1. KURSK STATE MEDICAL UNIVERSITY
Department of Infectious diseases.
1
Suhadini Kulatunga
Group No. 4
6th
year- 1st
semester
Medical Faculty
KURSK - 2014

2.  A recent study of children aged 16 years or
younger with meningococcal disease found
that classical signs such as haemorrhagic
rash, meningism and impaired
consciousness did not tend to appear until
after 13 to 22 hours.
 More nonspecific features such as leg pain,
cold hands and feet and abnormal skin colour
appeared much earlier with a median onset
of 7-12 hours.

3.  These earlier features are therefore very
important in early diagnosis and therefore in
the earlier initiation of potentially life-saving
treatment.[7]
 The same study divided the clinical features
into early, classic and late features, as follows
below.

4.  Early features:
 Leg pain.
 Thirst.
 Diarrhoea.
 Abnormal skin colour.
 Breathing difficulty.
 Cold hands and feet.

5.  Classic features (develop later):
 Haemorrhagic rash: Early on, the rash may be
nonspecific or absent. By the time the typical
purpuric or petechial rash develops, the patient is
gravely ill. Therefore, don't wait for the classic
rash before admitting the patient.
 Neck pain or stiffness.
 Photophobia.
 Bulging fontanelle.

6. Late features:
 Confusion or delirium.
 Seizures.
 Unconsciousness.

7. There can be,
 suppurative
 allergic (cutaneous vasculitis, athritis)
 neurologic complications.
But, the main complication is acute
adrenal insufficiency(WhF syndrome) due
to effect on adrenal glands, which can
leads to death.

8.  Waterhouse–Friderichsen syndrome (WFS) or
hemorrhagic adrenalitis or Fulminant
meningococcemia, is defined as adrenal gland
failure due to bleeding into the adrenal glands,
caused by severe bacterial infection (most
commonly the meningococcus Neisseria
meningitidis).
 Another definition is; acute and severe
meningococcemia with hemorrhage into the
adrenal glands

9.  Occur usually in infants or children younger than
10, occasionally in adults.
 The Waterhouse-Friderichsen syndrome may
develop in 10 to 20 percent of children with
meningococcal infection.
 This syndrome is characterized by:
Large petechial hemorrhages in the skin and mucous
membranes
Fever
Septic Shock
Disseminated Intravascular Coagulation

10.  Onset of the syndrome is dramatically
sudden.
 Nonspecific with fever (initially moderate,
then high), rigors, cough, vomiting, and
headache. Dysphagia, atrophy of the
tongue, and cracks at the corners of the
mouth are also characteristic features.

11.  Soon a rash appears; first macular, not much
different from the rose spots of typhoid, and
rapidly becoming petechial and purpuric with a
dusky gray color and sometimes large purpuric
cutaneous haemorrhages often followed by
necrosis and sloughing.
 Exhibits a cyanotic pallor, patients are alert but
pale with coldness and cyanosis of the
extremities due to generalized vasoconstriction.
 Hypotension and rapidly leads to septic shock.

16.  There is hypoglycemia with hyponatremia and
hyperkalemia, and the ACTH stimulation test
demonstrates the acute adrenal failure.
 Leukocytosis but if leukopenia is seen, it became a very
poor prognostic sign.
 C-reactive protein levels can be elevated or almost
normal.
 Thrombocytopenia , with alteration in prothrombin time
(PT) and partial thromboplastin time (PTT) suggestive of
diffuse intravascular coagulation (DIC).
 Acidosis and acute renal failure can be seen as in any
severe sepsis.
 Meningococci can be readily cultured from blood or CSF
or smears of cutaneous lesions.

17.  The treatment is as that for meningococcal infection,
fulminant meningococcemia is a medical emergency and
needs to be treated with adequate antibiotics as fast as
possible.
 Ceftriaxone is an antibiotic commonly employed today.
Ceftriaxone is a third-generation cephalosporin
antibiotic. Like other third-generation cephalosporins, it
has broad spectrum activity against Gram-positive and
Gram-negative bacteria. In most cases, it is considered
to be equivalent to cefotaxime in terms of safety and
efficacy.
 Benzylpenicillin was once the drug of choice with
chloramphenicol as a good alternative in allergic
patients.

18.  Addition of adrenal support with
hydrocortisone, given intravenously in a dose
of 200 mg per square metre body surface per
four hours. Hydrocortisone can sometimes
reverse the hypoadrenal shock.
 Hypovolaemia is treated with colloids,
dopamine and coagulation factors.
 Sometimes plastic surgery and grafting is
needed to deal with tissue necrosis.

19.  Routine vaccination against meningococcus is
recommended by the Centers for Disease Control
for;
1. All 11–18 year olds
2. People who have poor splenic function (who, for
example, have had their spleen removed or who
have sickle-cell disease which damages the
spleen)
3. Who have certain immune disorders, such as a
complement deficiency.

20.  Shock, extensive haemorrhage within the skin
and fall into coma.
 Death usually after a few hours, adrenal
insufficiency being the immediate cause.
 Patients who recover may suffer from extensive
sloughing of the skin and loss of digits due to
gangrene.
 MENINGITIS GENERALLY DOES NOT OCCUR.

21.  A 4 year old, previously healthy boy has a short history
of cough and malaise, which had also affected other
family members. On attending the accident and
emergency department he was found to have a fever of
39°C, an erythematous, blanching skin rash, mild
pharyngitis, and cervical lymphadenopathy. A diagnosis
of viral infection was made and he was sent home. Five
days later his condition worsened, with shock and a
confluent haemorrhagic rash. His temperature remained
high and he was noted to be tachypnoeic. Clotting
parameters, including D dimers, were abnormal and his
platelet count was low, consistent with disseminated
intravascular coagulation. Despite resuscitation, he died.
CLINICAL SCENARIO

22.  At necropsy there were signs of upper airway
infection and bilateral basal
bronchopneumonia, with consolidation.
Massive haemorrhage was present in the right
adrenal gland, but not the left. There was no
evidence of meningitis or haemorrhage
elsewhere. Microvascular thrombi were not
seen on histology.

23. The cause of death was given as acute
adrenal haemorrhage as a result of
meningococcal septicaemia. Family
members were given antibiotic
prophylaxis and the consultant in
communicable diseases was informed.
Blood cultures and skin scrapings taken
before death were unhelpful.

24.  Blood and pleural fluid taken aseptically at
necropsy grew a heavy pure growth of β
haemolytic streptococcus group A. Other
surface swabs also grew streptococcus group
A. The isolates typed as the M1 strain and
contained genes for toxins A and B (the cause
of streptococcal toxic shock syndrome).
Polymerase chain reaction for meningococcal
DNA was negative.

25. Thank you. 