Epidemic meningitis and other clinical forms of meningococcal infection.

Question 1

what is the ETIOLOGY OF EPIDEMIC MENINGITIS ?

Answer 1

Neisseria Meningitidis

Question 2

CHARACTERISTICS OF NEISSERIA MENINGITIDIS?

Answer 2

gram-negative aerobic diplococcus

13 serogroups,
based on polysaccharide capsule, but just
six of these—A, B, C, X, Y, and W (formerly W135) are the majority

//beneath the capsule,
they are surrounded by an outer phospholipid
membrane containing lipopolysaccharide (LPS,
endotoxin
) and outer-
membrane proteins

gram Diplococcus 
Facultative intracellular
Aerobe
Bacterial growth on culture medium is usually challenging
SELECTIVE MEDIUM: THAYER-MARTIN AGAR
MALTOSE AND GLUCOSE FERMENTER

=========
VIRULENCE FACTOR

IgA1 protease

Capsular polysaccharides

Lipooligosaccharide (LOS): serum LOS levels correlate with severity of symptoms

Adhesins: pili and opacity proteins facilitate nasal colonization → systemic infection

Question 3

EPIDEMIOLOGY OF NEISSERIA MENINGITIDIS?

Answer 3

obligate human pathogen with no other reservoir and are most commonly found within the nasopharynx

worldwide disease, with 10% mortality rate

//patterns of disease: 
epidemic (small clusters of cases) //

endemic, and sporadic = infection is constantly
maintained at a baseline level in a geographic area without external
inputs)

sub-Saharanmeningitis belt of Africa
, where tens to hundreds of
thousands of cases exist

most cases are
sporadic

Question 4

RISK FACTORS FOR EPIDEMIC MENINGITIS ?

Answer 4

age
peak incidence in the first year of life due to absence of
specific adaptive immunity and very close contact with colonized
individuals
-
second peak of disease occurs in adolescents and young adults (15–25 years of age) in Europe and North America
-
hosts susceptibility:
cigarette smoking
-
winter or the dry season

=========

newborns in endemic regions usually have passive immunity from the mother
for up to 3m
-
age group: 6m of age due to loss of maternal Abs

teenagers & young adults
-
risk factors: asplenia, complement deficiency, exposure to cigarette smok

Question 5

what is the TRANSMISSION OF MENINGOCOCCUS ?

Answer 5

via respiratory droplet

Question 6

what is the PATHOGENESIS OF MENINGOCOCCUS?

Answer 6

meningococcus colonises the nasopharynx
sometimes asymptomatic due to the protective antibodies

adherence to the mucosa facilitated by the pili which helps to promote the formation of meningococcal micro colonies and biofilms

high exposure - colonisation usually brief leading to invasion

once they have acess to submucosa they are able to scavenge essential nutrients like iron and evade the host immune response

once the organism is inside the blood stream it also RELEASES THE ENDOTOXIN FROM
LIPOOLIGOSACCHARIDE

the meningococcal capsule avoid the phagocytosis

they spread through the blood stream into the meninges
- into choroid plexus - pus formation - increase intracranial pressure

inflammatory cytokines are induced

severity of disease depends on he level of endotoxin release - the endotoxin and and cytokines causes widespread endothelia injury - leads to increased vascular permeability - macroscopic porteinurea

capillary leak syndrome - hypovolemia , tissue edema and pulmonary edema

Question 7

what are the 4 CLINICAL MANIFESTATION OUTCOMES OF EPIDEMIC MENINGITIS

Answer 7

1. Asymptomatic carrier
2. Acute purulent infection
3. Fulminant meningocemia
4. Meningococcemia

Question 8

what is the INCUBATION PERIOD OF MENINGOCOCCUS ?

Answer 8

1-10 days

Question 9

what are the CLINICAL FEATURES OF MENINGOCOCCUS ?

Answer 9

25 percent asymptomatic - due to antibody production lining the nasopharynx

===============

meningococcemia
and acute meningitis

non blanching rash / petechia or purpura - which is often accompanied by fever

in severe cases - large purpuric lesions - purpura fulminans

some patient may not develop a rash

//these skin lesions are widespread endothelial necrosis and occlusion of all vessels in the subcutaneous tissue? //

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meningitis 
triad 
1) headache 
2) fever 
3) vomiting 

NECK STIFFNESS , KERNIG SIGN, BRUDZINSKI SIGN

drowsiness and confusion

photophobia

babies maybe positive LESAGUE SIGN - increased intracranial pressure will resulting in bulging fontanelle , poor feeding and crying

muscle and joint pain
hyperasthesia

in infats - fever could be absent !!
however may show loss of appetite , diarrhea , weight loss , seizure

up to 5yrs meningococcal meningitis = irritability , lethargy , committing , SEIZURES MOST PROMINENT FEATURE OF THIS DISEASE AT THIS AGE

Question 10

what is the CLINICAL MANIFESTATION OF ACUTE MENINGOCCOCEMIA AND FULMINANT DISEASE ?

Answer 10

starts with fever and rash - maculopaplar rash becomes more hemorrhagic in character and then later necrotic

rash characteristics

1) central necrosis
2) star shaped
3) affects lower legs asymmetrically - buttocks - abdomen - trunk - upper extremities –and then face

after 4-6 hrs of progression vomitting , loss of appetite

after 8 hrs - leg pain , cold hands and feet
aboard breathing

shock - tachycardia cardia , poor peripheral perfusion , tachypnea, oliguria
multi organ failure
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waterhouse friderichsen syndrome

endotoxins triggers the coagulopathy - leading to DIC - bilateral hemorrhagic destruction of the adrenal gland - waterhouse fridrichsen syndrome

Question 11

DIAGNOSIS OF MENINGOCOCCUS?

Answer 11

severe form, must be made by clinical appearance: rash and
status, because time must not be lost!!
It can lead to death within
hours

(CSF) is sent to the laboratory as soon as possible for analysis -
diagnosis is suspected, when there is evidence of Gram-negative diplococci

gold standard of diagnosis is microbiological isolation of N. meningitidis from a sterile body fluid specimen, which could be CSF or blood ,
GROWN IN CHOCOLATE AGAR PLATE, BUT ALSO ON THAYER-MARTIN AGAR.

-
PCR assay for DNA identification

Question 12

what is the TREATMENT FOR NEISERIA MENINGITIS ?

Answer 12

Early diagnosis to decrease mortality

early recognition of fever and headache with a rash -> antibiotic treatment, rapid transportation hospital, and stabilization in an
intensive care unit

1. Antibiotic Therapy:
Penicillin,
has good CNS penetration
-
alternative:
cephalosporins third generation - ceftriaxone and
cefotaxime
- or vancomycin
-
for acute disease: moxifloxacin, chloramphenicol

-
In increased ICP -> dexamethasone + mannitol
-
treat shock and DIC with volume expansion, ICU monitoring, inotropic
support, management of raised intracranial pressure, and the
correction of hemostatic metabolic abnormalities

========

waterhouse fridrichsen syndrome - iv steroids immediately

Question 13

what is the PREVENTION METHODS OF NEISSERIA ?

Answer 13

post exposure Chemoprophylaxis :
rifampin,
ceftriaxone, ciprofloxacin, or azithromycin
when in contact with meningococus

=========
Immunoprophylaxis
: immunization is the only rational approach to
prevention at a population level
-
1. MENINGOCOCCAL POLYSACCHARIDE VACCINES
-
-> contain the antigens in the outer polysaccharide or sugar capsule
that surrounds the bacterium
-
local reactions may occur, but rarely severe adverse effects
-
2. meningococcal conjugate vaccine or MCV4