lecture slide gm- organisms

N. meningitidis

• resides in man only

• usually sporadic cases
– mostly young children

• outbreaks
– adults
– crowded conditions
* e.g. army barracks
Neisseria meningitidis
upper respiratory tract infection
– adhesion pili –bloodstream-brain

Meningococcal meninigitis
• second most common meningitis
– pneumococcus, most common

• fatal if untreated

• responds well to antibiotic therapy
– penicillin

• Meningococcemia can kill more rapidly than any other infectious disease
• Early recognition is critical to implement prompt antibiotic therapy and supportive care.
• Treatment must be instituted rapidly because irreversible shock and death may occur within hours of the onset of symptoms.

• Cutaneous manifestations in meningococcemia may be important clues to the diagnosis. Skin involvement can be the most dramatic aspect of the disease and is often the first sign that leads to the clinical consideration of meningococcemia.
• Transmission of N meningitidis occurs from person to person through respiratory secretions

• The human upper respiratory tract is the only known reservoir.

• Carrier rates depend on age.

• 20-40% of young adults are carriers of N meningitidis.

• Overcrowded conditions (eg, schools, military camps) can significantly increase the carrier rate.
• Colonization and invasion of meningococci are facilitated by pili that attach to mucosal epithelial cells.
• concomitant viral infection may facilitate the invasion of N meningitidis into the bloodstream or lower respiratory tract.
• Once in the bloodstream, N meningitidis causes profound effects on small blood vessels
• direct invasion of endothelial cells and indirect damage from endotoxin release.
• Endotoxin from the lipopolysaccharide of meningococci causes endothelial cells, monocytes, and macrophages to release tumor necrosis factor-alpha, interleukin 1, interleukin 6, and interferon-gamma.
deleterious effects of these cytokines
• play a major role in the pathogenesis of meningococcemia by causing
severe hypotension
reduced cardiac output
increased endothelial permeability

• Multiple organ failure, shock, and death may ensue as a result
anoxia in vital organs
massive disseminated intravascular coagulation (DIC).

SPIROCHETES
• Gram negative
• long, thin, helical, motile
• axial filaments
• locomotion
• between peptidoglycan layer/outer membrane
• runs parallel

• transmission
– genital/genital
– in utero or during birth
Syphilis
• chronic
• slowly progressive

• primary lesion - chancre
– 10 to 60 days
– area of ulceration/inflammation
– many organisms
• Secondary (2-10 weeks later)
– systemic spread
– flu-like symptoms
– skin, particularly
– many organisms

Secondary syphilis
• characterized by a skin rash
1-6 months (commonly 6 to 8 weeks) after the primary
•
• symmetrical reddish-pink non-itchy rash on the trunk and extremities,
• rash do not involve the palms of the hands and the soles of the feet;

• condylomata lata

• most contagious
• Tertiary
• several years later
• rare
• skin,
• central nervous system
• delayed hypersensitivity
• few organisms
• control by immune response

Congenital syphilis
• syphilis present in utero and at birth
• born to a mother with secondary or tertiary syphilis
• According to the CDC
40% of births are stillborn
40-70% of the survivors will be infected
12% of these will subsequently die


• Manifestations of congenital syphilis include
• Hutchinson's teeth
• frontal bossing
• saddle nose
• poorly developed maxillae
• enlarged liver; enlarged spleen; petechiae; other skin rash; anemia; lymph node enlargement; jaundice
Microbiological diagnosis
• not culturable
• dark field microscopy
– actively motile organisms
– brightly lit against dark backdrop
– light shines at an angle
– reflected from thin organisms
– enters objective
• conventional light microsrcopy
– light shines through
– NOT visualized
Secondary and Tertiary Syphilis
- serology
• screening method
• antibodies to cardiolipin

• specific diagnosis
• antibodies to treponemal antigen
• no vaccine

• antibiotics (e.g. penicillin)
– effective
Leptospirosis
• an animal/rodent infection

• animal excretes the organisms in its urine

• bacteria survive for days even weeks in moist conditions but only for a few hours in salt water.

• infection is caught by direct contact with infected urine or a polluted water environment.

• Bacteria can enter through skin abrasions or via eyes, nose or mouth.
• <100 cases per year in US

• symptoms
– flu-like
– severe systemic disease
* kidney
* brain
* eye
Transmission
• infected urine
– rodents
– farm animals

• water

• through broken skin.

The Illness
• The usual incubation is 2 to 12 days.

• "flu" like illness occurs which resolves in 2-3 weeks

• fever, severe headache, pains in the back and calves, jaundice

• Many cases recover without specific treatment.

• Antibiotics during the first few days help in limiting infection.

• death may occur in about 15% of jaundiced patients, death without jaundice is virtually unknown.
Laboratory Diagnosis
• serology
• most readily culturable of spirochetes
– culture still extremely difficult

ANAEROBES AND PSEUDOMONAS - OPPORTUNISTIC INFECTIONS
Obligate (strict) anaerobes
• no oxidative phosphorylation
• fermentation
• killed by oxygen
• lack certain enzymes
– superoxide dismutase
* O2-+2H+ H2O2
– catalase
* H2O2 H20 + O2
– peroxidase
* H2O2 H20 /NAD to NADH

Polymicrobic anaerobic infection
• Many species in human flora
• Many grow simultaneously - opportunistic
conditions
• opportunistic growth
– injured tissue
* limited blood/O2

• no growth
– healthy tissues
* high O2 content

Polymicrobic anaerobic infection
• Simultaneous infection with facultative anaerobe
– diminishes O2 supply further
– aids growth of obligate anaerobes
Endogenous versus exogenous infection
• Two sources
– normal human flora
• endogenous
– environment (e.g. soil)
• exogenous
Source of spore-formers and non-spore formers
• Spore-formers (clostridia)
– exotoxins
– common in the environment (e.g. soil)
– found in normal flora
• Non - spore-formers
– no exotoxins
– mostly normal flora

Sites of anaerobes in
normal flora
• intestine
– major site
– 95-99% total bacterial mass
• mouth
• genitourinary tract

Bacteroides fragilis
• minor component of gut flora
• most common (strict) anaerobic infection after abdominal surgery
• Enterobacteriaceae (facultative anaerobes)
– commonly cause disease
– low numbers gut flora

• Strict anaerobes
– much less commonly cause disease
– high numbers gut flora

Strict anaerobe infectious disease
• Sites throughout body
• Muscle, cutaneous/sub-cutaneous necrosis
• abscesses
Problems in identification of
anaerobic infections
• air in sample (sampling, transportation)
– no growth

• identification takes several days or longer
– limiting usefulness

• often derived from normal flora
– sample contamination can confuse
LABORATORY IDENTIFICATION
• BIOCHEMICAL KITS
– e.g. API SYSTEM

• GAS CHROMATOGRAPHY
– volatile fermentation products
Bacteroides fragilis
• Major disease causing strict anaerobic
non-spore-former
Prominent capsule
anti-phagocytic
abscess formation

• Endotoxin
– low toxicity
– structure different than other lipolysaccharide
ANAEROBIC SPORE-FORMERS (CLOSTRIDIA)
• Gram-positive rods
– human intestine
– soil
PSEUDOMONAS
• Pseudomonads are motile
• Gram-negative rods
• utilize glucose oxidatively
• Members of this genus are classified into five groups based on ribosomal RNA homology.

• clinically important because they are resistant to most antibiotics

• capable of surviving in conditions that few other organisms can tolerate. They also produce a slime layer that is resistant to phagocytosis.

• often encountered in hospital and clinical work because it is a major cause of hospital acquired (nosocomal) infections.
• Its main targets are immunocompromised individuals
• burn victims
• and individuals on respirators
• patients with indwelling catheters.
• colonize the lungs of cystic fibrosis patients
• increasing the mortality rate of individuals with the disease.

• Infection can occur at many sites and can lead to
• urinary tract infections
• sepsis
• pneumonia
• pharyngitis
• other problems.
• Aerobic
• Gram-negative rod
• majority of human infections
• P. aeruginosa
Common in the environment
• water
• air
• soil
P. aeruginosa and compromised host
• Burns and wounds
– destruction of blood vessels
– phagocyte access limited
• cancer
– cytotoxic drugs
* destroy the immune system
• cystic fibrosis
– altered respiratory epithelium
– pneumonia
Identification
• Pigments
– pyocyanin (blue-green)
– fluorescein (green-yellow, fluorescent)

• biochemical reactions

• cultures have fruity smell

Pathogenesis
• Slime layer is anti-phagocytic

• Toxin A - ADP ribosylates EF2
– similar to diphtheria toxin
PLEOMORPHIC GRAM-NEGATIVE RODS
HAEMOPHILUS
BORDETELLA
BRUCELLA
PASTEURELLA
LEGIONELLA
HAEMOPHILUS
• a large group of Gram-negative rods that like to grow on blood agar
• Morphologically--tiny coccobacilli under the microscope
• Pleomorphic bacteria-- because of the many shapes they assume.
• A methylene blue stain of a smear can also help with identification.

• classified by their capsular properties into six different serological groups, (a-f).
common in children
normal flora of the nose and pharynx----
they can confer severe illness in patients that are immunosuppressed
• This species may exist with or without a pathogenic
• polysaccharide capsule.

• H. influenzae infection can lead to a variety of diseases:
Meningitis-
Epiglottitis-
Most of these infections occur in unvaccinated
children less than five years of age
• Haemophilus infection has also been associated with chronic bronchitis,
• pneumonia, bacteremia, conjuctivitis, and a host of other illnesses.
Meningitis-
• most common cause of bacterial meningitis in children between the ages of five months and five years.

• initial respiratory infection ---spread to the blood stream -------the central nervous system.

• common symptoms in infected babies.
• stiff neck
• lethargy
• absence of the sucking reflex
• coma
• death

• A vaccine is available, but is not always effective in very young children..

Epiglottitis-
• H. influenzae is the number one cause of this potentially fatal disease

• may cause airway obstruction in children between the ages of 2 and 4.

treatment.
• third generation cephalosporins are the drug of choice.

• Resistance may develop when ampicillin is used in treatment.

BORDETELLA
extremely small, strictly aerobic, Gram negative,
non-motile cocobacillus (short rod).
B. pertussis --most important species
the organism which causes whooping cough.
• This highly contagious bacterium makes its way
• into the respiratory tract via inhalation
Binds to and destroys the ciliated epithelial
of the trachea and bronchi
Pertusis
catarrhal stage
mild symptoms of rhinitis, mild cough and sneezing occur which last 1-2 weeks
paroxysmal stage
characterized by paroxysms of cough followed by a
prolonged and distressing inspiratory gasp (whoop).
toxins
• Pertussis toxin-
Tracheal cytotoxin
Hemoagglutinin-
KLEBSIELLA
Klebsiella pneumoniae
The most clinically important speciies of this genus
pathogenicity
attributed to its production of a heat-stable enterotoxin
large, non-motile bacterium produces large sticky colonies
when plated on nutrient media
• infections are common in hospitals where they cause
• pneumonia (characterized by emission of bloody sputum) and

• urinary tract infections in catheterized patients
may contain resistance plasmids (R-plasmids)
which confer resistance to such antibiotics as ampicillin
and carbenicillin.