Gram positive spore-forming rods

GRAM POSITIVE SPORE-FORMING
SPORE FORMING
RODS
NON-SPORE NON SPORE FORMING OBLIGATE
ANAEROBIC BACTERIA AND
ASSOCIATED INFECTIONS
JOSEPH ONGRÁDI ONGR DI
INSTITUTE OF MEDICAL MICROBIOLOGY
SEMMELWEIS UNIVERSITY
Budapest 2012

ALLOCATED IN SEVERAL TAXONOMIC UNITS
HERE: FUNCTIONAL GROUPINGS
GRAM POSITIVE
SPORE-FORMING RODS
CLOSTRIDIUM GENUS
ONLY!!!
NON-SPORE FORMING
ANAEROBIC BACTERIA
Gram + cocci and
rods
Gram – cocci and
rods
COMMON CHARASTERISTICS
CATABOLISM: ANAEROBIC (fermentation)
lack of the cytochrom system, superoxide dismutase,
catalase and peroxidase enzymes
TOXIC END PRODUCTS OF OXYGEN METABOLISM
OBLIGATE ANAEROBIC --------- AEROTOLERANT
SPECIMEN COLLECTION: transport media without O 2
CULTIVATION: removal of O 2 (GasPack, etc.)

GRAM POSITIVE
SPORE-FORMING RODS
Exogenous infections
1 species = 1 disease
Small number of species
more clinical entities
Varied pathomechanisms,
but molecularly well
characterized
Diagnosis: unambigous
Treatment: unambigous
Prevention: unambigous
DISTINCT CHARACTERISTICS
NON-SPORE FORMING
ANAEROBIC BACTERIA
Endogenous infections
Many species
Mixed infections: (polymicrobial)
more aerobic +
anaerobic species
similar clinical entities
Diagnosis: complicated
Treatment: difficult
Prevention: difficult
3

ENDOSPORE: ENSURES SURVIVAL
PRODUCED IN THE ENVIRONMENT (SOIL, WATER, AIR)
EXTREME RESISTANCE
(PARAMETERS AND BIOLOGICAL MONITORING OF STERILIZATION PROCEDURES)
Bacillus genus
Aerobic
Spore Ø < bacterium Ø
B. anthracis (flagella-, capsule+)
B. cereus (flagella+, capsule-)
enterotoxins: (food poisoning)
heat stabile: emetic
heat labile: diarrhoea
eye, wound infections, IVDA
B. subtilis: contaminant ,
bioterrorism model
B. megaterium: contaminant
B. mesentericus: contaminant
B. stearothermophilus, B. pumilis:
monitoring sterilization procedures
B. globigii: modelling bioterrorisms
Other Bacilii: insecticides
Clostridium genus
Obligate anaerobic
Spore Ø > bacterium Ø
Peritrichous flagella
(capsule: C. perfringens)
Exogenous infections
Endogenous: C. perfringens
C. difficile
Intensive metabolism,
gas production +/-
Neurotoxic (exotoxin):
C. tetani (non- invasive)
C. botulinum (toxicosis)
Histotoxic (invasive):
C. perfringens + C. septicum +
C. novyi + other
Enteral (nosocomial):
C. difficile (dysbacteriosis) 4

MORPHOLOGY: 5-10 µm x 1 µm
Square ends
Capsule (in host), central spore
(in nature)
CULTIVATION:
agar/bloodagar: medusa head
lecithinase (weak)
PATHOGENIESIS: cattle, sheep>
feces/carcasses>soil>saprophytic >
spores persist for decades in dry earth>
human infection
Capsule+exotoxin (protective antigen,
edema factor, lethal factor)
CLINICAL FINDINGS:
Skin anthrax:
animal products , scratch,wound, >
12-24 h latency> gelation edema>
malignant pustule>necrotic ulcer>
bacteremia>sepsis
Inhalation anthrax:
hemorrhagic lobular pneumonia,
edema>meningitis, sepsis, shock
„woolsorter's disease”
biological warfare (bioterrorism)
Intestinal anthrax: abdominal pain,
bloody diarrhea, vomiting, ascites

Intestinal
anthrax
Cutaneous anthrax
Respitarory anthrax

DIAGNOSIS:
Specimens: fluid or pus from pustules
blood, sputum, feces
staining, immunofluorescent staining
cultivation on blood agar
(no hemolysis, no swarming)
Serology: precipitation, hemagglutination
to detect animal or human antibodies
Ascoli test: immune serum + tissue extract
Animal infection: guinea pig and
mouse – sensitive, rat – resistant
PREVENTION: public health control measures
deep burial in lime-pits
autoclaving animal products
protective clothing
Vaccination: live attenuated vaccine for animals
humans (occupational risk): cell-free vaccine
TREATMENT: as early as possible!
penicillin (except in inhalation anthrax)
tetracyclin, erythromycin, clindamycin
7

WHAT IS BIOTERRORISM?
A BIOTERRORIST ATTACK IS
THE DELIBERATE RELEASE OF BACTERIA, VIRUSES, OTHER GERMS
OR TOXINS TO CAUSE ILLNESS, DEATH, DISRUPTION OR FEAR
IN HUMANS, LIVESTOCK, FOOD CROPS AND ENVIRONMENTAL
RESOURCES
39 MAJOR MICROORGANISMS AND BIOLOGICALS TO BE USED
(NATO categorization)
RECENT DEVELOPMENT:
corrosive microbes to destroy electric appliances, health care products,
gaskets
THE MOST LIKELY, PREDICTED METHOD OF NEXT BIOLOGICAL ATTACKS:
AEROSOLIZED AGENTS
8

CHARACTERISTICS OF BIOTERRORIST ATTACKS
SUDDEN AND UNEXPECTED ONSET
LARGE NUMBER OF CASES
TYPICAL, ATYPICAL OR UNKNOWN CLINICAL ENTITIES
THE EFFECT: DEADLY (SMALLPOX)
INCAPACITIVE, TEMPORARY (Q-FEVER)
SPREAD: CONTAGIOUS (PLAGUE)
NON-CONTAGIOUS (TOXINS)
THE FATE OF AFFECTED PERSONS: CURABLE (ANTHRAX)
INCURABLE (EBOLA)
SPREAD OF THE AGENT: aerosol (

BIOTERRORISM AGENT CATEGORIZATION
CATEGORIZATION
HOW EASILY THEY ARE TO OBTAIN, WEAPONIZE,
DISSEMINATE
HOW MUCH DEATH, THE SEVERITY OF ILLNESS
HOW MUCH DAMAGE, DISRUPTION OR FEAR THEY
MIGHT CAUSE
10

CATEGORY A
High priority agents (organisms, toxins) that pose
the highest risk to the public security:
easy spread or transmitted from person to person
high death rate, major public health impact
cause public panic, social disruption
require special action for public health preparedness
Variola major
Bacillus anthracis
Clostridium botulinum (toxin)
Yersinia pestis
Francisella tularensis
FILOVIRUSES (Ebola, Marburg viruses)
ARENAVIRUSES (Lassa, Junin, Machupo)
BUNYAVIRUSES (Crimean-fever, Rift-valley fever)
11

THE MOST IMPORTANT MICROORGANISMS FOR
BIOTERRORISM (II)
CATEGORY B
THE SECOND HIGHEST PRIORITY
MODERATELY EASY TO SPREAD
MODERATE ILLNESS RATES, LOW DEATH RATES
REQUIRE SPECIFIC ENHANCEMENTS OF LABORATORY CAPACITY
Brucella spp.
Burkholderia mallei
Burkholderia pseudomallei
Rickettsia prowazekii
Coxiella burnetti
Chlamydia psittaci
Alphaviruses (Venezuelan horse encephalitis)
Staphylococcus aureus (enterotoxin B)
Salmonella spp.
Escherichia coli O57:H7
Vibrio cholerae
Shigella spp.
Cryptosporidium parvum
2010 SU Dept. Public Health 12

THE MOST IMPORTANT MICROORGANISMS
FOR BIOTERRORISM (III)
CATEGORY C
EMERGING PATHOGENS THAT COULD BE ENGINEERED FOR THE FUTURE
EASILY AVAILABLE
EASILY PRODUCED AND SPREAD
ATYPICAL OR NEW DISEASES
POTENTIAL HIGH MORBIDITY AND MORTALITY RATES
MAJOR HEALTH IMPACT
NIPAH VIRUS, HANTA VIRUS
RECOMBINANT MICROBES (bacteria, viruses, fungi)
THE FUTURE
ADAPTING ANIMAL VIRUSES TO HUMANS (Iraq: camel smallpox virus)
ENHANCED PATHOGENICITY OF KNOWN MICROBES
insertion of IL-4 gene into mouse pox virus to inhibit immune functions (Australia)
Clostridium botulinum: to spread from person to person (Soviet Union)
Bacillus anthracis: insertion of more virulence genes to circumvent vaccination
(Soviet Union)
recombination of Ebola and HIV (Soviet Union)
insertion of antibiotic resistance genes to produce polyresistant bacteria (SU)
2010 SU Dept. Public Health 13

RISK OF ANTHRAX INFECTION
U.S. Postal Service distribution clerk Sheila Dickson-Ongrady uses gloves as she
sorts mail in Hamilton Township, N.J., facility Tuesday. An employee of the
facility is believed to have contracted inhalation anthrax (Laredo Morning
Times).

Saprophyte in the soil
MORPHOLOGY: flagella +, capsule –
CULTIVATION: swarming, hemolysis on blood agar
PATHOGENESIS:
1. Enterotoxin>food poisoning, intoxication
Emetic type (spores: soiI>rice, pasta) Diarrheal type (meat)
2. Other: eye infections (trauma, foreign body>
keratitis, end-, panophthalmitis) endocarditis, meningitis, osteomyelitis,
pneumonia, IVDA
OTHER BACILLI
Parasites of insects < commercial insecticides
Food poisoning?
DIFFERENTIAL DIAGNOSIS: biochemistry, phage typization
15

Tetanus (1888)
MORPHOLOGY: 2-5 µm x 1-2 µm,
flagella (specific antigen), terminal spore
CULTIVATION: obligate anaerobic
β-hemolysis on blood agar
PATHOGENESIS: 1884
EXOTOXIN=tetanospasmin (151 kD, A-B-C chains)
Released by bacteriolysis. Minimal wound>necroparasite>non invasive
germination and toxin production is aided by associated pyogenic infection,
calcium salts reducing oxidation-reduction potential
Toxin absorption in neurons>retrograde axonal transport to CNS >
circulation>fixed to gangliosides> postsynaptic inhibition of acetylcholine
inhibitory factor>generalized muscular spasms, hyperreflexia, seizures
=TOXEMIA
(tetanolysin=exotoxin, non pathogenic)
16

TETANUS
Opisthotonus
Trismus
Risus sardonicus Neonatal tetanus

CLINICAL FINDINGS:
5-7 days of latency>spasms>
convulsive tonic contraction of voluntary muscles>
lockjaw, hydrophobia, opisthotonus, interference with
mechanics of respiration>death. Fully conscious!
INFECTION: soil, horse stool (occupational disease),
spores in air
wounds, uterus, umbilical stump (90% in developing
countries), abortion, burns
iatrogenic: surgery, ointments, catgut, injections
mortality: 50-60%, 1 M cases/year worldwide
DIFFERENTIAL DIAGNOSIS: rabies, strychnin poisoning

TREATMENT:
1.Symptomatic: proper care of wounds, surgical debridement (no
hyperbaric oxygen) muscle relactants, sedation (external stimuli
precipitate tetanic seizures), assisted ventilation
2.Toxoid recall injection
toxoid + antitoxin iv. (earlier horse serum,
recently human serum: tetanus immunoglobulin, HTIG)
3. Antitoxin: before toxin becomes fixed onto nerves
4.Antibiotics (penicillin, tetracyclin to stop toxin production)
treatment of associated pyogenic infection
PREVENTION: toxoid - active immunization
DPT combination (childhood)
recall injections in every 10 years (toxoid 0.5 ml)
totally preventable, immunization is mandatory
Booster shot in the elderly population would be ideal!

SAPROPHYTE BACTERIA (SOIL, INTESTINAL TRACT, DUNG)
MORPHOLOGY: 7-8 µm x 1-2 µm, Gram+
spore Ø > bacterium Ø
Germination into bacterium > sporulation
C. perfringens: capsule
Peritrichous flagella: C. novyi, C. septicum,
C. histiolyticum, C. sporogenes,
C. tertium, C. bifermentans, C. fallax, C. sordelli, etc.
(90 species/20 human pathogens)
CULTIVATION: anaerobic, gas production
(aerotolerants: milk stormy fermentation, clot torn)
ANTIGENS: 12 types
BIOCHEMISTRY: 1. Toxins: α, β, …,τ
(α=lecithinase, LD 50 =50 ng, hemolysing, cell lysing, cardiotoxic
inhibition by antitoxin: Nagler-reaction)
toxinogenic strains: A-E
2. Enzymes: collagenase, hyaluronidase, proteinase, DNase, etc.
20

PATHOGENESIS: normal habitat in the gut (skin, vagina) flora
Pathogenical local effects = tissue necrosis:
1. >endogenous infections: Colon surgery, colon-carcinoma,
appendicitis>perforation,
uterus war, trauma, iatrogenic
foul-smelling discharge, edema malignum,
gas-phlegmone.
myositis: edema,myonecrosis,exsudate,rapid progression, crepitation (acetylene,
H 2 , etc), cellulitis
General effects = toxic: malaise, hypotonia, fever, vomiting, nervousity,
toxemia, shock, death.
21

GAS GANGRENE

3. Bacteremia (10-15%): death
4. C. perfr. "A" (C,D): food poisoning, meat dishes high protein content
protects bacteria form strong acidic pH
incubation: 9-15 h
symptomps: abdominal cramps, diarrhea

DIAGNOSIS: microscopy,
cultivation (chopped meat-glucose medium,
egg yolk medium),
biochemistry, gas chromatography,
toxin-neutralization (VERO-cells)
phage typization, DNA-probes
TREATMENT:
1. ANTITOXIN
(polyvalent: C. perfringens, C. septicum, C. novyi)
to detoxity patients rapidly
2. Antibiotics (penicillin, chloramphenicol, erythromycin,
tetracyclin). Metronidazol
3. Symptomatic care
promt and extensive surgical debridement,
hyperbaric oxygen
early amputation
PREVENTION: Cleansing of contaminated wounds
24

Pseudomembranous colitis
Iatrogenic: antibiotic-associated diarrhea
MORPHOLOGY: spores
CULTIVATION: obligate anaerobic. Resistant.
PATHOGENESIS: in normal flora (3% of adults)
colonization: in newborns
in adults during hospitalization from the hand of
personnel, endoscopes, devices
NON INVASIVE (yes: newborns, neutropenia)
TOXEMIA (plasmid, phage, regulation?)
toxin A: 440-500 kD enterotoxin (watery diarrhea)
toxin B: 360-470 kD cytotoxic (colon wall destruction)
Binding to gut wall: gradual > microabscesses >
contraction > bleeding>necrosis>inflammation>
protein loss>watery/bloody diarrhea
PROLONGED TREATMENT WITH ANTIBIOTICS
(aminoglycosid, clindamycin) > dysbacteriosis > selection
of resistant mutants > 4-9 days of incubation, abdominal
pain > diarrhea, fever, elevated number of WBC
(rarely: perforation, peritonitis, acute arthritis)
26

CLINICAL DIAGNOSIS: endoscopy
MICROBIOLOGICAL DIAGNOSIS:
1. Cultivation
(cycloserin, cefoxitin, fructose-agar, CCFA)
2. Phage typization
3. Toxin detection
toxin B on VERO cells (24h CPE) and neutralisation
toxin A detection: latex agglutination
toxin A+B: ELISA
PCR
TREATMENT:
1. Discontinuing administration of offending antibiotic
2. Antibiotics: vancomycin, metronidazol, bacitracin
3. Symptomatic: cholestyramin
(=toxin B binding, but: binds vancomycin)
4. Surgical (in case of perforation)
PREVENTION: vancomycin in case of carriers and hospitalized patients
medical personnel
disinfection of medical devices, endoscopes:
glutaraldehyde, Na-hypochlorite, iodine (sporocidal)
wearing gloves during physical examinations by health care personnel 27

Saprophyte, ubiquiter in nature, (soil, dung vegetables, meat products)
MORPHOLOGY: 3-8 µm x 1-2 µm, flagella, spore
CULTIVATION: blood agar, anaerobic
ANTIGENS: common "O", type specific "H"
EXOTOXINS: A-H (A, B, E /F/ human pathogenic)
150-165 kD, 2 chains, disulfide bonds. Phage control.
Heavy chain: binding to motor nerve endplates,
internalization, light chain blocks acetylcholine release
Extremely toxic: 1-2 µg lethal dose
Heat labile: 100 o C, 20 min
PATHOGENESIS: J. Kerner, 1820
1.Botulism (botulus = sausage), food poisoning spore > food (canned,vacuum
packed,smoked, spiced alkaline products, home canned vegetables) > germination >
eaten w/o cooking/baking (20', 100C) > toxin absorption from gut (INTOXICATION)
2.Spore > honey > colonization in infants>toxin production and absorption > poor
feeding, weakness, floppy baby > sudden infant death syndrome (1976)
Complete recovery
3.Wound infection > toxin absorption (1943)
EXOTOXIN in circulation > nerve endings > flaccid paralysis
28

CLINICAL FINDINGS: 1-2h—1-2 days of latency,
speech difficulty, double vision, inability to swallow,
muscular weakness, +/- gastroenteritis,
respiratory paralysis, cardiac arrest>no fever>death
Fully conscious. High mortality (65>25%)
Recovery without antitoxins in serum
DIAGNOSIS:
toxin detection:
leftover food, vomiting, stool (infants), approx. for 1 month toxinneutralization:
mouse injection, ELISA from sera: passive HA, RIA
TREATMENT: 1. Polyvalent (A,B,E) antitoxin
80.000 U horse serum: promtly administered
2.Symptomatic: adequate ventilation (for 100 days!)
3.Infants, wound infections: antibiotics (penicillin 10-20 MU/day)
Contraindicated: tetracyclin, aminoglycosid (due to nerve toxicity)
PREVENTION:
1. strict regulation of commercial canning food hygiene
2. home canning: boiling food for >20 min before consumption
toxic food (beans, corn, peas, fish, vacuum-packed fish in plastic bags)
spoiled, rancid, cans „swell”, innocuous appearance
29

GENUS Species Biochemistry Residence
Gram positive cocci
Peptostreptococci 13 Protein hydrolysis/ Mouth, vagina
Peptococci 1 utilization Mouth, respiratory tract,
Anaerob streptococci 3
vagina, skin
Gram positive rods
Acids
Propionibacteria 4 Propionic Skin, mouth, vagina
Bifidobacteria 8 Acetic/lactic Gut, mouth, vagina
Lactobacilli 56 Lactic Gut, mouth, vagina
Actinomyces 20 +/- fermentation Gut, mouth, vagina
Eubacteria 45 Butyric Gut, mouth, vagina
Mobiluncus 2 Hydrolysis Vagina, rectum 30

Gram negative cocci
GENUS Species Biochemistry/
characteristc
Residence
Veilonella 3 Lactic acid Mouth, vagina
Acidaminococci 1 Acetic/lactic acid Gut
Megasphera 1 Capronic acid Gut
Gram negative rods
Bacteriodes 18 Capsule Mouth, gut, vagina
Prevotella 16 Pigment Mouth, vagina
Porphyromonas 8 Pigment Mouth
Fusobacterium 4 Polymorph Mouth, gut, vagina
Leptotrichia 2 Elongated Mouth
CONTINOUSLY CHANGING TAXONOMY: genera, number of species,
new characteristics
31

40 species pathogenic in human
MICROBIOLOGY
Obligate anaerobic ---------- microaerophil
Moderate biochemical activity
Protein hydrolisis
Starch and carbohydrate fermentation:
CO 2, foul-smelling gases
32

Anaerobic streptococci:
S. hansenii
S. pleomorphus
S. parvulus
Residence:
mainly respiratory tract (particularly the pharynx)
Cultivation:
non-hemolytic or alpha-hemolytic
33

Peptostreptococcus micros
resident in the normal mouth flora
Produced diseases: periodontitis,
abscesses around tooth implants(24%)
hematogenic spread brain abscess
chronic sinusitis in children, nasopharyngitis, otitis media
retropharyngeal abscess, pulmonary abscess, erythema
Peptostreptococcus anaerobius
resident in normal mouth flora
Produced diseases: as P. micros
peritonitis appendicitis, diverticulitis, after abdominal surgery
postpartum endometritis, septic abortion
34

Peptococcus niger
Produced diseases: postpartum endometritis,
tuboovarial abscess
septic abortion
Coprococcus
Ruminococcus
Residents in the normal flora of human and animal
Sarcina ventriculi
Mostly in the gut flora of vegetarian people
Unusual high number in the stomach: cancer
Gaffkya
Resident in the normal gut flora
35

Pathomechanism:
~ 15%- of normal flora
Predominantly in dental plaques and periodontal pockets
Continously changing resident flora in the mouth and gut
Depending on age and nutrition (food habits)
Polymicrobial (mixed) aerobic +
anaerobic infection
1. aerobic bacteria growth
2. lack of normal oxygenization in tissues
3. tissue destruction/necrosis, anaerobic conditions
4. vast proliferation of anaerobic bacteria
5. abscess formation, suppuration, gangrene, gas production
36

Specimen collection:
aspiration, punction
Laboratory process:
smears, staining
Cultivation:
usually small, grey colonies or other dark pigments
no ideal selective media are available
other microbes overgrow gram positive anaerobic cocci
Identification at species level:
no concensus protocol or scheme, uncertain
carbohydrate fermentation, gas production
enzyme reaction (urease, phosphatase, etc.)
gas- liquid chromatography (GLC)
Common end products: acetate, butyrate, capronic acid
37

Penicillin resistance
(due to the mutations of penicllin binding proteins)
Resistance to metronidazole
(mainly the microaerophilic species)
Effective antibiotics:
clindamycin (depending on geographical location)
amoxicillin + clavulic acid
4th generation quinolones (e.g. trova- and clinafloxacin)
38

BACTEROIDES GENUS
intensive sugar fermentation
strictly anaerobic, very pleomorphic,
non-motile
polysaccharide capsule: B. fragilis
no lipopolysaccharide endotoxin
colonization: fimbriae
Normal inhabitants of the upper respiratory tract, intestinal
and female genital tract
10 11 organism/g stool
(B. caccae, B. merdae, etc.)
Produced anaerobic infections:
abdominal, brain, lung abcesses, empyema, PID
surgical infections, peritonitis (pus: foul smelling)
bacteremia endocarditis
Taxonomical changes: Bacteroides melaninogenicus
Porphyromonas gingivalis,
Prevotella melaninogenica
39

PORPHYROMONAS GENUS
Porphyromonas gingivalis
Oxygen tolerant, small black colonies
on chocolate agar
no carbohydrate fermentation,
but proteolytic
Porphyromonas endodontalis,
P. asaccharolytica
Residents of the normal mouth flora
Produced diseases: soft tissue infection following
human bites
40

PREVOTELLA GENUS
moderate carbohydrate fermentation
glucose fermentation acid production
saccharose fermentation!
proteolysis
pigment production
P. intermedia, P. melaninogenica (B. melaninogenicus),
P. denticola, P. loeschii
residents in the normal mouth flora
endogenous infections, inflammations
periodontitis, surgical wound infection
and abscesses
41

FUSOBACTERIUM GENUS
Pleomorphic rods, produce butyric acid
Convert threonine to propionic acid
Cystein, methionin: H 2 S production
F. nucleatum**, F. alocis, F. sulci,
F. necrophorum, F. periodonticum*
** and * in the normal mouth flora, others in the gut
** Prevotella/Porphyromonas coinfection
Fusospirochetosis: noma
Occassionally: Fusobacterium the only species
in an infection (e.g. osteomyelitis)
LEPTOTRICHIA GENUS
Pleomorphic rods
First isolation: anaerobic,
subcultures: elevate CO 2 level requirement
L. buccalis: resident in the normal mouth flora
in immunocompromised individuals: ulcerative gingivitis
Frequent coinfection with Treponema, Porphyromonas,
Fusobacterium species 42

Metronidazole (Klion)
Amoxicillin + clavulic acid (Augmentin)
Imipenem
Chloramphenicol
(severe side effects)
43

Acne (carbunculus,phegmone,sepsis): Propionibacterium
Skin (carbunculus): Eubacterium
Chronic sinusitis: Peptostreptococcus, Eubacterium
Post-maxillo-facial or periodontal surgery: Bacteroides,
Fusobacterium, Porphyromonas, Prevotella, Actinomyces,
Peptostreptococcus, Veilonella, Propionibacterium
Gingivitis ulcerans: Leptotrichia, Porphyromonas,
Fusobacterium (+Treponema)
Peritonsillar abscess: Fusobacterium
44

Brain abscess: Peptostreptococcus
Pulmonary abscess, empyema: Bacteroides, Porphyromonas,
Prevotella, Peptostreptococcus
Thoracal infection: Actinomyces
Hepatic- and perihepatic abscesses : Bacteroides
Peritoneal infections, peritonitis, bowel rupture, post-surgical
infection, war injury: Bacteroides fragilis, Gram+ anaerobic cocci,
Actinomyces
IUD in women, abscess, criminal (instrumental) abortus, salpyngitis,
uterus abscess: Bacteroides, Fusobacterium,
Peptostreptococcus, Mobiluncus
Bacterial vaginosis: Mobiluncus, Porphyromonas,
Prevotella, Gram+ anaerobic cocci (G.vaginalis)
Perirectal abscess, fistule: Bacteroides, Fusobacterium
45

Necrotising cellulitis in the limbs: gas gangrene clostridia
Joint infections: Gram+ anaerobic cocci
Leg ulcers: mixed infection (but: Clostridium)
Bacteremia, septicemia, endocarditis:
Bacteroides fragilis, Propionibacterium,
Clostridium, Mobiluncus
Infections in immunocompromised: Bifidobacterium,
Lactobacillus
46

LOCAL FACTORS
ENDOGENOUS INFECTIONS
dermal and mucosal wounds
diminished tissue oxygenization
(diabetes mellitus, angiopathy)
surgery (oral, abdominal, gynecological)
EXOGENOUS INFECTIONS
human or animal bites
SYMPTOMS
foul-smelling pus, exsudate < fatty acids
(diagnosis: gas chromatography)
abscess formation, necrosis, gas production
(differential diagnosis!)
47

MODEL: VAGINA
NEWBORN: sterile, colonization in few days
SMALL CHILDREN: mixed flora (cocci, bacilli)
FROM PUBERTY:
1. Aerobic and anaerobic Lactobacilli (Döderlein)
estrogen > glycogen fermentation of epithelial cells > lactic acid
production > pH 4-4.5
(~ treatment: 0.5% lactic acid)
2. Resident flora: Bacteroides, Mobiluncus, Gram+ cocci,
α-hemolysing streptococci, enterococci,
Gardnerella , Mycoplasma, Ureaplasma, staphylococci, Mobiluncus,
Candida species etc.
3. Transient flora: Enterobacter, staphylococci, streptococci, clostridia
Critical pH (preventing harmful microbes): 6.0-6.5
Anaerobic : aerobic ratio: 2-5:1
Sexual activity: individual and continously changing flora
48

BACTERIAL VAGINOSIS
Alterations in the ratio of the normal flora = dysbacteriosis >
inflammation
1. Decreased ratio of Lactobacilli in the flora
2. Activation of endogenous bacteria = endogenous infection >
increasing ratio > massive infection
3. Promoting factors
hormonal changes (age, menses, gravidity, oral contraception)
chemical effects: antibiotics, chemotherapy
mechanical effects: contraceptive barriers, IUD
4. Consequences: pH increase (alkaline) >
increasing ratio of all anaerobic bacteria (1000:1)
>genital discharge> „amin vaginosis”
>recurrent vaginal and urinary tract infections
(10 9 /ml Mobiluncus, Prevotella, Porphyromonas, Gram+
anaerob cocci, Myco-, Ureaplasma, Gardnerella, etc.)
infection of the sexual partners (non-gonorrhoic urethritis)
or the newborn at time of delivery
DIAGNOSIS: clue cells, presence of PMNL, amin-test 49

In the majority of cases:
mixed (aerobic + anaerobic) infection
Surgical debridement,
excision of all devitalized tissues
50

THERAPY ANAEROBES
Gram positive Gram negative
Recommended
without sensitivity test
Recommended
as determined
by sensitivity tests
Not
recommended
(resistant)
β-lactam + β-lactamase inhibitors:
e.g. Augmentin
imipenem
chloramphenicol
clindamycin metronidazole
tetracyclines
erythromycins
clindamycin
cefoxitin
moxalactam
other β-lactams
penicillines
clindamycin metronidazole
aminoglycosides
fluoroquinolones
51

www.bact.wisc.edu/Bact330/lectureanthrax
www.cdc.gov
52