Lecture 10 - Anthrax & Q fever Flashcards
What does the Q in Q fever stand for?
The ‘Q’ stands for ‘query’, the name being given since the cause of an 1935 outbreak of illness among abattoir workers in Australia fever was not known.
2 alternative names for Q fever
Query fever
Coxiellosis
Alternative name for Anthrax.
Woolsorters’ disease
ANTHRAX is a disease of
mammals and birds, caused by bacterium Bacillus anthracis, characterized by septicemia, toxemia, edemas and death.
Causative agent of anthrax.
Bacillus anthracis
Large, non-motile, Gram+ rod.
Multiplies only inside the body.
Over 1200 strains.
ANTHRAX is a disease of mammals and birds, caused by bacterium Bacillus anthracis, characterized by
(4)
septicemia, toxemia, edemas and death.
Two forms of Bacillus anthracis:
Two forms: vegetative and spore
Multiplies inside the body
Over 1200 strains
Stability of anthrax.
VERY resistant.
Spores can remain viable for decades in soil or animal products (e.g. wool).
Water <2 years,
milk <10 years,
silk threads <71 years
Spores are resistant to heat, sunlight, drying and many disinfectants.
Can be killed with formaldehyde or 2% glutaraldehyde; sterilizations.
Host range of anthrax.
all mammals, some birds
Highly susceptible: cattle, sheep and goats.
zoonosis!
Most clinical cases of anthrax are in what species?
wild and domesticated herbivores
Highly susceptible: cattle, sheep and goats.
Morbidity of anthrax.
Morbidity is hard to determine because of the spores.
Mortality of anthrax.
Clinical infections in ruminants and horses is usually fatal; pigs and carnivores often recover.
Humans: cutaneous form mortality 5-20% if not treated,
inhalation anthrax mortality 90-100%, GI anthrax 25-60%.
Distribution of anthrax in 2023.
Worldwide distribution, particularly common in Africa, Asia, Middle East.
Transmission of anthrax.
Route: usually oral but also inhalation.
Vegetative form via ingestion
Spores usually by inhalation
Cutaneous form by skin contact with infected animal tissues possible but more rare.
Excretion of anthrax.
Hemorrhagic exudates from mouth, nose and anus etc.
When exposed to oxygen –> form endospores and contaminate the soil.
Sporulation also occurs if a carcass is opened so necropsies should be avoided!
IP of anthrax
1-20 days (herbivores: 3-7 days)
1-7 days in humans
Clinical signs of peracute anthrax in Ruminants.
Peracute – common
Sudden death may be the only sign.
Staggering, trembling, dyspnea then rapid collapse, terminal convulsions and death.
Clinical signs of acute anthrax in Ruminants.
Acute – clinical signs apparent up to 2 days before death.
Fever, excitement then depression, stupor, disorientation, muscle tremors, dyspnea, congested MM; abortions, drop in milk production.
Occasionally subcutaneous swelling (ventral neck, thorax, shoulders).
Clinical signs of anthrax in horses. (3)
Horses typically develop acute dz.
Fever, chills, anorexia, depression, severe colic, bloody diarrhea.
Swelling (neck, sternum, lower abdomen, external genitalia) then death in 1-3 days.
Clinical signs of anthrax in pigs. (3)
Pigs usually get mild subacute to chronic disease.
Localized swelling and systemic signs (fever, enlarged LNs).
Occasionally: septicemia and sudden death.
Three forms of anthrax in humans:
cutaneous,
gastrointestinal and
inhalation anthrax
Clinical signs of cutaneous anthrax in humans.
This forms comprises 95% of all cases.
Spores enter the skin via abrasions or open wounds.
Papule then vesicle then ulcer then eschar (dead tissue sloughing off).
Case fatality 5-20% if not treated (septicemia and death); <1% if treated.
Describe gastrointestinal anthrax in humans.
Via ingestion of raw of undercooked contaminated meat.
Two syndromes: abdominal and oropharyngeal anthrax.
Severe gastroenteritis with ulcerated lesions.
Case fatality rate 25-75%.
Post mortem lesions of Q fever.
Placentitis:
Leathery and thickened
Purulent exudate may be found at the edges of cotyledons and intercotyledonary areas.
Thrombi and vascular inflammation
Aborted fetuses have non-specific lesions.
