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%.
Describe inhalatory anthrax in humans.
Clinical signs develop gradually and are nonspecific.
Death in 24-36 hours.
Case fatality rate is 75-90% (untreated).
Post mortem lesions of anthrax.
Avoid necropsy!! Spores will get you.
But in case you do:
Rigor mortis is absent or incomplete, carcass is bloated and decomposed rapidly.
Dark tarry blood from body orifices.
Edema (throat and neck) – in horses.
Signs of septicemia
GI lesions
DDx for anthrax in Ruminants
Blackleg
Botulism
Peracute babesiosis
Poisoning (plants, heavy metals, snake bite)
Lightning strike
Suspect anthrax when: (3)
High mortality rate in herbivores
Sudden deaths with unclotted blood leaking from orifices
Localized edema
Material for diagnosis of anthrax. (2)
Blood straight from the heart of a carcass anaerobically!
lymphatic tissue
Lab analyses for diagnosis of anthrax. (4)
Blood smears (Giemsa stain)
Bacterial culture
PCR
Serology – e.g. ELISA; mainly used in research
Treatment of anthrax.
ABs – may be effective if started early enough. + Supportive care.
Some strains are resistant to penicillin.
Ab are effective only against the vegetative form, not against spores.
Humans: Tx for cutaneous anthrax is usually effective (other forms you’re shit out of luck).
Prevention & control of anthrax.
Quarantines, effective carcass disposal, thorough decontamination.
To prevent sporulation: carcasses should not be opened. Burn them!
During outbreaks: prophylactic ABs for exposed & high-risk animals.
Vaccination: modified live vaccines for livestock, human vaccines exist.
Humans: postexposure antibiotic prophylaxis but not after cutaneous exposure.
Causative agent of Q fever.
bacterium Coxiella burnetii
Obligate intracellular,
Gram– pathogen
Q FEVER is a contagious bacterial disease mostly affecting
ruminants, caused by Coxiella burnetii,
characterized by abortions and other reproductive failures.
Q FEVER is a contagious bacterial disease mostly affecting ruminants, caused by Coxiella burnetii, characterized by
abortions and other reproductive failures.
Which bacterial family does Q fever causative agent belong to?
Family Coxiellaceae
Obligate intracellular,
Gram– pathogen
Stability of Coxiella burnetii
Forms spore-like structures that are highly resistant to environmental conditions.
Not true spores though!
E.g. viable up to 120 days in dust
At 4-6 °C in milk – survives up to 42 months.
Disinfection with10% bleach should clear it.
Coxiella burnetii has 2 distinct antigenic phases: explain.
2 distinct antigenic phases: I and II.
Morphologically identical, differ in biochemical characteristics (e.g. LPS composition).
Phase I is more infectious than II.
Organism develops antibodies first against II, then I.
Host range of Q fever.
many domesticated and wild animals, including mammals, birds, reptiles and arthropods
Zoonosis!
Clinical signs of Q fever in animals.
Most are asymptomatic
Q fever mainly affects which animal species?
Mainly affects ruminants – sheep, goats and cattle,
dogs and cats are the most common reservoirs.
Morbidity of Q fever.
U.S. cattle seroprevalence 1-82%
Sheep abortions 5-50% of the flock
So morbidity is intermediate to high.
Mortality of Q fever.
Animals: rarely die.
Humans: acute form mortality 0.5 - 2%, chronic 1-11% (<65%)
So mortality is mostly low.
Distribution of Q fever.
Europe & east asia.
Most recently in Turku, Finland!
Excretion of Coxiella burnetii.
milk, urine and feces, semen, placenta and reproductive discharges
Shedding of the pathogen for months or even years!
Transmission of Coxiella burnetii.
Direct contact, aerosols – wind!
Ingestion
Fomites
Insect vectors
Route: mainly respiratory
IP of coxiella burnetii
very variable
IP in humans:
2-48 days (typically 2-3 weeks)
Clinical signs of Q fever in animals.
In sheep, cattle goats:
May be asymptomatic.
But also reproductive failure: abortions, stillbirths, retained placenta, infertility, weak newborns, low birth weight; mastitis.
Most abortions occur near term.
In species other than the above: mostly asymptomatic. Reproductive failure common.
Q fever is highly virulent:
even just ONE bacterium alone is capable of causing disease.
so infectious dose is super low!
Forms of Q fever in humans. (3)
asymptomatic (50%),
acute and
chronic
Clinical signs of acute Q fever in humans.
Self limiting, flu-like.
Atypical pneumonia (30-50%)
Hepatitis; skin rash (10%); other signs (<1%): myocarditis, meningoencephalitis, pericarditis.
Hospitalization 2% and death 1-2%.
Clinical signs of chronic Q fever in humans.
1-5% of all those infected: mostly prior heart dz, pregnant women, immunocompromised ppl
Endocarditis occurs in (60-70%)
Other: granulomatous hepatitis, cirrhosis, osteomyelitis
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.
DDx for Q fever.
Brucellosis
Neosporosis
Leptospirosis
Listeriosis
Pasteurellosis
Chlamydiosis
Campylobacteriosis
Suspect Q fever when…?
you see plenty of reproductive failure
Material for diagnosis of Q fever. (3-6)
Vaginal discharges, the placenta or its fluids, aborted fetuses
Milk, urine, feces
Lab analyses for diagnosis of Q fever.
Identification of organism (e.g. Modified Ziehl-Neelson, no gram staining!)
PCR
Serology (IFA, ELISA, CF)
Isolation of organism – biosafety level 3!
Treatment of Q fever.
Tx: Abs (though its very hard to get rid of even with meds)
Tetracycline prior to parturition
Humans: doxycycline
Prevention of Q fever. (5)
Good husbandry:
tick prevention because they can transmit it physically but not via bites,
disposal of birth products.
Quarantine new and/or sick animals.
Vaccination – animal & human
but only in Australia.
Pasteurize milk
Disinfection with10% bleach
Eradication of Q fever.
Eradication not possible!
Too many reservoirs
Constant exposure
Stability of the agent in environment is too high.
