KHO, Jesette Christien (BSN-1E)

● isolation of 5 or more aerobes from the specimen

does not imply that the specimen was contaminated
ANAEROBIC BACTERIA Synergy
- Endogenous anaerobic bacteria are opportunists causing
- Bacteria that require a zero O2 tension for their growth disease when factors combine to produce an environment in
- The presence of O2 is either inhibitory or toxic to them tissue that promotes their growth
- Predominant normal microbial flora in the body, outnumber
the anaerobic bacteria, like in the GIT, Bacteroides. INDIVIDUAL STRAINS OF ANAEROBIC BACTERIA
- Anaerobes outnumber the facultative anaerobic bacteria - generally lack the full complement virulence factors that
(E.coli) by a ratio of 1000:1 provide for:
- Other pathogenic anaerobes (e.g., Clostridium botulinum and a. invasion of tissue
Clostridium tetani) b. resistance to host defense mechanism
● Soil and environmental inhabitants c. growth in tissue
● Are not considered part of human flora d. injury to host tissue
- person- to-person nosocomial spread of Clostridium difficile
among hospitalized patients -> an enormous clinical and TREATMENT
infection control dilemma - Therapeutic mainstays
● majority of anaerobic infections occurs when a - surgical drainage
patient’s normal flora gains access to a sterile site as a - resection of necrotic tissue
result of disruption of some anatomic barrier. - Effective concurrent of antimicrobial therapy is also
important
TWO MAJOR DIVISIONS OF ANAEROBES Antibiotics
1. Spore forming anaerobes - antimicrobial selection may be critical
2. Non-spore forming anaerobes ● most common clinical isolates are resistant to some
of the more frequently used antibiotic
GENERALITIES
Most pathogenic anaerobes are destructive, the lesions produced may ANTIMICROBIAL WITH THE HIGHEST ACTIVITY
be:
a. Tissue necrosis
Metronidazole ● inactive against
b. foul-smelling (putrid odor) discharges and purulent
aerobic and
drainage
facultative
c. manifestation of gas in soft tissues - crepitation
bacteria
LABORATORY DIAGNOSIS
- specimens are taken directly from a site Imipenem ● highly active
- normally sterile broad spectrum
- specimen that ​cannot​ be used: ● used primarily for
● voided urine serious infections
● feces
● sputum B-Lactam ● drugs with
- recommended collection technique – needle aspiration B-lactamase
- special transport or collection tube (gassed-out tube) inhibitor
- incubated in anaerobic Gas Pak jars combinations
(sulbactam and

clavulanic acid)
1. Clindamycin
2. Chloramphenicol
3. Cefoxin
4. Piperacillin
5. Mezlocillin
- procedure:
1. gram staining
2. CULTURE *almost all anaerobes are resistant to aminoglycosides
- anaerobics are very fastidious, requires enriched ____________________________________________________________
medium (cooked meat medium)

The study of the organisms had lagged on: GENUS CLOSTRIDIUM

- sensitivity to O2 (killed in the presence of O2)
- fastidious growth requirements (need enriched media for SPOREFORMING ANAERBOBES
growth)
- frequently occurring in mixtures of anaerobic and facultatively GENUS & SPECIES INFECTION
anaerobic organisms
- Provision of anaerobic environment for culture was technically C. tetani tetanus
difficult
● making it impossible to have pure cultures for study
C. perfringens Gas gangrene
ANAEROBIC BACTERIA AS ETIOLOGICAL AGENTS OF INFECTION
C. botulinum food poisoning
- anaerobic infections typically contain polymicrobic
- mixtures of anaerobic and aerobic bacteria C. difficile Pseudomembranous
KHO, Jesette Christien (BSN-1E)
● deep and lacerated or crushed wound of muscles
enterocolitis ○ vascular damage of major vessels and capillary beds
e.3. PRINCIPAL SETTING FOR INFECTION
1. Clostridium tetani ○ War: ​massive wounds of muscles contaminated with
soil, clothing and metal fragments
○ Civilian life​: automobile and motorcycle accidents;
gunshot wounds, compound fractures; industrial
accidents; surgical complications

STAGES OF INFECTION:
1. simple wound contamination:
CHARACTERISTICS - one or more histotoxic clostridia present
- Gram (+) sporeforming bacilli occur singly or in pairs; 2. anaerobic cellulitis
- spores oval (greater diameter than the vegetative cell) and - gas is prominent
terminal with drumstick or tennis racket appearance. - patient not extremely toxic
- most isolates have peritrichous flagella - over all prognosis better than the next category
- Resistant to various disinfectants and heat.
● not destroyed by boiling for 20 minutes 3. clostridial myonecrosis
- for practical purposes, autoclaving at 120˚C for 15 minutes will - profound toxemia
kill the organism - Extensive local edema
- Normally found in the soil, intestine of lower - variable amounts of gas
animals(horses) and in humans - massive tissue damage
- death in untreated cases
PATHOGENICITY
ADDITIONAL SETTINGS
CLINICAL INFECTION:​ TETANUS 1. Uterine infection
- incidence: decreasing in many parts of the world remains 2. Clostridial septicemia
common and uncontrolled in developing countries - bloodstream invasion may occur with malignancy and
- Release a powerful exotoxin, a neurotoxin known as may involve a localized myonecrosis
tetanospasmin​ which has affinity to the tissues of CNS - usually no history of external trauma
● Responsible for the signs and symptoms of tetanus; - may follow biliary tract or GIT surgery
● Does not invade blood stream - rapid Dx and Rx are essential because death may
- classically small puncture wound from a nail, splinter or thorn occur in untreated cases in <24 hrs after onset of
- Other settings: compound fractures, skin popping of drug infection
addicts, decubitus, varicose ulcers, external otitis, dental
extraction PREVENTION AND CONTROL
- most feared: ​tetanus neonatorum 1. Thorough cleaning of wound, debride all necrotic areas
2. Active immunization ( DPT vaccine , tetanus toxoid)
INCUBATION PERIOD:
- Short IP TREATMENT ​ ​(FOR UNVACCINATED INDIVIDUALS)
● 3-21 days 1. SUPPORTIVE CARE
- Long IP - muscle relaxants and oxygen to reduce spasms and
● 4-5 weeks maintain breathing
- until circulating toxin is metabolized
TWO TYPES: 2. PASSIVE IMMUNIZATION ​- ATS ( horse serum), hyperimmune
tetanus serum
- neutralize circulating tetanospasmin
LOCALIZED GENERAL
3. DEBRIDEMENT​ of primary wound, penicillin therapy
- Eliminate clostridial organism
● Rarely localized form ● Onset within a week
● Later onset ● High mortality in ____________________________________________________________
● less serious unvaccinated
● Twitching and spasm of individuals
muscle groups near ● Neuromuscular spams – 2. Clostridium perfringens
site of inoculation lock jaw, trismus
● Risus sardonicus –
clenching of jaw
(sardonic grin)
● Hyperextension of neck
and body –
opisthotonus
● Painful muscle spasm
often provoked by the
slightest stimulation
- Found in environment ( Soil, sewage),intestines of humans and
MODE OF TRANSMISSION animals
● (via entry of spores via contaminated materials into cut/wound) - Central/subterminal spore – boxcar/match box shaped
● C. tetani - punctured wound
○ Tetanus neonatorum – infected umbilicus CLINICAL INFECTION
1. WOUND AND SOFT TISSUE INFECTION
PREDISPOSING FACTOR ASSOCIATED WITH - Gas gangrene ( Clostridial myonecrosis)
KHO, Jesette Christien (BSN-1E)
- C. perfringens is responsible for 60-90% of clostridial
myonecrosis
- Brought about by release of α toxin which is
cytotoxic, attack muscles, necrosis with accumulation
of fluid and gas.
- (extremities, intestine, uterus)
2. FOOD POISONING
- Due to production enterotoxin
- Ingestion of contaminated meat
- Manifestation 8-24 hrs after ingestion abdominal pain
and diarrhea for 12-18 hrs
TREATMENT
1. Proper wound care and prophylaxis
2. Surgical debridement and penicillin/clindamycin
3. Amputation
PREVENTION AND TREATMENT
- Prophylactic antibiotics for planned surgical procedure
- Removal of necrotic material & drainage of abscess plus
antibiotic therapy
CLINICAL IMPLICATIONS
- Surgery and trauma promote endogenous spread of Normal
colonic flora on other sites
- Important cause of​ foul smelling abscess and ulcers ​(bed sores
in bedridden Px)
____________________________________________________________
CORYNEBACTERIUM ACTINOMYCETES NOCARDIA
1. Corynebacterium diphteriae

____________________________________________________________

3. Clostridium botulinum
- N flora of intestines in some individuals
- Resistant to certain antibiotics
a. Enterotoxin (Toxin A )– promotes fluid secretion and
intestinal haemorrhage
- “ Diphteria bacilli”
b. Cytotoxin ( Toxin B) – damages mucosal membranes
- Gram (+), non sporeforming, non-motile ,
- produce the most potent exotoxin, a nerotoxin which is
- presence of metachromatic granules
responsible for the signs and symptoms of botulism, a fatal
- Chinese –character” like appearance
neuroparalytic disease
- Botulinum toxin​ ⟶ blocks release of acetylcholine leading to
PATHOGENICITY
flaccid paralysis
- Release of Diphteria toxin
- Recovery period is long as nerve endings affected by the toxin
● inhibits protein synthesis
needs to regenerate
● leads to cell death and disease manifestation
CLINICAL INFECTIONS:
CLINICAL INFECTION
1. PSEUDOMEMBRANOUS COLITIS
1. DIPTHERIA
- Px on antibiotic therapy ( Penicillin & clindamycin) develops
- Natural infection of humans
profuse, foul smelling, bloody diarrhoea
- Acute infection – communicable, common in children
1.2 TREATMENT
1.2 TRANSMISSION
- Discontinuation of antibiotics – mild cases
– inhalation of droplet spray
- Tx with Metronidazole, vancomycin – more serious
cases
1.3 INCUBATION PERIOD
- 1-7 days
2. FOOD-BORNE BOTULINISM
- Results from ingestion of preformed toxin in contaminated
CLINICAL MANIFESTATION
food ( improperly canned/preserved foods)
1. RESPIRATORY DIPTHERIA
- Weakness and dizziness, blurred vision, fixed and dilated pupils,
- Fever, chills, sore throat
dry mouth, flaccid paralysis, death from respiratory paralysis (
- Cervical lymph nodes become edematous and tender
3-7 days)
- Exudate develops into a thick Pseudomembrane
2.1 INCUBATION PERIOD
(dead cells, bacteria, fibrin) covering the nasal
- 18-36 hrs
mucosa, tonsils, uvula and palate
- Pronounced swelling – bullneck appearance
2.3 PREVENTION AND TREATMENT
- Proper canning/ preservation of food
2. SYSTEMIC TOXEMIA
techniques
- Complication causing damage to distant organs
- Heating of canned food, destroys toxin
- Myocarditis, neuropathy, renal tubular necrosis
● Toxin and bacteria are heat labile,
SPORES – HEAT STABLE
LABORATORY DIAGNOSIS
- Trivalent antitoxin
1. SMEARS
- Gram staining
4. Clostridium difficile - Methylene blue stain
5. Bacteroides fragilis - Metachromatic granules
- Gram (-)
- non-sporeforming, anaerobic colonizers of GIT, GUT 2. CULTURE
- Encapsulated, pleomorphic, produce foul smelling short chain - Loeffler’s medium
fatty acids ● enhance pleomorphic appearance
- Weak endotoxin activity ● Black colonies on K tellurite Blood agar
- Broad antibiotic resistance
KHO, Jesette Christien (BSN-1E)

- ELEK plate method

● determine if toxin producer
- Schick Test
● assess immune status of individual
- intradermal injection of diphteria toxin
● Immune – no skin reaction
● Non-immune – localized edema, necrosis

PREVENTION AND TREATMENT

- Isolate patient and Treat contacts
- Active immunization]
● DPT immunization - Gram (+) (WEAKLY)
- Passive immunization - non sporeforming rods
● antidiphteria serum, hyperimmune diphteria serum - may produce filament with branching
- Antibiotic therapy - Slow growing, AEROBIC, found in soil and aquatic envt.
● penicillin, erythromycin - Partially acid fast

2. Actinomyces Israelii TRANSMISSION

- Gram (+) rods, Slow growing, facultative anaerobic, non – acid - Acquired through inhalation of organism
fast, tendency to form chains or filaments
- N flora of mouth of cattle and man (URT, GIT) CLINICAL INFECTION:
1. NOCARDIOSIS
- Bronchopulmunary disease
- inhaled organisms colonize oropharynx, then into lower airways
(lungs) – may develop pneumonia
- May disseminate to CNS – brain abscess
-
-
-
-
CLINICAL INFECTION -
1. ACTINOMYCOSIS -
-

- Chronic suppurative, granulomatous infection

- characterized by pyogenic lesions with interconnecting sinus
tracts containing granules
a) Cervicofacial​ – tissue swelling, fibrosis, scarring along
draining snus tracts at the angle of jaw and neck.
Occur following oral/dental trauma LUMPY JAW
b) Thoracic​ – with history of aspiration
c) Abdominal & Pelvic​ – following surgery or trauma
d) Genital ​– IUD devices

TREATMENT
1. Surgical debridement
2. PCN treatment

3. Nocardia asteroides