CHN_3_for_RN_all_topics.pptxrrfggbnm5ttgw

Wsdcvbmhgf

1. Juba Institute of Health Sciences Prepared by Mike Malou Lual)

2. Course Code. GNP 222 Placement. 2 ND Year 2 nd Semester Theory Hours. 60 hours Practical Hours. 100 Hours Total Hours. 160 Hours Credits. 12.6

3. Course objectives At the end of the Course the student should be able to. Describe the basic concept of epidemiology Describe factors influencing the causation of diseases Describe common communicable diseases Describe the principles of control and prevention Describe the epidemiology study Method.

4. Learning objectives At the end of this session, Student will be able to. Define Epidemiology Analyze and describe Epidemiology Describe theories of causation of disease and their evolution Describe causation of diseases

5. Definition and concept of epidemiology Epidemiology is the study of the factors that influence the distribution and determinants of disease occurrence among human populations. Epidemiology deals with the study of disease in population groups, as opposed to clinical medicine that deals with disease in individual persons. Various characteristics of time, place and person influence disease distribution while determinants include characteristics of host, agent and environment.

6. Continue….. Epidemiology is the study of patterns of disease and injury in human populations and the application of this study to the control of health problems. The study of the distribution and determinants of health-related states or events in specified populations and the application of this study to control of health problems (Last JM, 1988).

7. Descriptive epidemiology concept Diseases occur in some people, in some places, sometimes. Only a few persons in the population get disease while others do not, even when they are susceptible; and some diseases only attack certain people and not others. Some diseases occur during certain times of the year and only in some places.

8. Continue…. For example, malaria occurs during the wet season in geographic areas that favour the breeding of mosquito and only affects a few persons while others remain healthy. Also, measles occurs mainly among children while adults are virtually free of it. These differentials in disease occurrence are due to the characteristics inherent in times, places and persons.

9. 1. Distribution of disease Place Time Person

10. In addition to describing the distribution of disease, epidemiology provides the basis for identification and analysis of causal factors or determinants of disease and, hence, for planning for the prevention and control of disease and for the promotion of health.

11. Concept of causation of disease Definition Cause of disease : is an event, condition, characteristic or a combination of these factors which plays an important role in producing the disease. The causes of disease can be classified in to two:

12. 1.Primary causes – these are the factors which are necessary for a disease to occur, in whose absence the disease will not occur. The term ”etiologic agent” can be used instead of primary cause for Infectious causes of diseases. For example “Mycobacterium tuberculosis” is the primary cause (etiologic agent) of pulmonary tuberculosis.

13. 2. Risk factors (contributing, predisposing, or aggravating factors) . These are not the necessary causes of disease but they are important for a disease to occur. A factor associated with an increased occurrence of a disease is risk factor for the exposed group; and a factor associated with a decreased occurrence of a disease is a risk factor for the non-exposed group. Risk factors could be related to the agent, the host and the environment. The etiology of a disease is the sum total of all the factors (primary causes and risk factors) which contribute to the occurrence of the disease.

14. It is the interaction of the agent, the host, and the environment which determines whether or not a disease develops, and this can be illustrated using the epidemiologic triangle.

15. The epidemiologic triangle Host Environment Agent

16. The epidemiologic triangle, depicts the relationship among three key factors in the occurrence of disease or injury: agent, environment , and host. An agent is a factor whose presence or absence, excess or deficit is necessary for a particular disease or injury to occur. The environment includes all external factors, other than the agent, that can influence health. These factors are further categorized according to whether they belong in the social , physical , or biological environments.

17. The social environment encompasses a broad range of factors, including education, unemployment, culture regarding diet; and many other factors pertaining to political, legal, economic, communications, transportation, and health care systems. Physical environmental factors- are factors like climate, terrain, and pollution. Biological environmental influences- include vectors, humans and plants serving as reservoirs of infection. From the perspective of epidemiologic triangle, the host, agent, and environment can coexist harmoniously . Disease and injury occur only when there is altered equilibrium between them.

18. 3.1. Natural history of disease The “natural history of disease” refers to the progression of disease process in an individual over time, in the absence of intervention. There are four stages in the natural history of a disease. These are: 1. Stage of susceptibility 2. Stage of pre-symptomatic (sub-clinical) disease 3. Stage of clinical disease 4. Stage of disability or death

19. 1. Stage of susceptibility In this stage, disease has not yet developed, but the groundwork has been laid by the presence of factors that favor its occurrence. Example: unvaccinated child is susceptible to measles.

20. 2. Stage of Pre-symptomatic (sub-clinical) disease In this stage there are no manifestations of the disease but pathologic changes (damages) have started to occur in the body. The disease can only be detected through special tests since the signs and symptoms of the disease are not present.

21. Continue…. Examples: • Detection of antibodies against HIV in an apparently healthy • Ova of intestinal parasite in the stool of apparently healthy children. The pre-symptomatic (sub-clinical) stage may lead to the clinical stage, or may sometimes end in recovery without development of any signs or symptoms.

22. 3. The Clinical stage At this stage the person has developed signs and symptoms of the disease. The clinical stage of different diseases differs in duration, severity and outcome. The outcomes of this stage may be recovery, disability or death. Examples: Common cold has a short and mild clinical stage and almost everyone recovers quickly. Polio has a severe clinical stage and many patients develop paralysis becoming disabled for the rest of their lives.

23. Rabies has a relatively short but severe clinical stage and almost always results in death. Diabetes Mellitus has a relatively longer clinical stage and eventually results in death if the patient is not properly treated.

24. 4. Stage of disability or death Some diseases run their course and then resolve completely either spontaneously or by treatment. In others the disease may result in a residual defect, leaving the person disabled for a short or longer duration. Still, other diseases will end in death. Disability is limitation of a person's activities including his role as a parent, wage earner, etc Examples: Trachoma may cause blindness Meningitis may result in blindness or deafness. Meningitis may also result in death.  

25. A schematic diagram of the natural history of diseases and their expected outcomes.

26. Healthy person   Sub clinical disease   Clinical disease   Recovery Disability Death 

27. Traditional disease causation theory A. Naturalistic disease causation theory: according to this theory the causes of disease were believed to be: External factors: e.g. -drinking polluted water eating contaminated foods bitten by animals, snakes,etc Contagium: e.g. through physical contact (sexual, kissing, sharing …) with ill people. Interpersonal conflicts: e.g. fighting each other

28. Personal excessive: e.g. eating / drinking, prolonged exposure to sun, rain, etc.,excessive crying and the like B . Magico – religious factor: here the causes of disease were believed to be: • god, kole, zar, dache, Atete • Magic factors: evils eye, sorcery, witch craft, ancestry ghosts, magagna, etc. And people believed that disease which is caused by magical factors is more serious and stayed for prolonged time

29. Theories of disease causation: i. Theories of the pre-modern era ii. Germ theory of disease iii. Biomedical model iv. Epidemiological triad v. Dever’s epidemiological model vi. Theory of multifactorial causation vii. Web of Causation viii. Wheel of disease causation ix. Other theories

30. i. Theories of the pre-modern era: These theories were in play before the existence of microorganisms was established, till the end of the 18th century. a. The demonic theory: According to this theory, the disease is a result of being possessed by demons, or evil spirits. Hence the sick person

31. was subjected to sorcery to rid the body of the evil occupant. B. The punitive theory: For a long time, the disease has been thought to be caused as a punishment for any bad deed done, as an outcome of the outrage (crime) of Gods. Hence the diseased individual is to appease (settle) the deity (Idol) to rid himself of the disease.

32. C. The miasmatic theory: It is the notion of bad air. Breathing in certain areas was proposed to cause disease, such as air around swamps, marshes and air at night times was thought to cause an array of diseases.

33. D. Theory of four humors: It proposes that the body is constituent of four humor; blood, phlegm, (Mucus) yellow bile and black bile. Any mbalance in these resulted in disease. Bloodletting was considered the most common method of treating disease. The Ayurveda believes that the imbalance of the three Doshas (tridosha) is the reason behind disease causation. While the Chinese medicine considers a discrepancy between the male (yang) and female (yin) principle resulting in disease.

34. ii. Germ theory of disease: The demonstration of bacterial presence in the air by Louis Pasteur and Anthrax is caused by bacteria by the turn of the 18 th century caused a drastic shift in the understanding of disease causation. Thus, focus from empirical causes such as bad air and wrath of God was altered to scientifically plausible causes like the presence of specific microorganisms.

35. The germ theory implies the causal effect is one to one, i.e. a single microorganism is the culprit behind a specific disease. Eg. Mycobacterium tuberculosis bacteria and the occurrence of tuberculosis. But that seldom is the case, as many diseases cannot be explained by this one to one causal relation but in reality, an interaction of various other contributory factors.3

36. iii. Biomedical Model: This envisions the healthy human body as an efficiently functioning machinery, and any resulting aberration as malfunction of the component organs. E.g. Hypothyroidism caused by improper functioning of the thyroid gland. But the human body seldom functions independently of its surrounding environment.

37. iv. Epidemiological triad: It proposes the disease is an outcome of imbalance of interactions between three essential components, Host, Agent, and Environment. Disease is caused when a susceptible host is exposed to the causative agent, in a compatible environment. It’s a broader concept and overcomes the limitations of germ theory. Intercepting any of the three links provides a means of halting the disease process, thereby highlighting areas for focus preventive efforts.5

38. v. Dever’s epidemiological model: This model highlights the interplay of four factors namely: Human biology, Lifestyle, Environment and Health system. All of which can have a positive or a negative effect.

39. Human biology includes genetics along with complex physiological systems, factors that are related to maturation and aging. While, lifestyle factors include daily habits, customs, and traditions; environmental factors are all the living and non-living factors that surround us.

40. vi. Multifactorial causation: Pettenkofer proposed that disease is a result of many factors as opposed to germ theory where the idea of a single cause was used. Improvements in public health and medicine brought about a decline in communicable diseases. But other non communicable ailments were on a rise which could not be explained based on the germ theory of disease. Hence single cause was deemed to be oversimplifying etiology of a disease where factors such as social, cultural, genetics, and economic factors were overlooked.

41. vii. Web of causation: Was proposed by MacMahon, Pugh, and Ipsen (1960), who argued that multiple factors causing a disease cannot be explained using a linear causal relation as, there are complex precursors to each causal component in the chain that have their respective complex interactions that overlap each other. Hence giving the metaphorical appearance of a complicated web of interactions rather than a linear causal relation.

42. viii. Wheel of disease causation: This was proposed by Mausner and Kramer in 1985. It eliminates the agent as a sole cause of disease, but emphasizes the complex interaction of physical, biological, and social environments. It also introduces genetics into the mix. The outer circumference is divided between environmental factors comprising of social, and physical factors. The core depicts the genetic component.

43. Levels of Disease Prevention The major purpose in investigating the epidemiology of diseases is to learn how to prevent and control them. Disease prevention means to interrupt or slow the progression of disease. Epidemiology plays a central role in disease prevention by identifying those modifiable causes. There are three levels of prevention

44. 1) Primary prevention:- The main objectives of primary prevention are promoting health, preventing exposure and preventing disease. Primary prevention keeps the disease process from becoming established by eliminating causes of disease or increasing resistance to disease. Primary prevention has 3 components. These are health promotion, prevention of exposure, and prevention of disease.

45. A. Health promotion: - consists of general non-specific interventions that enhance health and the body's ability to resist disease. Improvement of socioeconomic status, provision of adequate food, housing, clothing, and education are examples of health promotion. B. Prevention of exposure: - is the avoidance of factors which may cause disease if an individual is exposed to them. Examples can be provision of safe and adequate water, proper excreta disposal, and vector control.

46. Continue…. Primary preventive measures apply before a disease manifests with sign and symptoms. Examples: Eating well balanced diet, Regular exercise program Maintaining weight • No smoking • Moderation of alcohol • Information on alcohol substance • Nutritional counseling • Environmental control • Safe water Supply • Good food hygiene • Safe waste management • Vector and animal reservoir control • Good living and working condition • Stress management . etc

47. 2. Secondary prevention includes the early detection of actual or potential health hazards. This allows for prompt intervention and possibly a cure of a disease or condition. It is directed forwards health maintenance for patients experiencing health problems. Secondary prevention has two sub-levels early detection (diagnosis) of disease b. prompt treatment e.g. hypertension screen and acute care. Secondary prevention increases awareness of: breast self – examination testicular self-examination mammography pap smear BP screening Blood glucose screening Teaching breast self - examination Antibiotic treatment of streptococcal pharyngitis aimed at preventing rheumatic fever “Caution” of cancer.

48. 3. Tertiary Prevention is aimed at avoiding further deterioration of an already existing problem. Rehabilitative efforts are sometimes tertiary preventive measures. It deals with rehabilitation and return of client to a status of maximum function within the limit posed by the disease or disability and preventing further decline in health. This level of prevention occurs after a disease caused extensive damage. Examples -Rehabilitation after stroke -Smoking cessation program for clients with emphysema.

49. Unit two. Concept of infectious disease transmission Definition Communicable disease (infectious disease) – is an illness due to a specific infectious agent or its toxic products that arises through transmission of that agent or its products from an infected person, animal, or reservoir to a susceptible host, either directly or indirectly through an intermediate plant or animal host, vector, or the inanimate environment. Components of the infectious process The infectious process of a specific disease can be described by the following components, which constitute of the chain of disease transmission .

50. 1. The Agent 2. Its reservoirs 3. Its portal of exits 4. Its mode of transmission 5. Its portals of entry 6. The human host I. The Agents The agents in the infectious process range from viral particles to complex multi-cellular organisms II. Reservoirs A reservoir is an organism or habitat, in which an infectious agent normally lives, transforms, develops and/or multiplies. Reservoirs for

51. Continue.. infectious agents may be humans, animals, plants or other inanimate object Some diseases with human reservoirs are: 􀂃 Most bacterial and viral respiratory diseases 􀂃 HIV/AIDS/Sexually Transmitted Infections (STIs), measles, typhoid etc. All infected humans, whether showing signs and symptoms of the disease or not, are potential sources of infection to others. A person

52. who does not have apparent clinical disease, but is a potential source of infection to other people is called a Carrier. An example of carrier is a person infected with HIV. . A person infected with HIV might not have the signs and symptoms but he/she is capable of transmitting the infection to others Some diseases are transmitted to human beings from animals. These diseases are called zoonoses . Examples: Rabies, anthrax, etc.

53. Iii. Portal of Exit Portal of exit is the way the infectious agent leaves the reservoir. Possible portals of exit include all body secretions and discharges: Mucus, saliva, tears, breast milk, vaginal and cervical discharges, excretions (feces and urine), blood, and tissues. For example feces is the portal of exit for the eggs of hook worm.

54. Continue…. IV. Mode of Transmission Modes of transmission include the various mechanisms by which agents are conveyed to other susceptible hosts. Transmission may be direct or indirect. 1. 1. Direct Transmission 1.1 Direct contact : Occurs when there is contact of skin, mucosa, or conjunctiva with infectious agents directly from person or vertebrate animal, via touching, kissing, biting, passage through the birth canal, or during sexual intercourse. Example: HIV/AIDS/STIs, rabies

55. 1.2 Direct Projection : is transmission by projection of saliva droplets during coughing, sneezing, singing, spitting or talking. Example: common cold 1.3 Transplacental: is t ransmission from mother to fetus through the placenta. Example: syphilis, HIV/AIDS 2. Indirect transmission The following are the different types of indirect transmission.

56. 2.1 Vehicle-borne : Transmission occurs through indirect contact with inanimate objects fomites: bed sheets, towels, toys, or surgical instruments; as well as through contaminated food, water, IV fluids etc. 2.2 Vector-borne : The infectious agent is conveyed by an arthropod to a host. Vectors may be biological or mechanical. Biological vector : A vector is called biological vector if the agent multiplies in the vector before transmission. Example: anopheles mosquito is a biological vector for malaria.

57. Continue….. Mechanical vector : A vector is called mechanical vector if the agent is directly infective to other hosts, without having to go through a period of multiplication or development in the vector. The vector simply carries the agent by its body parts (leg, proboscis etc) to convey it to susceptible hosts. Example: Flies are mechanical vectors for the transmission of trachoma.

58. 2.3 Airborne: which may occur by dust or droplet nuclei (dried residue of aerosols) Example: Tuberculosis. When pulmonary tuberculosis patients cough, they emit many aerosols which consists the agents of tuberculosis. When these aerosols dry droplet nuclei will be formed. These droplet nuclei will remain suspended in the air for some time. When another healthy susceptible individual breaths he/she will inhale the droplet nuclei and become infected with tuberculosis.

59. Continue…. V. Portal of entry - is the site where an infectious agent enters a susceptible host. Examples: Nasal mucosa is portal of entry for common cold Conjunctiva is the portal of entry for trachoma Injury site is portal of entry for tetanus VI. Susceptible human host: The susceptible human host is the final link in the infectious process. Host susceptibility or resistance can be seen at the individual and at the community level. Host resistance at the community (population) level is called herd immunity .

60. Herd immunity can be defined as the resistance of a population to the introduction and spread of an infectious agent, based on the immunity of a high proportion of individual members of the population, thereby lessening the likelihood of a person with a disease coming into contact with susceptibles . Example - If 90 % of the children are vaccinated for measles, the remaining 10 % of the children who are not

61. Continue….. vaccinated might not become infected with measles because most of the children (90 %) are vaccinated. That means transmission from infected person to other susceptible children will not be easier.

62. COMMUNICABLE DISEASES Introduction Communicable diseases are the most common diseases in Africa caused by different kinds of microorganisms. They are called communicable diseases because they are capable of being passed on easily from person to person or from animal to person..

63. Types of communicable diseases Infectious diseases: Tuberculosis/Leprosy Tetanus Septicemia Diarrhea/cholera Brucellosis Leptospirosis (Infectious disease caused spirochetes bacteria) Plague Typus Rabies Chicken pox Yellow fever Typhoid fever

64. Dengue HIV/AIDS   Parasitic diseases: Malaria Amoebiasis Gardiasis Schistosomiasis Intestinal helminthes Hydatid Kala azar Onchocerciasis Trypanosomiasis  

65. Sexually Transmitted Diseases: HIV/AIDS Gonorrhoea Syphilis Chlamydia infection Trichomonas vaginalis Monilliasis (infection of the mucus membrane of the mouth) chancroid Lymphogranoluma venerium Lymphogranoluma inguinale Veneral warts Genital herpes

66. Contact diseases: Scabies Pendiculosis Skin fungal Urticaria Cutaneous leishmaniasis  Zoonotic disease Brucellosis Tuberculosis    

67. Disease control The disease agent is permitted to exist in the community at a level where it ceases to be as public health problem. Aims at reducing: i. Incidence of disease ii. Duration of disease iii. Risk of transmission of infection iv. Financial burden to the community.

68. Disease Elimination Interruption of transmission of disease from large geographic regions or areas. • An important precursor for eradication. • e.g. Measles, Polio.

69. Disease Eradication Termination of all transmission of infection by extermination of the infectious agent. Tear out by roots. Cessation of infection and disease from the whole world. e.g. Small pox. Potential candidates: Polio, Measles, Dracunculiasis

70. Importance of communicable diseases Many of them are very common Some of them are very serious and cause disability Some of them cause epidemic Many are particularly serious and more common in infant and children Most of them are preventable  

71. COMMUNICABLE DISEASES

72. PRELIMINARIES What we need to know : EPIDEMIOLOGY (concept, aims and purpose & use) PREVALENCE INCIDENCE ENDEMIC EPIDEMIC

73. EPIDEMIOLOGY Concept Epidemiology is the study of the distribution and patterns of health-events, health-characteristics and their causes or influences in well-defined populations. Aims and purpose inform policy decisions and evidence-based medicine by identifying risk factors for disease and targets for preventive medicine and public policies Use It is the cornerstone method of public health research and practice Cluster of Cholera Epidemic in London (1854) Plague Epidemic in Europe (1348)

74. Epidemiological Study Methods Descriptive Studies Analytical Studies Case / Control Studies Cohort Studies

75. Epidemiological Study Methods Descriptive Study Qualitative or quantitative study of the experience of a single patient, or small group of patients with a similar diagnosis . This study is purely descriptive and cannot be used to make inferences about the general population of patients with that disease. EXAMPLE = Survey Research is always based on a sample of the population and the success of the research is dependent on the representativeness of the population of concern.

76. Epidemiological Study Methods Analytical Study A statistical study in which action will be taken because a cause/effect relationship has been established between a certain risk factor or treatment and a certain disease or condition. The aim being to improve practice in the future

77. Epidemiological Study Methods Case / Control Studies =>A group of individuals that are disease positive (the "case" group) is compared with a group of disease negative individuals (the "control" group from the same population). The case control study looks back through time at potential exposures that both groups (cases and controls) may have encountered

78. Epidemiological Study Methods Case / Control Studies A = exposed cases B = exposed controls C = unexposed cases D = unexposed controls Odds ratio (OR), which is the ratio of the odds of exposure in the cases (A/C) to the odds of exposure in the controls (B/D), i.e. OR = (AD/BC). If the OR is clearly greater than 1 , those with the disease are more likely to have been exposed.   CASE CONTROL EXPOSED A B UNEXPOSED C D

79. Epidemiological Study Methods Cohort Studies Cohort Studies select subjects based on their exposure status. The study subjects should be at risk of the disease under investigation at the beginning of the cohort study; They should be disease-free when the cohort study starts. The cohort is followed through time to assess their later outcome status. EXAMPLE: a cohort of smokers and non-smokers over time to estimate the incidence of lung cancer.

80. Epidemiological Study Methods Cohort Studies A = exposed cases B = exposed NON-cases C = unexposed cases D = unexposed NON-cases Relative Risk (RR), is the probability of disease for a person in the exposed group, Pe = A / (A+B) over the probability of disease for a person in the unexposed group, Pu = C / (C+D), i.e. RR = Pe / Pu. RR > 1 shows association: those with the exposure were more likely to develop disease.   CASE NON CASE TOTAL EXPOSED A B A+B UNEXPOSED C D C+D

81. PREVALENCE & INCIDENCE OF A COMMUNICABLE DISEASE INCIDENCE RATE = New Cases of a certain disease in 1 Year PREVALENCE RATE = Current Number of people affected by a certain disease in 1 Year MORTALITY RATE = Number of people who died by a certain disease in 1 Year RECOVERY RATE = Number of people who got cured by a certain disease in 1 Year

82. Factors Influencing Causation of Diseases Host Agent Source Transmission Epidemiologic Triad HOST AGENT ENVIRON_MENT HOST RESERVOIR TRANSMISSION AGENT

83. PRELIMINARIES ENDEMIC EPIDEMIC When the balance between Host, Environment and the Agent is constant =>an infection is maintained in the population without the need for external inputs When the balance is shifted towards the Agent =>many new cases of a certain disease, in a given human population, and during a given period, occur.

84. Principles of Control and Prevention of diseases Attacking the source Interrupting the Transmission Protecting the Host Attacking the Source Interrupting Transmission Protecting the Host Treatment Immunization Isolation Chemoprophylaxis Reservoir Control Notification Environmental Sanitation Immunization Personal Hygiene Behaviour Change Vector Control Disinfection and Sterilization Immunization Chemoprophylaxis Personal Protection Better Nutrition.

85. Common Communicable Diseases Tuberculosis Leprosy Poliomyelitis Whooping cough Measles Chicken Pox Bacillary Dysentery Amoebiasis EACH CONDITION UNDER THE HEADING : Definition Cause/Predisposing Factors Pathophysiology Clinical Features Diagnosis SPECIFC AND GENERAL MANGEMENT Investigations and rationale Specifc Management Drug dose course General Management Health messages Follow up Care Role of RHN +

86. Common Communicable Diseases Cholera Typhoid & Paratyphoid Brucellosis Rabies Anthrax Tetanus STIs & HIV EACH CONDITION UNDER THE HEADING: Definition Cause/Predisposing Factors Pathophysiology Clinical Features Diagnosis SPECIFC AND GENERAL MANGEMENT Investigations and rationale Specific Management Drug dose course General Management Health messages Follow up Care Role of RHN +

87. Tuberculosis Definition Systemic,Chronic, communicable disease, caused by Mycobacterium Tuberculosis. In most cases lungs are involved (PTB) but any organ can be affected. 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

88. Tuberculosis Cause/Predisposing Factors Exposure to the bacillus Infection with TB Bacillus, after exposure Disease following infection 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.

89. Tuberculosis Pathophysiology Activated macrophages surround the place where MB have settled. Enlargement of LNs at the tracheal bifurcation. LN + Solitary lesion => PRIMARY COMPLEX. IF THE Immune Syst. Weakens, MB are able to prevail and spread to other parts of the lungs. Caseation and CAVITATION Rupture of blood vessel => haemoptysis Spread to other parts of the body Time

90. Tuberculosis Clinical Features Diagnosis Direct sputum examination using Ziehl-Nielsen staining. Ziehl-Nielsen staining of material of affected tissues Culture of AFB Chest X-Ray Tuberculin skin test (Mantoux Test) Early Symptoms/Signs Late Symptoms and Signs Productive cough for more than 2-3 wks POSITIVE Tuberculin Test Unexplained loss of weight Night sweats Blood stained sputum Enlargement of lymph nodes Difficulty in breathing Severe weight loss Symptoms of other organ involved

91. Tuberculosis Investigations and rationale SPUTUM TEST => At least 3 early morning specimens (sputum, NOT SALIVA!) Ziehl-Nielsen staining of tissue material & Culture of AFB => Require qualified personnel in hospital setting Chest X-Ray => Highly more expensive in comparison to microscopy Tuberculin skin test (Mantoux Test) POSITIVE TEST = INDURATION OF ABOVE 10mm people with active disease usually have large swelling/blisters people vaccinated with BCG may have a P+ve test Immunosuppressed pts may have a weak pos. response.

92. Tuberculosis Specific Management It implies CASE FINDING AND CORRECT CLASSIFICATION OF PATIENTS for proper treatment. CASE DEFINITON 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

93. Tuberculosis Drug dose course General Management Intensive Phase + Continuation Phase Directly Observed Treatment (TB-DOTs) Follow up Care Normally monthly F’Up visits. Treatment adherence, monitoring and record keeping. Complications. Side effect of the drugs, Interactions with other drugs. 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

94. Tuberculosis Health messages All TB patients are to be advised NOT TO SPIT ANYWHERE CARELESSLY! Use s 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 Role of RHN Heath education, monitoring treatment adherence (TB-DOTs), record keeping ad notification. BCG immunization.

95. Leprosy Definition Chronic infectious disease of human beings, caused by Mycobacterium Leprae . It mainly affect the peripheral nerves and the skin . It is not a fata disease BUT IT IS A CRIPPLING DISEASE. Leprosy currently 1 MILLION PEOPLE in Arica, Asia, South America and the Pacific. Between 2 and 3 MILLION PEOPLE have been left permanently disabled because of Leprosy. Prevalence => about 4.1/10,000 in the 11 endemic Countries.

96. Leprosy 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 ML through intact skin. Pathophysiology ML multiplies within macrophages of the skin or in the nerve fibers . More in cooler parts of the body (face and limbs). Inflammatory reaction ( Cellular Response ) in this structures. Hypo-pigmented areas in the skin ( INDETERMINATE ). Many Indeterminate lesions heals spontaneously. Lesions that do not heal may develop in TUBERCULOID, BORDERLINE , or LEPROMATOU S Leprosy.

97. Leprosy Pathophysiology Depending on the degree of cellular response: TUBERCULOID Leprosy. Strong focal response to bacteria. Lymphocytes infiltrates the nerves and destroy the fibers (anesthesia). Few or absent AFB. Invasion of trunk nerves. LEPROMATOUS Leprosy Little response. Few Lymphocytes seen. Nerves twigs are not infiltrated and mass of bacilli can be seen. Late damage to trunk nerves. BORDERLINE Leprosy. Features of both TL and LL. Lymphocytes are present but there is only slight infiltration of fine nerve twigs. Unstable: it may go towards TL or LL. Wide spread nerve damage.

98. Leprosy Pathophysiology: SUMMARY The Incidence of Leprosy increase in communities where we find: many untreated infectious cases Social conditions like overcrowding, poor houses, social customs . Many susceptible new comers in the area ML is introduced in a previously leprosy-free area Lepromatous (3.5%) Sub-clinical Infect. Susceptible Host Indeterminate Healing (70%) Tuberculoid Immunity Response Contact High Low Borderline

99. Leprosy Clinical Features TUBERCULOID Leprosy INDETERMINATE Leprosy Duration of Onset: SHORT (max 3-6 mths) Skin lesions: One Patch, (max 2-3) Not well defined edges Surface FLAT Loss of feeling: SLIGHT Trunk nerves NON involved SKIN SMEAR NEGATIVE LEPROMATOUS Leprosy BORDERLINE Leprosy NERVE DAMAGE AND DISABILITY Sensory Nerves => Anesthesia Motor Nerves => Paralysis Autonomic Nerves => Impaired circulation, skin atrophy, loss of sweating

100. Leprosy Clinical Features TUBERCULOID Leprosy INDETERMINATE Leprosy LEPROMATOUS Leprosy BORDERLINE Leprosy Skin lesions: very many Possibly well defined edges Outline often irregular Some loss of feeling NO central healing Some color changes in patch regular or irregular Symmetrical Often many trunk nerves involved somehow early SKIN SMEAR:RANGE FROM NEGATIVE TO POSITIVE NERVE DAMAGE AND DISABILITY Sensory Nerves => Anesthesia Motor Nerves => Paralysis Autonomic Nerves => Impaired circulation, skin atrophy, loss of sweating

101. Leprosy Clinical Features TUBERCULOID Leprosy Skin lesions: few, raised or flat, large or small Well defined edges regular or irregular Always some loss of feeling Often central healing Some color changes in patch regular or irregular Asymmetrical 1 r 2 trunk nerves involved SKIN SMEAR NEGATIVE INDETERMINATE Leprosy LEPROMATOUS Leprosy BORDERLINE Leprosy NERVE DAMAGE AND DISABILITY Sensory Nerves => Anesthesia Motor Nerves => Paralysis Autonomic Nerves => Impaired circulation, skin atrophy, loss of sweating

102. Leprosy Clinical Features TUBERCULOID Leprosy INDETERMINATE Leprosy LEPROMATOUS Leprosy Many Skin lesions: nodules, raised patches, flat patches areas of thick skin. Well defined edges regular or irregular OTHER ORGANS INVOLVED: eyes, hands, feet and testicles. Symmetrical Many trunk nerves involved but late in the disease SKIN SMEAR: STRONGLY POSITIVE BORDERLINE Leprosy NERVE DAMAGE AND DISABILITY Sensory Nerves => Anesthesia Motor Nerves => Paralysis Autonomic Nerves => Impaired circulation, skin atrophy, loss of sweating

103. Leprosy Clinical Features TUBERCULOID Leprosy SKIN SMEAR NEGATIVE INDETERMINATE Leprosy SKIN SMEAR NEGATIVE LEPROMATOUS Leprosy SKIN SMEAR: STRONGLY POSITIVE BORDERLINE Leprosy SKIN SMEAR:RANGE FROM NEGATIVE TO POSITIVE TYPE I or TYPE II REACTIONS TYPE I = Rapidly changed in Imm. Resp. (inflamm.). Common in unstable form of Leprosy (BT,BB,BL), during the 1 st year of Rx. TYPE I I + Erythema Nodosum Leprosum : reaction between dead ML and Ab. Especially in L and BL CAUSES: Other diseases , malnutrition, worms, TB, malaria etc… Stress Hormonal changes: pregnancy, menstruation, abortion, child birth, puberty Other drugs: iodine Immunization: BCG Infected wounds/Osteomyelitis REACTIONS ARE NOT CAUSED BY TREATMENT: Start MDT at the highest possible dosage

104. Leprosy 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.

105. Leprosy Investigations and rationale Sites of Predilection : site where the nerves are superficial and so, enlarged nerves are more easily palpable (see figg 10.19-24). Facial Nerves => over the jaw joint ( lagophtalmos and/or dropped mouth ). Trigeminal Nerve => over the eyebrows ( anest. of the cornea ) Greater Auricolar N. => post. border of the St./Cl./Mast. Muscle. Ulnar N. => medial side of the elbow ( “blessing hand” ) Median N. => middle of the inner side of the wrist ( “claw hand” ) Radial N. => radial site of the wrist ( “wrist drop” ) Peroneal N. => outer side of the knee ( “drop foot” ) Tibial N. => behind medial malleolus ( “clawing toes” )

106. Leprosy Specific Management : Classification according to the Mycobacterial concentration. GROUPS SUB-GROUPS OPERATIONAL GROUPING INDETERMINATE (I) I PAUCIBACILLARY TUBERCULOID (T) TT T   BORDERLINE (B) BT BB BL MULTIBACILLARY LEPROMATOUS (L) L LL  

107. Leprosy Drug dose course: W.H.O. RECOMMENDED DRUG MANGEMENT OF: PAUCI-BACILLARY LEPROSY (9 months) MULTI-BACILLARY LEPROSY (2-3 years) MDT (2 drugs) 0-5 years 6-14 years 15 years and above Dapsone daily self-administered (or by care giver) at home 25mg 50mg 100mg Rifampicin 4WEEKLY supervised in health centre 150mg 300mg 600mg MDT (4 drugs) 0-5 years 6-14 years 15 years and above Dapsone daily self-administered (or by care giver) at home 25mg 50mg 100mg Rifampicin 4WEEKLY supervised in health centre 150mg 300mg 600mg Clofazamine 4WEEKLY supervised 100mg 200mg 300mg Clofazamine daily self-administered 50mg (alternating days) 50mg daily 50mg daily

108. Leprosy General Management Proper care of the skin Proper care of minor wounds Provision of (orthopedic) shoes Physiotherapy Health education Follow up Care => treatment of complications (neuritis oedema, new paralysis, eye conditions –iritis, corneal ulcers, lagophtalmos-).

109. Leprosy 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, neg. attitudes => spend 3-4 visits repeating that Leprosy is curable, thus need to complete Rx ). Complete the full course of Rx even if patches disappear). Give 2-3 months of Rx to patients living far from H/C.

110. Leprosy Role of RHN Outpatient care Case holding: proper registration of patients, drug adherence, monitoring and record keeping of follow up. On each visit : signs of disease progression /remission. Direct ulcer care . Health education about self care for ulcer and disability, 1st aid measures, spread of the disease in overcrowded sites Others : home visits to the sick, distribution of shoes and/or food.

111. Poliomyelitis Definition Acute viral disease of the nervous system , as a result of the infection with POLIO VIRUS with a wide range of clinical presentations (from asymptomatic infection to paralytic d’se). Infantile paralysis or “polio” 3 types of POLIO Virus

112. Poliomyelitis Cause/Predisposing Factors Polio virus is very common in Africa. Most adults got he infection in childhood, just as they got measles. Detectable in faeces and pharyngeal secretions => faecal-oral or oral-oral route Persons with asymptomatic infections ( children ) are the reservoir.

113. Poliomyelitis Pathophysiology Following ingestion => replication in lymphoid tissue of pharinx and intestine (excretion). Viremia Infection of CNS The anterior horn cells f the spinal cord are susceptible to the infection and are damaged Destroyed. Inflammation of the neurons Anterior poliomyelitis. The right anterior corn in the cervical region is shrunken, and there is atrophy of all the white columns on that side. From a woman, aged 50, who was the subject of infantile paralysis of the right arm.

114. Poliomyelitis Clinical Features From minor illness (flu like syndrome)… To major Illness : Pre-paralytic stage : high fever and meningeal signs Paralytic stage : progressive spread of asymmetric flaccid paralysis in 24 hours Post paralytic stage : residual disability

115. Poliomyelitis Diagnosis Normally the diagnosis is based on clinical picture. However it is possible to isolate the virus from pharynx and fecal material. Investigations and rationale Antibodies are formed against Polio virus but it is more important to look for SERO-CONVERSION

116. Poliomyelitis Specific Management PRE-Paral. Stg . => Absolute bed rest; avoid injections. PARAL. Stg . => passive mobilization to avoid contractures POST-Paral. Stg . => physiotherapy (active + passive mobil.) Isolation of the patients. Drug dose course => NO SPECIFIC DRUG IS AVAILABLE General Management Community based physiotherapy, support to the parents (to learn PKT and to build simple exercise tools). Follow up Care Referral to H/C or Spec. Hospitals Orthopedics devices Surgical correction of deformities

117. Poliomyelitis Health messages Importance of FULL COURSE IMMUNIZATION Oral vaccine (Sabin) cover 3 types of virus. Given in combination, routinely to CHILDREN UNDER 5 or: At birth DPT1 => 6 weeks DPT2 => 10 weeks DPT3 => 1 4 weeks Poliomyelitis is a NOTIFIABLE DISEASE Role of RHN Health education, Immunization, empowerment of affected care takers, referral to specialized health facilities.

118. Whooping cough Definition Air borne infection of the respiratory tract caused by the Gram-negative bacillus Bordetella Pertussis , spread by droplets of secretions. The germ damages the cells of the respiratory tract. This produce a very sticky mucous that blocks the bronchioles.

119. Whooping cough Cause/Predisposing Factors Most African children are exposed early in life to other infected children, b’se of social contacts (extended families). Pathophysiology Destruction of respiratory tract cells Sticky mucous Irritation of bronchial mucosa => violent access of cough for weeks r months Impaired breastfeeding = vomiting => malnutrition

120. Whooping cough Clinical Features Incubation period 7-10 days Typical cough with whoop and sticky secretions Difference between younger and older children Clinical Picture Children < 3Months Children > 3Mts Remarks CATARRHAL PERIOD (14 days) Little cough Nasal discharge Cough Nasal discharge Like common cold PAROSYXMAL PERIOD (6 wks -3mts) Attacks of breathing arrest Cyanosis, Poss. B’Pneumonia Typical attacks of cough with whooping followed by vomiting. Sticky secretion Sub-conjunctival haemorrhage Diagnosis is typical in older children (often missed in younger children) Diagnosis ; based on CLINICAL HYSTORY and WBC >30,000 with LYMPHOCYTOSIS

121. Whooping cough Specific Management Maintenance of nutrition and hydration Oxygen therapy and (GENTLE) sucking. Avoid sedatives and cough depressants Drug dose course Antibiotics do not shorten the paroxysmal stage. Oral Erytromicin reduces period of infectivity. Broad spect. ABC for WC complicated with Pneumonia. General Management Isolation of known cases Prevent WC with Immunization (DPT) Immunization of contacts Follow up Care => ensure FULL COURSE OF IMMUNIZATION

122. Whooping cough Health messages Maintenance of nutrition and hydration . Breast feeding is encouraged after an attack. Oral Erytromicin reduces period of infectivity. Children who are contacts of known cases can be given Erytrom. or CAF together with Immunization. Prevent WC with Immunization (DPT). Role of RHN Health education, Immunization, referral to specialized health facilities (O2 therapy) W. Cough is a NOTIFIABLE D’SE

123. Measles Definition Acute general infection caused by a virus (Morbilli Virus, Paramyxoviurs), spread through infective invisible droplets. The clinical features are the result of the reaction of the body. Found all over the word, in Africa children develop measles before the age of 3 years.

124. Measles Cause/Predisposing Factors Before it becomes clear that the child has got measles, it has already spread to close contacts. Malnutrition => low immunity => infection. Pathophysiology The virus particles come from the secretions of the respiratory tract.

125. Measles Clinical Features UNCOMPLICATED MEASLES (in well nourished children) Fever, conjunctivitis rhinitis, stomatitis –Koplic’s spots) and skin rash. COMPLICATED MEASLES (in malnourished children) Dyspnea, nasal flaring, Hoarseness barking cough and stridor Mouths sores => impaired sucking Diagnosis based on typical clinical signs.

126. Measles Specific Management UNCOMPL. M . => Treat as outpatient. Ensure proper fluid intake and 5 meals /day. Tepid sponging. COMPL. M. => exclude meningitis, otitis media, diarrhoea and pneumonia. Treat accordingly if found. Treat convulsions with Phenoarbitone Drug dose course Use Paracetamol (no Antiobiotic unless complications require it). Give ONE SINGLE DOSE OF Vit. A (200,000 IU), or DAILY in COMPL . M. General Management Immunization of all children under 5 both sick and healthy, particularly if admitted in children wards and not immunized

127. Measles Health messages Measles vaccine takes 8-10 days to give protection (Measles’ incubation period: 12 days). Complications occur often in malnourished children. All children under 5 are to be immunized . Role of RHN Health education, Immunization, Monitoring and treating Possible Complications .

128. Chicken Pox Definition Mild viral disease, caused by an Herpes Virus (Varicella-Zoster Virus HZV). Very common children disease , it can occur in infant as congenital infection and. In the adult HZV can remain latent in the nervous ganglia, assume the characteristics of Herpes Zoster

129. Chicken Pox Cause/Predisposing Factors Spread though infectious droplets from the respiratory tract. Skin scabs are not infectious. Pathophysiology The disease leaves an immunity against HZV but, in certain people the virus remains latent in the nervous ganglia and can be reactivated in case of immuno-suppression A case of Herpes Zoster of the ophthalmic branch of the trigeminal nerve in HIV+ve Patient

130. Chicken Pox Clinical Features Typically: Mild fever and sore throat Maculo-papular rash from the trunk to the armpits and limbs. Then, STARRY SKY RASH, with different stages of development. In HZV = Dermatomeric distribution of blisters Diagnosis: clinical .

131. Chicken Pox General Management Chicken pox requires only supportive treatment. Calamine lotion can relieve itching. Chicken pox is already infectious in the incubation period: no prevention measures. Specific Management HZV is highly symptomatic and painful. Daily Bathing and soaks. Avoid scratching (bacterial super infection) Drug dose course In infection less than 24hrs, Acyclovir 800mg 5 times a day fro 5-7 days . Painkillers and antidepressant are at times required. Follow up Care => reactivation of latent HZV (Immunosuppression?)

132. Chicken Pox Health messages Very common children disease. No major complications. Avoid bacterial super infection of rash. Possibility to develop HZV in the future (ISS) Role of RHN Health education, reassurance of the parents, supportive treatment. Follow up.

133. Bacillary Dysenteryq1 Definition Acute diarrhoeal disease, characterized by bloody stools, fever, vomiting and abdominal cramps. It is also known as Shigellosis.

134. Bacillary Dysentery Cause/Predisposing Factors Gram –ve bacilli of Shigella Spp. Carried by horse-flies During dry season, when water availability reduces. Limited chance of wash eating utensils and hand-washing. Malnutrition . Pathophysiology F AECES F LIES F INGERS F OOD The 4F RULE The incubation period is short (1-4days). Gastro-enteritis with bloody, mucous stools (destruction of the mucosa). Toxemia. Contraction of the anal sphincter. Hypovolemic shock and electrolytic imbalance

135. Bacillary Dysentery Clinical Features Acute Fever Abdominal cramps Tenesmus Mucous and bloody stools Diagnosis Stools exam: many RBC and WBC (PMN & Macrophages) Shygella Spp. Found in the stool culture

136. Bacillary Dysentery Investigations and rationale The stool culture is required to rule out Entoamoeba hystolitica. Anemia, not common. Leucocytosis >15,000.

137. Bacillary Dysentery Specific Management In case of severe symptoms rehydration, + antibiotics . In uncomplicated disease, only rehydration . Drug dose course (tetracycline, ampicillin or cotrimoxazole), better after culture sensitivity. Nalidixic acid and fluoroquinolones (not in chlidren) Spasmolytics (Hyoscine - Buscopam) General Management Stopping the fecal-oral transmission

138. Bacillary Dysentery Health messages Check the water supplies (epidemic) Health education on preparation of rehydration fluids. HANDWASHING!!!!!! USE OF LATRINES, REFUSE DISPOSAL AND PERSONAL HYGIENE Avoid use of antibiotics in mild cases Role of RHN Health education, rehydration therapy and education of the parents, supportive treatment. Follow up.

139. Amoebiasis Definition An infection caused by a pathigenic amoeba, Entamoeba hystolytica . Most infections remain asymptomatic but, in certain circumstances the amoeba may invade the bowel wall, causing amoebic dysentery. Cause/Predisposing Factors The only infectious form is the cyst, so a patient with amoebic dysentery is unlikely to spread the disease, since Trophozoites are destroyed in the stomach. Endemic in area with poor sanitary conditions. Amoebiasis occurs in families or spread through institutions (schools etc…) but odes not in epidemics

140. Amoebiasis Pathophysiology 1: Lyfe Cycle Ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation in the small intestine: trophozoites are released. Trophozoites migrate to the large intestine. Binary Multiplication: Trophozoites + Cysts. Cysts are passed in the feces.

141. Amoebiasis Pathophysiology 2: Disease Development In many cases, the trophozoites remain confined to the intestinal lumen ( Non-invasive infection ) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients the trophozoites invade the intestinal mucosa (Intestinal disease). In others, they invade, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs ( Extra-intestinal disease)

142. Amoebiasis Clinical Features Amoebic Dysentery Bottle shape ulcers in the intestinal lumen => amoeboma Insidious onset of amoebic dysentery with abdominal discomfort. Mild loose stools or frank diarrhoea. In severe cases, dark blood contained in stools, toxic + dehydrated patient. Alternating diarrhoea to constipation Amoebic liver abscess : hepatomegaly; CXR shows elevation of right emi-diaphragm. Other Extra-hepatic sites : skin, lungs, brain

143. Amoebiasis Diagnosis Stool examination stained with Lugol solution, positive for Cysts of Entamoeba hystolitica Trophozoites may also be seen in diarrhoea stools Investigations and rationale Entamoeba hystolityca’s cyst & Trophozoites are to be differentiated from those of Entamoeba coli . Entoamoeba hystolytica cyst: Typically 4 nuclei are seen after staining with Lugol

144. Amoebiasis General Management Asymptomatic patients: no Rx recommended Specific Management Drug dose course Invasive disease => Metronidazole 1.4 gr daily for 3 days. Or Metronidazole 800mg TDS for 5days. Or Tinidazole 2gr OD for 3 days Children: Metronidazole 25mg/Kg/day Hepatic Amoebias => Metronidazole 1.4gr daily for 3 days . Aspiration can be performed in Hospital setting.

145. Amoebiasis Health messages Healthy carriers who pass cysts in the stools are responsible for the spread in the community. Boiling of drinking waters will kill the cysts. HAND WASHING! People handling food should be screened. The most important control method is PROPER DISPOSAL OF FAECES . Role of RHN Health education, treatment of invasive disease, referral to specialized H/C for further care

146. Cholera Definition Acute intestinal disease, characterized by sudden onset of profuse watery stools, vomiting, rapid dehydration and circulatory collapse. Between 19 th and 20 th Cent.: 7 pandemics. Current pandemic sustained by EL TOR Genotype.

147. Cholera Cause/Predisposing Factors Cholera is caused by Vibrio cholerae , a Gram Positive Bacillus, curved and motile. Water-borne d’se. Fecal-Oral route. V. chol. is sensitive to gastric acid and so A LARGE NUMBER OF BACIILI needs to be INGESTED TO CAUSE DISEASE . Reservoir => CARRIER population (normally asymptomatic: only 1-2% of infected persons develop typical symptoms). Pathophysiology The Vibrios are confined to the intestinal lumen. Toxin release, that is responsible of large loss of water and electrolytes in the stools.

148. Cholera Clinical Features Incubation period 2-3 days. Fever often low grade or absent. Typical features in 3 stages : Passage of important watery stools (3-12 hrs)=> RICE WATER STOOLS . Vomiting begins. Abd & muscle cramps. Collapse from dehydration : dry inelastic skin. Low to un-recordable BP. Renal block. SHOCK. RECOVERY PHASE . Spontaneous or with Rx Diagnosis Cholera should be suspected in any outbreak of diarrhoeal disease . Isolation of V. cholerae in rectal swab (sent to lab in Cary Blair transport medium). Sensitivity culture helps to find adequate antibiotic. treatment.

149. Cholera General Management Do not refer suspected cholera case but inform District Health office. Organize temporary hospitals. Stools and vomit ( infectious ) are disposed in pit latrine and septic tanks. Use cholera beds REHYDRATION: oral (&NGT) or Intravenous. Specific Management Drug dose course Tetracycline can speed the recovery. Single dose 2gr. OR Doxycycline 300mg single dose. If resistance to Tetacycline => Cyprofoxacine 30mg/kg (mx 2gr) single dose OR Cotrimoxazole 2 tabs BID x3days In CHILDREN < 8YRS DO NOT USE TETRACYCLINE . Erythromycin 40mg/kg/day in 3 divided doses x 3days.

150. Cholera Health messages Most cholera infections are asymptomatic but are spread in the environment by carriers. Do not refer a suspected case but notify t to district office. Prompt rehydration with glucose/electrolytes solutions saves most of cholera cases . Surveillance of disease is the key . It includes: morbidity and mortality reports, field investigations, laboratory investigations. Role of RHN Notification of cholera cases to the district office. Surveillance of epidemic in catchment area. Health education on proper disposal of faeces and safe drinking water practice.

151. Typhoid & Paratyphoid Fever Definition Systemic infectious disease cause by Salmonella typhi or Salmonella para-typhi , transmitted through food and water contaminated with faeces or urine of a patient carrier. Paratyphoid fever is less water-borne b’se it requires a higher infective dose in water, where multiplication does not occur. Gastric acidity is an important defence against the development of the disease.

152. Typhoid & Paratyphoid Pathophysiology Ingestion (the organism remains in the lumen and it can be found in the stool exam during the 4 days of incubation period.) Penetration through intestinal mucosa . From sub-mucosa => mesenteric LNs => thoracic duct => bloodstream ( TRANSIENT PRIMARY BACTERAEMIA ). Transport to LIVER & SPLEEN => multiplication. SECONDARY BACTERAEMIA => involvement of other organs: gall bladder => cholecystitis and Peyer’s Patches => infiltration and inflammation => ulcers.

153. Typhoid & Paratyphoid Clinical Features Incubation: 10-20 days for S. typhi; 1-10 for S. paratyphi. Duration about 4 weeks: 1 st WEEK 2 nd WEEK 3 rd WEEK 4 th WEEK Non specific: Headache, Malaise Raising remittent fever Patient looks toxic and apathetic. Sustained high temperature. Splenomegaly & abd. distension Rose spots on upper abd. & lower chest. Patient more toxic and ill. Weak. Delirium and confusional state. Pronounced abd. distension. Diarrhoea with foul green-yellow stools. Death may occur.   Fever, mental state and abd. distension improve. Slow convalescence

154. Typhoid & Paratyphoid Diagnosis Based on isolation of the organism from blood or bone marrow. Investigations and rationale WIDAL TEST (serology of the antibodies against H or O antigen) HAS MANY LIMITATIONS . Anti-O appear first in acute infection => high title of Anti-O means acute infection . Anti-H appear later but remain longer => help to recognize the type of enteric fever (H = flagellar antigen). In endemic countries, patients have higher Anti-H title: here Widal test lacks sensitivity.

155. Typhoid & Paratyphoid General Management Management of dehydration and electrolytic imbalance. No diet restriction Parasympaticolytics (anticholinergic) for colics. Specific Management Drug dose course Cyprofloxacine 500mg bid x 7-10 days CAF & Cotrimoxazole are alternatives A vaccine is available and recommended 10 days before trip in endemic areas. Follow up Care: with treatment the prognosis is good but antibiotics may prolong the elimination of bacteria

156. Typhoid & Paratyphoid Health messages Fecal oral route. Existence of asymptomatic carriers. Role of RHN Notification of diagnosed cases to the district office. Health education on proper disposal of faeces and safe drinking water practice.

157. Brucellosis Definition Zoonosis transmitted to humans form infected animals. Its clinical features are not specific. It is also known as undulant fever. Causative GRAM –ve organisms are : Brucella abortus , from cattle; Brucella melitensis , from goats; Brucella suis , from pigs.

158. Brucellosis Pathophysiology Brucellae are phagocytized by neutrophils . The glycoprotein Lipopolysaccharide (LPS) is responsible of the pathology Macrophages become parasitized with bacteria. Involvement of other organs . Cause/Predisposing Factors Occupational hazard of farmers vet-doctors, cattle keepers and pastoralists. Transmitted through the ingestion of untreated milk, milk products, raw meat, bone marrow . Possible inhalation during contact with tissues and animal body fluids. No communicability from human to human

159. Brucellosis Clinical Features Incubation period: 5-21 days Fever, chills, headache, sweating & generalized ( SEVERE ) joint pain. Splenomegaly is common Diagnosis Combined clinical features and possibility of contacts=> suspicion. GOLD STANDARD: culture of Bone marrow (better than blood’s) Serology: Anti-Brucella Title > 1:160

160. Brucellosis Investigations and rationale The serology may lack specificity and sensitivity Widal test can also be positive in Brucellosis. X ray of the skeleton : justified when pain is very well localized, also given the possibility of osteomyelitis.

161. Brucellosis Specific Management Drug dose course Adults : Streptomycin 1gr IM daily for 2 weeks + Doxycycline 100mg bid for 6weeks (up to 12) Children <8yrs: Gentamicine 7.5mg/Kg IM daily in 1-3 doses for 5-7 days Cotrimoxazole 24mg/Kg bid for 6weeks Pregnant Women: Rifampicin 600-900mg od for 6 weeks

162. Brucellosis Health messages Boil milk before drinking and possibly treat dairy products (pasteurization) before ingestion. Cook meat and other derivatives. Screening of relatives of an identified case. Track the source of infection (animal farm? Single animal? Butchery shop?). For those individual exposed to occupational hazards => recall safe practice of handling discharges and carcasses . Importance of animal immunization. Role of RHN Health education, treatment of identified cases. Follow up for treatment completion.

163. Anthrax Definition Endemic disease of the domestic herbivores caused by the bacterium Bacillus anthracis , that, when passed to humans, caused a cutaneous lesion , gastro-intestinal infection with overwhelming pneumonia and disseminated disease . From Greek “Anthrax” = “black”. Farmers and wool workers seem to be at higher risk, although wool workers may become more resistant with time.

164. Anthrax Clinical Features Incubation period: 2-3 days. CUTANEOUS : Small skin papule with a central vesicle => many vesicles surrounding a central dry lesion with a black scar. Normally on head/neck. PULMONARY : fever, chills, cyanosis and dyspnoea develop rapidly. Often fatal. INTESTINAL : vomiting diarrhoea and haematemesis or dysenteric stools. Diagnosis Bacteriological diagnosis from the skin lesion, sputum, or faeces according to the manifestation.

165. Anthrax Specific Management Drug dose course Intravenous Penicillin at high doses remains the drug of choice. Vaccine under development. General Management Anthrax spores originate from animal died with the disease and released in the environment. The spores may be ingested inhaled or they can enter the skin . It is recommended not to eat the meat of animals that fell sick. Disposal of carcasses Disinfection of factory environment (wool factories and textiles).

166. Anthrax Health messages Occupational hazard for wool/textile workers. Threat of bio-terrorism Safe disposal of carcasses of dead animals. Proper disinfection of infected work settings. Role of RHN Health education, treatment of disease in specialized settings

167. Rabies Definition Acute viral disease that affect mammals (zoonosis), incidentally transmitted human beings by the bite of an infected (rabid) animal. Cause/Predisposing Factors Agent: Rabies Virus that has preference for salivary glands and nervous tissue. The main animal reservoirs are: wild animals like jackals, mongooses, hyena. domestic animals like dogs and cats

168. Rabies Pathophysiology

169. Rabies Clinical Features Incubation period: from 2 weeks to 1 year, depending on: Bite size Distance of the bite from the brain Dose of virus discharged Earliest symptoms: increasing severe pain in the wound FURIOUS RABIES => anxiety, violent behaviour, seizures, hallucinations PARALYTIC RABIES => depression, paralysis of the limbs and spasm of the pharyngeal muscles (Hydrophobia). Diagnosis History of animal bite (animal dead after 10 days) No immunization received.

170. Rabies Investigations and rationale What are the condition of the wound? Is/Was it possible to monitor the animal that bit the patient? Was immunization given? Are specialized test available? Have symptoms started yet?

171. Rabies General Management Observe the animal for 10 days : Healthy ? => NO RABIES Escaped ? => refer patient for immunization . Looks rabid ? => carefully catch & lock it. Inform district and refer patient for immunization . Already dead? (brought to H/C) => carefully bury the carcasse. Inform district and refer patient for immunization . Treat the wound Cleaning Disinfection No sutures or closing Tetanus and antibacterial prophylaxis when indicated.

172. Rabies Specific Management = Immunization with PVRV/PCEC/HDCV + Rabies Antiserum, when required . Immunization: Drug dose course recommended by W.H.O. Standard Intramuscular regimen (HDCV: 1ml dose IM on deltoid on days 0,3,7,14, 28) OR PVRV 0.5 ml, same administration. EXPENSIVE!!! NB: Available Vaccines HDCV: 1ml x amp. Expensive! PVRV: 0.5ml x amp PCEC PDEC

173. Rabies Specific Management = Immunization with PVRV/PCEC/HDCV AND/OR Rabies Antiserum . Drug dose course recommended by W.H.O. 8 sites intradermal regimen (HDCV or PCEC) Day 0 : 0.1 ml id in 8 sites (deltoid Rt & Lt; supra-scapular Rt & Lt; Lower abdomen Rt & Lt; thigh Rt & Lt;). Day 7 : 0.1 ml id in 4 sites (deltoid Rt & Lt; thigh Rt & Lt;). Days 28 and 91 : 0.1 ml id in 1 site (deltoid). Cheaper than the above and more effective. Longer follow up. NB: Available Vaccines HDCV: 1ml x amp. Expensive! PVRV: 0.5ml x amp PCEC PDEC

174. Rabies Specific Management = Immunization with PVRV/PCEC/HDCV AND/OR Rabies Antiserum . Drug dose course recommended by W.H.O. 2 sites intradermal regimen (PVRV 0.5ml x amp.) Days 0, 3 and 7 : 0.1ml id at 2 sites (deltoids) Days 28 and 91 : 0.1ml id at 2 sites (deltoids) NB: Available Vaccines HDCV: 1ml x amp. Expensive! PVRV: 0.5ml x amp PCEC PDEC

175. Rabies Specific Management = Immunization with PVRV/PCEC/HDCV AND/OR Rabies Antiserum . POST EXPOSURE TREATMENT for those who had previous vaccination Wound care 2 booster doses IM on days 0 and 3 PRE EXPOSURE IMMUNIZATION OF HIGH RISK WORKERS IM Dose on days 0,3,28

176. Rabies Specific Management: Decision Table Type of exposure Circumstances Recommended treatment Indirect contact, NO bite, NO licks. Rabid animal Serum + Vaccine Stop treatment if animal remains healthy for more than 10 days. Licks on the skins, scratches, abrasions, minor bites (covered areas of arms, trunk and legs); minor exposure. i) Suspected as rabid, unprovoked attack by cat or dog Start Vaccine Stop treatment if animal remains healthy for more than 10 days.   ii) Rabid: wild animal or animal NOT available for observation Serum + Vaccine Licks of mucosa, major bites (multiple or on face, head, finger and neck) Suspect or rabid domestic or wild animal NOT available for observation Serum + Vaccine Stop treatment if animal remains healthy for more than 10 days N.B.: Observation period applies only to dogs and cats. All unprovoked bites in endemic areas are to be considered suspect, unless proved negative by lab investigations. In general, exposure to rodents and rabbits seldom, if ever, requires anti-rabies treatment.

177. Rabies Health messages Refer for immunization all suspected and certain case or if the animal is not available for observation. Follow up for completion of immunization course. Continue monitoring patient. There is no treatment of manifested disease. Rabies is a NOTIFIABLE DISEASE. Immunization of domestic animals. Role of RHN Health education, immunization and treatment, follow up, notification to health district office

178. Tetanus Definition Neurological disorder, caused by a toxin produced by Clostridium tetani . It is characterized by i ncreased muscle tone and spasms , e.g. painful contractions of voluntary muscles. Cause/Predisposing Factors C. tetani is a GRAM+ rod which f orms terminal spores and is an OBLIGATE ANAEROBIC . It normally lives in animal (&human) bowel and when it is passed in the faeces it forms spores that are very resistant. Spores enter the body through a contaminated (deep penetrating, necrotic) wound .

179. Tetanus Pathophysiology After the spores enter the wound the aerobic bacteria consume all the oxygen and the environment becomes favorable to C. tetani . Tetanus toxin in transported through the axons to the central nervous system… … and from there back to the motor neurons particularly of the extensor muscles . The contraction of facial muscles gives the “risus sardonicus”(devil’s grin). More generalized contractions develop (opystotonus). 1 5 4 2 3

180. Tetanus Clinical Features Incubation period: 5-21 days “ Risus sardonicus ”(devil’s grin). More generalized contractions develop ( opystotonus ) Painful spasms + period of apnoea In Tetanus neonatorum : inability to suck, then spasms ad apnoeas. ALWAYS FATAL! Diagnosis History of contaminated wound in non immunized patient. Or contaminated umbilical cord (mother non immunized during pregnancy).

181. Tetanus Investigations and rationale The diagnosis is clinical and based on the history of immunization not occurred. It is important to enquire about the tetanus immunization any time a person come with a wound. Pregnant women need to get immunized before delivery if not done before, on previous pregnancies.

182. Tetanus Specific Management of manifested Tetanus Eliminate the source of toxin => Metronidazole IV (or penicillin). Neutralize unbound toxin => Tetanus Anti-toxin : 10,000 IU Intravenous or Intramuscular to adults and children Prevent muscle spasm Diazepam (Valium) at high doses: Start with 10-40mg intraven. Give the same dose at the same time through NGT increase the dose (up to 500mg/day) if spasm continue. Diazepam can be alternated to chlorpromazine 100mg   06h-09h 09h-12h 12h-03h 03h-06h 06h-09h 09h-12h 12h-03h 03h-06h DZP                 CPZ                 Drug given Drug NOT given This scheme can be used for Rabies as well

183. Tetanus General Management Cleaning of the wound with spirit or disinfectant. No operative procedures on the wound of a patient with established tetanus. Nursing in quiet dark rooms, in semi prone position . Close attention to fluid support Respiratory support Follow up Care Change position every 2 hours. Raise the foot of the bed. Medication chart. Immunize against tetanus all recovery patients.

184. Tetanus Health messages for Prevention and Control Proper surgical treatment of wounds (removal of foreign bodies/necrotic tissue). Active immunization First three doses given in childhood (DPT 1,2,3) If primary immunization was completed and injury occurs later in life => 1 BOOSTER DOSE (protective for 7-10 years).

185. Tetanus Health messages for Prevention and Control If no proper primary immunization any patient with a wound receives SHORT TERM PASSIVE IMMUNIZATION WITH ANTI-TETANUS SERUM (ATS, that can give reactions) Patients are managed with penicillin and a booster of TT. Very contaminated wounds are treated with Human Tetanus Immunoglubulins (HTIG)

186. Tetanus Health messages for Prevention and Control Tetanus neonatorum is prevented by active immunization of the mother, during pregnancy . The antibodies generated by the mother pass the placenta and are transferred to the foetus. The newborn obtains antibodies passively from the mother. Vaccine: Tetanus Toxoid (TT) Recommended Timing Expected Protection TT1 1 st Contact or 1 st ANC visit NO PROTECTION TT2 4 wks after TT1 3 YEARS TT3 6 months after TT2 or during next pregnancy 5 YEARS TT4 1 year after TT3 or during next pregnancy 10 YEARS TT5 1 year after TT4 or during next pregnancy ALL CHILD BEARING YEARS

187. Tetanus Role of RHN Health education , particularly to pregnant women, people exposed to occupational hazards (farmers, garners…) and children . Promotion of and participation to Immunization campaigns. Treatment and follow up of patients with contaminated wounds and assessment of immunization status. Management (nursing) of patients with manifested tetanus (treatment, position, sedation and fluid balance chart…).

188. STIs & HIV/AIDS Definition Sexually transmitted diseases (STDs) and sexually transmitted infections (STIs) are communicable diseases or infections whose predominant mode of transmission is through sexual contact , be it hetero-sexual or homo-sexual. STIs refer to conditions that are normally in a pre-clinical stage ( symptoms not developed yet ) STDs refer to conditions in clinical stage . HIV/AIDS will be treated separately.

189. STIs & HIV/AIDS Risk Factors BIOLOGICAL Microbiological characteristic Hormonal factors Immunological profile

190. STIs & HIV/AIDS Risk Factors INDIVIDUAL (BEHAVIOURAL ) Age of sexual intercourse Multiple partners Frequency of partner change Frequency of exposure Sexual practices Substance abuse

191. STIs & HIV/AIDS Risk Factors SOCIAL (BEHAVIOURAL) Use (or not) of barrier methods Monogamy or polygamy Inadequate health seeking behaviour Compliance with treatment Self medication Inadequate partner treatment social and cultural conditioning

192. STIs & HIV/AIDS Risk Factors DEMOGRAPHIC => sexual activity is greatest between adolescence and 2 nd -3 rd decades of life. Countries with a high proportion of youngsters might see many cases of STI/Ds. Marital status Employment patterns. SOCIO-ECONOMIC => Poverty Urbanization Prostitution Promiscuity “Sex-for-food”, “sex-for-school fees”, etc… Low educational level

193. STIs & HIV/AIDS Clinical Features STIs presenting with GENITAL DISCHARGE Gonorrhea Urethritis due to Chlamydia trachomatis or N.S.U. Trichomoniasis Bacterial vaginosis Candidiasis STIs presenting with GENITAL ULCER /Sores/Swelling/Lumps in the groin Syphilis Chancroid Lymphogranuloma venereum Condilomata acuminata (venereal warts) Herpes Simplex Molluscum Contagiosum Scabies Pediculosis Pubis (crab lice infestation) Granuloma inguinale STIs presenting as DISEASE ELSEWHERE IN THE BODY Syphilis Gonorrhea HIV/AIDS Chlamydia infection Hepatitis A, B or C

194. STIs & HIV/AIDS Diagnosis Laboratory diagnosis is very advanced for STIs and many organisms can be identified by very specific tests. It is possible to amplify genetic material of organisms difficult to detect ( PCR ). Where these facilities are not available: Syndromic approach

195. STIs & HIV/AIDS Investigations and rationale Wet preparations and simple GRAM stains can be done for venereal discharge. Serological tests for Syphilis (VDRL, TPHA, RPR) need to be done on all cases of genital ulcer . All patients with STIs should be offered HIV test . All patients should be informed on the need to inform and treat their partner(s)

196. SYNDROMIC APPROACH TO STIs URETHRAL DISCHARGE Patient complains of urethral DISCHARGE & DYSURIA Take history and examine. Milk urethra if necessary Discharge confirmed? Any other genital disease? TREAT FOR GONOCOCCAL INFECTIONS AND CLAMYDIA TRACOMATIS Educate & counsel Promote condom use and provide condoms Manage and treat partner Offer HIV counseling and testing (if available) Ask the patient to return in 7days if symptoms persist Use proper flow chart Educate & counsel Promote condom use and provide condoms Offer HIV counseling and testing (if available) Review in 7days if symptoms persist YES YES NO NO

197. SYNDROMIC APPROACH TO STIs LOWER ABDOMINAL PAIN Patient complains of LAP Take history Including gynecological) and examine (abdominal & vaginal) ANY OF THE FOLLOWING PRESENT? Missed/overdue period? Recent delivery/abortion/discharge? Abdominal guarding or rebound tenderness? Abnormal vaginal bleeding? Abdominal mass? Is there cervical excitation tenderness? lower abdominal tenderness? vaginal discharge? Manage for PID Review in 3 days Continue Rx until completed Educate & counsel Promote condom use and provide condoms Offer HIV counseling and testing (if available ) Refer for surgical/gynecological opinion. Before referral set up an IV line and apply resuscitatory measures if necessary YES NO YES YES Patient has improved? YES Any other illness found? NO Manage appropriately YES NO Refer NO

198. SYNDROMIC APPROACH TO STIs VAGINAL DISCHARGE Patient complains of VAGINAL DISCHARGE, VULVAL ITCHING OR BURNING Take history and examine; assess risk Abnormal vaginal discharge or vulvar erythema? Lower abdominal tenderness? TREAT FOR CANDIDA ALBICANS HIGH PREVALENCE OF GC/CT? YES Any other genital disease? YES Use proper flow chart Use proper flow chart LAP NO NO TREAT FOR BACTERIAL VAGINOSIS & TRICOMONAS VAGINALIS YES YES TREAT FOR GONOCOCCAL INFECTIONS AND CLAMYDIA TRACOMATIS, BACTERIAL VAGINOSIS & TRICOMONAS VAGINALIS NO NO YES Vulvar oedema, curd-like discharge, escoriations? Educate & counsel Promote condom use and provide condoms Offer HIV counseling and testing (if available) NO YES Educate & counsel Promote condom use and provide condoms Offer HIV counseling and testing (if available) YES

199. SYNDROMIC APPROACH TO STIs GENITAL ULCERS Patient complains of GENITAL SORE or ULCER Take history and examine Only vesicles present? Ulcer(s) HEALED? CONTINUE RX FOR OTHER 7 DAYS YES Sore or Ulcer present ? YES NO TREAT FOR HSV2 TREAT FOR SYPHILIS IF INDICATED YES NO NO YES Educate & counsel , condom use and provision, HIV counseling and testing, offer Partner’s NO YES Educate & counsel Promote condom use and provide condoms Offer HIV counseling and testing (if available) ASK PATIENT TO RETURN IN 7 DAYS YES TREAT FOR SYPHILIS and CHANCROID. TREAT FOR HSV2 Ulcer(s) IMPROVING? Refer Educate & counsel Promote condom use and provide condoms Offer HIV counseling and testing (if available)

200. STIs & HIV/AIDS Specific Management => Drug does course Gonorrhea Azytromicine 1gr single p.o. single dose OR Norfloxacyn 800mg or (Cypprofloxacine 500mg) p.o. single dose . IF SYMPTOMS PERSISTS: Metronidazole 2gr single dose. Clamydia infections (LGV) Doxycycline 100mg daily for 2 weeks : IN PREGNANCY: Erythromycin 500mg qid for 2 weeks .

201. STIs & HIV/AIDS Specific Management => Drug does course Non-Gonococcal (Non Specific) Urethritis) => Clamydia t . &/or Ureoplasma ureolyticum . Doxycycline 100mg bid x 5-7 days OR Erythromicin 500mg qid x 7days FOR PERSISTENT/RECURRENT CASES: Erythromicin 500mg qid x 7days COMBINED WITH Metronidazole 400mg bid x 5days.

202. STIs & HIV/AIDS Specific Management => Drug does course Syphilis BENZATHINE PENICILLIN 2.4 MU intramusc . (half on each buttock) single dose (or weekly for 4 doses in case of syphilis longer ha 1 year). IN CASE OF ALLERGY TO PENICILLIN: Erythromycin 500mg qid x 10 days . Trichomoniasis Metronidazole 2gr single dose swallowed under supervision. OR Metronidazole 400mgtds x5 days OR Tinidazole 2gr single dose .

203. STIs & HIV/AIDS Specific Management => Drug does course Vaginal Candidiasis Nystatine (or Clotrimazole) pessary (intravaginal) 1 od at night time x 7-10 nights Oral Fluconazole 400mg start and 200mg od x 10-14 days Herpes Simplex Virus (HSV-2) Acyclovir 800mg 5 times per day for 5-7days

204. STIs & HIV/AIDS Health messages Holistic approach=> the “4C”: COUNSELLING to prevent further transmission COMPLIANCE to take full course medication CONDOM use if one cannot abstain from sex CONTACT TRACING : always treat partner(s) Reducing rate of sexual partner change Reducing efficiency of transmission (safer sex practices) Reducing duration of infectiousness (treatment of patients and partners) Population level approaches targeting: the core groups of transmitters (CSWs) and the groups at risk (students, soldiers, labourers, hotel and bar workers)

205. STIs & HIV/AIDS Role of RHN Health education, treatment and follow up, counseling, provision of skills and/or family planning and/or barrier methods.

206. Some notes on: HIV/AIDS Definition The Acquired Immunodeficiency Syndrome (AIDS) is a systemic viral disease caused by the Human Immunodeficiency Virus ( HIV ) with a latency or asymptomatic period which ranges from few months to as many as 17 years . The progression of the disease is variable but ends up in immunodeficiency of the body which results in death from opportunistic infections and tumors .

207. Some notes on: HIV/AIDS Cause/Predisposing Factors HIV attacks Lymphocytes CD4. With the destruction of CD4 cells, immunity falls and opportunistic infections prevail.

208. Some notes on: HIV/AIDS Cause/Predisposing Factors HIV attack CD4 and is present in all body fluids. However it reaches MINIMAL INFECTIOUS CONCENTRATION in: Blood Semen Vaginal secretions

209. Some notes on: HIV/AIDS Clinical Features The disease develops through stages according to the decreased number of CD4 cells: STAGE 1: ASYMPTOMATIC STAGE 2: MILD DISEASE STAGE 3: ADVANCED DISEASE STAGE 4: SEVERE DISEASE (AIDS ) DEATH PRIMARY INFECTION

210. Some notes on: HIV/AIDS Diagnosis of HIV Once HIV has infected a person, his/her Immune System reacts, producing antibodies that are not protective but are a marker of occurred infection. These antibodies are used to make diagnosis of HIV infection. HIV tests are based on the detection of antibodies Anti-HIV. These tests cannot be used in children les than 18 months because during this period we still find antibodies produced by the mother.

211. Some notes on: HIV/AIDS The “Window Period” If recent exposure or high risk, have occurred and the test shows a negative result , this can mean that: either the person is not infected with HIV or is infected but it has not yet developed the antibodies against the virus This is the so called “Window Period” that can last from 3 to 6 months!. Antibodies are not detectable (too few). BUT THE PERSON IS INFECTIOUS Repeated HIV testing can be offered after 8 weeks.

212. Some notes on: HIV/AIDS Prevention and Control of HIV ABC Prevention Model: A = ABSTAIN B = BE FAITHFUL to your partner C = use CONDOM continuously & consistently

213. Some notes on: HIV/AIDS Prevention and Control of HIV ABC Prevention Model: The ABC approach has long been used as the foundation of ‘comprehensive’ HIV prevention programmes around the world. ABC’s sole focus is on sexual transmission —a focus that fails to address other modes of HIV transmission. The approach falls short to include testing, care and treatment for people living with HIV as well as the empowerment of people infected and affected to most effectively address the epidemic. The ABC approach implies that people who are HIV positive have failed at abstinence and being faithful. It also suggests that people should abstain and that condoms are a last resort.

214. Some notes on: HIV/AIDS Prevention and Control of HIV S.A.V.E. Prevention Model S = Safer Practices A = Access to Treatment V = Voluntary Counselling and Testing E = Empowerment The SAVE response originated as a reaction to build on the strengths and shortcomings of the ABC approach

215. Some notes on: HIV/AIDS Prevention and Control of HIV: S.A.V.E. Prevention Model Safer practice Availability of Medication Voluntary Counselling and Testing Empowerment Abstinence Being faithful Correct and consistent use of condoms (male and female condoms) Positive prevention PMTCT that involves fathers Screening blood products and clean medical equipment Safe medical control practices Clean needles, harm reduction for drug users and safe scarification practice Male circumcision PRE & POST exposure prophylaxis Treatment as prevention Safer traditional practices Medication: Treatment services: Information, care and support Counselling and testing for HIV. To prevent HIV transmission. Testing for sero-discordancy Education Economic empowerment Gender empowerment Meaningful involvement and inclusion of PLHIV and affected communities. Promoting inclusion and social transformation

216. Some notes on: HIV/AIDS Prevention and Control of HIV: Prevention from mother to child transmission (PMTCT)

217. Some notes on: HIV/AIDS Prophylaxis drugs For OIs: Prophylaxis with Cotrimoxaole or Dapsone Isoniazid Fluconazole ARVs work like the brakes of this car Treatment of HIV: Treatment with Antiretrovirals (ARVs)

218. Unit three Measurements of Morbidity and Mortality Learning Objectives At the end of this unit the student is expected to: Describe the differences between ratio, proportion and rate Calculate the most important morbidity and mortality measures

219. Measurement of health Epidemiology is mainly a quantitative science. Measures of disease frequency are the basic tools of the epidemiological approach. Health status of a community is assessed by the collection, compilation, analysis and interpretation of data on illness (morbidity), death (mortality), disability and utilization of health services .

220. The most basic measure of disease frequency is a simple count of affected individuals. Such information is useful for public health planners and administrators for proper allocation of health care resources in a particular community. However, to investigate distributions and determinants of disease, it is also necessary to know the size of the source population from which affected individuals were counted.

221. One of the central concerns of epidemiology is to find and enumerate appropriate denominators in order to describe and compare groups in a meaningful and useful way. Such measures allow direct comparisons of disease frequencies in two or more groups of individuals. Ratios, proportions, and rates Ratio A ratio quantifies the magnitude of one occurrence or condition to another. It expresses the relationship between two numbers in the form of x: y or x/y X k Example: The ratio of males to females (M:F) in South Sudan.

222. The ratio of male malaria patients to female malaria patients. Proportion A proportion quantifies occurrences in relation to the populations in which these occurrences take place. It is a specific type of ratio in which the numerator is included in the denominator and the result is expressed as a percentage. Example: The proportion of all births that was male Male births x 100 Male + Female births Rate Rate is the most important epidemiological tool used for measuring

223. diseases. Rate is a special form of proportion that includes time. It is the measure that most clearly expresses probability or risk of disease in a defined population over a specified period of time, hence, it is considered to be a basic measure of disease occurrence.

224. Continue….. Accurate count of all events of interest that occur in a defined population during a specified period is essential for the calculation of rate. Rate = Number of events in a specific period x k Population at risk of these events in a specified Period Example: The number of newly diagnosed pneumonia cases in 1999 per 1000 under five children.

225. Measurements of morbidity Morbidity rates are rates used to quantify the occurrence of disease. Measures of morbidity include incidence, period prevalence, and point prevalence rates. Incidence rate The incidence of a disease is defined as the number of new cases of a disease that occur during a specified period of time in a population at risk for developing the disease.

226. Continue…. Incidence rate = Number of new cases of a disease over a period of time X K Total Population during the given period of time The critical element in the definition of incidence is new cases of disease. Because incidence is a measure of new events (i.e. transition from a non-diseased to a diseased state), incidence is a measure of risk.

227. Continue… The appropriate denominator for incidence rate is population at risk but knowing the population at risk is difficult at this level. Hence, total population can be used as a denominator. Another important issue in incidence is the issue of time. For incidence to be a measure of risk we must specify a period of time and we must know that all of the individuals in the group represented by the denominator have been followed up for that entire period.

228. The choice of time period is arbitrary: We could calculate incidence rate in one week, one month, one year, 5 years, and so on. Incidence rates can be used to make statements about the risk of disease. If the incidence rate of a certain disease is high in one area, then the risk of acquiring that disease by other healthy individuals will be high. Example. In Torit 2020 there were 50 new cases of relapsing fever in “Magui X”. The average total population of “Magui X” was 5000.

229. Calculate the incidence rate of relapsing fever in “Magui X” in Magui 1995. Answer- Incidence rate = 50 X 1000 = 10 new cases per 1000 population 5000. That means out of every 1000 people living in “Magui X”, 10 of them acquired relapsing fever in Magui 2020. Another commonly used measure of morbidity is attack rate. Attack rate is a type of incidence rate which is mainly used during epidemics .

230. Attack Rate Attack rate = No. of new cases of a specific disease reported during an epidemic X k Total population at risk during the same time On Tir 7, 1995, 100 people were invited by Ato Alemitegnaw for dinner. All of them ate the food that was served for dinner. The next day (Tir 8, 1995) 90 of the 100 people who ate that food developed diarrhea. Calculate the attack rate of diarrhea which occurred on Tir 8, 1995.

231. Attack rate = 90 X 100 = 90 cases of diarrhea per 100 people, 100 That means out of 100 people who ate the food served by Ato Alemitegnaw, 90 of them developed diarrhea on Tir 8, 1995. Uses incidence rate Incidence rate is important as a fundamental tool for etiologic studies of diseases since it is a direct measure of risk. If the incidence rate is significantly higher in one area, then the cause of that disease can be systematically searched.

232. Prevalence rate Prevalence rate measures the number of people in a population who have a disease at a given time. It includes both new and old cases. The major type of prevalence is point prevalence rate. Point Prevalence rate : measures the proportion of a population with a certain condition at a given point in time. Point prevalence rate can be determined by conducting cross-sectional study. Point Prevalence rate = All persons with a specific Condition at one point in time X K Total population

233. Example: One health extension worker conducted a survey in one of the nearby elementary schools on Hidar 10, 1996 to know the prevalence of trachoma in that school. The total number of students in that school was 200. The health extension worker examined all the 200 students for trachoma. Hundred students were found to have trachoma.

234. Calculate the point prevalence rate of trachoma for that school. Point prevalence rate= 100 X 100 = 50 trachoma patients per 100 students 200 on Hidar10,1996 That means 50 % of the students in that elementary school were affected by trachoma on Hidar 10, 1996.

235. Uses of prevalence rate Planning health facilities and human resource Monitoring chronic disease control programs like tuberculosis control program 6.4 Measurements of Mortality Mortality rates and ratios measure the occurrence of deaths in a population using different ways. Rates whose denominators are the total population are commonly calculated using either the mid - interval population or the average population.

236. This is done because population size fluctuates over time due to births, deaths and migration. Population count at the beginning + Population count Average population = at the end of the time interval considered Below are given some formulas for the commonly used mortality rates and ratios.

237. 1. Crude Death rate (CDR) CDR = Total no. of deaths reported during a given time interval X 1000 Estimated mid interval population The Crude Death Rate measures the proportion of the population dying every year, or the number of deaths in the community, per 1000 population. It reflects the risk of death in that community or country.

238. Currently the Crude Death Rate in Ethiopia is 12.6 per 1000 population (1995 health & health related indicators, MOH). That means out of 1000 total population about 13 people die each year. 2. Age- specific mortality rate = No. of deaths in a specific age group during a given time X 1000 Estimated mid interval population of specific age group One example of age specific mortality rate is Infant Mortality Rate .

239. Unit four Epidemiological studies

240. Source of Epidemiological data and Epidemiological studies Epidemiology is research-oriented subject and data for description of the distribution of disease and analyzing determinants may be obtained from two main sources. These are a) Routine statistics, and b) Field surveys. Data generated in the process provision of health care and in other health related activities. This is referred to as routine statistics. Data may also be collected from field surveys and used for epidemiologic purposes

241. Types of epidemiologic studies Epidemiology is a tool for describing disease and health states in medical and public health practice. Epidemiological studies may be classified according to their purpose, i.e. descriptive or analytic , or in the way they are assembled and conducted, i.e. observational or experimental .   Descriptive studies are those that describe the patterns of occurrence and distribution of disease in different human populations defined by person, place and time.

242. In this type of study, the characteristics of patients with a specific disease or diseases are described. This is usually useful in the early stages of disease investigation before detailed epidemiological studies can be done. Such descriptions may be in the form of service records and reports or case studies or case series. These only give the initial indications of possible correlations between disease and causal factors inherent in geographic areas or ecological zones, time periods or season or individuals or groups of persons

243. A case series is the simplest form of a descriptive study. Health service reports are commonly used to describe the occurrence and distribution of disease among the users of the services provided. Analytic studies are those which describe the relationship or association between the occurrence of disease in different human populations and the factors that influence the occurrence. The studies test hypotheses about diseases and their causal factors as a step towards the identification of causes and prevention of disease. Analytic studies are further subdivided into observational and experimental.

244. Observational studies , also referred to as non-interventional studies, are analytic studies in which observations and measurements are made on and data collected from individuals or populations and analyzed, and conclusions and deductions are made based on this. Observational studies are useful for the description of disease in populations and for the analysis of aetiology or causation of disease.

245. Experimental studies , also referred to as interventional studies, are analytic studies in which conditions of study are deliberately changed before observations and measurements are made and data collected and conclusions and deductions are made based on this. Experimental studies are useful for the evaluation of the efficacy of new preventive and therapeutic measures.

246. PRINCIPLES OF EPIDEMIC MANAGEMENT Epidemic management has been described as the process of anticipating, preventing, preparing for, detecting, responding, and controlling epidemics in order that the health and economic impacts are minimized. 9  It is an all-embracing term that described all that needs to be done before, during, and after epidemics. It involves anticipating or predicting the occurrence of an outbreak such that it could be prevented.

247. However, if the outbreak could not be totally prevented, it involves preparedness so that there is a readiness to respond. Early detection through a sensitive surveillance system is required to know when and where the outbreak occurs to limit its spread. Most importantly, a coordinated and rapid investigation is required to describe the outbreak and identify interventions. Following which an effective response will be required to implement appropriate control measures. An epidemic management would not be complete without an evaluation to identify what went right and wrong before and during the outbreak.

248. From the foregoing, preparedness is a subset of epidemic management. Epidemic preparedness constitutes all the activities that have to be undertaken from the national to the health facility levels to be ready to respond effectively to disease outbreaks. Moreover when all the activities are put together in a plan, and then we have an epidemic preparedness and response plan (EPR). The elements of an epidemic preparedness will include to ensure that routine surveillance system can detect outbreaks as soon as it occurs, and to ensure that staff are organized to confirm, investigate, and respond to outbreaks.

249. Although epidemic management requires adequate knowledge of medical and/or public health, effective management requires proper coordination of all the specialty areas involved in response activities. Information could be obtained rapidly from reference books and/or disease specialists.  Figure 1  illustrates the EOC conceptual model for coordinating responses to an epidemic.

250. Figure 1 Epidemic management using an emergency operating center model

251. Although laboratory testing may not be required in all epidemics, the laboratory experts are involved in specimen transportation, transfers, and diagnosis. The needs to educate the general population and special groups such as the health workers are usually necessary during epidemics. The coordinating team is made up of representatives of the technical subgroups, the logistics and administrative personnel and headed by the representative of the Commissioner for Health