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GRAM POSITIVE BACILLI

Mycobacterium group
Mycobacterium tuberculosis

 Acid fast bacilli; appears singly or in groups and may form


long chains in liquid culture
 Obligate aerobes
 Very slow growers (2-3 weeks)
 Requires high oxygen tension
 Grown in Lowenstein-Jensen medium
 Colonies are non-pigmented, rough, wrinkled, cauliflower-
like
 Can survive outside the host for days but can be killed by
prolonged exposure to sunlight and pasteurization
VIRULENCE FACTORS
 Cord factor
 Distrupt mitochondria
 Lipids
 hydrophobic
 Mycolic acid
 Wax- D
 Adjuvant activity
 Sulfatides
 Neutral red test
Pathogenesis
 May infect any organ in the body but pulmonary
tuberculosis is the most common form
 May become disseminated (miliary type) and
involve other organs
 Produce no toxins
 Predisposing factors:
 Chronic fatigue
 Sedentary lifestyle
 Malnutrition
 Overcrowding
 Occupational hazards
Primary TB
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 Infectious dose 10 cells
 Phagocytosed by alveolar macrophages and
multiply intracellularly
 After 3-4 weeks immune system attacks, forming
tubercles, granulomas consisting of a central core
containing bacilli surrounded by WBCs – tubercle
 If center of tubercle breaks down into necrotic
caseous lesions, they gradually heal by
calcification.
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Secondary TB
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 Ifpatient doesn’t recover from primary
tuberculosis, reactivation of bacilli can occur.
 Tubercles expand and drain into the bronchial
tubes and upper respiratory tract.
 Gradually the patient experiences more severe
symptoms.
 violent coughing, greenish or bloody sputum, fever,
anorexia, weight loss, fatigue
 Untreated, 60% mortality rate
Extrapulmonary TB
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 During secondary TB, bacilli


disseminate to regional lymph nodes,
kidneys, long bones, genital tract, brain,
and meninges.
 These complications are grave.
Diagnosis
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1. In vivo or tuberculin testing
Mantoux test – local intradermal injection of
purified protein derivative (PPD); look for red
wheal to form in 48-72 hours- induration;
established guidelines to indicate
interpretation of result based on size of
wheal and specific population factors
1. X rays
2. Direct identification of acid-fast bacilli in
specimen
3. Cultural isolation and biochemical testing
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Management and Prevention of
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TB
 6-24 months of at least 2 drugs from a
list of 11
 One pill regimen called Rifater
(isoniazid, rifampin, pyrazinamide)
 Vaccine based on attenuated bacilli
Calmet-Guerin strain of M. bovis used in
other countries
TUBERCULOSIS
Mode of transmission:

 Droplet inhalation
 Ingestion of contaminated milk and milk
products
 Kissing
 Skin contact
Constitutional signs and symptoms

 Afternoon rises in temperature (low grade


fever)
 Chronic, non-productive cough
 Anorexia
 Loss of appetite
 Easy fatigability/general body weakness
 Hemoptysis
2 principal lesions
 Exudative type
 Acute inflammatory reaction in the lungs
(pneumonia-like)
 May completely resolve, may lead to massive
necrosis, or convert into the reactive type
 Reactive type
 Chronic granuloma (tubercle) with caseation necrosis
 Heals by fibrosis of calcification

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Immunity
 Cellular immunity controls growth and
spread of bacteria while humoral immunity
is short-lived and non-productive
 BCG (Bacillus of Calmette and Guarin)
vaccine is given ID, usually at birth
 Tuberculin test (Mantoux test) detects the
exposure to the bacilli

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Diagnosis

 Acid fast staining of specimen: sputum,


washings, exudates, CSF, urine
 Culture in Lowenstein-Jensen medium,
glycolated agar medium, potato medium,
or biologic medium (guinea pigs)
 Biochemical tests: (+) niacin test, (+)
nitrate reduction test, (-) catalase test

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Other methods:

 Radiometric methods using radioactive


tarcers
 Electrophoresis
 Gas chromatography
 Mycodot
 Antibiotic sensitivity test – to determine
resistance to drugs
Management
 Physicaland mental rest
 Good nutrition
 6 months (short course) anti TB thearpy
 Isoniazid– mainstay of management
 Rifampicin
 Pyrazinamide
 Ethambutol
 Streptomycin

12/09/09 20
Mycobacterium leprae
 Commonly known as Hansen’s bacillus
 Acid fast bacilli arranged in pallisade
 Obligate intracellular organisms
 Grown only in a biologic medium: in foot
pads of mice, chimps, armadillo
Mycobacterium leprae: The Leprosy
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Bacillus
 Strict parasite – has not been grown on
artificial media or tissue culture
 Slowest growing of all species
 Multiplies within host cells in large
packets called globi
 Causes leprosy, a chronic disease that
begins in the skin and mucous
membranes and progresses into nerves
Epidemiology and Transmission of
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Leprosy
 Endemic regions throughout the world
 Spread through direct inoculation from
leprotics
 Not highly virulent; appears that health
and living conditions influence
susceptibility and the course of the
disease
 May be associated with specific genetic
marker
Course of Infection and
Disease
24  Macrophages phagocytize the bacilli, but
a weakened macrophage or slow T cell
response may not kill bacillus.
 Incubation from 2-5 years; if untreated,
bacilli grow slowly in the skin
macrophages and Schwann cells of
peripheral nerves
2 forms possible:
 tuberculoid – superficial infection without skin
disfigurement which damages nerves and causes
loss of pain perception
 lepromatous – a deeply nodular infection that
causes severe disfigurement of the face and
extremities
Diagnosis
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 Combination of symptomology, microscopic


examination of lesions, and patient history
 Numbness in hands and feet, loss of heat
and cold sensitivity, muscle weakness,
thickened earlobes, chronic stuffy nose
 Detection of acid-fast bacilli in skin lesions,
nasal discharges, and tissue samples
Diagnosis
 Nasalscrappings and tissue sample
 Lepromin skin test
 Fernandez-24-48 hrs
 Mitsuda- 4 weeks
Mycobacterium leprae
Pathogenesis
 Causes leprosy (Hansen’s disease)
 Transmission requires prolonged contact
 2 types
 Tuberculous type
 (+)tuberculin test
 Implies good cellular response
 Good prognosis

 Lepromatous type
 (-)
tuberculin test
 Poor cellular response to infection
 Poor prognosis
Management
 Dapsone: mainstay of management,
lifetime maintenance
 Rifampicin
 Ethionamide
Other mycobactrium
Mycobacterium kansasii
 Photochromagen: produce pigments in
light but not in the dark
 Produce tuberculosis-like symptoms
Mycobacterium avium-
intracellulare
 Produce little pigment
 Produce overt tuberculosis among AIDS
patients
 opportunistic
Mycobacterium avium-
intracellulare
Mycobacterium scrofulaceum
 Scotochromagen: produce pigments when
grown in the dark
 Saprophytic in adults with chronic lung
disease
 Produce scrofula in young children with
cervical lymphadenitis
Mycobacterium marinum et
ulcerans
 Occurs in water contaminated by bird
droppings
 Causes swimming pool granulomas
(superficial skin ulcers)
Mycobacterium fortuitum et
cheloni
 Rarelyproduce systemic and superficial
disease in man
 Contaminates porcine valves used in
human cardiac surgery
Bacillus group
Bacillus anthracis
 Forms long chains giving a bamboo pole
appearance
 Spore formers
 grown in blood agar medium forming
medusa head colonies
 Zoonotic infection
Bacillus anthracis
Pathogenesis
 Causes anthrax
 Types of anthrax
 Cutaneous anthax: manifest with malignant
skin pustules
 Pulmonary anthrax: woolsorter’s disease
 Intestinal anthrax: enteritis
Cutaneous Anthrax
 The most common naturally occurring form of
anthrax.
 Ulcers are usually 1-3 cm in diameter.
 Incubation period:
 Usually an immediate response up to 1 day
 Case fatality after 2 days of infection:
 Untreated (20%)
 With antimicrobial therapy (1%)
Cutaneous Anthrax

CDC, Cutaneous Anthrax—Vesicle Development


Inhalation Anthrax
 The infection begins with the
inhalation of the anthrax spore.

 Spores need to be less than 5


microns (millionths of a meter)
to reach the alveolus.

 Macrophages lyse and destroy


some of the spores.

 Survived spores are


transported to lymph nodes.

Inhalation Anthrax, Introduction, DRP, Armed Forces Institute of Pathology


Inhalation Anthrax
• At least 2,500 spores have to
be inhaled to cause an
infection.

• Disease immediately follows


germination.

• Spores replicate in the lymph


nodes.

• Bacterial toxins released


during replication result in
mediastinal widening and
pleural effusions (accumulation
of fluid in the pleural space).

Inhalation Anthrax, Introduction, DRP, Armed Forces Institute of Pathology


Inhalation Anthrax
 Death usually results 2-3 days after the onset of symptoms.
 Natural infection is extremely rare (in the US, 20 cases were
reported in last century).
 Inhalation Anthrax is the most lethal type of Anthrax.
 Incubation period:
 1–7 days
 Possibly ranging up to 42 days (depending on how many
spores were inhaled).
 Case fatality after 2 days of infection:
 Untreated (97%)
 With antimicrobial therapy (75%)
Gastrointestinal Anthrax
 GI anthrax may follow
after the consumption of
contaminated, poorly
cooked meat.

 There are 2 different


forms of GI anthrax:
1) Oral-pharyngeal
2) Abdominal

 Abdominal anthrax is
more common than the
oral-pharyngeal form.

http://science.howstuffworks.com/anthrax1.htm
GI Anthrax
 GI anthrax cases are uncommon.
 There have been reported outbreaks in Zimbabwe,
Africa and northern Thailand in the world.
 GI anthrax has not been reported in the US.
 Incubation period:
 1-7 days
 Case fatality at 2 days of infection:
 Untreated (25-60%)
 With antimicrobial therapy (undefined) due to the rarity
Treatment
 Before 2001, 1st line of
treatment was penicillin G
 Stopped for fear of
genetically engineered
resistant strains
 60 day course of antibiotics
 Other Drugs
 Ciprofloxacin
 Doxycycline
 For inhalational, need another
antimicrobial agent
 clindamycin
 rifampin
 Chloramphenicol
http://nmhm.washingtondc.museu  Vaccine
m/news/anthrax.html
 Toxoid (protective antigen)
 Effective in short term but not
long term
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Laboratory identification
 Stain
 Culture
 Ascoli’s test- precipitin band ring
Management
 Penicillin G
 Vaccine
 Premier et Diexeme vaccine
 Sobernheim vaccine
 Sterne vaccine
Other bacillus
 B. cereus
 B. subtilis
 B. thuringensis
 B. polymyxa
 B. licheniformis
Bacillus cereus
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 Common airborne and dustborne; usual methods of
disinfection and antisepsis are ineffective
 Grows in foods, spores survive cooking and
reheating
 Ingestion of toxin-containing food causes nausea,
vomiting, abdominal cramps and diarrhea; 24 hour
duration
 No treatment
 Increasingly reported in immunosuppressed
Clostridium group

anaerobic spore forming bacteria


Gas gangrene group
 C. perfringens
 C. novyi
 C. sporogens
 C. histolyticum
 C. bifimentans
 C. sordelii
Toxigenic group
 C. tetani
 C. botulinum
General characteristics
 All are motile except c. perfringens
 All are non encapsulated except c.
perfringens
 All are singly hemolytic except c.
perfringens
 All with swollen sporangia except c.
perfringens and c. bifimentans
 All are lactose non fermenter except c.
perfringens
 All are sucrose non fermentative except c.
perfringens
 All are glucose fermenters except c. tetani
and histolyticum
 All are strict anaerobe except c.
histolyticum
Clostridium tetani
 Anaerobic spore-former
 With terminal spore giving a drumstick
appearance to the bacteria
 Produces tetanus and tetanus neonatorum
 Produces toxins:
 Tetanospasmin – causes spastic contraction of
skeletal muscles, lock jaw, risus sardonicus
 Tetanolysin – destroys RBC
Tetanus
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 Clostridiumtetani
 Common resident of soil and GI tracts of animals
 Causes tetanus or lockjaw, a neuromuscular disease
 Most commonly among geriatric patients and IV drug
abusers; neonates in developing countries
Pathology
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 Spores usually enter through accidental puncture
wounds, burns, umbilical stumps, frostbite, and
crushed body parts.
 Anaerobic environment is ideal for vegetative cells to
grow and release toxin.
 Tetanospasmin – neurotoxin causes paralysis by
binding to motor nerve endings; blocking the release
of neurotransmitter for muscular contraction inhibition;
muscles contract uncontrollably
 Death most often due to paralysis of respiratory
muscles
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Clostridium tetani
Management
 DPT vaccine
 Tetanus antitoxin
 Tetanus immunoglobulin
 Penicillin
Clostridium perfringens
 Causes gas gangrene
 Anaerobic
 Encapsulated
 non-motile
Pathogenesis
 Interrupt blood supply to infected wound
resulting in ischemia and necrosis
 CHO from dead tissues are fermented by the
bacteria causing gas formation
 Bacteria produces enzymes that destroys
collagen and proteins
 A mild food intoxicant when ingested
 Bacteria is an indicator of fecal contamination,
usually found in soil and intestinal tract of
humans and animals
Gas Gangrene
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 Clostridium perfringens most frequent clostridia
involved in soft tissue and wound infections -
myonecrosis
 Spores found in soil, human skin, intestine, and
vagina
 Predisposing factors – surgical incisions,
compound fractures, diabetic ulcers, septic
abortions, puncture wounds, gunshot wounds
Virulence Factors
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 Virulence
factors
toxins –
alpha toxin – causes RBC rupture, edema and
tissue destruction
collagenase
hyaluronidase
DNase
Pathology
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 Not highly invasive; requires damaged
and dead tissue and anaerobic conditions
 Conditions stimulate spore germination,
vegetative growth and release of
exotoxins, and other virulence factors.
 Fermentation of muscle carbohydrates
results in the formation of gas and further
destruction of tissue.
Management
 Debridement of wound
 Amputation
 Penicillin G
Clostridium botulinum
 Motile
 Unencapsulated
 anaerobic
Pathogenesis
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 Spores are present on food when gathered
and processed.
 If reliable temperature and pressure are not
achieved air will be evacuated but spores will
remain.
 Anaerobic conditions favor spore germination
and vegetative growth.
 Potent toxin, botulin, is released.
 Toxin is carried to neuromuscular junctions
and blocks the release of acetylcholine,
necessary for muscle contraction to occur.
 Double or blurred vision, difficulty
swallowing, neuromuscular symptoms
Treatment and Prevention
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 Determine presence of toxin in food,
intestinal contents or feces
 Administer antitoxin; cardiac and
respiratory support
 Infectious botulism treated with penicillin
 Practice proper methods of preserving
and handling canned foods; addition of
preservatives.
Clostridium botulinum
Clostridium botulinum
Clostridium Botulinum
Pathogenesis
 Causes botulism (food poisoning)
 Transmitted by ingesting contaminated
smoked, pickled, canned foods
 Produce a very potent neurotoxin that
causes paralysis of respiratory muscles
leading to respiratory and cardiac arrest,
diplopia and meningitis within 72 hrs. after
ingestion
Wound Botulism
(Clostridium botulinum)

 Deep wound - anaerobic


environment – BT leaks into blood
 BT binds neurons, internalized,
prevent acetylcholine release in
neuromuscular junction, prevent
muscle contraction – hence,
flaccid paralysis
 Antitoxin, supportive therapy and
antibiotics
Management
 Type-specificantitoxin
 Supportive respiratory assistance
 Vaccine
 Proper food preparation
Clostridium difficile

 Nosocomial (hospital-acquired infection)


 Causes pseudomembranous colitis,
manifests with:
 Fever
 Bloodydiarrhea
 Abdominal cramps
 Toxins released in the GI tract causes
necrosis of the mucosal surface of the colon
and formation of a pesudomembrane
 May lead to toxic megacolon
 Treatment: Vancomycin, Metronidazole
Clostridium difficile
Clostridium difficile
Other gram positive bacilli
Lactobacillus acidophilus
 Mouth
 G.I.
tract
 Stomach- Boa’s oppler’s bacilli
 Vagina- Doderlein’s bacilli
Listeria monocytogenes
 With peritrichous flagella
 Listeriosis- disseminated granuloma or
abscess
 Infection tranplacentally that may leads to
purulent meningitis
 septicemia
Erysiphilothrix rhusophatiae
 Non suppurative lesions on hands and
fingers called erysipeloid

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