Meningitis Cerebrospinal fever
Meningitis caused by many M.O but the commonest type of meningitis is bacterial meningitis which caused primarily by 3 M.O: 1. Meningo-coccal meningitis (Neisseria meningitidis). 2. Streptococcus pneumoniae. 3. Haemophilus infuenzae type b (Hib). Those m.o constitutes 80-90% of all types of meningitis, 5-10% caused by TB meningitis, the rest of meningitis caused by other pyogens, bacteria, virus & even fungi.Meningococcal meningitis
CFR: Before Rx > 50 %.After Rx → 8 – 15 %.In addition 10-20 % of survivors will suffer from long-term squeal as epilepsy, hearing loss (once cranial nerves damage occur, it never return to normal). So the earlier the diagnosis, the least the complications and the better the prognosis.Diagnosis: Clinical picture. CSF examination and culture (lumber puncture). Blood culture. 2. Infectious agent: Neisseria meningitidis, 12 sero-groups, only 5 of which (A, B, C, and recently W-135 and X) can cause epidemics. These are important in prevention, control and vaccine preparation.
3. Occurrence: Distribution world-wide. Disease occurring sporadically, some time endemic, and in small outbreaks in most part of the world.
3. Occurrence: continueIn tropical Africa, the disease usually occur in dry season, & there is what is called “meningitis belt” in sub-Saharan Africa because of frequent epidemic waves (every 7-14 years) that have been occurring in that region with high rate of carriers up to 50% of population during epidemics and 25% during sporadic, including 25 African countries; which stretches from Senegal in the West to Ethiopia in the East (sero-group A).Last epidemic in 2009 (88 000 cases).
4. Reservoir: Humans. No animal reservoir. 5. Mode of transmission: Direct contacts including respiratory droplets from nose and throat of infected people. Up to 10-20% of people may be asymptomatic carrier with nasopharyngeal colonization. Less than 1% of them progress to invasive disease.
5. Mode of transmission: continue Polluted fomites transmission is insignificant i.e. indirect transmission is not an important route (since the M.O is delicate one and easily destroyed by U.V light and heat). Large population movement and overcrowding facilitate the circulation of virulent strains.
6. I.P: 2 – 10 days, commonly 3 – 4 days.7. Period of communicability: Without treatment until the M.O is no longer present in nose and mouth discharges.But usually disappear from nasopharynx within 24 hours after start antibiotic treatment.8. Susceptibility:Susceptibility to clinical disease is low and decrease with age; this induces a higher ratio of carriers to cases.There is group-specific immunity of unknown duration follows even sub-clinical infections.
9. Method of control: A) preventive measures: Public health education about the need to reduce droplet infection. Avoid overcrowding in living quarters, work places as school, camps & ships. Vaccines: quadrivalent ACYW-135 vaccine (no vaccine effective against group B meningococci). This vaccine is safe, effective in adults & children above 2 years, but do not elicit long term protection particularly in children under 5 years of age. (so not used in routine childhood immunization program).
Quadrivalent A,C,Y,W-135 used in: Outbreak control. High risk groups:- Hajj pilgrims, military groups. Travelers to countries where disease is epidemic. From December 2010, a new meningococcal A (MenAfriVan) conjugate vaccine is being introduced nationwide in African countries. Highly effective for adults and children, low price and long term protection.
B) Control of patient, contacts and environment: 1. Reporting: class II. 2. Isolation: respiratory isolation, usually at hospital for 24 hours after start RX. 3. Concurrent disinfection & terminal disinfections. 4. Quarantine: not applicable.
B) Control of patient, contacts and environment: continue 5. Protection of contacts: Daily surveillance of house-hold contacts for early signs and symptoms of illness. Prophylactic chemotherapy for house contacts, close friends in schools (not all the class), military personnel, young children in day-care. By using rifampicin (300 mg twice daily for 2 days in adults), or ciprofloxacin (500 mg, single dose). Generally immunization not recommended. 6. Investigation of contacts and source of infection: None.
7. Specific Rx: Penicillin in high doses given parenteral is the drug of choice; ampicillin and chloramphenicol are also effective. Treatment should be start as early as possible, even before identification of M.O. The patient should be given rifampicin prior to discharge from hospital to ensure elimination of the M.O.
C- Epidemic measures: Careful surveillance, early diagnosis, and immediate treatment of suspected cases. Immunization campaign must be implemented for children 2-5 years of age if an outbreak occur in a large institution when group A,C,Y,W-135 are responsible. Reduce overcrowding & ventilating living quarters. Mass chemoprophylaxis is usually not effective in controlling outbreaks, except for small population (e.g. a single school) given to all members at the same time [sulfadiazine 0.5 gm for children, 1 gm for adult twice daily for 2 days]. Rifampicin not recommended as mass chemoprophylaxis.
Haemophilus meningitis
It was the most common bacterial M. in child aged 2 months – 5 years before Hib vaccine wide spread.Infectious agent: Haemophilus infuenzae type b (Hib).Occurrence: worldwide, 2 months – 3 years, unusual > 5 years.Reservoir: Humans6.7.8. I.P and others: same.9. Method of control: A) preventive measures:Vaccines: routine childhood immunization (introduce in Iraq since end of 2011):1st dose → age 2 months (Hib+DPT+HB)2nd dose → age 4 months (Hib+DPT)3rd dose → age 6 months (Hib+DPT+HB)Booster → age 18 months (Hib+DPT)B) Control of patient, contacts and environment:5. Protection of house contacts: By using rifampicin.7. Specific Rx: Ampicillin parenteral is drug of choice, chloramphenicol, ceftriaxone are also effective. The patient should be given rifampicin prior to discharge from hospital.
Pneumococcal meningitis
High CFR, fulminating disease (see Pneumonia). Vaccination is the mainstay of prevention. In USA pneumococcal vaccine in routinely recommended for below 2 years children.Viral meningitis
Infectious agent: a variety of viruses [mumps virus in 25% of cases……..]Recovery usually complete.Dysentery
Amoebic BacillaryDx: GSE Cyst or trophozoid microorganism and RBC inside (fresh stool)
Infectious dose: large no.Low (10 – 100 S.) Aetiology: E. histolytica Group A: S. dysenteriae 15 sero Group B: S. flexneri 8 Group C: S. boydii 20 Group D: S. sonnei 1Transmission: feco-oral (cyst) feco-oral (direct, indirect) sexual (oral-anal)
Reservoir: Man Man
Occurrence: Young adults 2/3 of cases in < 10 years rare <5 Y, very rare < 2 Y rare < 6 months infants
Epidemics: Rare (sporadic cases) Occur in epidemics (S. dysenteriae-1)
Amoebiasis
Shigellosis
Clinical: chr., not bedridden Acute, bedridden, toxemic not toxic, no tensmus tensmus, cramp, vomiting
Complication: amoebic liver S. dysenteriae-1 → convulsion, abscess, amoboma, anal lesion toxic megacolon, perforation, hemolytic uremic syndrome. S. flexneri → reactive arthropathy (Reiter syndrome) in HLA: B27 I.P: Variables (days, months,short 1 – 3 daysyears) usually 2-4 weeks CFR: Low High in complicated cases (20% in hemolytic uremic syndrome in hospital).
Amoebiasis
Shigellosis
Prevention (same as typhoid fever) 1- Health education. 2- Personal hygiene. 3- Sanitary disposal of feces.
Amoebiasis
Shigellosis
Vaccination: None No commercial vaccine is available.
Rx: Flagyl + tetracycline Self-limiting within 4-7 day.or Tinidazol Mainly supportive (fluid replacement)if abscess→ surgery. Methiprine → ↓duration &severity of disease (ampicillin or ciprodar). Anti-motility is contra indicated.
Cancer and Infections
Infectious agents are now recognized as a causes of or risk factor in malignancy diseases A. Viruses:DNA viruses HBV → hepatocellular Ca.EBV → nasopharyngeal Ca., Burkitt’s lymphoma and Hodgkin and non-Hodgkin lymphomas.HPV (16, 18) → Ca. cervix, vulva and anus.HHV-8 → Ca. cervix and Kaposi’s sarcoma. (Human Herpes-8)A. Viruses:RNA viruses HCV → hepatocellular Ca.HIV → Kaposi’s sarcoma and non-Hodgkin lymphomas.HTLV-1→lymphatic H malignancy (leukemia/lymphoma). (Human T-cell Lymphotrophic V.)