ETIOLOGY— SYMPTOM A TOLOGY 



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It lives in the naso-pharynx of healthy people whose opsonic index for the 

 germ is abnormally high, and it passes from these carriers to healthy people, 

 who may, according to their resistance, become carriers, temporary or per- 

 manent, of the germ, or victims to the disease. 

 Its aetiological relationship depends upon : — 



1 . Its presence in all cases of the true epidemic disease. 



2. Its pure culture from these cases, and the reproduction of the disease in 

 monkeys by inoculation of cultures. 



3. The sera of persons suffering from the disease can agglutinate and give 

 positive complement-fixation with meningococci obtained Irom other patients. 



4. It produces a protective mechanism in carriers which is lacking in sus- 

 ceptible persons. 



i-^f Pathology. — The meningococcus appears to enter the blood via the mucosa 

 of the nose and air sinuses, but it quickly leaves this fluid and enters the 

 cerebro-spinal fluid via the choroid plexuses, and perhaps by other routes. 

 Arrived in the cerebro-spinal fluid, it causes a cerebro-spinal meningitis. 



Morbid Anatomy. — In fulminating infections meningitis is absent, ard little 

 is to be seen beyond haemorrhages in various parts; while the cerebral vessels 

 are intensely congested and the perivascular subarachnoid spaces show 

 scattered patches of pus. 



In ordinary fatal cases there is considerable amount of purulent exudate 

 in the subarachnoid, the most intense being over the uppermost part of the 

 vertex. 



In chronic cases there may be but little sign of pus and no vascular conges- 

 tion, but the ventricles are distended by a quantity of fluid, the pressure of 

 which causes flattening of the convolutions. 



Symptomatology — General Remarks. — As seen in the tropics the disease is 

 of sudden onset, with or without a rigor, but with marked headache, 

 vomiting, and fever. The next day there is often some remission in the 

 symptoms, but with stiffness in the muscles of the neck and sometimes 

 Kernig's sign. On the third day vomiting returns, with headache and a 

 condition of resistant stupor, retraction of the head and Kernig's sign, and 

 from this time onwards the symptoms in fatal cases go from bad to worse, and 

 the patient dies within four to six days of the commencement of the attack. 

 If the case is to recover, the symptoms begin to abate about the seventh to 

 eighth day, the temperature falls to normal, and convalescence begins. 



Slightly fuller details of this usual type may be given. 



Incubation Period. — Judging by persons who have left an uninfected area, 

 visited an infected and returned to the uninfected area, the incubation period 

 is short, varying from two to five days, and more usually about four days; 

 but there are obvious fallacies in this calculation, and it may perhaps be better 

 to admit that the length of time of the incubation period is only approximately 

 known. 



Attack. — The onset is sudden and may begin with a rigor in an adult or 

 convulsions in a child, but these may be absent. The patient feels very ill 

 and exhibits three so-called cardinal symptoms — viz., fever rising to 102° to 

 104° F., vomitihg, marked headache, which may be associated with severe 

 giddiness. As the first day progresses there may be pain and stiffness in the 

 neck and some retraction of the head. If the blood be examined at this early 

 stage of the disease, only a moderate amount of leucocytosis, amounting to 

 about 10,000 cells per cubic millimetre, will be found, while the differential 

 count will show an enormous preponderance of polymorphonuclear leucocytes, 

 amounting to over 90 per cent, in some cases. 



Blood cultures are usually very successful at this early stage of the disease, 

 but not later in uncomplicated cases. By direct examination of blood films 

 Gram-negative diplococci can be seen in about i per cent, of the polymorpho- 

 nuclear leucocytes examined, while a very few similar organisms may be 

 found outside the cells. Even at this early stage of the disease the cerebro- 

 spinal fluid is usually more or less turbid, and shows a variable number of 

 white cells, which may amount to 20,000-30,000 per cubic millimetre, and of 

 which some 98 per cent, are polymorphonuclear leucocytes, while the remain- 



