95. Anthrax (aetiology, epidemiology, pathogenesis, clinical signs, post mortem lesions in different host species).

Question 1

Anthrax history?

Answer 1

Anthrax NOTIFIABLE DISEASE, ZOONOSIS

• Bacillus anthracis,
• Gram Positive

History

• Pollender 1849;
• Koch; Pasteur 1881 (made 1st vaccine);
• Azary 1881;
• Ascoli-Valenti 1910

Question 2

Aetiology?

Answer 2

Aetiology

• Relatively uniform (Clone A and B),
• metachromatic staining
• (unique toluidine blue Æ pink capsule, blue bacteria),
• easy culture: S colony Æ drop-like, if no O2: flat R
• Spore: can survive harsh environment
• excellent resistance
• 5 antigens:
• capsule (co2 presence)
• cell wall (identified with Ascoli test)
• oedema factor
• lethal factor
• protective antigen (these 3 factors form the exotoxin ʹ importance virulence factor)
• Virulence factors:
• Capsule very wide ʹ good protection (plasmid): made from D-Glutamic acid which gives complete protection to the bacteria (can only find L AAs in animals (eucaryotes)ʹ body cannot do anything with the DAAs (cannot decompose so it protects the bacteria from phagocytosis))
• Toxin (plasmid)
• Resistance
• Vegetative bacterium: medium
• Spore (soil ʹ manure ʹ disinfectants ʹ not so much heat): survive several decades in the soil (the bacteria itself is not that resistant but the spore is extremely resistant)

Conditions of spore formation:

• oxygen! (in the infected host there is no spore production, the O2 is not available b/c it is bound to the Hb),
• min. 12 oC (warm summer, spore formation is faster ʹ few hours)
• water (in the carcass)

Question 3

Epidemiology?

Answer 3

Epidemiology

• Obligate pathogen (no predisposing factors needed)
• Susceptibility: (Ov most) ruminants, horse, dog, cat, human (not as susceptible), swine, (birds quite resistant)
• Zoonosis
• Source of infection: soil (resistant spore ʹ survive for long time 50-60 years), diseased or dead animal (replicates onlyin the infected host, very rare to replicate in the environment, would need special conditions),
• shed with discharge or when dead animals are buried they could be the source of infection
• It is not transmitted from animal to animal (no direct spread)
• Infection from: PO
• Soil, pasture: soil disturbance (excavation, digging); environmental effects (drought, flooding); soil will be infected for a long time (people forget about the previous infection)
• Water, Infected meat (Carnivorous animals, source of human infection)
• Role of scavengers (mammals, birds): oxygen exposure, transport
• Raptors can be quite resistant, but spores can be present in the gut & they can spread the disease over some distances!

Question 4

Pathogenesis?

Answer 4

Pathogenesis

• Infection (spore)
• PO: throat, intestine, germination (veg bacterium) typical local lesions at sight of entry;
• bloodstream, septicaemia (107-108 cfu/ml ʹ extremely high cell count: b/c they have a capsule which cannot be decomposed by the host);
• toxin (local lesions, block of the respiratory centre
• Lethal factor: stops resp centre ʹ die due to suffocation
• Human: Aerogenic infection or wound
• Entrance of anthrax toxin (partly responsible forthe local lesions)
• Protective antigen will help the uptake of the toxin ʹ forming a channel

Question 5

Clinical signs?

Answer 5

Clinical signs

• Incubation time 3-5 days (OIE 20 days)
• Animals can be already dead within half a day!
• Influenced by host species, amount of spore
• Cattle (typical disease, very susceptible): per acute
• (high fever, depression, ataxia, bleeding from orifices, non-clotted blood)
• after ~1 hour of ataxia they die
• Horse: acute (fever, depression, colic, SC oedema) ʹ dont die as quickly as cattle
• Carnivores (not as susceptible ʹ slower disease): acute (1st sign = pharyngitis (voice changes), haemorrhagic enteritis, vomiting)
• Swine (not as susceptible): local lesions (throat, intestine): do not want to eat b/c swallowing painful
• Bird: rare, fever, generalised disease, haemorrhagic diarrhoea
• Die b/c of suffocation ʹ foam: nasal discharge = haemorrhages

Question 6

Pm Lesions?

Answer 6

PM lesions

Acute:

• suffocation,
• no rigor mortis,
• incomplete clotting of blood,
• dark blood (anthrax means coal),
• enlargement of spleen,(4 times size in cattle)
• LNs enlarged and haemorrhagic,
• haemorrhages,
• oedema,
• enteritis,
• carbuncle
• (oedematous region), kidney
• In pigs: the PM lesions can be different: enlarged LN quite common (in gut), necrosis in tonsils/LN of gut
• Local: pharynx, tonsils, gut, LNs enlarged