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Year : 1991  |  Volume : 57  |  Issue : 1  |  Page : 19-21

Cutaneous manifestations in acute meningococcal meningitis

Correspondence Address:
N Chakrabarty

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Twenty three army recruits with acute meningococcal meningitis were admitted to a military hospital during February-March 1986. Of the 23 patients 11 developed cutaneous lesions, 3 had associated herpes simplex, 6 had arthritis/artharalgia and 3 got conjunctivitis. Maculopapular lesions were the commonest cutaneous manifestation although pinkish macules, purpura and cutaneous vasculitis were also seen. All the patients were treated with intravenous pencillin and other supportive measures.

Keywords: Acute meningococcal meningitis, Cutaneous manifestations

How to cite this article:
Chakrabarty N, Verma A K, Singh G. Cutaneous manifestations in acute meningococcal meningitis. Indian J Dermatol Venereol Leprol 1991;57:19-21

How to cite this URL:
Chakrabarty N, Verma A K, Singh G. Cutaneous manifestations in acute meningococcal meningitis. Indian J Dermatol Venereol Leprol [serial online] 1991 [cited 2020 Oct 24];57:19-21. Available from:

Meningococcal meningitis is a well de­scribed clinical entity. Its neurological mani­festations are largely well understood. At times it may cause cutaneous lesions which may be quite a intriguing. The recent epidemic of me­ningococcal meningitis in an army camp has offered an opportunity to define its pattern. Similar report on the subject has focused our attention on the situation. [1]

  Materials and Methods Top

Twenty three patients of acute meningo­coccal meningitis were studied in detail. Patients were examined in the morning and evening for the development and progress of cutaneous lesions. Haemolgobin, total and differential white cell count, platelet count and blood culture were done in all cases. CSF examination for diplo­cocci, cell counts, biochemistry and culture were done before starting treatment. Smears from skin lesions were stained with Gram stain for the demonstration of gram negative diplococci. Skin biopsy was performed in 4 cases - 2 with maculopapular lesions and 2 with necrotizing ulcers.

  Results Top

All patients were male army recruits aged between 17 and 21 years. Eleven (47.82%) out of 23 developed various types of skin lesions [Table 1], six patients (54.54%) had mixed le­sions with one type predominant, but all the patients having pinkish macules and vasculitis did not have any other lesion. Widespread le­sions on face, trunk, limbs and soles were seen in patients with maculopapular and purpuric lesions.

One case of vasculitis had ulcers on lips, upper and lower extremities and the other one had on buttocks and lower limbs. Initially dark patches appeared on the lips and skin. After 24 to 36 hours bullae appeared on the patches which burst in 2 days leading to shallow ulcers covered with crusts. Cutaneous lesions were observed within a few hours to 3 days and vasculitis from 7 to 10 days.

Twenty one patients (91.3%) had fever but two patients were afebrile. Six patients (26.1%) developed arthritis/arthralgia and three (13.1%) developed conjunctivitis and herpes labialis. One patient (4.4%) had mucous membrane in­volvement.

The fulminating case on admission had few purpuric spots on the trunk and extremities and was afebrile. However he developed generalised purpuric and ecchymotic lesions within 4 hours and expired 2 hours thereafter.

Total white counts varied from 4,500/cmm to 22,100/cmm. Platelet counts were within normal limit in all cases except the fatal case who had a count of 70,000 cmm. CSF cell (Polymorphs) counts varied from 450 to 2100/ cmm, sugar and chloride were decreased and protein was raised in all cases.

The maculopapular lesions showed oedema of epidermis and infiltration of the basal cell layer with polymorphs. The blood vessels of upper and mid dermis were oedematosus and dilated and had perivascular infiltration with polymorphs. Ulcerative lesions showed pro­nounced changes in the blood vessels in both superficial and deep dermis. There was oedema, arteriolar thrombosis, and necrosis associated with intense perivascular and periappendiceal infiltration with polymorphs and mononuclear cells. The lumen as well as the wall of the blood vessels were infiltrated. No gram negative diplococci could be demon­strated in the biopsy specimen. The maculopapular and pink macules disappeared within 6 to 8 days and purpuric spots within 7 to 11 days. The ulcers healed between 9 to 13 days.

  Comments Top

Meningococcal meningitis primarily affects children and occurs frequently in winter [2]. Outbreak in crowded relatively close groups like recruits in a training Camp [3] and in military barracks have been reported from western countries [4],[5] All the patients were from rural areas and had undergone 4 to 10 weeks of military training. These individuals either did not have any resistance against meningococcus or were unusually susceptible to infection.

Cutaneous lesions were seen in 47.82% although higher incidence had been reported. [2] The cutaneous lesions can be divided into pure cutaneous lesions consisting of macules, maculopapules, purpura and ecchymosis.

Cutaneous lesions associated with other complications are cutaneous vasculitis, arthritis and eye lesions.

Association of other skin infection like herpes simplex was seen in patients.

Maculopapular lesions were the common­est and the second commonest were the pinkish macules mostly distributed on trunk, palms and soles. The skin lesions appeared in crops and were polymorphic but one type was predomi­nant. The macular, maculopapular and petechial skin lesions are caused by the damage of small dermal blood vessels either due to direct inva­sion by meningococcus [6] or the effects of en­dotoxin via dermal Schwartzman reaction [7]. Vasculitis is mostly due to immunes complex reaction [8],[9] and skin biopsies showed features of Leucocytoclastic vasculitis.

Fulminating meningococcemia often causes wide spread intravascular coagulation [9],[10],[11] with high mortality and the fulminant case in the present study had all the features of wide spread intravascular coagulation.

Rare complications like gangrene, bacterial endocarditis, pneumonia and nephritis were not seen.

  References Top

1.Ramesh V Remjis, Sehgal SK : Cutaneous in­volvement in acute meningococcemia, Ind J Dermatol Venereol Leprol, 1987; 53 : 264 - 266.  Back to cited text no. 1    
2.Narain JP and Mukherjee D : Va,cine against me­ningococcal disease, Ind pediat, 1985; 22 : 405­407.  Back to cited text no. 2    
3.Weinberg AN and Swartz MN : Gram-negative coccal and bacillary infections : Dermatology in general medicine, 4th ed, Editors, Fitzpatrick TB, Elsen AZ Wolff K, Mc Graw Hill, Newyork, 1987 ; P 212.  Back to cited text no. 3    
4.Roberts SOB and Highest AS : Meningococcal in­fections : Text book of Dermatology, 4th ed, Edi­tors, Rook A, Wilkson DS, Ebling FJ, Oxford Uni­versity Press, Bombay, 1987; 755-756.  Back to cited text no. 4    
5.Buchan PA : An out break of meningococcal dis­ease : Implications for community medicine, NZ Med J, 1984; 97 : 860.  Back to cited text no. 5    
6.Sotto MN, Langer B and Shimozus H : Pathogen­esis of Cutaneous lesions in acute meningococcemia in humans light, immunoflourescent and electron microscopic stud­ies of skin biopsy specimen, J Infect Dis. 1976; 133 : 506 - 514.  Back to cited text no. 6    
7.Davis CE and Arnold L : Role of meningococcal endotoxin in meningoccal purpura, J Exp Med, 1974; 140 : 159 - 171.  Back to cited text no. 7    
8.Greenwood BM, Whittle HC and Brycesson ADM : Allergic complications of meningococcal disease II, Immunological investigations Brit Med J, 1973; 2 : 737 - 740.  Back to cited text no. 8    
9.Dalldrof FG and Jenetter JG : Fatal meningococ­cal septicemia, Arch Pathol. 1977; 101 : 6-9.  Back to cited text no. 9    
10.Mc Gehee WG Rapaport SI and Hjort PF : Intra­vascular coagulation in fulminant meninge coccemia, Ann Int Med. 1967; 67 250 - 259.  Back to cited text no. 10    
11.Winkelestein A, Songster CL and Caras TS : Fatal meningococcemia and disseminated intravascular coagulation, Arch Int Med, 1969; 124 : 55-59.  Back to cited text no. 11    


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