communicable disease course, master of community medicine university of Khartoum

1. By;
Randa Abdalla

2. Contents:
 Introduction
 History
 Epidemiology
 Causative organism
 Transmission
 Clinical manifestation
 Management
 Prevention and control

3. Introduction
 Malignant pustule, Malignant oedema, Woolsorter
disease,Ragpicker disease.
 From the Greek word anthrakos for coal
 Caused by spores
 Primarily a disease of domesticated & wild animals
 Herbivores such as sheep, cows, horses, goats.
 Anthrax zones
 Soil rich in organic matter (pH < 6.0)

4. History of Anthrax (Early history)
 Although anthrax dates back more than 3,000 years,
it was not recognized as a disease until the 18th
century.
 1500 B.C - A “plague of boils” in Egypt affected the
Pharaoh’s cattle. ‘Boils’ are symptomatic of anthrax.
 1600s - The “Black Bane” thought to be anthrax, in
Europe kills over 60,000 cattle.
 1700s - There are some accounts of human cases.

5. History (1800s)
 Early 1800s - The first human cases of cutaneous anthrax
in the US and UK were reported in men who contracted the
disease after having been in contact with infected
livestock.
 The disease was called Wool Sorter’s disease or Rag
Picker’s disease because it affected workers in those
trades.
 1868 - Anthrax was observed under a microscope.
 1876 - German bacteriologist Robert Koch confirmed
bacterial origin of anthrax.

6. History (Early 1900s)
 1915 - German agents injected horses, mules, and cattle
with anthrax . This was the first recorded use of anthrax
as a biological weapon.
 1937 - Japan started a biological warfare program in
Manchuria, including tests involving anthrax.
 1942 - UK demonstrated experiments using anthrax at
Gruinard Island off the coast of Scotland.
 1943 - United States began developing anthrax weapons.
 1945 - In Iran an anthrax outbreak killed more than 1
million sheep.

7. History (Late 1900s)
 1950s and 60s - U.S. biological warfare program continues
after WWII at Fort Detrick, Maryland
 1969 - President Nixon ended United States' offensive
biological weapons program, but defensive work still
continues.
 1970 - Anthrax vaccine for humans was approved by U.S.
FDA.
 1978-80 - The world's largest outbreak of human anthrax
via insect vectors or contaminated meat struck Zimbabwe,
Africa where more than 10,000 cases were recorded and
over 180 people died.
 1979 - In Soviet Union, aerosolized anthrax spores were
released accidentally at a military facility, affecting 94 and
killing 64 people.

8. History (Recent years)
 1991 - About 150,000 U.S. troops were vaccinated for
anthrax in preparation for Gulf War.
 1990-93 - The cult group, Aum Shinrikyo, released
anthrax spores in Tokyo, fortunately no one was injured.
On February 27, 2004, the leader of this group was given
a sentence of death at a district court in Tokyo.
 1995 - Iraq produced 8,500 liters of concentrated anthrax
as part of the biological weapon program under Saddam
Hussein’s administration.
 2001 - Letters containing anthrax spores were mailed to
many places in the US such as NBC, New York Times,
and Media in Miami. In Florida, a man died after inhaling
anthrax at the office.

9. Outbreaks in Thailand
 This picture is 9 days
after the onset of
symptoms of oral-
pharyngeal anthrax.
 1982 - In rural Northern
Thailand, an outbreak of 52
cases of cutaneous anthrax
and 24 cases of oral-
pharyngeal anthrax occurred.
 Oral-pharyngeal anthrax: an
unusual manifestation of
human
infection with B. anthracis.
 1987 - 14 cases of both oral-
pharyngeal and abdominal
anthrax occurred.
 Caused by the consumption of
contaminated water and
buffalo meat.

10. Natural Outbreaks in North Dakota
 The highest occurrence of
Anthrax outbreaks in the US
 1989-1999 - 26 cases of
infected livestock were
reported.
 2000 - 33 cases were reported
during July-September.
 Total of 180 animals (beef
cattle, horses, and bison) died
and one person was infected
with cutaneous anthrax.

11. Epidemiology
 Distribution worldwide
 Not common in West. Common in Africa ( Zimbabwe),
S.E. Asia, China, South America, Turkey, Pakistan, India
 Human to human or animal to animal transmission is rare (
not contagious)
 Grazing animals become infected through ingestion of
spores in the soil ( Carcasses become the source)

13. Causative organism
 - Etiologic agent: Bacillus anthracis Cohn 1875.
 - Large (8 x 1.2 mm) Gram positive, nonmotile,
weakly hæmolytic; central spores, straight ends,
encapsulated in vivo, produces long chains.
 - Pathogenic to herbivores, man, lab animals.

14.  - Habitat: Parasitic; persists in “cursed” fields.
 - Sporulation only in aerobic conditions.
 - Capsule antigen: poly D-glutamic acid g-peptide
 - Immunogenic protein toxin, edematizing, lethal.

15. Bacillus anthracis: culture

16. (blue)
(red)

17. STAGES OF INFECTION
 Encounter: organism and body surfaces
 Adhesion: generalized and receptor-specific
 Initial multiplication  in situ colonization
 Invasión  breaching of anatomic barriers
 Lymphatic stage  invasion of bloodstream
 Generalized infection, metastases.

18. Transmission

19. Transmission:
 Contact with tissues of animals (cattle, sheep, goats,
horses, pigs and others) dying of the disease.
 Biting flies that have partially fed on such animals.
 Contact with contaminated hair, wool, hides or
products made from them (e.g. drums, brushes, rugs).
 Contact with soil associated with infected animals or
with contaminated bone meal used in gardening.

20. Transmission cont.
 Inhalation anthrax results from inhalation of
spores in risky industrial processes—such as
tanning hides and processing wool or bone—
with aerosols of B. anthracis spores in an
enclosed, poorly-ventilated area.
 Intestinal and oropharyngeal anthrax may arise
from ingestion of contaminated undercooked
meat; there is no evidence that milk from
infected animals transmits anthrax.

21. Transmission cont.
 The disease spreads among grazing animals
through contaminated soil and feed; and
among omnivorous and carnivorous animals
through contaminated meat, bone meal or
other feeds derived from infected carcases.
 Accidental infections may occur among
laboratory workers.

22. Transmission cont.
 Anthrax is not transmitted person to person.
 Articles and soil contaminated with spores in
endemic areas may remain infective for
many years.

23. Clinical manifestations

24. Clinical manifestations:
 Anthrax is an illness with acute onset.
 characterised by several distinct clinical forms including:
1. a skin lesion
2. a respiratory illness
3. abdominal distress
 Ninety percent of cases are cutaneous anthrax

25. Cutaneous Anthrax
• Mainly in professionals( Veterinarian, butcher, Zoo
keeper
• Spores infect skin- a characteristic gelatinous edema
develops at the site (Papule- Vesicle-Malignant Pustule-
Necrotic ulcer)
• 80-90% heal spontaneously ( 2-6wks)
• 0-20% progressive disease – develop septicemia
• 95-99% of all human anthrax occur as cutaneous
anthrax

26. Site of Malignant pustule
 Head: usually no complication
 Face: severe, superinfection; gangrene near eye
 Neck, breast or chest wall: massive edema, over thorax and
sometimes involving scrotum
 Shoulders, arms: may be multiple, small lesions
 Forearms, fingers: atypical on palms
 General symptoms, fever, chills, depend on site.
 Weakness, hypotension are danger signs.

28. Notice the edema and typical lesions

30. Intestinal Anthrax
• Due to in ingestion of infected carcasses
• Mucosal lesion to the lymphatic system
• Rare in developed countries
• Extremely high mortality rate

31. Intestinal Anthrax
 Nausea, anorexia, vomiting, fever
 Progresses to severe abdominal pain and
bloody emesis and diarrhea
 Ascites may develop on day 2 - 4
 Death 2 to 5 days after onset of symptoms
 Very difficult to diagnose

32. Cecal Lesion
from eating undercooked Carabao... (AFIP)

33. PULMONARY ANTHRAX
• Require very high infective dose ( > 10,000 spores)
• Acquired through inhalation of spores ( Bioterrorism -
aerosol)
• Present with symptoms of severe respiratory infection( High
fever & Chest pain)
• Haemorrhagic mediastinitis
• Progress to septicemia very rapidly
• 10 7 to 10 9 bacilli/ ml of blood at the time of death
• Mortality rate is very high > 95%

36. Anthrax Meningitis
 Usually a complication of anthrax septicemia.
 Subarachnoid haemorrhage is a common
feature
 Very often fatal

37. Anthrax meningitis:
Subarachnoid Haemorrhage
(AFIP)

38. Anthrax - Disease in
animals
 Fulminating, acute, subacute or chronic.
 Apoplectic death: “fall” - animals found dead.
 Acute: excitable, then depressed, cardiac and
respiratory distress, trembling, staggering, convulsions.
 Edematous lesions, blood exudes, incoagulable.
 Death in 1-2 days, or 4-5.
 Chronic infection in more resistant animals: pigs.

39. Diagnosis:
 Clinical; symptoms and signs.
 Incubation period—From 1 to 7 days,
although incubation periods up to 60 days
are possible

40.  Laboratory confirmation requires at least
one of the following:
1. isolation of Bacillus anthracis from a clinical
specimen
2. demonstration of B. anthracis in a clinical
specimen by immunofluorescence
3. significant antibody titres developing in an
appropriate clinical case.

41. Management

42. Management:
 Investigation
Obtain a history of travel and contact with imported
animal
 Restriction
Standard infection control precautions apply for all
direct clinical care. Although a cutaneous lesion
will be sterile after 24 hours’ treatment, dressings
soiled with discharges from lesions should be
burned and reusable surgical equipment
sterilised.

43. Treatment
 The case should be under the care of an infectious
diseases physician.
 Penicillin is the drug of choice for cutaneous
anthrax and is given for 5–7 days.
 Tetracyclines, erythromycin and chloramphenicol
are also effective.
 The U.S. military recommends parenteral
ciprofloxacin or doxycycline for inhalation anthrax
though the duration of treatment is not well defined.

44.  Counselling
Advise the case and their caregivers of the
nature of the infection and its mode of
transmission.
 Management of contacts

45. Vaccination
 Cell-free filtrate
 At risk groups
 Veterinarians
 Lab workers
 Livestock handlers
 Military personnel
 Immunization series
 Five IM injections over 18-week period
 Annual booster
9/19/2015

46. Methods of control—
 A. Preventive measures:
Immunize high-risk persons , Educate employees ,
Control dust, wash, disinfect or sterilize, immunize and
annually reimmunize all domestic animals at risk….etc.
 B. Control of patient, contacts and the immediate
environment
Report to local health authority, Isolation,
Concurrent disinfection, Investigation of contacts,
Specific treatment….etc.

47.  C. Epidemic measures
 D. Disaster implications
 E. International measures; Sterilize imported
bone meal before use as animal feed. Disinfect
wool, hair and other products when indicated and
feasible.

48. Prevention
 Control in animals. Annual vaccination protects.
 Disposal of animal carcasses: disinfect with oil,
burn, bury deep, covered with quicklime.
 Spores will NOT form inside the carcass, and
putrefaction kills the Bacillus. Flies feeding on
incoagulable blood may be a problem.

49. An anthrax death. Notice flies
feeding on blood and secretions

50. Burning a carcass in a hole... Not deep enough

51. Question
The most common naturally occurring form of
anthrax is:
a. Cutaneous
b. Gastrointestinal
c. Inhalational
d. Ocular
e. Mediastinal

52. Question
After low-level germination at the site of entry
to the body, anthrax may be taken up by:
a. Basophils
b. Eosinophils
c. Lymphocytes
d. Macrophages
e. Neutrophils

54. Thank
you…