large Gm+ rod, non-motile, endospore forming, catalase-positive, facultative anaerobe, encapsulated in glutamate polymer

B. anthracis habitat

soil, especially near active breakouts. wool, fur, hides that have been exposed

B. anthracis source

lethal livestock pathogen, most natural human infections from contaminated animal products, environmental endospores are introduced into compromised skin, inhaled or ingested, utilised as a biological weapon

Anthrax spore exposure routes

anthrax spores can persist in the environment for decades, leading to various routes of human exposure

anthrax spores - meat processing

workers handling infected carcasses/products can be exposed via cuts or abrasions, inhalation during hide, wool, bone processing. consumption of undercooked/contaminated meat

Anthrax spores - farming process

direct contact with infected animals/products, handling of contaminated feed, exposure during burial/disposal of infected animals → contaminated soil, grazing animals on pastures from previous outbreaks

Anthrax spores - gardening and soil

spores can remain viable in soil for decades, particularly in alkaline soils with high organic content. gardeners can be infected through abrasions.

Anthrax spores - historic farmland development

construction on sites of previous anthrax outbreaks can disturb dormant spores, excavation work may expose spores that have been buried for years

B. anthracis epidemiology

naturally occurs infrequently and sporadically, common in agricultural regions in central/south america, sub-saharan africa, central/southwestern Asia and southern/eastern europe. Breakouts in the western world are rare

Anthrax Clinical disease - cutaneous

most common, 1-7 days → painless ulcer necrotic centre, ~20% mortality without treatment

Anthrax clinical disease - inhalation

inhaled spores in alveolar spaces, macrophages engulf, spores germinate, spread to lymph nodes and bloodstream. ~80% mortality

Anthrax clinical disease - GI

spores consumed, evade stomach acid due to hard capsule, spores germinate etc. ~25-75% mortality

anthrax V factors - endospores

highly resistant dormant structures, hard protein coat resists environmental stress, germinate into vegetative cells when conditions are favourable, primary form for transmission

Anthrax V factors - Poly-D-glutamyl capsule

encoded by genes on pXO2 plasmid, composed of poly-D-glutamic acid, antiphagocytic, provides protection

Anthrax V factors - anthrax toxin (AB exotoxin)

encoded by genes on the pXO1 plasmid (217 genes), consists of three protein components making → Protective antigen (PA)