COMMUNICABLE DISEASES NOTES COMMUNICABLE DISEASE - an illness caused by an infectious agent or its toxic products that are transmitted

directly or indirectly to a well person through an agency, a vector or an inanimate object. CONTAGIOUS DISEASE - a term given to a disease that is easily transmitted from one person to another through direct or indirect means. INFECTIOUS DISEASE - is those that are transmitted not only by ordinary contact but requires direct inoculation of the organism through a break on the skin or mucous membrane INFECTION - the implantation and successful replication of an organism in the tissue of the host resulting signs and symptoms as well as immunologic response. ISOLATION - the separation of an individual suffering from a communicable disease from other persons. QUARANTINE - the limitation of freedom of movement of persons or animals which have been exposed to communicable disease/s for a period of time equivalent to the longest incubation period of that disease. SPORADIC DISEASE - these are diseases that occur occasionally and irregularly with no specific pattern. EPIDEMIC DISEASE - is a disease that occurs greater than expected number in a specific area over a specific time. PANDEMIC - is an epidemic that affects several countries or continents. ENDEMIC DISEASE - is those that are present in a population or community at times PATHOGNOMONIC SIGN - pointing out the nature of sickness or disease making the true diagnosis recognizable. STAGES OF INFECTION Incubation Period: time between the entry of microorganism into the body and the onset of the symptoms. Prodromal Period: the time from the onset of non- specific symptoms such as fatigue, malaise, fever and irritability with specific symptoms of infection appears. Full Stage Illness Period: during this period specific symptoms develop and become evident. Convalescent Period: extends from the time the symptoms start to about until the person returns to the normal state of health CHAIN OF INFECTION Causative Agent/ Infectious Agent: any microbe capable of producing a disease. Reservoir or Source of Pathogen Growth: is a place where pathogen can survive but may or may not multiply. The Portal of Exit: the path or way in which the organism leaves the reservoir Mode of Transmission: the means by which the infectious agent passes from the portal of exit from the reservoir to the susceptible host.

 Portal of Entry: the venue where the organism gain entrance into the susceptible host. Susceptible Host: the human body has many defenses against the entry and multiplication of organism.

DEFENSES AGAINST INJURY 1. Intact Skin and mucous membrane - first line of defense 2. Mononuclear Phagocyte System (MPS) 3. Inflammatory response 4. Immune system MONONUCLEAR PHAGOCYTE SYSTEM (MPS) Consists of monocytes and macrophages and their precursor cells known as the Reticuloendothelial system (RES) which consists of: 1. Fixed phagocytes macrophages of the liver, spleen, bone marrow, lungs and lymph nodes 2. Mobile or wandering phagocytes- monocytes in the blood and macrophages found in connective tissues, known as Histiocytes Functions of MPS: Recognition & phagocytosis of foreign material such as microorganism Removal of old & damaged cells from circulation Participation in the immune response

INFLAMMATION is a pathophysiologic response that serves to defend the tissues against microorganisms, injury or irritation and to prepare the tissue for repair (local and non-specific) . It is the bodys almost uniform systemic response to any insult or injury. first response of the immune system to infection or irritation characterized by the following quintet: redness (rubor), heat (calor), swelling (tumor), pain (dolor) and dysfunction of the organs involved (functio laesa). INFLAMMATORY RESPONSE Is a sequential reaction to cell injury. Incorrectly used as synonym for infection. INFLAMMATION IS ALWAYS PRESENT WITH INFECTION, BUT INFECTION IS NOT ALWAYS PRESENT WITH INFLAMMATION. ACUTE INFLAMMATORY RESPONSE Occurs when first line of defense is broken by cellular injury Injury can be caused by: trauma or surgery chemical agents temperature extremes invasion of micro-organisms oxygen/nutrient deprivation (ischemic damage) genetic/immune defects (e.g. autoimmune) INFLAMMATORY RESPONSE First Stage Vascular and Cellular response Second Stage Exudate production Third Stage Reparative phase VASCULAR RESPONSE Vascular permeability after cell injury, the capillaries in the area briefly undergo vasoconstriction after the release of histamine & other chemicals by the injured cells, the vessels dilate resulting in hyperemia, which raises filtration pressure CLINICAL ASPECTS OF ACUTE INFLAMMATION Redness (rubor) An acutely inflammed tissue appears red, for example skin affected by sunburn, cellulitis due to bacterial infection or acute conjunctivitis. This is due to dilatation of small blood vessels within the damaged area.

Heat (calor) Increase in temperature is seen only in peripheral parts of the body, such as the skin. It is due to increased blood flow (hyperaemia) through the region, resulting in vascular dilatation and the delivery of warm blood to the area Swelling (tumor) Swelling results from edema, the accumulation of fluid in the extra vascular space as part of the fluid exudate, and to a much lesser extent, from the physical mass of the inflammatory cells migrating into the area. Pain (dolor) For the patient, pain is one of the best known features of acute inflammation. It results partly from the stretching and distortion of tissues due to inflammatory oedema and, in particular, from pus under pressure in an abscess cavity. Some of the chemical mediators of acute inflammation, including bradykinin, the prostaglandins and serotonin, are known to induce pain Loss of function (functio laesa) a well-known consequence of inflammation, was added by Virchow (1821-1902) to the list of features drawn up by Celsus. Movement of an inflamed area is consciously and reflexly inhibited by pain, while severe swelling may physically immobilize the tissues

CELLULAR RESPONSE Margination/Pavementation phagocytes line up at the walls of the blood vessels Diapedesis/Emigration phagocytes move out of the blood vessels by squeezing through the blood vessel walls Ameboid motion slithering (glide or slide like a snake) through the tissue spaces Chemotaxins injured tissues release substances which exert magnet-like force or chemicals to the phagocytes to bring them to the area of injury Phagocytosis engulfing or ingestion of microorganisms, foreign particles or other cells by phagocytes

ACUTE INFLAMMATORY RESPONSE Chemical mediators: Histamine released from mast cells & basophils Plasma factors: kinins and clotting factors Prostaglandins: stimulate inflammatory response Cytokines: enhance inflammatory response

Interferons: stimulate immune cell production & enhances the bodys defenses against viral & parasitic infections Tumor necrosis factor (TNF): produced by macrophages in response to infection with gram-negative bacteria

MANIFESTATIONS OF INFLAMMATION Local symptoms: rubor (redness) > blood flow to area tumor (swelling) > capillary permeability calor (heat) > blood flow to area dolor (pain) stretching of nerves by swelling Systemic Changes: Fever Leukocytosis Increase in circulating plasma proteins Septic Shock: < BP, > HR, > RR infection Scar tissue formation CHRONIC INFLAMMATION Can occur as a distinct process without much acute inflammation Some micro-organisms have cell walls that are very high in lipid & wax content, making them relatively insensitive to degradation by phagocytes These bacteria continue to stimulate inflammation (e.g. tuberculosis & syphilis EXUDATE PRODUCTION Fibrinogen Thromboplastin Platelets REPARATIVE PHASE Regeneration Fibrous tissue formation Granulation Tissue Resolution and Repair Healing: Minor injury: return to normal structure & function Extensive damage: infection with abscess or granuloma formation repair takes place

 Repair: Replacement of destroyed tissue with scar tissue fill in the wound cover, seal, or shrink the wound Cell Repair or Healing WOUND HEALING Primary Intention: minimal tissue loss wound edges are close together no infection & little scarring Secondary Intention: wounds requiring a lot of tissue replacement heal from bottom upward extensive scarring staphlycocus may be present Regeneration occurs when the injured cells & tissues are replaced by new cells & tissues that are identical in nature & function to the damaged cells Scar formation involves replacement of damaged tissue cells by fibrous/connective tissue formation such as in the healing of tendons, fascia, connective tissues, & collagenous structure Dysfunctional Wound Healing May occur at any phase of wound healing insufficient repair (e.g. dehiscence) excessive repair infection Etiological Causes: Diabetes Mellitus, anti-inflammatory agents Hypoxemia, hypovolemia, poor nutrition Age (infants vs. elders) NURSING INTERVENTIONS FOR CLIENTS WITH INFLAMMATION 1. Promote rest. 2. Reduce swelling: Position elevate the affected body part to promote venous return. Heat and Cold Application cold application during the 1st 24 -48H; heat application may be used later & when swelling has subsided. 3. Relieve pain. 4. Increase excretion of microorganisms by adequate hydration. 5. Provide adequate nutrition. high caloric, high protein, with Vitamins A and C-rich foods 6. Pharmacotherapy Analgesic/Antipyretic: aspirin, acetaminophen, paracetamol, mefenamic acid Antiinflammatory: non-steroidal anti-inflammatory drugs (NSAIDs): ibuprofen, piroxicam Antimicrobials: antibiotics to control infection

7. Surgery Incision and Drainage to remove inflammatory exudates & promote healing process Debridement - to remove necrotic/ dead tissues

Below is a list of the chemical signals that are produced, which cells produce them and the effects that they have on the metabolism. Cytokines involved in the Inflammatory Response Producing cell Action Macrophages T cells T cells T cells T cells Stimulation of various cells, e.g. T cells, acts to initiate inflammation, induces hypothalamus to increase body temperature Causes proliferation of activated T and B cells, induces antibody synthesis Induces growth and differentiation of immune cells in bone marrow Promotes B cell growth and differentiation Induces differentiation of B cells, and activates some Microphages

Cytokine Interleukin-1 Interleukin-2 Interleukin-3 Interleukin-4 Interleukin-5 Interleukin-6 Interleukin-10 Interleukin-12 Interleukin-13 GammaInterferon Tumor Factor Necrosis

T cells, Costimulator of T cells, induces growth in B cells Macrophages T cells Macrophages T cells Activates B cells and inhibits Macrophage function Activates T cells and NK cells Induces proliferation of B cells and differentiation of T cells

T cells, NK cells Activates Macrophages Macrophages Causes activation of some Microphages. Induces inflammation and fever. Induces catabolism of muscle and fat, thus leading to cachexia (bodily wasting)

Transforming Growth Factor Lymphotoxin Histamine

T cells, Inhibits T cell growth and Macrophage activation Macrophages T cells Mast cells Similar to TNF, activates Microphages Not actually a cytokine, but an important chemical mediator that induces blood vessel dilation and increases cell wall permeability

As you can see from the list above, the cells of the immune system communicate and cooperate in a complex fashion. An important point to note is that invading organisms, if they interfere with any of the chemicals above, or the cells that produce them, can cause a profound change on the bodys immune response to that organism.

IMMUNITY
Immunity - a condition of being secure against any particular disease. Types of Immunity: Natural or Innate Artificial or Acquired Sub clinical: Immunity acquired through constant exposure to a particular disease or organism Innate: Native or Natural Resistance Not produced by an immune response One type of natural immunity that exists at birth Species specific For example, we are not prone to infectious agents that cause illness in other species (e.g. canine distemper) Acquired: formed after birth Produced by an immune response Active: following an exposure to antigen or immunization Passive: does not involve the hosts immune response T lymphocytes or preformed antibodies are transferred to host Temporary - such as tetanus, rabies exposure, snake bite IMMUNE RESPONSE Key Cells are Lymphocytes Recognize micro-organisms 2 types develop in bone marrow T - Cells: lymphokine, macrophages, cytotoxic, helper, suppressor, Mature in thymus and move to the spleen B - Cells:(10-20% of lymphocytes) Mature in bone marrow and move to the spleen Infection causes maturation into Plasma Cells Plasma Cells secrete antibodies antigen receptors Cell Mediated Immunity (CMI) T - Cells (helper & killer) fight invading microbes and destroy infected cells To boost CMI the immune system produces cytokines (soluble molecules) govern the development of antigen-specific immunity Interferon, Interleukin-2, Interleukin 12 Interferon elicits uninfected neighboring cells to produce antiviral proteins Humoral Immunity: Immune system depends on the production of antibodies made by mature, antibody secreting B - Cells To strengthen this response the immune system releases cytokines Interleukin-4, IL 6, IL-10 T - Cells (CMI) are essentially responsible for stimulating antibody production by B - Cells

IMMUNE FUNCTION Fetal Last trimester: fetus is able to produce an immune response to various infections IgG is not sufficient and maternal transfer occurs Figure 6-21, p. 193 Neonate IgG is near adult levels and then drops by 5-6 mos. Human infant is immunologically immature at birth Elder Immunologically at risk declined function with age Decreased T-cell and specific antibody function Increased autoantibodies that attack normal tissue Infections, cancers and autoimmunity take place

INFLAMMATORY VS. IMMUNE

Inflammatory response nonspecific occurs in the same manner whether an initial or second exposure Immune response antigen specific has a memory The success of a pathogen is dependent upon Virulence and portal of entry Gram negative are most problematic Trick the phagocytes Harm vessels by forming clots E-coli is very aggressive pathogen Can move from local site to septicemia Compromised host is at extreme risk Sepsis to death can occur from gram negative or positive Immunosuppression Immune deficiency can be Primary:Inherited X-Linked: A Gamma-Globulinemia SCID: Severe Combined Immunodeficiency Secondary: Acquired Neoplasia of Immune System Hodgkins Disease: Neoplasm of Lymphoid Cells AIDS: A depletion syndrome of the T - Cells Use of corticoid steroids Iatrogenic immunodeficiency: Caused by RX for Neoplasias

VECTOR/VEHICLE BORNE DISEASES DENGUE FEVER/ DENGUE HEMORRHAGIC FEVER (BREAKBONE FEVER; DANDY FEVER/ HEMORRHAGIC FEVER; THROMBOCYTOPENIC PURPURA) CAUSATIVE AGENT: Flavirus 1, 2, 3, 4; Arbovirus; Westnile; Chinkungunya; Onyonyong virus. MODES OF TRANSMISSION: By the bite of an infected Female Aedes Aegypti PATHOGNOMONIC SIGN: Herman sign: maculopapular rash starts at distal portion of the extremities with blanched areas. CLINICAL MANIFESTATION: GRADE I: Fever Accompanied with non specific symptoms (myalgia, anorexia and vomiting) and (+) Tourniquet Test (Rumpel leads test): more than 20 petechia/ square inch. GRADE II: All signs of grade 1 plus spontaneous bleeding from the nose, gums etc. GRADE III: Circulatory Failure. GRADE IV: Profound shock. DIAGNOSTIC EXAMS Torniquet test / Rumple Leads test Hematocrit level Platelet count NURSING INTERVENTIONS Administer medications as needed. Vitamin K to promote blood clotting. Antipyretics for fever. No aspirin. Control bleeding Avoid shock Symptomatic / supportive care 4 oclock habit by DOH C hemically treated mosquito nets L arvivorous fishes E nvironmental sanitation A nti-mosquito soaps N ymph tree / eucalyptus tree Isolation of the infected person (sleeping under the mosquito net) Case finding and reporting

PREVENTION AND CONTROL: THE INFECTED INDIVIDUAL, CONTACTS AND ENVIRONMENT: Recognition of the disease. Isolation of patient. Epidemiological investigation. Case finding and reporting. Health education. CONTROL MEASURES: Avoid too many hangings clothes inside the house. Residual spraying with insecticides. Eliminate vectors by: Changing water and scrubbing sides of lower vases once a week. Destroy breeding places of mosquito by cleaning surrounding, proper disposal of rubber tires, empty bottles and cans. Keep water containers covered. MALARIA (AGUE) CAUSATIVE AGENT: Plasmodium Falciparum Plasmodium Vivax Plasmodium Malariae Plasmodium OvalE MODES OF TRANSMISSION: Through bite of an infected female Anopheles Mosquito. Through blood transfusion. Shared contaminated needles. DIAGNOSTIC TEST Malarial Smear Quantitative Buffy Coat CLINICAL MANIFESTATIONS Cold stage Presence of chills mostly 10 to 15 minutes Hot stage Fever, headache Diarrhea, nausea and vomiting Nose bleeding Last for 4 to 6 hours Diaphoretic stage Sweating Generalized body malaise Decreased pulse rate, temperature and respiratory rate

Others Anemia Hepatomegaly Splenomegaly

PREVENTION AND CONTROL: INSECTICIDE-TREATMENTOF MOSQUITO NET: HOUSE SPRAYING: RECOMMENDED ANTI-MALARIA DRUGS: Drugs acting on sexual blood stages of the parasites (blood schizonticides) which are responsible for clinical manifestation Chloroquine Sulfadoxine Quinine Quinidine Sulfate Primaquin Antipyretics for fever Symptomatic / supportive care PREVENTIVE MEASURES: Wearing of clothing that covers arms and legs in the evening. Avoiding outdoor night activities, particularly during the vectors peak biting hours from 9pm to 3 am. Using mosquito repellents such as mosquito lotion, coils, soap or other personal protection measures advocated by the DOH. Planting of Neem tree or other herbal plants which are mosquito repellents as advocated by the DOH. Zooprophylaxis- the typing of domestic animals like carabao, cow etc. near human dwellings to deviate mosquito bites from human to these animals. NURSING INTERVENTIONS 4 oclock habit by DOH C hemically treated mosquito nets L arvivorous fishes E nvironmental sanitation A nti-mosquito soaps N ymph tree / eucalyptus tree Isolation of the infected person (sleeping under the mosquito net) Mass screening MBS Mass Blood Smear collection House spraying (fumigation) 0n stream-seeding On stream-clearing

FILARIASIS
ELEPHANTIASIS; BARBADOS LEG; ELEPHANT LEG; MORBUS HERCULUS) CAUSATIVE AGENT: Wuchereria Bancrofti CLINICAL MANIFESTATION: ASYMPTOMATIC STAGE: No clinical signs and symptoms of the disease. Presence of microfilariae in the peripheral blood. ACUTE STAGE: Lymphadenitis (inflammation of the lymph nodes). Lymphangitis (inflammation of the lymph vessels). In some cases, the male genitalia are affected leading to funiculitis, epidydimitis, or orchitis (redness, pai(nful and tender scrotum). CHRONIC STAGE: Hydrocoele (swelling of the scrotum). Lymphedema (temporary swelling of the upper and lower extremities). Elephantiasis (enlargement and thickening of the skin of the lower and upper extremities, breast and genitals). DIAGNOSTIC TEST Physical examination and history taking Nocturnal Blood examination (NBE) Immunochromatographic Test (ICT) PREVENTION AND CONTROL: MEASURES AIMED TO CONTROL THE VECTOR: Environmental sanitation such as proper drainage and cleanliness of surrounding. Spraying with insecticides. MEASURES AIMED TO PROTECT THE INDIVIDUAL AND FAMILIES IN ENDEMIC AREAS: Use mosquito nets. Use of long sleeves, long pants and socks. Application of insect repellants. Screening of the house. Health education. NURSING INTERVENTIONS Administer Diethylcarbamazine Citrate (DEC) or Assist in surgical therapy Lymphovenous anastomosis Chyluria Symptomatic / supportive care 4 oclock habit by DOH C hemically treated mosquito nets L arvivorous fishes E nvironmental sanitation A nti-mosquito soaps N ymph tree / eucalyptus tree On stream clearing TREATMENT: Diethylcatbamazine Citrate (DEC) or Hetrazan: An individual treatment kills almost all microfilaria and a good proportion of adult worms. Drug is given to patients with clinical manifestation and microfilariae.

SCHISTOSOMIASIS
(BILHARZIASIS; SNAIL FEVER) Causative Agent: TYPES: Schistosoma Japonicum (Oriental Schistosomiasis) Schistosoma Mansoni (Endemic in the Philippines) Schistosoma Haematobium MODES OF TRANSMISSION: Through ingestion of contaminated water. Through the skin. The disease is transmitted through an intermediary host Oncomelania CLINICAL MANIFESTATION: Swimmers itch Hepatomegaly and spleenomegaly. Bloody mucoid stools, dysentery like that comes on and off for 2 weeks. Malnutrition Weakness Accumulation of fluid in the abdominal cavity (ascites) Inflammation of the skin and itching DRUG OF CHOICE Administer Praziquantel (Biltricide). Alternative drugs include Oxamniquine for S. mansoni Metrifonate for S. haematobium. NURSING INTERVENTIONS Symptomatic / supportive care : Measure abdominal girth Proper waste disposal Use of molluscicides Apply 70% alcohol after exposure to water Use of rubber boots Water can be treated with iodine or chlorine, standing 48-72 hours before use Improve irrigation and cultural practices

LEPTOSPIROSIS
WEILS DISEASE, MUD FEVER, TRENCH FEVER, FLOOD FEVER, SPIROKETAL JAUNDICE, JAPANESE SEVEN DAYS FEVER, HEMORRHAGIC JAUNDICE, CANICOLA FEVER, SWINEHERDS DISEASE, ICTEROHEMORRHAGIC SPIROCHETOSIS CAUSATIVE AGENT: A spirochete: Leptospira Interrogans. Leptospira icterohemorrhagiae (most virulent) causing Weils diseases MODES OF TRANSMISSION: Ingestion or contact with the skin and mucus membrane with the infected urine The break of skin. CLINICAL MANIFESTATION: Mimic the signs and symptoms of Hepatitis. CLINICAL MANIFESTATIONS Leptospiremic phase Fever, headache Nausea and vomiting Cough, chest pain Myalgia Conjuctivitis, jaundice Hematemesis, hematuria, hepatomegaly Immune phase DIAGNOSTIC TEST Agglutination test CSF analysis Culture and Sensitivity DRUG OF CHOICE Administer medications, as ordered Penicillin and other B lactam antibiotics Tetracycline (Doxycycline) Erythromycin in patients to allergic to penicillin. NURSING INTERVENTIONS Symptomatic / supportive care Environmental sanitation Eradication of rats Use of rubber boots PREVENTION AND CONTROL: Improved education of people at particular risk e.g. farmers, miners, etc. to increase their awareness and enable early diagnosis and treatment. Use of protective clothing boots and gloves especially by workers with occupational risks. Stringent community wide rat eradication program. Remove rubbish from work and domestic environment to reduce rodent population. Segregate domestic animals potentially infected from mans living, Segregate working and recreation areas. Isolation of patient and concurrent disinfection of soiled articles. Report all cases of Leptospirosis. Investigation of contacts and source of infection. Chemoprophylaxis in groups at high risk of infected host.

Cholera
Causative agent: Vibrio cholerae, Vibrio comma (ogawa and inaba) Mode of transmission: direct or indirect fecal contamination of water or food supplies by soiled hands, utensils, or mechanical carriers such as flies Incubation period: from a few hours to five days (average 3 days) ASSESSMENT Clinical manifestations - acute colicky pains in the abdomen - mild diarrhea (yellowish) - marked mental depression - headache, vomiting - fever, may or may not be present Collapse stage after one or two days - profuse watery stools (grayish-white or rice water) - thirst - severe/violent cramps in the legs and feet - thickly furred tongue - sunken eyes - ash-gray colored skin Reaction stage after 3 days - Increased consistency of stools - Skin becomes warm and cyanosis disappear - Peripheral circulation improves - Urine formation increases Diagnostic Exam: a. Positive ( + ) stool exam/vomitus PLANNING AND IMPLEMENTATION 1. Drugs - Tetracycline 2. Replacement of fluids and electrolytes 3. Isolation 4. patient should be spared all unnecessary efforts during the acute stage 5. Buttocks should be kept clean with warm and soap, rubbed dry and its applied 6. Antiseptic mouthwash in case of vomiting Fluids is given as soon as they can be tolerated

HEPATITIS
Types I. Type A (Infectious Hepatitis) Incubation period: 15-45 days Mode of transmission: fecal/oral route Occurs in crowded living conditions; with poor personal hygiene or from contaminated food, milk, water or shellfish II. Hepatitis B (Serum hepatitis, SH virus, Viral Hepatitis, Transfusion Hepatitis, Homologous Serum Jaundice) Incubation period: 50 180 days Mode of transmission: Blood & body fluids (saliva, semen, vaginal secretions) Often from contaminated needles among IV drug abusers; intimate/sexual contact

III. Type C (Non-A, Non-B Hepatitis) Incubation period: 7 50 days Mode of transmission: by parenteral route; through blood & blood products, needles, syringes ASSESSMENT 1. Pre-icteric stage Anorexia Right upper quadrant discomfort Nausea & vomiting Hepatomegaly Fatigue Splenomegally Constipation or diarrhea Lymphadenopathy Weight loss 2. Icteric Stage - Fatigue - light colored stools - lymphadenopathy - jaundice - continued hepatomegaly with tenderness Post icteric stage - fatigue but increased sense of well-being - hepatomegaly: gradually decreasing

- weight loss - dark urine - splenomegally - pruritus

3.

Diagnostic Exam 1. all three types a. SGPT, SGOT, alkaline phosphatase, bilirubin, ER all increased in preicteric b. Leukocytes, lymphocytes, neutrophils all decreased c. Prolonged PT 2. Hepa A a. Hepa A (HAV) in stool before onset b. Anti HAV (IgG) appears soon after onset of jaundice, peaks in 1-2 months and persist indefinitely c. Anti-HA (IgM); positive in acute infection lasts 4-6 weeks 3. Hepatitis B a. HbsAg (surface antigen) positive; develops 4-12 weeks after infection b. Anti-HbsAg negative in 80% cases c. Anti HBC associated with infectivity: develops 2-16 weeks after infection d. ABeAG associated with ineffectively and disappears before jaundice e. Anti-Hbe present in carriers, represents low infectivity f. No specific serologic tests

PLANNING AND IMPLEMENTATION Management 1. Promote adequate nutrition small, frequent meals of high CHO, moderate to high protein, high vitamin, high calorie diet, avoid very hot/cold foods 2. Ensure rest/relaxation 3. Monitor/relieve pruritus cool, moist compresses, emollient lotion 4. Administer corticosteroid as ordered 5. Isolation procedures as required 6. Provide client teaching and discharge planning with regards to: a. Importance of avoiding alcohol b. Importance of not donating blood c. Recognition/reporting of signs of inadequate convalescence d. Avoidance of persons with known infections 7. Drugs liver protector (e.g. essentiale, Jectofer, Interferon drug)

Typhoid Fever (enteric fever)

Causative agent: Salmonella typhosa Incubation period: Mode of transmission: Infected urine and feces Sources: contaminated food and water ASSESSMENT Clinical manifestation 1. Gradual onset - severe headache, malaise, muscle pains, non-productive cough - chills and fever, temp. rises slowly - pulse is full and slow - skin eruption irregularly spaced small rose spots on the abdomen, chest and back; fades on 3-4 days - splenomegally 2. second week - fever remains consistently high - abdominal distention and tenderness , constipation or diarrhea - delirium in severe infection - coma-vigil look: pupils dilate and patient appears to stare without seeing - sultus tendium twitching of the tendon sets 3. Third week - gradual decline in fever and symptoms subsides Diagnostic Exam a. White blood cell count leukopenia b. Blood or bone marrow culture c. Positive urine and stool cultures in later stage d. Blood serum agglutination ( + ) at the end of 2nd week PLANNING AND IMPLEMENTATION Prevention: Decontamination of water sources, milk pasteurization, individual vaccination of high risk persons, control of carriers

Management 1. Drugs

- Chloramphenicol, Ampicillin - Sulfamethoxazole - Trimethoprim - Furazolidone 2. Intravenous infusions to treat dehydration and diarrhea 3. Nursing Care - Give supportive care - Position the patient to prevent aspiration - Use of enteric precautions - TSB for high fever - Encourage high fluid intake - Give the meds as prescribed - Monitor for complications

MEASLES (Rubeola, Morbilli, 7 day measles)

Causative agent: Paramyxovirus Incidence: Endemic in all large cities of the world recurring in epidemic form every 2 years usually occurs during cold weather Mode of transmission: Nasal throat secretions, droplet infection, indirect contact with articles Incubation period: 8 20 days ASSESSMENT Stages 1. incubation period (average of 10 days) 2. pre-eruptive stage or stage of invasion ( 3- 6 days) - from the appearance of the first sign/symptom to the earliest evidence of the eruption - fever, severe cold - frequent sneezing - profuse nasal discharge - eyes are red and swollen with mucopurulent discharge (lids stick together) - Stimsons sign (puffiness of lower eyelids with definite line of congestion on the conjunctivae) - Redness of both ear drums - Vomiting, drowsiness - Hard, dry cough - Kopliks spot (appears on 2nd day): small, bright, red macules or papules with a tiny or bluish-white specks on the center and can be found on the buccal cavity - Macupapular rashes: (seen late in 4th day) appears first on the cheeks or at the hairline - True measles rash: slightly elevated sensation to touch - Appears first on the face and spreads downward over neck, chest, trunk, limbs and appearing last on the wrist and back of the hand

3. Eruptive stage - characterized by a general intensification of all local constitutional symptoms of the preeruptive stage with the appearance of bronchitis and loose bowels - irritability and restlessness - red and swollen throat - enlargement of cervical glands - fever subsides 4. Desquamation stage - follows after the rash fades - follows the order of distribution seen in the formation of eruption Diagnostic Exam No specific diagnostic exam except only for the presence of leukopenia PLANNING AND IMPLEMENTATION Prevention Management: 1. drugs antibiotics Sulfadiazine 2. Isolation 3. Meticulous skin care-warm alcohol rub to prevent pressure sores 4. Good oral and nasal hygiene- increase oral fluids 5. Proper care of the eyes-screen to avoid direct light; wear dark glasses 6. Ears should be cleaned after bath if there discharges pt. Should lie the affected ear down or towards the bed 7. Give ample of fluids during febrile stage

GERMAN MEASLES (Rubella, Rotheln, Roseola, 3-day measles)

An acute infectious disease characterized by mild constitutional symptoms, rose-colored macular eruption that may resembles measles, enlargement, and tenderness.

Causative agent: Myxovirus Incidence: Occurs mostly in spring and seen mostly in children over 5 years of age Mode of transmission: Direct contact Incubation period: 14-21 days Pathognomonic Sign: Forcheimers Spot a pinkish rash on the soft palate. ASSESSMENT Clinical manifestations - fever, cough - loss of appetite - enlargement of lymph nodes - sweating - leukopenia - vomiting (in some cases) - headache, mild sore throat - desquamation follows the rash - Enanthem of uvula with tiny red spots - rash (cardinal symptom) accompanied with cervical adenitis: begins on the face including the area around the mouth; oval, pale, rose-red papules about the size of a pinhead; covers the body within 24 hours and gone by the end of Fourth day Prevention: vaccination Management 1. Isolation (Catarrhal stage_ to prevent infection to others 2. Bed rest for first few days 3. Meticulous skin care especially after the rash fades 4. Good oral and nasal hygiene (use of petroleum jelly if lips become dry) 5. No special diet is necessary / increase fluid intake Prognosis: very favorable

VARICELLA (Chicken pox)

Causative agent: Varicella zoster virus (airborne) Incidence: Occurs before the 6th year especially in winter Mode of transmission: Droplet infection, direct contact Incubation period: 2-3 weeks ASSESSMENT Clinical manifestations - slight fever: first to appear - body malaise, muscle pain - eruption (maculopapular) then progresses to vesicle (3-4 days) ; begins on trunk and spreads to extremities and face (even on the scalp, throat and mucus membranes) - intense pruritus - vesicles ended as a granular scab - irritability PLANNING AND IMPLEMENTATION 1. Isolation in a room by itself 2. Provide a well-ventilated, warm room to the patient 3. Warm bath should be given daily to relieve itching; use a calamine lotion 4. Avoid injuring the lesions by using soft absorbent towel and the patient should be potted dry instead of rubbed dry 5. Maintain good oral hygiene. If lesions are found in the mouth or nasal passages, antiseptic prep may be used. 6. Diet should be regular

MUMPS (Infectious or epidemic parotitis)

Causative agent: Filterable virus, member of myxovirus family Mode of transmission: Direct contact with a person who has the disease or by contact with articles which is contaminated Incubation period: 14 21 days ASSESSMENT Clinical manifestations - pain in the parotid region - headache - earache - difficulty to open the mouth wide Diagnostic Exam a. Moderate leukocytosis b. Complement fixation test

- General malaise - sorethroat - fever

c. Skin test for susceptibility to mumps

PLANNING AND IMPLEMENTATION 1. Drugs - Aspirin for fever, cortisone 2. Isolation 3. Absolute bed rest to prevent complications (at least 4 days) 4. Daily bath should be given 5. Soft bland diet for sore jaw 6. Advise male to wear well-fitting support to relieve the pull of gravity on the testes and blood vessels 7. TSB for fever 8. Ice pack / collar application

PULMONARY TUBERCULOSIS (Phthisis, consumption)

- A communicable disease characterized by the formation of tubercle Bacillus in tissues undergoing necrosis and calcification by direct or indirect spread Causative agent: Mycobacterium tuberculosis Mode of transmission: Nasopharyngeal secretions, drinking infected cows milk, droplet infection Incubation period: less than 1 month ASSESSMENT Clinical manifestations - cough with yellow mucoid sputum - afternoon low - grade fever - anorexia - weight loss - night sweats, fatigue, malaise - hemoptysis, chest and back pain - dyspnea Diagnostic Exam a. Sputum examination to be done early in the morning b. Chest X ray c. Mantoux Skin Test positive result means client has had contact but does not signify active disease is present. DIRECT OBSERVED TREATMENT SHORT COURSE (DOTS): CATEGORY AND TREATMENT REGIMEN: Category 1: This treatment regimen is to be prescribed to 1. New pulmonary TB patients whose sputum is (+). 2. Seriously ill patients with severe forms of: 3. Smear negative PTB with extensive parenchymal involvement. 4. Extra pulmonary TB (TB Meningitis, TB Pericarditis, Pleurisy, Potts disease, Intestinal TB). Intensive Phase: The following drugs are given daily for 2 months: Isoniazid + Rifampicin+ Pyrazinamide+ Ethambutol. Maintenance Phase: INH + Rifampicin given daily for the next 4 months Category 2: This treatment regimen is to be prescribed to previously treated patients who are: 1. Relapses 2. Failures Intensive Phase: INH + RIF + PZA + ETH + Streptomycin for the 1st 2 months; followed by Streptomycin + RIF + PZA + ETH for 1 month.

After 3 months of treatment with (-) sputum result patient will proceed to maintenance phase. (+) sputum the phase will continue for 1 more month.

Maintenance Phase: INH + RIF + ETH will be given daily for 5 months. Category 3: This treatment regimen is to be prescribed to: New PTB patient whose sputum is negative for 3 months and CXR results is minimal PTB. Extra-pulmonary Intensive Phase: INH + RIF + PZA daily for 2 months. Maintenance Phase: INH + RIF daily for 2 months. PLANNING AND IMPLEMENTATION 1. Increase body resistance by providing adequate rest and sleep 2. Promote adequate nutrition by providing well-balanced diet 3. Instruct client to prevent spread of disease by covering nose and mouth when sneezing and coughing; and maintaining adequate ventilation 4. Provide frequent oral hygiene 5. Hand washing is required after direct contact with the client or contaminated articles 6. Monitor administration of medications 7. Chemoprophylaxis

INFLUENZA (La Grippe of Flu)

- a highly contagious disease characterized by sudden onset of aches and pains Causative agent: Influenza virus A, B, C Mode of Transmission: Droplet infection, contact with nasopharyngeal secretions Incubation period: 24-48 hrs ASSESSMENT Clinical Manifestation 1. Respiratory most common - Fever - anorexia - Chills - muscles pains and aches - Coryza - sore throat - Bitter taste - pain behind the eyeballs 2. Intestinal - Vomiting - severe abdominal pain - Fever - obstinate constipation - Severe diarrhea 3. Nervous - headache - aching of the muscles and joints - Fever PLANNING AND IMPLEMENTATION 1. Provide adequate rest and good ventilation 2. Tepid sponge bath to reduce the temperature 3. Monitor vital signs 4. Provide adequate nutrition 5. Assist the patient in conserving strength when she is very weak 6. Drugs - antibiotics - sulfonamides

PERTUSSIS (Whooping cough) Causative agent: Hemophilus pertussis or Bordetella pertussis, An aerobic and anaerobic bacterium Mode of transmission: Nasopharyngeal secretions Incubation period: 7 to 21 days ASSESSMENT Clinical manifestations 1. Invasive or catarrhal stage (7 to 14 days) - Fever, watery eyes, sneezing - Cough is worse at night (slight, dry, irritative) - Restlessness 2. Spasmodic Stage (4 to 12 weeks) - Pathognomonic sign: cough with a peculiar inspiratory crowning sound which becomes the typical whoop - Paroxysmal cough 3 to 10 times during expiration with prolonged inspiratory phase - The whoop follows the end of a series of short explosive coughs with no time to catch a break between cough - Protrusion of eyeballs, protruded tongue - Swollen head and neck veins - Abdominal hernia 3. Convalescent stage symptoms subsides Diagnostic exam a. Cough plate Bordet-Gengou test, agar plate PLANNING AND IMPLEMENTATION 1. Provide quiet and non-stimulating room 2. Keep patient warm and out of drafts or wind 3. Mouth and nose must be kept clean 4. Small frequent feedings to lessen vomiting 5. A light but nutritious diet with plenty of fruit juices but no seasoned foods 6. Fluids given between meals 7. Apply abdominal binder for hernia 8. Oxygen inhalation 9. Dug-antibiotics (Penicillin, Erythromycin, Azithromycin, Clarithtromycin )

SCABIES
Causative agent: itch mite, Sarcoptes scabiei Incubation period: 1 to 2 weeks Mode of transmission: direct contact with infected persons, indirect contact trough soiled bed linens, clothing and others. ASSESSMENT Clinical manifestations - Intense itching especially at night - Sites between fingers or flexor surfaces of wrists and palms, around nipples, Umbilicus, in axilllary folds, near groin or gluteal fold, penis, scrotum. Diagnostic Exam: presence on skin of female mite, ova an feces upon skin scraping PLANNING AND IMPLEMENTATION 1. Take a warm soapy shower/bath to remove scaling debris from crusts. 2. Apply prescribed scabicide such as a. Lindane lotion (Kwell) 1% b. Crotamiton (Eurax) cream/lotion c. 6-10% precipitate of sulfur in petrolatum Encourage to change clothing frequently

TETANUS (Lockjaw )
Causative Agent: Clostridium tetani an anaerobic bacterium Mode of Transmission: Break in skin integrity Otitis media Tooth decay Incubation Period: 5 10 days Clinical Manifestations: Trismus Difficulty in swallowing and breathing Risus Sardonicus Urinary and bowel incontinence Opisthotonus Pain, redness and swelling due to inflammatory response Rigidity of abdominal muscles and extremities Diagnostic Exam History of the wounds Wound Culture PLANNING AND IMPLEMENTATION 3 Objectives of Medical management o Neutralize toxins o Kill the bacteria o Prevent muscle spasm NURSING CARE Avoid stimulation to avoid muscle spasm o 3 types of stimuli exteroceptive outside environment of patient interoceptive within the environment of patient proprioceptive somebody in charge Provided a quiet and well ventilated room to avoid stimulation Always have padded tongue depressor to maintain patent airway Preventive Measures Immunization with DPT for infants and TT1-TT5 for pregnant mother Proper Wound care with use of 3% hydrogen peroxide or povidone-iodine solution. Avoidance of Wound

MENINGITIS
(Epidemic Cerebrospinal Meningitis, cerebrospinal fever) An acute contagious disease due to inflammation of meninges of the CNS. Kinds of Meningitis 1. Staphylococcal Meningitis 2. 3. Streptococcal Meningitis 3. Pneumococcal Meningitis Causative Agent: Neisseria Meningitides (most common) Mode of Transmission: Droplet contact Contact with nasopharyngeal secretions Incubation period: 2 10 days ASSESTMENT Clinical Manifestation o Headache o photophobia o malaise o irritability o Chills and fever o Vomiting o Seizures and decreasing level of consciousness o Signs of meningeal irritation: Kernings Sign Brudzinski sign Diagnostic exam a. Lumbar Puncture b. Blood Culture PLANNING ANG IMPLEMENTATION 1. Drugs antibiotics. IV 2. Provide nursing for increased ICP, seizures and hypothermia. 3. Provide bed rest; keep room quiet and dark if client has headache or photophobia. 4. Maintain fluid and electrolyte balance. 5. Monitor Vital signs and Neurochecks frequently Preventive Measures: Proper disposal of nasopharyngeal secretions

RABIES (Hydrophobia)
Causative agent: Rhabdo virus Mode of transmission: Saliva of infected animal Bite of dog Although rare, it can also be transmitted via airborne droplets. Incubation period: 3 8 weeks for rabid animals 10 days to 10 years for man ASSESSMENT Clinical manifestation 1. for RABID ANIMALS a. dumb form - complete change in disposition - animal becomes withdrawn - very affectionate and walking to and from - paralysis and copious flow of saliva b. furious form - vicious, agitated, then become paralyzed, emits excessive saliva and dies 2. for MAN a. invasive stage - numbness on site of bite - headache - malaise - restlessness - fever - photosensitivity - apprehension b. excitement stage hydrophobia - spasms of laryngeal and pharyngeal muscle *Maniacal - climbing the wall and excessive salivation paralytic stage - laryngospasms stopped - last for how many seconds or hours

c.

Diagnostic Exam: a. Fluorescent Rabies Antibody specimen: blood of an individual b. Brain Biopsy of the Animal c. 10 days observation of the animal PLANNING AND IMPLEMENTATION 1. Provide a dim, quiet and non-stimulating room for the patient 2. Wear gown, mask and gaggles 3. All noises no matter how minor should be avoided 4. Restrain the patient when needed 5. Stimulation of any senses by fluids must be avoided 6. Anti-rabies vaccine Preventive Measures 1. Isolation 2. Provide comfort for the patient 3. Wear PPE 4. Clean and dress the wound 5. Take precaution to avoid being bitten by the patient during excitement stage.

POLIOMYELITIS (Infantile Paralysis, Geine-Medin disease)

Causative Agent: Legio debilitans Type I Brunhilde Type II Lansing type III Leon Portal Entry: Nasopharynx Feces Mode of Transmission: direct contact from one person to another Incubation Period: 7 - 14 days Pathophysiology Clinical Manifestation Invasive or abortive stage: tonsillitis, abdominal pain, anorexia, nausea, vomiting diarrhea. Pre-paralytic stage: Haynes sign(head drop), Pokers sign(Opisthotonus) Paralytic stage: flaccid paralysis Types of Paralysis Spinal Paralysis Bulbar paralysis Bulbo-spinal paralysis Laundrys Paralysis

Diagnostic Exam a. Muscle testing b. Lumbar puncture c. Stool exam d. Electromyelography determines the extent of muscle involvement e. (+) Pandys test increased protein in the cerebrospinal fluid PLANNING AND IMPLEMENTATION 1. Maintain complete bed rest during acute period 2. Provide respiratory ventilation if respiratory paralysis occurs 3. Assist with physiotherapy 4. Prevent potential complication

DIPTHERIA
Causative agent: Corynebacterium diphtheriae or Klebs Loffler bacillus Mode of transmission: a. Discharges from respiratory passages b. Saliva Incubation period: 1 to 7 days ASSESSMENT Clinical manifestations a. Nasal Diphtheria - irritating, bloody discharges with excoriated nares and upper lip - pseudomembrane in nasal septum - fever - cervical or sub-maxillary glands enlarged - nose almost or completely stopped up b. Pharyngeal Diphtheria - sore throat - pseudomembrane on throat and uvula - fever - tonsillitis with exudative membrane - redness and warmth - bull neck appearance, due to edema c. Laryngeal Diphtheria - hoarseness of voice - initiative :croupy cough - cyanosis - profuse perspiration - difficulty of breathing - inflammation of larynx thus obstructing passage of air to the lungs d. Wound Diphtheria - diphtheritic infection from wounds or burns e. Mucous Membrane Diphtheria - may appear on any mucous membrane such as conjunctiva, mouth Diagnostic Exam: a. Nose and throat culture there must be 3 consecutive negative result b. Schicks test determines susceptibility and immunity to diphtheria c. Maloneys Test determine hypersensitivity to diphtheria anti-toxin PLANNING AND IMPLEMENTATION 1. Provide, liquid or soft diet with minimal protein 2. Maintain good oral hygiene 3. Maintain patent airway 4. Drugs anti-diphtheria serum to neutralize toxins - Epinephrine and corticosteroids - Penicillins 5. Tracheostomy if respiratory obstruction occurs 6. Throat irrigation to ease the pain and clear the throat of mucus and fragments of membranes Prevention 1. Active immunization of all infants (6 weeks) and children with 3 doses of Diphtheria 2. Pasteurization of milk. 3. Education of the parents. 4. Reporting of the cases to the Health Officer for proper medical

LEPROSY (Hansens disease, Hansenosis, Leprae, Leontiasis)

Different forms o Lepromatous leprosy- causes damage to skin, nerves, upper respiratory tract, testes and eyes. o Tubercoloid leprosy- mostly affects the peripheral skin o Dimorphous leprosy- poses both the characteristic of Lepromatous and Tubercoloid leprosy. The skin lesions present are poorly differentiated.

Causative agent: Mycobacterium leprae (acid-fast bacillus) Mode of transmission: Prolonged intimate skin-to-skin contact, nasal secretions Incubation period: 6months - 8years ASSESSMENT Clinical manifestations 1. Early stage - loss of sensation - paralysis of extremities - absence of sweating (anhydrosis) - nasal obstruction - loss of hair (eyebrows) - eye redness

change in the skin color ulcers that does not heal muscle weakness

2. Late symptoms - contractures - Leonine appearance (due to nodular and thickened skin of the forehead and face) - Madarosis (falling of eyebrows) - Synecomastia - Sinking of bridge of nose 3. Cardinal signs - presence of Hansens bacilli in a smear of biopsy material - presence of localized areas of anesthesia - peripheral nerve enlargement Diagnostic Exam a. Lepromin Reaction a positive test develops a nodule at the site of inoculation (first and third week) b. Wassermann Reaction PLANNING AND IMPLEMENTATION Prevention: 1. Separate infants from Lepromatous parents at birth 2. Segregate and treat open cases of leprosy 3. Require public health supervision and control of cases of Hansens disease Medical Management 1. Multiple drug therapy a. Paucibacillary treatment six months or until negative ( - ) results occurs Rifampicin once a month Dapsone once a day b. Multibacillary treatment for 2 consecutive year or until negative ( - ) for leprosy test Rifampicin once a month Lamprene once a day Dapsone once a day Full, wholesome, generous diet Alcohol or TSB may be used for high fever Patient should have a daily cleansing bath and change of clothing Good Oral Hygiene Normal elimination should be maintained Meticulous skin care for ulcers

2. 3. 4. 5. 6. 7.

Prognosis: The longer the time of active disease, severe lesions, the more rapidly they have advanced without ability to produce the Lepromin Reaction the poorer the prognosis Case under 21 years old high relapse rate

d.

SEXUALLY TRANSMITTED DISEASES

Gonorrhea (Strain, Clap, Jack, Morning drop, G.C. Gleet)
- an infectious disease which causes inflammation of the mucus membranes of the genitourinary tract. Causative agent: Neisseria gonorrheae Mode of transmission: sexual contact Incubation period: 2 to 5 days ASSESSMENT Clinical manifestations 1. Male - Burning sensation in the urethra upon urination - Passage of purulent (yellowish) discharge - Pelvic pain - Fever - Painful urination 2. Female - Burning sensation upon urination - Presence or absence of vaginal discharges - Pelvic pain - Abdominal distention - Nausea and vomiting - Urinary frequency Diagnostic Exam 1. Culture and sensitivity

Female: Papa smear or cervical smear Male: Urethral smear 3. Blood exam VDRL PLANNING AND IMPLEMENTATION 1. Educate men and women to recognize signs of gonorrhea and to seek immediate treatment 2. Monitor urinary and bowel elimination 3. Important to treat sexual partner, as client may become reinfected 4. Make arrangements for follow-up culture 2 weeks after therapy is initiated 5. Drugs - Penicillin: drug of choice - Tetracyclines - Ceftriaxone sodium (Rocephin) - Amoxicillin (Augmentin)

2.

SYPHILIS (Lues, Pox, Bad blood disease)

a contagious disease that leads to many structural and cutaneous lesions

Causative agent: Treponema pallidum Mode of transmission: Sexual contact Incubation period: 3 to 6 weeks ASSESSMENT Primary Syphilis - Chancre on genitalia, mouth or anus - Serous drainage from chancre - Enlarge lymph nodes - Maybe painful or painless - Highly infectious 2. Secondary Syphilis - Skin rash on palms and soles of feet - Reddish copper colored lesions on palms of hands and soles of feet - Condylomas: lesions/sores that fused together - Erosions of oral mucus membranes - Alopecia - Enlarged lymph nodes - Fever headache, sore throat and general malaise

3. Tertiary Syphilis - Gumma: the characteristic lesion - Cardiovascular changes - Ataxia - Stroke, blindness Diagnostic Exam 1. Positive test for syphilis a. Venereal Disease Research Laboratory (VDRL) b. Rapid plasma Reagin Circle card test (CRPR-CT) c. Automate Reagin Test (ART) d. Fluorescent treponemal antibody absorption test (FTA-ABS) e. Wassermann test f. Khan Precipitation test g. Kline, Hinton and Mazzin tests 2. Dark field examination 3. Culture and sensitivity test PLANNING AND IMPLEMENTATION 1. Strict personal hygiene is an absolute requirement 2. Assist in case finding 3. Instruct client to avoid sexual contact until clearance is given by physician 4. Encourage monogamous relationship 5. Explain need to complete course of antibiotic therapy 6. Drugs- Penicillin, Tetracyclines/Kithramycin

HIV/ ACQUIRED IMMUNE DEFICIENCY SYDROME (AIDS)

- an acquired immune deficiency characterized a defect in natural immunity Causative agent: Retrovirus, Human immunodeficiency virus (HIV-1 and HIV-2) previously referred to as human Tlymphotropic virus type II (HTLV-III) Mode of transmission: Blood, sexual contact, contaminated needles, perinatal transmission Incubation period: 6 months to 9 years ASSESSMENT Clinical manifestations - Anorexia - fatigue - Dyspnea - night sweats - Fever - diarrhea - Enlarged lymph nodes - HIV encephalopathy: memory loss, lack of coordination, partial paralysis, mental deterioration - HIV wasting syndrome, emaciation - Positive test for HIV antibody - Positive test for presence of HIV itself - Opportunistic infection: pneumocystis carinii, cytomegalovirus, Kaposis sarcoma Diagnostic Exam 1. ELISA test (enzyme-linked immunosorbent assay) a screening test

2. Western Blot- a confirmatory test Drug of Choice AZT - Azidothymidine - antiretroviral drugs which are medications for the treatment of infection by retroviruses, primarily HIV. Different antiretroviral drugs restrain the growth and reproduction of HIV. PLANNING AND IMPLEMENTATION 1. Provide frequent rest periods 2. Provide skin care 3. Provide high-calorie, high protein diet to prevent weight loss 4. Provide good oral hygiene 5. Provide oxygen and maintain pulmonary function 6. Provide measures to reduce pain 7. Protect the client from secondary infection; carefully assess for early signs 8. Encourage verbalization of feelings 9. Teach client the importance of: a. Informing sexual contacts of diagnosis b. Not sharing needle with other individuals c. Continuing medical supervision