Communicable diseases Essen simple books

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1. COMMUNICABLE DISEASES

2. DEFINITION Communicable disease is an illness that occurs due to a specific infectious agent or its toxic products capable of being directly or indirectly transmitted from man to man,animal to animal or from the environment to man or animal Communicable or infectious diseases are diseases that can spread ,directly or indirectly from one person to another.

3. CAUSES Pathogenic microorganisms such as Bacteria Viruses Parasites fungi .

4. TUBERCULOSIS Definition: Is a Systemic , Chronic, communicable disease caused by a gram negative bacillus called Mycobacterium Tuberculosis Causative organism: Mycobacterium Tuberculosis.

5. Mycobacterium tuberculosis

6. Mode of transmission : The disease is spread through droplets containing Mycobacteria, released through coughing, sneezing, spitting by a sputum positive infected person in close contacts with vulnerable hosts. Incubation period: 2 to 12 weeks

7. Types: Pulmonary tuberculosis whereby the lungs are infected. Extra pulmonary tuberculosis in which other parts of the body other than the lungs are infected.

8. E pidemilogy Tuberculosis is endemic in most developing countries including sub-Saharan Africa. According to WHO if TB control is not strengthened, between 2000 and 2020 over 1BILLION people will be infected , 200 MILLION will develop clinical disease and 35MILLION will die

9. Pathophysiology of TB TB infection begins when a susceptible host inhale mycobacteria and becomes infected. The bacteria are transmitted through the airways to the alveoli where they are deposited and begin to multiply (PTB ). The bacteria can also be transported through the lymphatic system and bloodstream to other parts of the body such as kidneys,bones,cerebral cortex e.t.c hence extra pulmonary TB

10. The body’s immune system respond by initiating an inflammatory reaction,the phagocytes,neutrophils and macrophages engulf much of the bacteria while the TB-specific lymphocytes lyse(destroy)the bacilli and normal tissue . The tissue reaction results in accumulation of exudate in the alveoli causing bronchopneumonia. Initial infection usually occurs 2 to 10 weeks after exposure . Granulomas (new tissue mass of live and dead bacilli)are surrounded by macrophages which form a protective wall,they are then transformed into a fibrous tissue mass ,the central part called a ghon tubercle .

11. The material (bacterial and macrophages) become necrotic forming a cheesy mass,which calcifies and forms a collagenous scar . At these point ,the bacteria become dormant and there is no further progression of active disease. After initial exposure and infection, active disease may develop because of A compromised or inadequate immune system response. Active disease may also occur with reinfection and activation of dormant bacteria.

12. In this case ,the ghon tubercle ulcerates, releasing the cheesy material into the bronchi,The bacteria becomes airborne resulting in further spread of the disease,then the ulcerated tubercle heals and forms scar tissue

13. Tuberculosis

14. Clinical manifestation:

15. Symptoms of Extra pulmonary TB ORGAN AFFECTED SYMPTOMS Kidney Blood in urine Meninges Headache and confusion Spine Backache

16. Diagnosis A complete history taking Physical examination to assess patient’s general health e.g. weight loss Sputum smears and Culture of acid fast bacilli(AFB) using fluorescence microscopy (more sensitive)or Ziehl Neelsen staining(Obtain early morning sputum ). Chest x-ray : reveals lesions in the upper lobes. Tuberculin skin test( mantoux test)-reveals if patient has been exposed to mycobacterium tuberculosis bacteria.

17. Specific management Specific management implies the following Case finding. Correct classification of patients for proper treatment.

18. Case definition New case Patient never had treatment for TB before or had anti TB drugs < 1 month Relapse Patient was previously treated and declared cured or treatment completed and who now has PTB +ve Treatment after failure Patient is started on re-treatment after failing previous treatment Treatment after default Patient with PTB+ve who was on treatment but interrupted treatment for>2 months Transfer in Pt transferred from another centre to continue treatment Others Any TB pt that does not fit in one of the above definitions

19. Anti TB drugs Rifampicin (R) Ethambutol (E) Isoniazid (H) Pyrazinamide (Z) Streptomycin (S)

20. Doses Isoniazid (H) 1Omg/Kg (range 10-15mg/Kg),maximum dose 300mg/day. Rifampicin(R) 15mg/kg(range 10-20 mg/kg) maximum dose 600mg/day . Pyrazinamide (Z) 35mg/kg(30-40mg/kg Ethambutol (E) 20mg/kg (15-25 mg/kg) Streptomycin(S) 15 mg/kg IM,no more than 1g/day.

21. Drug dose course CATEGORY TB PATIENTS DAILY TB TREATMENT INITIAL PHASE CONTINUATION PHASE I All new AFB+ve TB All severe EPTB 2HRZE 4HR II Relapse, treatment failure and AFB+ve after default 2HRZES + 1HRZE 5HRE III All new AFB-ve TB All non severe EPTB Children with TB except for those in I and II 2HRZE 4HR

22. Summary of antiTB treatment regimen Intensive Phase + Continuation Phase 2 months of intensive phase 4 months of continuation phase

23. NOTE: Directly Observed Treatment (TB-DOTs) The patient must be hospitalized during the intensive phase (2months) after which sputum smear should be done before proceeding to the continuation phase. Once patient has been on TB treatment for 2 weeks,they are safe to interact .

24. Follow up Care: Normally monthly follow up visits. Treatment adherence. Monitoring and record keeping. Complications. Side effect of the drugs. Interactions with other drugs

25. Health messages All TB patients are to be advised the following NOT TO SPIT ANYWHERE CARELESSLY! Use container with a cover for spitting Dispose sputum carefully in pit latrine or fire . Wash and sterilize container in the sun. Eating tools dried up in the sun.

26. Recommendations for preventing transmission of TB in health care settings Early identification and treatment of persons with active TB. Maintain high index suspicion for TB to identify cases rapidly. Promptly initiate effective multi drug anti -TB therapy based on clinical and drug resistance surveillance data .

27. 2 . Prevention of spread of infectious droplet nuclei by source control methods and by reduction of microbial contamination of indoor air by doing the following : Isolate all patients who are suspected or confirmed to have active TB and who may be infectious. Persons entering the isolation room should use disposable particulate respirators or masks . Continue isolation until there is clinical evidence of reduced infectiousness .

28. example Cough has substantially decreased. Number of mycobacterium tuberculosis on subsequent sputum smears is decreasing . Surveillance for TB transmission Maintain surveillance among the following: Health care workers by routine mantoux tests TB cases among patients

29. If drug resistance is suspected, continue precautions till sputum smear is negative for AFB.

30. Role of N/M Heath education. Monitoring treatment adherence (TB-DOTs). Record keeping and notification BCG immunization. Surveillance for TB through screening

31. Prevention Proper sputum disposal Cough and sneezing etiquette BCG immunization

32. LEPROSY Definition: Chronic infectious disease of human beings with a predilection to the superficial nerves and skin. Causative organism : Mycobacterium Leprae . Incubation period: 6 years (range 1-12 yrs)

33. Mycobacterium Leprae

34. Cause/Predisposing Factors It is very likely that Leprosy is transmitted by sneezing, coughing spitting, and unhygienic nose cleaning habits. Opportunity for contact e.g. overcrowding. Unlikely penetration of the mycobacterium leprae through intact skin . It is not a fatal disease but it is a crippling disease. The mycobacterium leprae multiplies in macrophages of the skin and nerve fibres(Schwann cells ). Schwann cells are glial cells that wrap around the nerve fibre in the peripheral nervous system.

35. The organisms multiply best in the cooler parts of the body so that the skin of the face and limbs and their more superficial nerves are invaded first . Leprosy currently 1 MILLION PEOPLE in Africa, Asia, South America and the Pacific . Between 2 and 3 MILLION PEOPLE have been left permanently disabled because of Leprosy.

36. Pathophysiology of leprosy An inflammatory reaction occurs as a result of the mycobacterial invasion of these structures. A small vague hypo pigmented macule appears (indeterminate )as there is no indication as to why it will develop . Most indeterminate lesions heal spontaneously ,many are never noticed and those which do not heal may develop into tuberculoid ,borderline or lepromatous leprosy . The development of different forms of leprosy depends on the host’s cellular immunity This depends on the ability of the host to develop cellular immunity against mycobacterium leprae.The following can occur ( hence the different types of leprosy)

37. Types of leprosy Tuberculoid leprosy There is a strong focal cellular reaction to the bacteria. The intracutaneous nerves are infilterated by lymphocytes and completely destroyed resulting in sensory loss(anaesthesia.) AFB are usually few or absent Invasion of peripheral nerve trunks is early

38. Clinical manifestation: The skin patches are few in number, raised or flat and asymmetrically distributed, with well defined edges .

39. There is little sweating (dry surface) Loss of hair Loss of sensation Often central healing Hypopigmentation Paralysis-nerves are always involved in the early course of illness Skin smear is usually negative

40. TUBERCULOID LEPROSY

41. Lepromatous leprosy There is little cellular response Very few lymphocytes are found Nerve twigs are not infilterated by lymphocytes Masses of bacilli are seen Damage to peripheral nerve trunks is late

42. Clinical manifestation: Skin lesions are many e.g. nodules ,raised patches ,flat red patches. Other organs involved eyes, hands ,feet and testicles .

43. Many nerve trunks are involved late in the disease. Smears are strongly positive.

44. Borderline leprosy Shows features of both the tuberculoid type and lepromatous type. Lymphocytes are present. There is slight infiltration of the fine nerve twigs. AFBs occur in moderate numbers Due to the instability of the type ,widespread damage to peripheral nerves may occur.

45. Clinical manifestation: Skin lesions are very many. Edges may be well defined. Outline often irregular, raised or flat. Some loss of feeling . No healing centre. Symmetrical. Many nerve trunks are often involved fairly early. Smears range from negative to positive.

46. Diagnosis Demonstration of one or more of the following : Hypo-pigmented skin patches with loss of sensation Abnormally large peripheral nerves at predilection sites Acid Fast Bacilli (AFB) in skin smear at the edge of an active (spreading, raised or red) lesion.

47. Predilection sites Sites where the nerves are superficial and so, enlarged nerves are more easily palpable. Facial Nerves :over the jaw joint (lagophtalmos and/or dropped mouth) Trigeminal Nerve over the eyebrows (anesthesia of of the cornea)

48. Greater auricular nerve : posterior border of the Stenocleidomastoid muscle. Ulnar Nerve: medial side of the elbow (“blessing hand”)

49. Classification of leprosy For purposes of treatment, patients can be divided into 3 groups depending on the number of skin lesions and nerves involved Paucibacillary single lesion leprosy(one skin lesion ) Paucibacillary leprosy(2-5 skin lesions) Multibacillary leprosy(more than 5 skin lesions). Paucibacillary : presence of few bacilli Multibacillary : presence of many bacilli

50. NOTE: When skin smears are available and dependable ,any patient with positive skin smear ,irrespective of the clinical picture must be classified as multibacillary leprosy and must be treated with multidrug therapy regimen for multibacillary leprosy.

51. Management of leprosy Drug therapy 6 month regimen for paucibacillary ( PB)leprosy

52. 12 month regimen Multibacillary (MB)Leprosy AGE DAPSONE RIFAMPICIN CLOFAZIMINE ADULT 50-70 KG 100MG daily Self administered 600MG once a month (DOT) 50MG daily(self administered) plus 300MG) once a month(DOT) CHILD 10-14YRS 50MG daily self administered 450mg once a month (DOT) 50mg daily 150mg once a month supervised (DOT)

53. General Management Proper care of the skin Proper care of minor wounds Provision of (orthopeadic) shoes Physiotherapy Health education Follow up Care : treatment of complications (neuritis, oedema , new paralysis, eye conditions –iritis, corneal ulcers, lagophtalmos ).

54. Health messages Prevent further damage to insensitive limbs. Wash and inspect feet (1 st aid of small wounds). Wear shoes and do not walk long distances Leprosy is curable (shame, negative attitudes). Spend 3-4 visits repeating that Leprosy is curable, thus need to complete Rx )

55. Complete the full course of treatment even if patches disappear. Give 2-3 months of treatment to patients living far from health care centre .

56. Role of RN/RM Outpatient care: Case holding: proper registration of patients, drug adherence, monitoring and record keeping of follow up. On each visit : Check for signs of disease progression /remission. Direct ulcer care : clean and dress wounds. Health education about self care for ulcer and disability, first aid measures, spread of the disease in overcrowded sites. Others : home visits to the sick, distribution of shoes and/or food.