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117 Cards in this Set

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until recently, this organism was the most common cause of bacterial meningitis in children < 4 years
Haemophilus influenzae (type b)
(Hib) affected 41 per 100,000 children under 5 in 1987, only 1.3 per 100,000 in 1998
What percentage of children infected with Hib developed meningitis?

What was mortality due to this diease?
60% developed meningitis

death rate due to this disease is 3-6%
Basic morphology, staining characteristics of Haemophilus influenzae
small, gram (-)
non-motile, non-spore-forming baccilus (or coccobacillus) with complex nutritional requirements (FASTIDIOUS)
Pathogenesis of Hib
-natural disease only in humans
-no known exotoxin, endotoxin not significant in pathogenicity, anti-capsular Abs are protective
-produces IgA protease
Hib transmission
respiratory aerosols between children
carrier rate of Hib in children may be:
30-50% (who may harbor unencapsulated strains)
disease caused by Hib starts as what?
NASOPHARYNGITIS (with otitis media or sinusitis)

BACTEREMIA may follow with involvement of the meninges
(epiglottitis is less common, but equally serious)
Hib bacteria infecting nasopharyngitis can spread where?
face (cellulitis) or joints (pyarthrosis, pus in joint)

in addition to epiglottitis, otitis media, sinusitis,
most serious complications of Hib infection
what is special about the types a-f of H. influenzae
possesses an ANTIPHAGOCYTIC polysaccharide capsule,

capsular carbohydrates provoke protective antibodies (capsule is the basis for serotyping)
how is type b H. influenzae different from types a, c, d, e, and f?
b has a ribose (5 carbon sugar) rather than hexose in its polysaccharide capsular structure
(no known if/how this unusual ring structure relates to the pathogenicity of the type b bacterium)
what type of colonies do encapsulated virulent strains of H. influenzae grow?
smooth colonies (spontaneously give rise to "rough" unencapsulated variants
what is required for Hib growth?
this facultative anaerobe requires:
2 growth factors (X (hemin) and V (NAD or NADP)
what does Staphylococcus provide for Hib that facilitates its growth?
V factor (NAD or NADP) (X & V factors also released from RBCs by the action of the hemolysins secreted by some species of Staph and Streptococci)
What will be seen on agar plates of H. influenzae and Staphylococci?
staphylococcal colonies will be surrounded by small SATELLITE COLONIES of H. influenzae
what type of medium is used to grow Hib?
chocolate agar (heated/lysed RBCs release both X and V)
are sugar fermentations useful in Hib Dx?
why do clinical samples of Hib not last for very long?
very susceptible to disinfectants and drying
Why was Hib particularly harmfum to children under age 4?
kids aquire passive immunity from mom that lasts for a few months

after 3 to 4 years, most children aquire active immunity from asymptomatic infection
vaccine for Hib
conjugate capsular vaccine (1988) effective
vaccine is capsule (PRP) linked to diptheria toxoid so as to have increased dependence of T cells and memory as compared to the previous formulation (only composed of capsule)

2004: version with synthetic carb moiety introduced
Dx of Hib
Hx and age of patient most important
cultures of blood and spinal fluid
-gram stain (-)
-CSF streaked on chocolate agar, incubated in CO2
-demonstrate requirement for X and V factors
-immunofluorescence or immunoelectrophoreses (to detect tybe b casular Ag) (sometimes latex agglutination test)
Treatment for Hib Meningitis
AMPICILLIN = drug of choice
(3rd generation cephalosporin used immediately since some isolates amp-resistant)

ampicillin + clavulanate (a beta-lactamase inhib), for amp-resistant strains)
long-term prognosis after recovery from Hib Meningitis
if treated early, mortality low

previously 1/3 of those who recovered had residual neuro damage (has been decreased with use of corticosteroids during Ab treatment to reduce inflammation and cytokine production due to LPS released as a result of bacteria lysis)
Hib prophylaxis
RIFAMPIN (or single dose of ciprofloxacin or cefriaxone)
what is non-typeable H. influenzae
DOES NOT HAVE polysaccharide CAPSULE
utilized cell-surface adhesions and LPS to colonize cell surfaces
no known role for toxins
how is growth and metabolism of non-typeable H. influenzae, different from typeable H. influenzae?
(identical to typeable strains)
How is pathogenesis of non-typeable H. influenzae different from typable strains?
generally non-typeable strains are restricted to the respiratory tract and infections of the ear
2nd most common cause of otitis media (after S. pneumoniae)
non-typeable H. influenzae
why is otitis media caused by non-typeable H. influenzae most common in kids?
immune system does not fight off infections of the respiratory tract as effectively

structure of the eustacian tube in young kids has straighter angle and shorter length- more prone to infections
non-typeable H. influenzae causes respiratory infections in patients with:
underlying respiratory issues (COPD, chronic bronchitis, CF), sinusitis, conjunctivitis and otitis media
non-typeable H. influenzae colonization starts in the nasopharynx with preferential adhesion to respiratory mucus, non-ciliated cells and damaged epithelium, what surface structures contribute to adhesion?
a) peritrichous pili
b) cell surface adhesions: Hap; Hia; HMW1/2; P2 and P5 porins; OapA OM protein; LPS
Hap adhesion is found in what organisms?
typeable and non-typeable H. influenzae
HMW 1/2 adhesion is expressed by:
non-typeable H. influenzae (but not typable) strains
Hia adhesion is expressed in:
non-typeable H. influenzae strains lacking MHW1/2
Hsf: is a homologue of what?
found in what H. influenzae strains?
homologue of Hia found in TYPEABLE strains
LPS in non-typeable H. influenzae may bind to what receptor?
the PAF (platelet activating factor) receptor
Invasion of non-typeable H. influenzae (Haemophilus) is thought to occur via what 3 possible mechanisms?
a) MACROPINOCYTOSIS (gets cell to engulf it)
b) PARACYTOSIS: passes bt cells to invade sub-epi space (OM protein required)
c) LPS binding to PAF may also facilitate invation
What happens post non-typeable H. influenzae invasion?
TBA (not yet known)
Characteristics of immunity to non-typeable H. influenzae
1) passive immunity from mom only lasts a few months
2) adults are susceptible (not clear that long-term immunity develops to non-typeable strains as in Hib)
4) NO VACCINE currently
Dx non-typeable H. influenzae
demonstrate requirement for X and V factors
typing is not typically informed, unless isolates are from invasive infections (eg meningitis)
Treatment of non-typeable H. influenzae
AMOXICILLIN for localized infections (~20-35% of isoaltes are resistant to amoxicillin)
Alternative: AUGMENTIN (amp + beta lactamase inhibitor (clavunate)) or CEFTRIAXONE
Why can non-typeable H. influenzae infections be persistent and recurrent?
Haemophilus ducreyi
emerging STD in US (chanroid = soft chancre, ragged ulcer on genetalia) more common in Africa and Asia

Haemophilus aegypticus
(Koch-Weeks bacillus) produces a purulant conjunctivities, common in hot climates
Haemophilus parainfluenzae
occasional cause of pharyngitis and bacterial endocarditis
the cause of whooping cough
Bordetella pertussis
Whooping cough characteristics
begins with mild upper respiratory symptoms, followed by acute inflammation of trachea, bronchi and bronchioles with a paroxysmal cough, lasting 1-4 weeks
general properties of Bordetella pertusis
small, gram (-) cocco-bacillus (similar in appearance to H. influenzae
-strict AEROBE
-no requirement for X and V factors (unlike H. influenzae)
-B. pertussis requires VERY FRESH media for growth (so most labs have switched to PCR to detect organism from washes of nasal cavity)
-found only in humans, no known animal reservoir
4 Toxins (virulence factors) expressed by Bordetella pertussis
a) Pertussis toxin
b) Calmodulin-stimulated adenylate cyclase toxin
c) Dermonecrotic toxin
d) Tracheal cytotoxin
Pertussis toxin
(virulence factor expressed by Bordetella pertussis)
ADP-ribosylating toxin that catalyzes transfer of ADP-ribobse from NAD to G-proteins in target cells, eg:
-Inhibiting AC, causing ACCUMULATION of cAMP
-affects PLC and ion channels
combined axn causes lymphocytosis, sensitization to histamine, and enhanced insulin secretion
Calmodulin-stimualted adenylate cyclase toxin
(virulence factor expressed by Bordetella pertussis)
catalyzes the production of cAMP from ATP and is activated by endogenous calmodulin

increased cAMP may impair leukocyte fxn and even cause cell death
Dermonecrotic toxin
(virulence factor expressed by Bordetella pertussis)
(aka mouse lethal toxin or heat-labile toxin)
causes vascular SM contraction resulting in ischemic necrosis of lung tissue
Tracheal cytotoxin
(virulence factor expressed by Bordetella pertussis)
causes ciliostasis, inhibits DNA synthesis and ultimately kills tracheal epithelial cells
Bacterial colonization by Bordatella pertussis is mediated through several factors:
-PILI mediate attachment to ciliated epi cells of upper Resp. tract and decrease ciliary activity
-FHA (pilus-like filamentous humagglutinin)
-PERTACTIN (surface molecule plays role in colonization)
acute local inflammation, + mucous secretions, and patchy ulceration of resp. epi follow. may result in - O2 supply or pneumonia
does Bordatella pertusis invade bloodstream?
How are virulence factors of Bordatella pertussis regulated?
expression of genes coding virulence factors is regulated at TRANSCRIPTIONAL level by "TWO COMPONENT" SYSTEM:
transmembrane sensor protein that responds to host environmental cused to phosphorylate a cyto response regulator protein that binds DNA to activate transcription from appropriate promoters
Clinical features of Bordatella pertussis:
incubation period:
incubation: 7-10 days
CATARRHAL STAGE: runnin nose, low-grade fever, mild occasional cough
PAROXYSMAL STAGE: bursts of counging, high-pitched "whoop" and occasional vomiting, patients can become cyanotic during cough attacks (more frequent at night) *infants don't WHOOP
how has incidence of whooping cough been diminished?
IMMUNIZATION 120,000 cases in 1950 to 2000 by 1997
why has pertussis not been eliminated?
neither immunization nor the disease produces lifelong immunity

old, heat killed vaccine (part of DTP) had potential side effects of encephalopathy and permanant neuro sequelae (led to fewer infants receiving vaccine in 80/90s)

new lower-risk vaccines with specific pertussis antigens (safer and more effective) DTaP
how is Bordatella pertussis transmitted?
aerosolized droplets during sneezing/coughling (very contagious)
what cuases the "Whoop" in whooping cough caused by Bordatella pertussis/
inspiration through a narrowed glottis following, long series of coughts
Why are infants susceptible to whooping cough?
Ab xing placenta not adequate protection for passive immunity
when are Abs in children infected with whooping cough found?
only several weeks after infection
Dx of whooping cough
1) Hx of contact, classic cough, marked lymphocytosis
2) Isolation of organism by naso-pharyngeal swab or cough plate, colonies grow slowly. ID by appearance of colony, gram stain (-) biochem rxns. rapid direct fluorescein labeled Ab test for naso-pharyn specimens
Antibiotic used for Bordatella Pertussis
ERYTHROMYCIN = drug of choice
alternatives: TETRACYLCIN, CHLORAMPHENICOL (not sensitive to penicillin or ampicillin)
B. parapertussis can cause what?
sporadic cases of whooping cough

(similar virulence factors to B. pertussis, but does not carry gene for pertussis toxin)
B. bronchiseptica causes:
respiratory illness in animals and only occassionally in humans

(similar virulence factors to B. pertussis, but does not carry gene for pertussis toxin)
agent of meningococcal meningitis
agent of gonorrhea
common features of MENINGOCOCCUS and GONOCOCCUS
1) Gram (-) diplococci
2) Require rich medium for isolation
3) readily killed by drying, heat, disinfectants
4) no known animal reservoir
5) oxidase (+)
6) both ferment GLUCOSE
7) secrete an IgA1 protease
8) Pili and OMPs may contribute to colonization (&morphology on agar)
9) LOS (contains no O side chains, but still endotoxic and mediates resistance to serum bactericidal activity)
How can one distinguish MENINGOCOCCUS and GONOCOCCUS and non-pathogenic NEISSERIAL species?
SUGAR FERMENTATION TESTS: (glucose, maltose, lactose & sucrose)
N. gonorrhoeae: glucose (+)
N. meningitidis: glucose & maltose (+)
non-pathogenic Neisseria: ferments all sugars except sucrose
LOS, endotoxic component of both N. gonorrhoeae and N. meningitidis (lacks O-side chain seen in LPS)

mediates resistance to serum bactericidal activity
multiplication of MENINGOCOCCUS occurs where?
outside of cells, but not once phagocytized
what does endotoxin from MENINGOCOCCUS do?
damages walls of small vessels
N. meningitidis lives where?
in NASOPHARYNX (carrier rate varies, may be ~5% in general population, but higher in homes where there has been a cause of meningococcal meningitis)
basis of classification of MENINGOCOCCUS into serogroups:
differences in composition of polysaccharide capsule (bacteria of groups A, B, and C are most important)
which is encapsulated MENINGOCOCCUS or GONOCOCCUS?
basis for serotypes within each serogroup:
differences bt outer membrane proteins
appearance of virulent MENINGOCOCCUS colonies
virulent strains are encapsulated and have SMOOTH colonise, on articifical media rough colonies (unencapsulated, relatively avirulent are often produced)
how is MENINGOCOCCUS transmitted
person to person (airborne respiratory droplets)
most often in crowded conditions
MENINGOCOCCUS carrier state may last how long? what symptoms might occur?
from days to many months, in some a mild pharyngitis and fever are all that occur
incidence of severe disease caused by MENINGOCOCCUS:
how does it occur?
1/50,000 per year

bacteria progress from nasopharynx to bloodstream
incubation period of MENINGOCOCCUS
days to a week, most serious consequence = meningitis
MENINGOCOCCUS prediliction for what age group?
<5 years, highest incidence in first year (but after maternal Abs are gone ~ NOT neonates)
most common meningitis in neonates is due to:
group B Strep or E. coli K1
incidence of MENINGOCOCCUS increases by how much in epidemics?
without treatment mortality from MENINGOCOCCUS meningitis is about what?
with treatment it can be less than what?
w/o treatment ~ 85%

w/ treatment <1%
how does MENINGOCOCCUS capsule contribute to pathogenicity?
has antiphagocytic properties

contributes to virulence
MENINGOCOCCUS have organotropism, what does that mean?
localize preferentially in specific organs:
MENINGES (also skin, eyes and lungs)
what is Waterhouse-Friderichsen syndrom?
an uncommon occurence in MENINGOCOCCUS infection: MENINGOCOCCEMIA (may cause adrenal failure, circulatory collapse and shock with rapid death)
If most adults have Abs that confer immunity to MENINGOCOCCUS, why do outbreaks occur?
when diverse groups are brought together, exposure to new serotypes causes outbreaks
Clinical picture of MENINGOCOCCUS
clinical picture of upper Respiratory infection, high fever and signs of meningitis. Patechiae may appear followed by ecchymosis from leaky blood vessels
blood, CSF, nasopharyngeal secretions cultured and examined for gram-neg diplococci.
can further id with:
-sugar fermentation test (4 hrs) or
-latex agglutination test (10mins) based on capsule Ag in CSF
must be prompt, intravenous PENICILLIN = drug of choice
or 3rd generation cephalosporins (CEFTRIAXONE)
Prophylaxis in household MENINGOCOCCUS contacts
RIFAMPICIN (because effeciently secreted in saliva) or CIPROFLAXACIN (bc so potent)
have been tested with moderate success
QUADRIVALENT vaccine available for groups A, C, Y, and W-135. mainly for epidemics or military
Why does MENINGOCOCCUS Type B capsule not immunogenic?
composed of sialic acid, not recognized by C3b complement, thus does not stimulate recruitment of phagocytes
What does lumbar puncture determine when meningitis is indicated?
fever in neonate (suspect group B strep or E. coli K1)
patechial rash with neuro symptoms is indicative of N. meningitidis
How is endotoxin activity different in GONOCOCCUS (vs MENINGOCOCCUS)
not a major factor in disease state caused by GONOCOCCUS
GONOCOCCUS lives primarily where?
# of serotypes of GONOCOCCUS (based on what?)
100+ serotypes
based on antigenicity of pilus protein
GONOCOCCUS transmission:
STD, direct genital contact, resultin in genitourinary tract infection
-rectal and pharyngeal mucosa (non-path Neisseria also found in pharynx) and conjunctiva of newborns
how quickly is infection by GONOCOCCUS is established?
within an hour of exposure
how does GONOCOCCUS invade?
bacteria anchor to surface of epithelial cells using pili
-penetrate through surface cells and reach sub-epi CT w/in a few days
-followed by inflammation and yellow purulent urethral dicharge
incubation period for GONOCOCCUS in
males: symptoms appear in 2-3 days
females: most become symptomatic within 10 days (but a higher percentage of infected females remain asymptomatic)
where might GONOCOCCUS infection spread?
epididymis or prostate in males, to FALLOPIAN tubes in females
what do the Pili of GONOCOCCUS do?
associated with VIRULENCE, promote sticking to epithelial cells and impair phagocytosis by PMN leukocytes (non-piliated strains are not virulent)
probably the 2 most prevalent communicable bacterial diseases of humans?
gonorrhea (WW pandemic)
and infection with venereally-transmitted chlamydia trachomatis
carrier state of gonorrhea
common and asymptomatic (est. 1-10% of infected males are asymptomatic, even higher for females)
-can transmit infection
complications of disseminated gonorrheal disease
a) arthritis-dermatitis syndrome with spread to one or more joints and with skin lesions; joint infection may occur in the absence of prior overt genito-urinary symptoms
b) chronic pelvic inflammatory disease in females
clinical picture of gonorrhea
discharge + hx or exposure
lab dx of gonorrhea
-stained smears of fresh exudate (gram - diplococci within PMN leukocytes)
-culture should be done before Tx is started (oxidase +, gram - diplococci)
-dx might be difficult in chronic cases
treatment for gonorrhea
drug resistance = major problem

IM-Ceftriaxone and 10 day oral tetracycline or doxycycline for chlamydia (assumed present also)

single-dose Pen not recommended
3 major forms of gonococcal resistance:
a) Plasmid-mediated penicillinase producing N. gon (PPNG)
b) Plasmid mediated tetracycline resistant N. gon (TRNG)
c) Chromosome-mediated resistant N. con (CMRNG) {includes Pen, Tet, and some cephalosporins-- related to mutations affecting permeability; level of resistance low; treatment failure rare)
Opthalmia neonatorum
once ause of 50% of blindness in children

Prophylactic Tx of newborn required by law: Tetracycline or Erythromycin ointment (or dilute (1%) silver nitrate)
Immunity against GONOCOCCUS
can be demonstrated after infection, but weak for unknown reasons

hence, repeated attacks are common

high degree of Antigenic variation may contribute to this
Vaccine for GONOCCOCUS
No vaccine yet