Cominicable Abebaw

Commmunicable Disease

UNIT ONEINTRODUCTION TO COMMUNICABLE DISEASES AND ITS CONTROL

Introduction to terminologiesCommunicable diseases -These are illnesses due to specific infectious agent or its toxic products which arise through transmission of that agent or its toxic products Communicable disease is also named as Infectious disease or Contagious disease

Communicable diseases can be conveniently divided based on the mode of transmission or the causative agent A Based on mode of transmission 1 Airborne diseases- -Need droplet nuclei or dust for transmission Eg Tuberculosis 2 Vehicle borne disease - Need non-living substance or object for transmission Eg Cholera 3 Vector Borne disease -Need vectors for transmission Eg Malaria 4 Other sexually transmitted Diseases contact diseases etc B Based an the Biologic agent 1 Bacterial diseases eg syphilis gonorrhea etc 2 Protozoal diseases eg Malaria 3 Viral diseases eg HIVAIDS 4 Helminthes diseases eg Ascariasis 5 Fungal diseases eg candidiasis

Etiology causative organism or infectious agent -Agent capable of causing infection or infectious diseaseClassification of infectious agent by size and sort1 Metazoa (multicellular organisms eg helminthes) They are made up of many cells Most of them are visible by naked eye Eg Tape worm2 Protozoa (unicellular organisms eg amoeba Plasmodium)Single-celled organisms that are smaller and can only be seen by a microscope3 Bacteria (eg Tpallidum Mtuberculosis)They are smaller than protozoa simple single celled amp seen under a microscope4 Rickettsia and Chlamydia are smaller and can only multiply with in cells5 Viruses -Smallest of all which canrsquot even be seen with an ordinary microscope6 Fungus egCalbicans

Reservoir -Any person animal arthropod plant soil or substance (or a combination of these) in which an infectious agent normally lives multiplies amp spreads

Types of reservoirs1 ManThere are a number of important pathogens that are especially adapted to man such as measles typhoid M meningitis gonorrhea and syphilis The cycle transmission is from man to man2 AnimalsSome infective agents have their reservoir in animalEg Bovine TBc - cow to man Brucellosis ndash cow pigs and goats to man Anthrax ndash cattle sheep goats horses to man Rabies ndash dogs foxes etc to man3 Non-living things as a reservoirEgCbotulinum etiology of botulism Ctetani etiology of tetanus Cwelchi etiology of gas gangrene all of them use soil as reservoir Carrier -It is an infected person or animal that does not have apparent clinical disease but is a potential source of a diseaseTypes of carriersA Healthy or asymptomatic carriers -These are persons whose infection remains unapparent through out its course B Incubatory or precocious carriers -These are individuals or persons who excrete the pathogens during the incubation period (before the onset of symptoms)C Convalescent carriers-These are those who continue to harbor the infective agent after recovering from the illnessD Chronic carriers -The carrier state persists for a long period of timeEg Typhoid fever Hepatitis B virus infectionPortal of exit (mode of escape from the reservoir ) -The site through which the agent escapes from the reservoir Eg GIT = bacillary dysentery amoebic dysentery cholera etc Respiratory = TBc common cold etc Skin and mucus membrane = syphilisPortal of entry -The site in which the infectious agent enters to the susceptible hostEg Mucus membrane = syphilis HIV Respiratory tract = TBc pertusis GIT = bacillary dysentery amoebic dysentery cholera etcPeriod of communicability or communicable period-The period during which an infectious agent is transmitted from the infected person to the susceptible host Susceptible host -A person or animal not possessing sufficient resistance against a particular pathogenic agent Incubation period -The time interval between infection of the host and the first appearance of symptoms and signs of the diseaseProdromal period -The time interval between the onset of symptoms of an infectious disease and the appearance of characteristic manifestations Eg In measles from the onset of fever and coryza to the development of characteristic signs like koplickrsquos spots and rashes

Prepatent period -The period in people between the time of exposure to a parasite and the time when the parasite can be detected in blood or in stoolEndemic -A disease that is usually present in a population or in an area at a more or less stable levelEpidemics -The occurrence of any disease in a given population in excess of the usual frequency in that populationPandemic -An epidemic disease which occurs world wide (world wide epidemics)Sporadic -A disease that occur in a population at occasional and irregular intervalsInfection -The entry and development or multiplication of an infectious agent in the body of man or animalInfestation -For persons or animals the lodgment development and reproduction of arthropods on the surface of the body or in the clothing Eg Louse infestation

Chain of disease transmission -Refers to sequence of factors of a chain that are essential to the development of the infectious agent and progression of disease

It has six components 1 The agent 2 Its reservoirs 3 Its portal of exits 4 Its mode of transmission 5 Its portal of entry and 6 The human host

1 The agent They range from smaller viruses to complex multicultural organisms( worms) Infections agents may bring about pathologic effect through different mechanisms

These mechanisms include 1 Direct tissue invasion2 Production of a toxin 3 Allergic reaction 4 Immune suppression

2 Reservoirs They include organisms or habitat in which an infectious agent normally lives

transforms develops or multiplies amp spreads They include human beings vertebrate animals invertebrates (arthropods

molluscs) amp environmental sources like plants soil water etc For some diseases humans are the only reservoirs eg STDs measles Pertussis Diseases with environmental reservoirs include cholera (water) Tetanus amp

ascariasis (soil) 3 Portal of exit

It is the way through which the infectious agent leaves its reservoir Possible portal of exit include all body secretions amp discharges mucus saliva

tears breast milk vaginal amp urethral discharges excretions (feces amp urine) blood etc

4 Mode of Transmission It includes the various mechanisms by which agents are conveyed or passed to a

susceptible host Transmission may be direct or indirect

1 Direct transmission11 Direct contact = refer to the contact of skin mucosa or conjunctiva from another

person or vertebrate animal through

- Touching Eg Eye- hand ndasheye Nose-hand-mouth Mouth- hand- mouth

Feces-hand- mouth Skin- skin

- Kissing - Sexual intercourse eg syphilis HIV AIDS - Biting eg rabies - Passage through birth canal (eg gonococcal ophthalmia neonatarum)

12 Direct projection = droplet created by expiration activities such as

coughing sneezing spitting talking singing etc

- Saliva droplets are emitted amp can reach another host directly at distances of up to one meter Eg Common cold

13 Trans placental transmission

- It is transmission of diseases from mother to her fetus through the placenta

Eg TORCHS (Toxoplasmosis Rubella Cytomegalovirus infection Herpes simplex infection syphilis others including HIVAIDS)

2 Indirect transmission

21 Airborne

Two types of particles can result in airborne transmission a) Dust - are small infectious particles that arise from soil clothes bedding contaminated floors and be suspended by air currents

b) Droplet nuclei -are small residues resulting from evaporation of fluid (droplets) from respiratory discharge emitted by an infected host They usually remain suspended in the air for long periods of time

22 Vehicle borne

A vehicle is any non- living substance or object by which an infectious agent can be transported and introduced in to a host

Eg food water milk fomites towels clothes etc23 Vector borne-

A vector is an organism (usually an arthropod such as an insect tick or louse) which transports an infectious agent to a susceptible host or to a suitable vehicle

5 Mode of entry - It is a way in which the infectious agent enters susceptible host6 Human host - Human being that accepts or allow the infection to occurInfectivity -The ability of an agent to invade and multiply in a hostPathogenecity -The ability of an agent to produce clinically apparent diseaseVirulence -The ability of infectious agent to produce severe disease among infected personsImmunogenicity -The ability of an agent to produce specific immunityUnapparent infection -The presence of infection in a host with out recognizable clinical signs and symptoms It can be identified only by laboratory means (blood) Asymptomatic sub clinical and occult infections are synonymous (other names) Host -A person or other living animal that affords substance or lodgment to an infectious agent under natural conditions Nosocomial infection -An infection occurring in a patient in a hospital or other health care facility in whom it was not present or including at the time of admissionPathogen- is an infectious agent that can cause clinically apparent infectionInfectious agent - is an agent that is capable of causing infection or infectious diseasePattern of communicable disease - different diseases are common in different places and at different times Why To understand this we need to consider the agent the host and the environment The agents need a suitable environment in which to grow and multiply and thus be able to spread and infect another host If they are not successful in doing this they die out There is there fore a balance between the agent the host and the environment which can be shown as HOST

AGENT ENVIRONMENT (The host agent environment triad)

UNIT TWOGENERAL METHODS OF PREVENTION AND CONTROL OF

COMMUNICABLE DISEASESDisease prevention -Inhibiting the development of a disease before it occurs or if it occurs interrupting or slowing down the progression of diseasesDisease control -Involves all the measures designed to reduce or prevent the incidence prevalence and consequence of a disease to a level where it can not be a major public health problemThere are three levels of prevention1 Primary prevention The objectives here are to promote health prevent exposure and prevent disease

A) Health promotion - any intervention that promotes a healthier and happier life This consists of adequately paid jobs education and vocational training affordable and adequate housing clothing and food emotional and social support relief of stress daily physical exercise balanced diet amp etc

B) Prevention of exposure - any intervention which prevents the coming in contact between an infectious agent and a susceptible host This includes actions such as provision of safe and adequate water proper excreta disposal vector control safe environment at home(proper storage of insecticides and medicines) at school and at work(proper ventilation monitoring of harmful substances in factories)

C) Prevention of disease - This occurs during the latency period between exposure and the biological onset of the disease An example for this is immunization NB Immunization against an infectious organism does not prevent it from invading the immunized host but prevents it from establishing an infection Breast feeding is an example of intervention that acts at all three levels of primary Prevention

=gtHealth promotion by providing optimal nutrition for a young child either as the sole diet up to six months of age or as a supplement in later age

=gtPrevention of exposure by reducing exposure of the child to contaminated milk =gtPrevention of disease after exposure by the provision of ant-infective factors including antibodies WBCs and others2 Secondary prevention This is applied after the biological on set of the disease but before permanent damage sets in =gtThe objective here is to stop or slow the progression of disease so as to prevent or limit permanent damage through early detection and treatment of diseases Eg Breast cancer (prevention of invasive stage of the disease) Trachoma (prevention of blindness) Syphilis (prevention of tertiary or congenital syphilis)3 Tertiary prevention After permanent damage sets in the objective of tertiary prevention is to limit the impact of that damage The impact can be physical (physical disability) psychological social(social stigma)and financial Rehabilitation refers to the retraining of remaining functions for maximum effectiveness Rehabilitation should be seen in a very broad sense not simply limited to the physical aspect

Principles of communicable disease controlThere are three principles

1 Attacking the source2 Interrupting the mode of transmission and3 Protecting the host (decreasing susceptibility)

1 Attacking the source =gt Domestic amp Wild animals as reservoirs

i Immunization ii Destruction of infected animals eg Rabies

=gtHumans as reservoirs i Isolation of infected persons amp separation of infected persons from others for

the period of communicabilityii Treatment

Of cases (clinical) and carriers

Mass treatment ndash where large proportion are known to have a diseaseiii Quarantine ndash the limitation of freedom of movement of apparently healthy

persons or animals who have been exposed to a case or infectious disease Cholera plague and yellow fever are the 3 internationally quarantinable

diseases by international agreement bc these diseases are very infectious2 Interrupting transmission

For Transmission by ingestioni Purification of waterii Pasteurization of milk iii Inspection procedures designed to ensure safe food supply iv Improve housing conditions

For Transmission by inhalation i Chemical disinfections of airii Improving ventilation

Transmission by vector or intermediate hostsi Vector ndash control measures

ii Environmental manipulation 3 Measures that reduce host susceptibility

i Immunization ii Chemoprophylaxis iii Better nutrition iv Personal hygiene -Protective measures primarily with in the responsibility of the individual that promote health and limit the spread of infectious disease chiefly those transmitted by direct contact It includes - = Washing hand in soap and water immediately after evacuating bowel or bladder and always before handling food or eating = Keeping hands and unclean articles or articles that have been used for toilet purposes by others away from the mouth nose eyes genitalia and wounds = Avoiding the use of common or unclean eating utensils drinking cups towels hand kerchiefs combs hair brushes and pipes = Avoid exposure of other persons to spray from the nose and mouth as in coughing sneezing laughing or talking = Washing hands thoroughly after handling a patient or the patientrsquos belongings = Keeping the body clean by frequent soap and water baths

NB- Effective control of disease is most likely when a combination of methods ndash attacking the source interrupting transmission and protecting the host is used at the same

UNIT THREE

Prevention and control of feco ndash orally transmitted diseases

Common features 1 The causative organisms are excreted (portal of exit) is the stools of infected

persons (or rarely animals) 2 The portal of entry for these diseases is the mouth3 Feco-oral transmission occurs mostly through unapparent fecal contamination of

food water and hands 4 In feco - oral transmission of disease food takes a central position bc it can be

directly or indirectly contaminated via polluted water dirty hands contaminated soil or flies

5 The five ldquoFsrdquo which play an important role in fecal oral disease transmission are finger flies fomites food and fluid

Feces Soil Food Mouth Flies

Finger NB ndash There are also diseases that are mainly transmitted through fecally contaminated water rather than food General prevention methods of feco-orally transmitted diseases

1 Early case detection and appropriate Rx of cases 2 Safe human excreta disposal3 Control of flies 4 Safe water supply5 Hand washing and sanitary handling of food and utensils 6 Control and check up of food handlers7 Avoid eating of un cooked foods

Classification of feco-orally transmitted disease 1 As a result of fecally contaminated water

are mainly transmitted through contaminated water rather than food 1) Typhoid fever2) Amoebiasis3) Giardiasis 5) Bacillary dysentery 4) Cholera 6) Infectious hepatitis

2 As a result of fecally contaminated soil These infections are acquired through exposure to fecally contaminated soil

1) Ascariais 4Enterobiasis2) Hook worm 5Strongloidiasis 3) Trichuriasis

3 As a result of direct contact with feces These are diseases transmitted mainly through direct contact with feces of the

infected person1) Poliomyelitis 2) Hydatid disease or echinococious

TYPHOID FEVER

Definition It is a systemic infectious disease characterized by high continuous fever malaise and involvement of lymphoid tissues (of intestine) Etiology - Salmonella typhi-Gram negative bacilli

Salmonella enteritidis (rare cause) EPI - It occurs world wide particularly in poor socioeconomic areas In endemic areas the disease is most commonly in preschool and school aged children (5-19 years) Reservoir - humans Mode of transmission - by water and food contaminated by feces and urine of patients and carriers Flies may infect foods in which the organisms then multiply to achieve an infective doseIncubation period - 1 ndash 3 weeks Period of communicability As long as the bacilli appear in excreta usually from the first week through out convalescenceAbout 10 of untreated patients will discharge bacilli for 3 months after onset of symptoms and 2 - 5 become chronic carriersSusceptibility and resistance - susceptibility is general and increased in individuals with gastric achlorhydria or those who are HIV positive Relative specific immunity follows recovery from infection but inadequate to protect against subsequent ingestion of large no of organisms Clinical ManifestationsFirst Week - mild illness x-zed by fever rising stepwise (ladder type) for 4- 5 days with associated chills myalgia dry cough epistaxis poor appetite anorexia lethargy malaise and general aches Dull and continuous frontal headache is prominent Nose bleeding vague abdominal pain and constipation occur in 10of pts Second week - sustained to (fever) severe illness with weakness mental dullness or delirium abdominal discomfort and distension Diarrhea is more common than 1st week and feces may contain blood Rash on upper abdomen shoulder chest and back slightly raised rose-red spots fade on pressure not visible on dark skinned person Hepatospleenomegally may occurThird week - patients continue to be febrile and increasingly exhausted If no complications occur pt begins to improve and temperature decrease gradually In this week increased toxemia GI hemorrhage melena paralytic ileus perforation rigid abdomen coma amp death are also may occurClinical Manifestations suggestive of typhoid fever 1 Sustained fever (ladder fashion) 2 Rose spots - small pallor blanching slightly raised macules usually seen on chest

and abdomen in the 1st week in 75 of white people 3 Relative bradycardia - slower than would be expected from the level of temperature 4 Leucopenia - WBC count is less than 4000ml of blood Diagnosis =gtBased on clinical grounds but this confused with wide variety of diseases ( Malaria Typhus fever Bacillary dysentery Amoebic liver abscess Relapsing fever Non typhoid salmonellosis etc) =gtWidal amp weil flex test=gtBlood culture (first week) feces or urine culture (2nd and 3rd week) bone marrow

culture (most sensitive) Treatment

ndash CAF or ndash ciprofloxacin or ndash ceftriaxone for seriously ill pts

_ Ampicillin or co-trimoxazole for carries (usually for 4 weeks) amp mild cases

Prognosis - Untreated 10 die - Treated 01 diePrevention

1 Treatment of pts and carriers 2 Education on hand washing particularly food handlers pts and child care givers3 Sanitary disposal of feces and control of flies 4 Provision of safe and adequate water 5 Safe handling of food 6 Exclusion of typhoid carriers and pts from handling of food and patients 7 Immunization for people at special risk eg Travelers to endemic areas

NB - In paratyphoid fever the disease is almost same to the typhoid fever except in the following points-- The cause of Paratyphoid is Salmonella para typhi- It is less severe- The course of disease tends to be shorter and milder than typhoid fever- The onset is often more abrupt with acute enteritis- The rash may be more abundant and the intestinal complications less frequent Complications of Typhoid fever clubs GI Hemorrhage Perforation clubs Myocarditis clubs Meningism Convulsions clubs Arthritis clubs Bronchitis clubs Bronchitis clubs Leucopenia thrombocytopenia DIC

BACILLARY DYSENTERY (SHIGELLOSIS)Definition - An acute bacterial disease involving the large and distal small intestine caused by the bacteria of the genus shigella Etiology - Four species or serotypes of shigella

1 Group A = shigella dysentriae (most common cause) 2 GP B = flexneri3 GP C = boydi4 GP D = sonnei

Enteroinvassive E-coli may rarely cause bacillary dysenteryEPI- It occurs world wide and is endemic in both tropical and temperate climates Outbreaks commonly occur under conditions of crowding and where personal hygiene is poor such as in jails institutions for children day care centers mental hospitals and refugee camps Reservoir - Humans Mode of transmissionMainly by direct or indirect fecal-oral transmission from a patient or carrierIncubation period - 12 hrs ndash 4 days (usually 1-3 days)

Period of communicability -during acute infection and until the infectious agent is no longer present in feces usually with in four weeks after illnessSusceptibility and ResistanceSusceptibility is general The disease is more severe in young children the elderly and the malnourished Breast-feeding is protective for infants and young childrenClinical manifestation Fever rapid pulse vomiting and abdominal cramp are prominent Diarrhea usually appears after 48 hrs with dysentery supervening two days later Generalized abdominal tenderness Tenesmus is present and feces are bloody mucoid and of small quantity Dehydration is common and dangerous- it may cause muscular cramp oliguria and shock Diagnosis -Based on clinical grounds - Stool microscopy (presence of pus cells) -Stool culture confirms the diagnosis Treatment ndash Fluid and electrolyte replacement ndash Cotrimoxazole or

- Ciprofloxacin or- Gentamycin or- Ampicillin

Prevention and control1 Detection of carriers and Rx of the sick 2 Hand washing after toilet and before handling or eating food 3 Proper excreta disposal especially from pts convalescents and carriers4 Adequate and safe water supply 5 Control of flies 6 Cleanliness in food handling and preparation

AMOEBIC DYSENTERY AMAEBIASIS)Definition - an infection due to a protozoa parasite (E histolytica) that cause intestinal or extra ndash intestinal disease Etiology - Entameba histolytica EpI - It occurs world wide but most common in the tropics and subtropics Prevalent in area with poor sanitation in mental institutions and homosexualsMode of transmissionFecal-oral transmission by ingestion of food or water contaminated by feces containing the cystIncubation period - variable It ranges from few days to several months or years but most commonly 2-4 weeksPeriod of communicability During the period of passing cysts of E histolytica which may continue for years Susceptibility and resistance-Susceptibility is general

Life cycle

Clinical Manifestations Starts with a prodormal episode of diarrhea abdominal cramps nausea vomiting and tenesmus With dysentery feces are generally watery containing mucus and blood Acute amoebic dysentery poses limited danger

Diagnosis - Demonstration of entamoeba histolytica cyst or trophozoite in stool microscopyRx Metronidazole or Tinidazole

Prevention and control 1 Adequate Rx of cases 2 Provision of safe drinking water 3 Proper disposal of human excreta and hand washing following defection 4 Clearing and cooking of local foods (eg Raw vegetables) to avoid eating food

contaminated with feces

Transmission1 Cysts ingested in food water or from hands contaminated with feces

Human host2 Cysts excyst forming

trophozoites 3 Multiply amp invade the

intestine 4 Trophozoites encyst 5 Infective cysts passes in

feces Trophozoites passed in feces disintegrate

Environment 6 Feces containing infective cysts contaminate the environment

GIARDIASISDefinition - a protozoan infection principally of the upper small intestine EPI - Occurrence ndash world vide distribution Children are more affected than adults The disease is highly prevalent in areas of poor sanitation amp overcrowding living situations Reservoir Humans Mode of transmission-- Feces to mouth transfer of cysts from feces of infected personsPeriod of communicability-entire period of infection often months Susceptibility and resistance Asymptomatic carrier rate is high Infection is frequently self-limited Persons with AIDS may have more serious and prolonged infection Life cycle - Similar to E histolytica Clinical Manifestation - Ranges from asymptomatic infection to severe failure to thrive and mal absorption - Associated with symptoms of chronic diarrhea steatorrhea abdominal cramps bloating frequent loose and pale greasy stools fatigue and wt loss- Young children usually have diarrhea but abdominal distension and bloating are frequent -Adults have abdominal cramps diarrhea anorexia nausea malaise amp bloating - Many pts complain of sulphur testing (belching) Diagnosis Demonstration of G lamblia cyst or trophozoite in feces Treatment Metronidazole or Tinidazole Prevention and control

1 Good personal hygiene and hand washing before food and following toilet use 2 Sanitary disposal of feces3 Protection of public water supply from contamination of feces 4 Case Rx 5 Safe water supply

CHOLERADefinition-An acute illness caused by an enterotoxin elaborated by vibrio cholera Etiology - Vibrio cholera EPI - Has periodic out breaks in different parts of the world and given rise to pandemics Endemic predominantly in children Reservoir- Humans Mode of transmission - by ingestion of food or water directly or indirectly contaminated with feces or vomitus of infected person Incubation period - few hours to 5 days (Usually 2-3 days) Period of communicability - for the duration of the stool positive stage usually only a few days after recovery Antibiotics shorten the period of communicability Susceptibility and Resistance Variable Gastric achlorhydria increases risk of illness Breast fed infants are protected

Clinical ManifestationAbrupt painless watery diarrhea the diarrhea looks like rice water In severe cases several liters of liquid may be lost in few hours leading to shock amp sudden deathSeverely ill pts are cyanotic have sunken eyes and cheeks scaphoid abdomen poor skin turgor and thready or absent pulse Loss of fluid continues for 1-7 daysDiagnosis- Based on clinical grounds - Stool Culture Treatment (1) prompt replacement of fluids and electrolytes

- Rapid IV infusions of large volumes- Isotonic Normal saline solution alternating with isotonic Ringer lactate

(2) Antibiotics like TTC are very effective Prevention and control

1 Safe disposal of human excreta and control of flies 2 Safe public water supply 3 Hand washing and sanitary handling of food4 Control and mgt of contact cases5 Case treatment

GASTROENTERITISIt is an inflammation of stomach and intestine by bacteria virus and poisons Acute diarrheal disease is a clinical syndrome of this disease Additionally nausea and or vomiting and often fever are also foundDiarrheal disease affects all the population but severity varies in different age groups Dehydration occurs rapidly in children and is a common cause of deathOccurrence =gtLow birth weight children and premature children easily get Ecoli infections=gtIn the weaning period new type of foods are introduced to children They are then exposed to a variety of micro-organisms (pathogenic and non pathogenic) =gtMalnutrition =gtBecause of poor economic and educational status of mothers of developing countries in general bottle fed children develop diarrheal disease Because they do not have the facility to clean the bottle properly and they do not have enough money to buy adequate amount of milk and other artificial feeds The child gets fed with poorly prepared diluted feeds and inevitably gets diarrhea=gtTravelers diarrhea occurs in people who are exposed to a new environment It is thought to be the guts response to new intestinal flora acquired through feco oral contact but other factors like changes in food amp contamination may also contributeNB Many organisms can cause diarrhea but it is difficult to prove the particular organism that is responsible But Bacteria like Ecoli and Rota-viruses are common causes There are many strains of Ecoli that can cause gastroenteritis

IP l0 hrs to 6 days for most strains Mode of transmission - through contamination of H20 food etc Clinical Manifestation ndash Acute onset of watery diarrhea that is usually mild and self limiting Malaise anorexia amp abdominal cramps may occur Some strains can result in bloody or mucoid diarrhea Toxins are released from these organisms which increase intestinal fluid secretion amp lead to diarrhea

Diagnosis - Clinical Features- Stool examination shows fecal leukocytes- Isolation of specific organism in stool specimen (culture)

Treatment - Rehydration (ORS)- Cotrimoxazole or- Ciprofloxacin for resistant strains

ASCARIASISDefinition - A helminthic infection of the small intestine generally associated with few or no symptoms Etiology ndash Ascaris lumbricoids EPI - Common where sanitation is poor School children (5-10 yrs) are most affected Highly prevalent in moist tropical counties Reservoir - Humans amp ascarid eggs in soil Mode of transmission- Ingestion of infective eggs from soil contaminated with human feces- Or uncooked food contaminated with soil containing infective eggs but not directly from person to person or from fresh feces Incubation period- 4-8 weeks Period of communicability As long as mature fertilized female worms live in the intestine Usual life span of adult worm is12 months Susceptibility and resistance susceptibility is general

Life cycle

Transmission 1 Infective eggs ingested in food or from contaminated hands

Human host 2 Larvae hatch in intestine 3 Migrate through liver and lungs 4 Pass up trachea and are swallowed 5 Worm mature in small intestine 6 Eggs produced and passed in feces

Environment (Envrsquot) 6 Eggs become infective (embryonated) in soil in 30-40 days 7 Infective eggs contaminate the envrsquot

Clinical ManifestationMost infections go unnoticed until large worms passed in feces and occasionally the mouth and nose

- Migrant larvae in lung amp trachea may cause itching wheezing and dyspnea fever productive cough of bloody sputum

- Abdominal pain may arise from intestinal or duct (billiary pancreatic) obstruction

- Serious complications include bowel obstruction due to knotted or intertwined worms

Diagnosis ndash Microscopic identification of eggs in stool sample - Adult worms pass from anus mouth or noseTreatment- Albendazole - Mebendazole - Piperazine - Levamisole Prevention and Control

1 Rx of cases2 Sanitary disposal of feces3 Prevent soil contamination in areas where children play 4 promote good personal hygiene (hand washing)

TRICHURIASIS( whip worm)Definition - It is a nematode infection of the large intestine (Caecum amp upper colon)Etiology - Trichuris trichuria (whip worm) EPI occurs ww esp in warm moist regions Common in children 3-11 years of ageReservoir- Humans Mode of transmission - indirect particularly through ingestion of contaminated vegetables Not immediately transmissible from person to person Ip ndash indefinite Period of comm several years in untreated carriers Susceptibility amp Resistance susceptibility is universal Life cycle

Transmission1 Infective eggs ingested in food or from contaminated hands

Human host 2 Larvae hatch Develop in small intestine migrate to Caecum 3 Become mature worms 4 Eggs produced and passed in feces

Envrsquot 5 Eggs become infective (embryonated) in soil after 3 weeks 6 Infective eggs contaminate the envrsquot

Clinical Manifestation - Most infected people are asymptomatic Abdominal pain tiredness nausea and vomiting diarrhea or constipation are complaints by patients Rectal prolapse may occur in heavily infected very young childrenSeverity is directly related to the number of infecting wormsDiagnosis Stool microscopy (eggs in feces) Treatment Albendazole or Mebendazole Prevention and control

1 Sanitary disposal of feces2 Maintaining good personal hygiene (ie washing hands and vegetables and other

soil contaminated foods) 3 Cutting nails esp-in children 4 Rx of cases

ENTEROBIASIS (OXYURIASIS PIN WORM INFECTIONS)Definition A common helminthic infection of Large intestine (Caecum) Etiology caused by Enterobius vermicularis EPI- it occurs world wide affecting all socioeconomic classes Prevalence is highest in school-aged (5-10 yrs) Infection usually occurs in more than one family memberReservoir- Humans Mode of transmission direct transfer of infective eggs by hands from anus to mouth=gtOr indirectly through clothing bedding food or other articles contaminated with eggs of the parasite Ip 2-6 weeksPeriod of communicability - As long as gravid females are discharging eggs on perianal skin Eggs remain infective in an indoor environment for about 2 weeks Susceptibility and resistance susceptibility is universalLife cycle

1 Ingestion of eggs by man2 Larvae hatch in duodenum and migrate down to caecum 3 Adult worms mature in caecum4 Gravid females migrate through the anus to the perianal skin and deposit eggs

(usually during the night) 5 Eggs become infective in a few hors in perianal area

Clinical Manifestation - perianal itching disturbed sleep irritability and some times secondary infection of the scratched skin The worm may also invade vaginaDiagnosis Stool microscopy for eggs or female worms Treatment Mebendazole 100mg Po stat or Albendazole-400mg Po stat Prevention and control

1 Educate the public about hygiene (ie hand washing before eating or preparing food )

2 keeping nails short and discourage nail biting3 Rx of cases4 Reduce over crowding in living accommodations 5 Provide adequate toilets

STRONGLOIDIASISDefinition An often asymptomatic helminthic infection of the duodenum and upper jejunum (Can be through out the small intestine)Infectious Agent ndash Strongloides stercoralisEPI- It occurs in tropical and temperate areas more common in warm and wet regions Reservoir ndash HumansMode of transmission - infective (filariform) larvae penetrate the skin and enter venous circulation IP 2-4 weeks Period of communicability as long as living worms remain in the intestine up to 35 yrs in cases of autoinfection Susceptibility and resistance susceptibility is universal Patients with AIDS or an immuno - suppressive medications are at risk of disseminationLife cycle

1 Infective filariform larvae penetrate skin amp enter circulation Eg feet 2 larvae reaches lung pass up trachea and swallowed 3 Become mature worms in small intestine4 Eggs laid Hatch rhabditiform larvae in intestine 5 Rhabditiform larvae

- passed in feces or- become filariform larvae in intestine causing autoinfection

6 In soil larvae become free living worms produce more rhabditiform larvae 7 Become infective filariform larvae in the soil

Clinical Manifestation pneumonia occurs during heavy larval migration Mild peptic ulcer like ss epigastric discomfort to severe watery diarrhea Heavy infection may result in malabsorption syndrome

Diagnosis- Identification of rhabditiform larvae in stool specimen microscopy Treatment- Albendazole 400mg Po per day for 03 days - Or thiabendazole 500 mg Po BID for 03 daysPrevention and control

1 Proper disposal of human excreta 2 personal hygiene including use of foot wear 3 Case Rx

HOOK WORM DISEASE(ANCYLOSTOMIASIS AND NECATORIASIS)

Definition A common chronic parasitic infection of small intestine with a variety of symptomsInfectious Agent ndash Ancylostoma duodenale and Necator americanus EPI- Widely endemic in tropical and subtropical countries where sanitary disposal of human feces is poor Common in area where soil is wet Reservoir-HumansMode of transmission - through skin penetration by the infective larvae (Filariform) 18

IP- Few weeks to many months depending on intensity of infection and iron intake of the hostPeriod of communicable infected people can contaminate the soil for several years in the absence of Rx Susceptibility amp Resistance susceptibility is universal Life cycle

1 Infective filariform larvae penetrate the skin amp enter circulation2 Larvae migrate to lung pass up trachea and are swallowed 3 Become mature worms in small intestine (attach to wall and suck blood) 4 Eggs produced and passed in feces 5 Eggs develop Rhabditiform larvae hatch in soil 6 Develop in to infective filariform larvae in about 1 week 7 Filariform larvae contaminate soil

Clinical Manifestation 1 Larval migration to the skin

Produces transient (short lasting) localized maculopapular rash associated with itching called ground itch

2 Larval migration to lungs Produces cough wheezing and transient pneumonitis

3 Blood sucking in intestine Light infection ndash no symptom Heavy infection ndash result in symptoms of PUD like epigastric pain and

tenderness Further loss of blood leads to anemia manifested by exertional dyspnea weakness and light headedness

Diagnosis Demonstration of eggs in stool specimen Treatment - Mebendazole 200 mg PO BID for 03 days

- Albendazole 400mg PO stat - Levamisole

Prevention amp control1 sanitary disposal of feces2 wearing of shoes3 Case Rx

POLIOMYELITISDefinition Acute viral infection most often recognized by the acute onset of flaccid paralysis Etiology Polioviruses (type I II and III) EPI =gtOccurs world wide prior to the advent of immunization =gtIt is primarily a disease of infants and young children ie 70-80 of cases are less than three years of age =gtmore than 90 of infections are unapparent and =gt Flaccid paralysis occurs in less than 1 of infections Reservoir Humans especially children Mode of transmission primarily person to person spread principally through the feco- oral route In rare instances milk food stuffs and other materials contaminated with feces have been incriminated as vehicles

IP Commonly 7-14 days Period of communicability As long as the virus is excreted (Usually less than 60days) Susceptibility and resistance susceptibility is common in children but paralysis rarely occurs Infection confers (gives) permanent immunityClinical Manifestation

- Usually asymptomatic or non ndash specific fever is manifested in 90 of cases

- If it progresses to major illness severe muscular pain stiff neck and back pain with or without flaccid paralysis may occur

- Paralysis is asymptomatic and occurs with in 3 to 4 days of illness - The legs are more affected than other parts of the body - Paralysis of respiratory and swallowing muscle is life threatening

Clinical course of the disease 1 Asymptomatic (unapparent infection) ndash90-95

-Show no signs and symptoms2 Abortive infection ndash occurs in 4-8 of cases

- SS of URTI ndash fever sore throat myalgia- SS of GI ndash anorexia nausea vomiting loose stool stomach upset stomach

aches 3 Non-paralytic poliomyelitis

- There is involvement of CNS without signs of paralysis amp subsides without sequel

- Signs of meningeal irritation head ache fever nuchal rigidity 4 Paralytic poliomyelitis

- Flaccid paralysis of a group of muscles associated with fever myalgia neck rigidity

Diagnosis Based on clinical and epidemiological grounds Treatment symptomatic Prevention and control

1 Educate public about the advantage of immunization in early child hood 2 Safe disposal of human excreta

Unit 4 20

AIR-BORNE DISEASESINTRODUCTION

Air-borne diseases are diseases transmitted through dissemination of microbial agent by air to a suitable portal of entry usually the respiratory tract The organisms causing the diseases in the air-borne group enter the body via the respiratory tract When a patient or carrier of pathogens talks coughs laughs or sneezes heshe discharges fluid droplet nuclei The smallest of these remain up in the air for sometime and may be inhaled by a new host Droplets with a size of 1-5 microns are quite easily drawn in to the lungs and retained there

Droplets that are bigger in size will not remain air-borne for long but will fall to the ground Here however they dry and mix with dust When they contain pathogens that are able to survive drying these may become air-borne again by wind or something stirring up the dust and they can then be inhaled

Air-borne diseases obviously will spread more easily when there is overcrowding as in over crowded class rooms Public transport canteens dance halls and cinemas Good ventilation can do much to counteract the effects of overcrowding Air borne diseases are mostly acquired through the respiratory tract

Common cold (Acute Viral Rhinitis or coryza)Definition An acute catarrhal infection of the nasal mucus membrane Infections agent Rhino viruses (100 serotypes) are the major causes in adults Para influenza viruses respiratory syncytial viruses (RSV) influenza and adenoviruses are additional causes of common cold EPI it occurs world wide both in endemic and epidemic forms Many people averagely have one to six colds per year Greater incidence in the highlands Incidence is high in children under 5 years and gradually declines with increasing age Reservoir HumansMode of transmission inhalation of air-borne droplets and articles freshly soiled (contaminated) by discharges of nose and throat of an infected personIP usually 48 hrs varying with the agentPOC 24 hrs before on set and for 5 days after onset SampR susceptibility is universal Repeated infections (attacks) are most likely due to multiplicity of agents Clinical features - Coryza sneezing lacrimation pharyngeal or nasal irritation chills and malaise Dry or painful throat Diagnosis Based on clinical grounds Treatment No effective Rx but supportive measures like

1 Bed rest 4 Anti pain2 Steam inhalation 5 Balanced diet intake 3 High fluid in take

Prevention amp control 1 Educate the public about the importance of hand washing covering the mouth when coughing and sneezing 2 Sanitary disposal of nasal and oral discharges 3 Avoid crowding in living and sleeping quarters esp in institution 4 Provide adequate ventilation

Influenza 21

Definition An acute viral disease of the respiratory tract (especially trachea) Infections agent Three types of influenza virus (A B amp C) EPI Occurs in pandemics epidemics and localized outbreaks Reservoir Humans are the primary reservoirs for human infection Mode of transmission Air-borne spread predominates among crowded populations in closed places such as school buses IP short usually 1-3 daysPOC 3-5 days from clinical onset in adults up to 7 days in young children PR when a new subtype appears all children and adults are equally susceptible Infection produces immunity to the specific infecting agent Clinical picture Fever headache myalgia prostration sore throat and cough Cough is often severe and protracted but other manifestations are self limited amp last long with recovery in 2-7 days Diagnosis based on clinical ground Treatment same as common cold namely

1 Antipain and antipyretic2 High fluid intake3 Bed rest4 Balanced diet

Prevention 1 Educate the public in basic personal hygiene esp the danger of unprotected coughs and sneezes and hand to mucus membrane transmission 2 Immunization (with available killed virus vaccines for (A amp B types) may provide 70-80 protection) 3 Amantadine hydrochloride is effective in the chemo prophylaxis of type A virus but not others It is used both for Rx (4-5days) and prophylaxis (as long as epidemics lasts) 100mg PO BID

Measles (Rubella)Definition An acute highly communicable viral diseaseEtiology measles virus EPI Prior to wide spread immunization measles was common in child hood so that more than 90 of people had been infected up to age 20 few went through life without any attack The maximum incidence is bn 6 months and 5 yearsReservoir Humans Mode of transmission

Airborne droplets released when an infected person sneezes or coughs Contact with nose and throat secretions of infected people Cases can infect others for several days before and after they develop symptoms Spreads easily in over crowded areas (schools military barracks health facilities

etc)IP 7-18 days from exposure to onset of fever POC slightly before the ss appear to four days after the appearance of the rashS and R All those who are non-vaccinated or have not had the disease are susceptible Permanent immunity is acquired after natural infection or immunization

Signs and symptoms

High fever which begins approximately 10 -12 days after exposure and lasts for several days

A characteristic slight raised red blotchy rash appears on the third to seventh day beginning inside the cheeksamp on the buccal mucosa as small white spot (this is called koplikrsquos spot) then under the ears then on the face and neck gradually spreads to the body and then to the hands amp feet and lasting 4-7 days

Runny nose conjunctivitis coryza cough red and watery eyes and Leucopoenia is common Complications like otitis media pneumonia diarrhoea encephalitis croup

(laryngotracheo bronchitis) may result from viral replication or bacterial super infection

Diagnosis = Based on clinical and epidemiological grounds = Fever and rash plus one of these Cough coryza or conjunctivitis Complications

bull Unimmunized children under 5 years and infants are at highest risk of measles and its complications

bull Pneumonia is the most common cause of death as the virus weakens the immune system

Complications are due to 1 Bacterial infection

2 Measles virus which damages respiration and intestinal tracts 3 Vitamin A deficiency

1 Acute complicationso Bronchopneumonia- the most important complication and responsible

for most deaths o Diarrhoea (dysentery and persistent diarrhoea) o Laryngo-tracheo bronchitis o Conjunctivitis and corneal ulceration o Ottitis media mastoiditis o Stomatitis o Appendicitis o Malnutritiono Acute encephalitis-rare complications o Febrile convulsions AGE in children lt2yrs

2 Long term complication o Increase susceptibility to other infection (damages immune system) o Blindnesso Sub acute sclerosing pan encephalitis

Treatment No specific Rx General nutritional support and Rx of Dehydration Antibiotics are given only to ear and severe respiratory infection Vitamin A two doses in 24 hours Rx of complication

Nursing care1 Advise pt to have bed rest2 Relief of fever3 Provision of non- irritant small frequent diet 4 Shorten the finger nails

Prevention 1 Educate the public about measles immunization2 Immunization of all children (lt5 years of age) who had contact with infected

children 3 Provision of measles vaccine at nine months of age 4 Initiate measles vaccination at 6 months of age during epidemic and repeat at 9

months of age

Pertussis (whooping cough)Definition An acute disease of the respiratory tract caused by bacteriaInfections agent Bordetella pertusis EPI it is an endemic disease common to children esp young children every where in the world The disease is mostly affects amp dangerous in children age less than one year and non-immunized Many children that contract pertussis have coughing spells that lasts for eight weeksReservoir- Humans Mode of transmission direct contact with discharges from respiratory mucus membrane of infected persons by air borne route amp by handling objects freshly soiled with nasopharyngeal secretions Ip 1-3 weeks POC ranges from 7 days after a person has been exposed to until three weeks after the start of the coughing Highly communicable in early stage Infectiousness decreases after onset of therapy S and R Susceptibility to non immunized individuals is universal One attack usually confers prolonged immunity but may not be life long

Signs and symptoms The disease has insidious onset and 3 phases

1 Catarrhal phase- Last 1 ndash 2 week- Cough and rhinorhea

2 Paroxysmal phase - Explosive repetitive and prolonged cough - Child usually vomits at the end of paroxysmal cough - Expulsion of clear tenacious mucus often followed by vomiting - Lasts 2-4 weeks -Whoop (inspiratory whoop against closed glottis) between paroxysms - Child looks health bn paroxysms- Cyanosis and sub conjunctival haemorrhage due to violent cough

3 Convalescent phase - The cough may diminish slowly in 1-2 weeks time or may last long time- After improvement the disease may recur

Diagnosis difficult to distinguish it from other URTI - History and physical examination at phase two ensure the diagnosis - Marked lymphocytosis

Treatment Erythromycin 30-40mgkg PO QID for 10days - Antibiotics for super infection like pneumonia bc of bacterial invasion due to

damage to cilia Nursing care

1 Proper feeding of the child high fluid intake 2 Encourage breast feeding immediately after an attack of each paroxysm3 Proper ventilation-continuous well humidified oxygen administration 4 Reassurance of the mother (care giver) 5 Steam inhalation

Prevention o Educate the public about the dangers of whooping cough and the advantages of

initiating immunization at 6 weeks of ageo Consider protection of health worker at high risk of exposure by using

erythromycin for 14 days o Vaccination (DPT)

Complications 1 Loss of appetite 6 Bronchiectasis 2 Middle ear infection 7 Re activation of latent TB3 DHN 8 Pneumothorax4 Bacterial pneumonia 9 Emphysema5 Convulsions and seizures 10Encephalopathy

11 Debility and emaciation Diphtheria

Definition An acute bacterial disease of the mucus membrane of the RT involving primarily tonsils pharynx nose occasionally other mucus membranes or skin and some times the conjunctiva or genitalia Infections agents corynebacterium diphtheriae EPI Disease of colder months involving primarily non-immunized children less than 15 years of age It is often found among adult population groups whose immunization was neglected Unapparent cutaneous and wound diphtheria cases are much more common in the tropics 25

Reservoir HumansMode of transmission contact with a pt or carrier ie with oral or nasal secretion or infected skin raw milk has served as vehicle IP usually 2-5 days POC variable Usually 2 weeks or lessS and R susceptibility is universal Prolonged active immunity can be induced by diphtheria toxoid Clinical picture Characteristic lesion marked by a patch or patches of an adherent greyish membrane with a surrounding inflammation (pseudo membrane)

-Throat is moderately sore in pharyngotonsillar diphtheria with cervical lymph nodes some what enlarged and tender in severe cases there is marked swelling and oedema of neck- sore throat cervical adenopathy or swelling and low grade fever accompanied by nasal discharge systemic toxicity hoarseness stridor palatal paralysis with or without pseudo membrane - Patient may recover within 6 ndash 10 days - But late effects of absorption of toxin appearing after 2-6 weeks including cranial

and peripheral motor and sensory nerve palsies and myocarditis (which may occur early) and are often severe

Complications

bull Abnormal heart beats which may lead to heart failure

bull Inflammation of heart muscles and valves (lead to chronic heart disease and heart failure)

bull The most severe complication is respiratory obstruction as a result of laryngotracheobronchitis (croup) followed by death

Diagnosis Bacteriologic exam of discharges from lesions Based on clinical and epidemiological grounds

Treatment1 Diphteria antitoxin 2 Erythromycin 500mg for 2 weeks but 1 week for cutaneous form or 3 Procaine penicillin IM for 14 days or

Single dose of Bezanthine penicillin IM Newborn 150000IU once(stat) 1-12 months 300000IU once 2-6years 600000IU once 7-10 years 900000 IU once Over 10 years 1200000 IU 0nce Adult12 to 24 Million IU once

NB- primary goal of antibiotic therapy for pts or carriers is to eradicate C- diphtheriae and prevent transmission from the pt to other susceptible contacts

Prevention1 Immunization of infants with diphtheria toxoid( DPT)2 Concurrent and terminal disinfection of articles in contact with pt and soiled by

discharges of pt 3 Single dose of B penicillin (IM) or erythromycin 7-10 days course (PO) is

recommended for all persons exposed to diphtheria Antitoxic immunity protects against systemic disease but not against local

infection in the nasopharynx

Definition An acute bacterial disease that causes inflammation of the meninges (esp the pia and arachnoid space) the coverings of the brain There may also be varying involvement of the brain parenchymaInfectious agent 1 In neonates Gram-ve bacilli-Ecoli Proteus species

Group B streptococci 2 Preschool child Haemophilus influenza B

Neisseria meningitides (meningococcus) Streptococcus pneumonae

3 Older children and Adults N meningitidis(A B C X Y Z w135) strep Pneumonae

=gtMeningococcus (N Meningitidis) is responsible to Meningococcal meningitis amp type A is know to cause epidemics

EPI - Epidemics occurs irregularly - Common in children and young adults - It is a disease of individuals with poor general health and commonly happen in

crowded situations Reservoir ndash Humans Mode of transmission ndash Direct contact with respiratory droplets from nose and throat of infected person Ip- Varies from 2-10 days commonly 3-4 days POC- until the meningococci are no longer present in discharges from nose and mouth Meningococci usually disappear from the nasopharynx with in 24 hrs after initiation of proper RxSusceptibility and Resistance

- Susceptibility is low and decreases with age - Immunocompromised persons are at high risk Pathogenesis Meninges (pia arachinoid ampdura mater) are congested and infiltrated with inflammatory cells A thin layer of pus formed and this may later organize to form adhesions This may cause obstructions to the free flow of CSF and impedes absorption of CSF leading to hydrocephalus or they may damage the cranial nerves at the base of the brain The CSF pressure rises rapidly the protein content increases and the glucose content decreases

The increased ICP (tension) impedes cerebral blood supply further results in ischemic damage

Clinical Manifestation- Sudden onset of fever intense head ache nausea and often vomiting Neck

stiffness drowsiness photophobia seizures are the usual presenting features- There may be purpuric or petechial rash and circulatory collapse- In severe cases the pt may be comatous and later there may be neurological

deficit Usual signs of meningeal irritations - Kernigs sign- pt feels back pain when one of the lower limbs is flexed at the knee

joint and extended forward in an elevated position Or when the pt is lying with his thigh flexed on the abdomen he cant completely extend his leg - Brudzinkis sign when the pts neck is flexed the two lower extremities get flexed

at knees and hip joint or raised up Or when passive flexion of the lower extremity of one side is made a similar movt is seen for the opposite extremity

- Neck rigidity (Nuchal rigidity ) on flexion of the neck Lateral rotation of the neck doesnt produce pain

Diagnosis Based on clinical and epidemiological grounds Lab investigations

WBC count ( specially neutrophils may be increased) CSF analysis by lumbar puncture

o Gram stain of CSF G-ve intra cellular diplococcio WBC-polymorphso Protein level increased possibly by increased capillary

permeability o Glucose ndash increased used up by brain decreased transport via

inflamed membraneo Physical appearance ndash turbido Pressure on withdrawing the needle

CT-to exclude cerebral abscesses or space occupying lesions NB Lumbar puncture is mandatory unless there is contraindicationTreatment

1 Admit the pt and administer high dose of crystalline penicillin IV- Crystalline 3 to 4 Million IU IV q 4 hourly and- CAF l g Iv QID and- Ampicillin 1 g IV QID- Monotherapy with ceftriaxone 100mgkgday IM BID- The usual duration of antibiotic Rx is 14days

2 Fluid replacement3 Mgt of seizures

- Control by diazepam 10mg IM or IV 4 Cerebral oedema mgt

- by IV manitol 1-2 days followed by oral glycerine (produce osmotic gradient bn the plasma and brain which in turn excrete through the kidneys)

Nursing care1 Maintain fluid balance (in put and out put)2 Maintain body temp to normal3 Timely administration of antibiotics4 Monitor vital signs5 Observe for any neurological disorders

Prevention and control1 reduce direct contact and exposure droplet infection2 Reduce over crowding in work places schools camps etc3 Vaccines containing group AC and Y strains4 Chemo therapy of case5 Chemo prophylaxis eg Rifampin 600mg po BID for 2 days or ciprofloxacin

500mg PO 6 Report to the concerned health authority

Meningococcal infections- Bacteraemia and meningitis are the most common infection caused by N

meningitides among an variety of infections- N- meningitidis is a gram ndashve diplococcus and has 13 serogroups- The natural habitat of these bacteria is the nasopharynx and they are continued

entirely to humans - Sero group A meningococci are the primary cause of epidemics especially in

Africa- In the lsquoMeningitis belt lsquo On sub-Saharan Africa the incidence of Meningococcal

do rises sharply toward the end of the dry and dusty season and falls with the onset of rains

- Outbreaks occur more frequently among the poorest segments of the population where overcrowding and poor sanitation are common

- Invasive meningococcal disease occurs almost exclusively in individuals who lack protective bacterial antibodies to the infecting strain

- Infants are protected from meningococcal infection for the first few months of life by passively transferred maternal antibodies and by a very low rate of meningococcal acquisition As maternal antibodies are lost susceptibility rises peaking at 6 to l2 months It then falls progressively as antibodies are acquired through colonization with closely related but non pathogenic bacteria such as N lactamica avirulent N meningitidis N lactamica colonizes the nasopharynx

Complication - The complication of meningococcal infections include Recurrent infection and damage to CNS

- Superinfection of the respiratory tract- Neurological complication may result from direct infection of brain parenchyma

- Cerebritis- Brain abscess- Injury to cranial innervations (seizures focal deficits amp paralysis)

- Cerebral edema amp raised ICP- Interruption of CSF pathway (hydrocephalus)- Effusion in to subdural space

TUBERCULOSISA systemic bacterial disease which primarily affects the lung but other organs may also be involved depending on the bacteria dissemination and the host resistance Infectious agent

- M tuberculosis- human tubercle bacilli (commonest cause) - M bovis-causes cattle and man infection - M avium-causes infection in birds and man

EPI- It occurs world wide however under developed areas are more affected - Affects all ages and both sexes but age groups bn 15-45 years are mainly

affectedMode of transmission

- Through aerosolized droplets mainly from persons with active ulcerative lesion of lung expelled during taking sneezing singing or coughing directly

- Untreated PTB+ cases are the source of infection - The risk of infection is related to the length of contact an individual shares

volume of air with an infections case ie intimate prolonged or frequent contact is required

- Transmission through contaminated fomites (clothes personal articles) is rare - Ingestion of unpasteurized milk transmits bovine TB Over crowding and poor housing conditions favour the disease transmission

Incubation period depends on the site of involvement - 4-12 weeks ndash PTBc- 3-6 mouth ndash meningeal milliary and pleural disease - Up to 3 yrs- GI bone joint amp lymph node disease - 8 yrs ndash Renal tract disease

Period of communicability- As far as the bacilli is present in the sputum Some untreated or inadequately

treated pts may be sputum positive intermittently for year NB-effective antimicrobial therapy usually eliminates communicability with in 2 weeks

- Extra pulmonary TB and children with primary TB are generally non-infections Susceptibility and resistance

- Every one who is non infected or non-vaccinated can be infected- Susceptibility to infection is highest among

o Children under 3 yrs oldo Adolescentso Young adults o The very oldo The immunocompromised

Children at greater risk of developing TB are 1 Children who are contacts of a newly diagnosed smear positive case 2 Children less than 5 years of age 3 HIV infected children 4 Severely malnourished children

HIV is an important risk factor for the development of HIV-associated TBc by facilitating

1- Reactivation reactivation of latent TB infection that was acquired prior to the HIV infection

2- Progression of recent infection= rapid progression of latent TB infection to TB disease following recent TB infection

3- Reinfection= a re infection with another strain of M tuberculosis Clinical manifestationTuberculosis has two major clinical forms

1 Pulmonary (80) of the total TB cases- Primarily occurs during child hold amp secondarily 15-45 yrs or later

2 Extra pulmonary (20) affects all parts of the bodyMost common sites are lymph nodes pleura GUT bone and joints meninges amp peritoneum

Early signs and symptoms - Productive cough for more than 3 weeks - Fever- Unexplained wt loss- Night sweats

Late signs and symptoms- Blood stained sputum - Difficulty in breathing- Severe wt loss- Severely diminished loss of appetite - Weakness- Symptoms of other organ involvement - Enlargement of lymph nodes

EPTBTB lymphadenitis

- Slowly developing and painless enlargement of lymph nodes followed by matting and drainage of pus

Tuberculosis pleurisy - Pain while breathing in dull lower chest pain slight cough breathlessness on

exertion TB of bones and joints

- Localized pain andor swelling discharging of pus muscle weakness paralysis and stiffness of joint

Intestinal TB- Los of wt and appetite - Abdominal pain diarrhoea and constipation - Mass in the abdomen - Fluid in the abdominal cavity (ascites)

Tuberculosis meningitis

- Head ache fever vomiting neck stiffness and mental confusion of insidious onset

Diagnosis1- Clinical Manifestations2- Sputum smears for AFB ndash the golden standard

However one positive result doesnt justify starting anti TB Rx since errors can never be excluded

3- Acid fast stain for AFB can be done for extra Pulmonary TB having discharge4- Radio logic examination ndash chest x-ray

- This is unreliable bc it can be caused by a variety of conditions or previous TB patients who are healed may have chest x-ray giving the appearance of active TB which requires Rx

5- Histopathological exam Biopsy for EPTB like TB lymphadenitis 6- Tuberculin skin test (TST or Montoux test) ndash Helpful in non-BCG vaccinated

children under 6 yrs of age Values of a negative tuberculin test

A tuberculin test is not significant or negative when the diameter of skin indurations is less than 10mm (or less than 5 mm in an HIV infected child) This is regardless of whether or not the child has had BCG A negative tuberculin skin test doesnrsquot exclude TB In other words a negative test is of no help in deciding that some one does not have TB Conditions that may suppress the TSF

- HIV infection- Malnutrition amp Cancer- Severe bacterial infections including TB- Viral infections like measles chicken pox glandular fever - Immunosuppressive drugs like steroids - Incorrect injection of PPD

Values of a positive TSTThe criterion for a significant or positive tuberculin test depends on whether a child has previously had BCG vaccination or not This is because a reaction to tuberculin is usual after a previous BCG for several years This reaction is usually a weaker reaction (diameter often less than 5mm) than the reaction to natural infection with M tuberculosis A tuberculin test is considered significant or positive when the diameter of skin indurations is 10mm or more However if the child is HIV infected tuberculin test is considered positive if the induration is 5mm or more A positive tuberculin test is only one piece of evidence in favour of the Dx of TB The younger the child and the greater the diameter of indurations the stronger is the evidence

7- Sputum culture- complex and sophisticated which takes several weeks 8- ESR9- Gastric washing for children10- Trans bronchial biopsy11- CT scan ndash tuberculoma12- CSF analysis ndash TB meningitis

13- Pleural fluid analysis and culture-TB pleurisy 14- Pericardial fluid analysis ndash TB pericarditis

ManagementCase definitions

1 Relapse (R) A pt who has been declared cured or treatment completed of any form of TB in the past but who reports back to the health service and is found to be AFB smear positive or culture positive

2 Rx failure (F) A pt who while on Rx remained smeary positive or became again smear positive at the end of the five months or later after commencing Rx

3 Return after default (D) Apt who had previously been recorded as defaulted from Rx and returns to the health facility with smear positive sputum

4 New case (N) Apt who has never had Rx for TB or has been on anti TB Rx for less than four weeks

5 MDR-TB A pt who is still smear positive at the completion of re treatment regimen

6 Defaulter A pt who has been on Rx for at least 4 weeks and whose treatment was interrupted for 8 or more consecutive weeks

7 Rx failure A pt who remains or becomes again smear positive at the end of 5 months or later during Rx A pt who was PTB-negative at the beginning and turned out smear positive at the end of the intensive phase

Drugs used for the chemotherapy of TB1 Streptomycin (S)2 Ethambutol (E) 3 Isoniazid (H)4 Rifampicin (R)5 Pyrazinamide (Z)

Phases of chemotherapy ndash Rx of TB has two phases 1 Intensive phase (initial) This phase consists of three or more drugs for the 1st 8 weeks for new cases and 12 weeks for re-treatment cases It renders the pt non-infectious by rapidly reducing the load of bacilli in the sputum and minimizing the danger of devt of drug resistance 2 Continuation phase This phase immediately follows the intensive phase and is important to ensure that the pt is permanently cured and does not relapse after completion of Rx This phase requires at least two drugs to be taken for 4-6 monthsTreatment categories

There are four diff Rx categories and corresponding Rx regimens 1 Category I short course chemotherapy for smear +ve PTB amp seriously ill

smear negative PTB and EPTB cases ndash New smear-positive PTB pts

- New smear-negative PTB pts who are seriously ill - Return after default from SCC who have smear negative PTB

Seriously ill includes - Life threatening disease - Acute disseminated miliary TB

- TB meningitis- TB peritonitis

- Risk of severe disability - Spinal TB- TB pericarditis- Bilateral TB pleural effusion - Renal TB- Extensive x-ray lesions without cavitations in immuno-

compromised pts eg DM HIV the Rx 2(ERHZ) 6 (EH) ie

Intensive phase- 2ERHZ ndash The drugs must be collected daily and must be swallowed under the direct observation of a health worker Continuation phase ndash 6 EH the drugs must be collected every month and self ndash administered

2 Category II (Re treatment regimen)This regimen is to prescribe for pts previously treated for more than one month with SCC or LCC and who are still smear positive

- Relapses- Treatment failures- Returns after default - PTB patients who become smear positive after 2 months of Rx- Re turn after default from re-treatment (only once re- treatment again) - Relapses after re treatment (only once re treatment again) Rx Intensive phase ndash 2 S(ERHZ)

- 1 (ERHZ) Continuation phase 5 E3 (RH) 3 3 ndash 3 times a week ie in alternate days

NB- The drugs must be taken under the direct observation of a health worker through out the duration of re-treatment

3 Category II- short course chemotherapy for smear negative PTB EPTB and TB in children

who are not seriously ill o New adult patient with smear negative PTBo New adult patents with EPTB (milder forms)

TB of the lymph nodes TB osteomyelitis (Bone TB) TB arthritis Adrenal TB TB with unilateral pleural effusion

Children bn 7 and 14 yrs old with any type of TB who are not seriously ill

Rx Intensive phase - 2 (RHZ)

Continuation phase ndash 6 (EH)

4 Category IV ndash chronic cases- Multi drug resistant cases of TB they are given the least priority - RxINH ndash prophylaxis for life long or second line anti TB drugs eg

Clarithromycin azithromycine Ofloxacine Protionamide Ethionamide Cycloserine Capreomycin Para aminosalicylic acid (PAS)

- This category is not being implemented in EthioPrevention and control

1 Health education esp for pts how to dispose sputum and MOT 2 Chemotherapy of cases 3 Chemoprophylaxis for contacts

INH for 06 months blindly or INH for 03 months then do PPD test

PPD test +ve continue for 03 months PPD ndashve stop INH and give BCG for the future

4 Immunization of infants with BCG5 Educate the public about the modes of disease transmission and methods of

control - Improved standard of living - Adequate nutrition - Healthy housing ventilation and sunlight exposure (windows open and transparent) - Environmental sanitation- Personal hygiene amp Active case finding and Rx

6 Isolation of PTB +ve case = decreases infectivity

Leprosy (Hansens disease)Definition A chronic bacterial disease primarily of the skin peripheral nerves and in lepromatous patients the upper air way and the eyes Infections agent M leprae acid fast rod shaped bacillus EPI Although common in rural tropics and subtropics socio-economic condition may be more important than climate itself Endemic in south and southeast Asia tropical Africa and Latin America Leprosy affects all ages and both sexes The age group mainly affected is between 15-45 yrs There are however special groups that are more vulnerable to developing the disease Factors related to poverty increase the risk of developing diseaseUnder normal circumstance only a very small proportion (less than 5) of all individuals who are infected by the leprosy bacilli will develop the disease during their life In the majority of people the immunological defence kills all the bacilli The disease has a long

incubation period on average ranging from 3 to5 years but it may vary from 6 months to more than 20 yrs Leprosy can cause severe disability mainly as a result of peripheral nerve damage

Reservoir untreated multi-bacillary leprosy pts discharging bacilli are the main reservoir of the disease Mode of transmission - Not clearly established House hold and prolonged close contact appear to be important Millions of bacilli are liberated daily in the nasal discharges of untreated lepromatous pts Cutaneous ulcers in lepromatous pts may shed large No of bacilli Organisms probably gain access (entrance) through the URTI and possibly through broken skin In children less than one year of age transmission is presumed to be transplacental IP 8 mouth to 20 yrs POC Infectiousness is lost in most instances with in 3 months of continuous and regular Rx with dapsone or clofazmin and with in 3 days of rifampicin Rx Susceptibility and resistance the presence and format leproly depend on the ability to develop effective cell mediated immunity Clinical Manifestations vary bn two polar forms lepromatous and tuberculoid leprosyLepromatous (multibacillary form) Nodules papules macules and diffused infiltrations are bilaterally symmetrical and usually numerous and extensive (six or more skin lesions)Involvement of the nasal mucosa may lead to crusting obstructed breathing and epistasis Ocular involvement leads to iritis and keratitis Tuberculoid (paucibacillary form) skin lesions are single or few are to five leprosy skin lesions sharply demarcated anaesthetic or hyperaesthetic and bilaterally symmetrical peripheral nerve involvement tends to be sever Borderline

Has features of both polar form and is more liable to shift towards the lepromatous form in untreated patients and toward the tuberculoid form in treated patients

Diagnosis cardinal signs for the diagnosis of leprosy are-1 Hypo-pigmented or reddish skin lesion(s) with definite loss of sensation 2 Definitively enlarged nerves at the sites of predilection andor damage to the

peripheral nerves as demonstrated by loss of sensation and weakness of the muscles of hands feet or face

3 The presence of AFB positive skin smears NB The finding of one of these three cardinal signs is diagnostic for leprosy The main aim of case-finding is to 1 Diagnose and treat leprosy cases early before irreversible damage has occurred 2 Interrupt transmission of the disease3 Prevent the occurrence of leprosy related disability

A pt is suspect for leprosy when presenting with 1 Reddish patches on the skin 2 loss of sensation on the skin 3 Numbness and tingling of the hands andor the feet 4 weakness of eyelids hands and feet 5 painful andor tender nerves

6 Burning sensation in the skin 7 Painless swelling in the face and ear lobes 8 Painless wounds or burns on the hands or feet

TREATMENT MDT regimen for MB leprosy Drugs 0-5yrs 6-14yrs gt15yrs Rifampicin 300mg 450mg 600mgClofazimine 100mg 150mg 300mgClofazimine 50 mg twice 50mg every 50mg daily

a week 0ther day Dapsone 25 mg 50mg 100mg

MDT regimen for PB leprosy Drugs 0-5yrs 6-14yrs gt15yrsRifampicin 300mg 450mg 600mgDapsone 25mg 50mg 100mg

Prevention and control1 HE2 Case detection and early Rx (particularly infectious mutibacilary)

3 Avoid contact with pt (isolation) 4 Disinfection of articles in contact with nasal discharges of infections pt

UNIT 5 Arthropod-borne

(Intermediate host-borne)or vector borne diseases

Introduction

Generally speaking a vector is any carrier of disease specially invertebrate hosts (insects or snails) Vector ndash borne disease

1 Mosquito ndash borne diseases - Malaria- Filariasis- Yellow fever

2 Flea-borne Diseases - Plague- Endemic typhus (flea-borne typhus)

3 Louse-borne Diseases - Epidemic typhus - Relapsing fever

4 Snail-borne Diseases - Shistosomiasis - Guinea worm infection (Dracunculiasis)

MALARIADefinition Malaria is an acute infection of the blood caused by protozoa of the

genus plasmodiumInfectious agent

- Plasmodium falciparum malignant tertian invades all ages of RBC RBC cycle is 42 hrs

- Plasmodium vivax benign tertian invades reticulocytes only RBC cycle is 48 hrs

- Plasmodium ovalae tertian invades reticulocytes only RBC cycle is 48hrs

- Plasmodium malarial quartan malaria invades reticulocytes only RBC cycle is 72 hrs

EPI- Endemic in tropical and subtropical countries of the world Affects 40 of the word population Children less than 5 yrs of age pregnant women and travellers to endemic areas are risk groups P falciparum 60 and p vivax 40 are common in Ethiopia Reservoir- humansMode of transmission

- By the bite of an infective female anopheles mosquito which sucks blood for egg maturation

- Blood transfusion hypodermic needles organ transplantation and mother to fetus transmission is possible

- Female Anopheles mosquitos are common vectors in Ethiopia

Incubation period ndash Varies with species - P falciparum-7-14days- P vivax -8-14 days- P Ovalae-8-14 days- P Malariae -7 -30 days

Period of communicability Mosquitoes are infective as long as infective gametocytes are present in the blood of patients Once infected mosquito remains infective for life Susceptibility and resistance Susceptibility is universal except in some host ndashresistance factors Non specific factors

- Hyperpyrexia-which is said to be schizonticidal - Sickle cell traits are resistant to p falciparum- Because of passive immunity infants are resistant in early life

Clinical Manifestations- Chills rigor fever head ache diarrhoea hallucinations abdominal pain

aches renal or respiratory symptoms amp jaundice etc Diagnosis

- Clinical Manifestations and epidemiological grounds- Blood film for hemo parasites - Chest x-ray to rule out pneumonia

Treatment Management of simple Pfalciparum malaria

1 For non ndashpregnant mothers Adults and children gt5kg Artemether-Lumefantrine two times daily for 3 days (4 tabs PO BID for 03 days) 2 For pregnant mothers and children lt5kg

- Quinine three times daily for 7 days (600mg PO TD for 07dys)

Management of severe (Complicated) Pfalciparum malaria 1 Quinine loading dose (20mgkg) in 500cc Dw to run over 4hrs 4hrs interval of

rest 2 Quinine maintenance dose (10mgkg) in 500cc DW to run over 4hrly until the pt

can take po At least for the 1st 48 hrs 3 Give IV glucose 40 (IV push or in the bag) simultaneously with quinine4 Nursing Management 5 Discharge the pt with quinine po or Artemether-Lumefantrine for the remaining

period of Rx 6 A loading dose should not be used in pts who has taken any anti malarial in the

preceding 24 hrs or mefloquine with in preceding 7 daysManagement of other forms of malaria

- Chloroquine po daily for 3 days (442)Complications

1 Cerebral malaria in a pt with falciparum malaria 2 Anaemia (Hglt5gdl)

- Due to Acute destruction of RBC amp Spontaneous bleeding3 Renal failure 4 Hypoglycemia (BGLlt40gde) 5 Fluid electrolyte and acid- base disturbances 6 Pulmonary edema 7 Circulatory collapse shock 8 Spontaneous bleeding

9 Hyper pyrexia Hyper parasitemia- Parasite load or density above 5 or +++++

10 Malarial haemoglobinuria Prevention and control

1 Chemo prophylaxis for travellers to endemic areas 2 Vector control

- Avoiding mosquito breeding sites - DDT spray or other chemicals - Personal protection against mosquito bite (use of bed net amp mosquito

repellent creams) 3 Chemo therapy of cases

FilariasisDefinition A disease caused by the reaction of the body to presence of worms in the lymphatic system Infectious agent ndash Nematodes

Wucheriria Bancrofti (vectors are culex Anopheles mosquito) EPIWidely prevalent in tropical and subtropical areas It is found in Gambella region (western Ethiopia) Reservoir Humans Mode of transmission - by bite of mosquito harbouring infective larvaeIncubation period one monthPeriod of communicability microfilariae may persist in human for 5-10 year or longer after infection The mosquito becomes infective about 12-14 days after an infective blood meal Susceptibility and resistance universal Repeated infections may lead to the severe manifestations such as elephantiasisClinical manifestationThe presence of worms in the lymph vessels causes allergic reactionThree phases may be distinguishedAcute phase = Lymphadenopathy Fever EosinophiliaSub acute phase= This occurs after about one year following acute phases

- lymphangitis epididymitis Recurrent attacks will sooner or later lead to hydrocele

Lung symptoms may be seenChronic phase

- After many years of repeated attacks lymph glands and lymph vessels become obstructed as a result lymphedema is seen in the legs (elephantiasis) or scrotum But may also be present in vulva breasts or arms

-Diagnosis

- Clinical and epidemiological grounds- History of travel to and residence in endemic areas

- Microfilaria in the peripheral blood film (BF) That is microfilarial appears in the peripheral blood during the night (nocturnal) in most parts of the world

Treatment Diethyl carbamazine (DEC)

- Day 1 ndash 50mg- Day 2 ndash 50 mg Po TID- Day 3 ndash 100 mg Po TID- Day 4-14- 2mgkg Po TID OR

Ivermectin 150-200 mcgkgd PO as single dose repeat q2-3mo Refer the pt for surgical Rx of hydrocele Prevention and control

1 Reducing the vector population 2 Mass and selective Rx3 Personal protection against mosquito bite

Epidemic Typhus (Louse -borne typhus)

Definition An acute rickettsial disease often with sudden onset

Infectious agent - Rickettsia Prowazeki

EpidemiologyOccurrence- In colder areas where people may live under unhygienic conditions and are louse-infected Occurs sporadically or in major epidemics for example during wars or famine when personal hygiene deteriorates and body lice flourish

Reservoir- Humans Infected lice die and donrsquot serve as a reservoir

Mode of transmission- The body louse and head louse are infected by feeding on the blood of a patient with acute typhus fever Infected lice excrete rickettsiae in their feces and usually defecate at the time of feeding People are infected by rubbing feces or crushed lice into the bite or into superficial abrasions (scratch inoculation)Incubation period- From 1 to 2 weeks commonly 12 daysPeriod of communicability- Patients are infective for lice during febrile illness and possibly for 2-3 days after the temperature returns to normal Infected lice pass rickettsiae in their feces within 2-6 days after the blood meal it is infective earlier if crushed The louse die within 2 weeks after infectionRickettsiae may remain viable in the dead louse for weeks

Susceptibility and resistance- Susceptibility is general One attack usually confers long-lasting immunity

Clinical Manifestation Early symptoms of fever headache mayalgia macular eruption appear on the body

Patient may have pneumonia renal or CNS involvement gastrointestinal disease skin rash singly or incombination1048707 Disease usually terminates by rapid lysis after 2 weeks of feverDiagnosis1048707 Based on clinical and epidemiologic grounds1048707 Serologic test (weil-felix agglutination test)Treatment Treatment consists of either tetracycline (25 mg kgd in four divided doses) or chloramphenicol (50ndash100 mgkgd in four divided doses) for 4ndash10 days

Prevention and control1 Delousing of clothes by insecticides or dipping into boiling water2 Public education on personal hygiene3 Treatment of cases4 Chemoprophylaxis for contacts

Endemic typhus (Flea-borne typhus) (Murine Typhus fever)Definition A rickettsial disease whose course resembles that of louse borne typhus but is milder Infections agent - Rickettsia typhi ( Rickettsia mooseri) EPI ndash occurs world wide found in areas where people and rats occupy the same buildingsReservoir Rats amp mice Infection is maintained in nature by a rat ndash flea-rat cycleMode of transmission Infected fleas defecate rickettsia while sucking blood contaminating the bite site and other fresh skin wounds Rarely inhalation of dried infective flea feces Incubation period = commonly 12 days Period of communicability Not directly transmitted from person to person Once infected fleas remain so for life (up to 1 year)Susceptibility and resistanceSusceptibility is general One attack confers immunity Clinical Manifestations

- Prodromal symptoms of head ache myalgia arthralgia nausea and malaise for 1 to 3 days Then abrupt onset of chills and fever Nearly all patients experience nausea and vomiting early in the illness

- The duration of untreated illness averages 12 days - Rash is present in only 13 of patients- Pulmonary involvement non productive cough and pneumonia

Dx - Epidemiological ground - Weil felix agglutination test (serology)

Rx - Doxycycline (single dose) OR 42

- Chloramphenicol or TTC 500mg Po QID for 7days Prevention and control

1 Destroy rats from burrows and harbourages 2 Use insecticides to abolish flea from living quarters 3 Treatment of patients

Relapsing feverDefinition An acute infectious bacterial disease characterized by alternating febrile periods (recurrent pyrexia attacks) Infections agent

Borrelia recurrentis causes of louse borne relapsing fever Borrelia duttoni ndash cause of tick ndashborne relapsing fever

EPI ndash Occurs in Asia eastern Africa (Ethiopia and Sudan) the high lands areas of central Africa and South America Reservoir Humans for Borrelia recurrentis Wild rodents and soft ticks for tick borne relapsing feverMode of transmission By crushing an infected louse so that it contaminates the bite wound or an abrasionIncubation period ndash usually 8 days Period of communicability Louse becomes infective 4-5 days after ingestion of blood from an infected person and remains so for life (20-40days) Susceptibility and resistance Susceptibility is general Clinical manifestations

- Sudden onset of illness with chills fever and prostration head ache myalgia and arthralgia

- There may be nausea and vomiting jaundice and liver swelling After 4-5 days the temperature comes down the patient stays free for 8-12 days and then a relapse follows with the same signs but less intense In untreated cases there may be up to 10 relapses Diagnosis

- clinical and epidemiological grounds - Blood film(BF)

Treatment1 Admit the pt2 Open vein (start IV line with Normal saline) before administering penicillin 3 Administer 400000 IU procaine penicillin IM stat 4 TTC 500 mg po QID during discharge for 3 days5 Chloramphenicol in infants and children can be used in place of TTC6 Nursing care (monitor vital signs amp any Reaction shaving hair)

Prevention and control1 Control of vectors (louse) 2 Personal hygiene 3 HE about hygiene and modes of disease transmission

4 Delousing of pts clothes and hisher family 5 Chemotherapy of cases and chemoprophylaxis (TTC) for contacts when risk of

acquiring the infection is highUNIT 6

Prevention and control of zoonotic diseasesIntroductionInfectious diseases transmitted between vertebrate animals and men are called zoonosis For most of these diseases man is a dead end of the transmission cycle This means under normal conditions man will not infect other human beings

1 When animals used as a food- Teaniasis- Brucellosis - Trichinellosis or trichinosis- Toxoplasmosis

2 Animal Bite diseases- Rabies

3 Direct contact diseases- Anthrax

4 Animal reservoir diseases- Leishmaniasis- African trypanosomiasis

Teaniasis Definition -Teaniasis is an intestinal infection with the adult stage of large tapeworms Cysticercosis is a tissue infection with the larval stage Infection agent Taenia saginata (beef take worm)

- Taenia solium (pork tape worm)EPI ndash Frequent where beef or pork is eaten raw or insufficiently cooked and where sanitary conditions permit pigs and cattle to have access to human faeces ReservoirHumans are definitive hosts of both species of Taenia cattle are the intermediate hosts for Taenia saginata and pigs for Taenia soliumMode of transmission

Eggs of Taenia saginata passed in the stool of an infected person are infectious only to cattle They develop into cysticercus bovis(larva) in the flesh of the cattle

In human infection follows after ingestion of raw or under corked beef containing cysticerci The adult worm develops in the intestine

Or in case of Taenia solium the larvae penetrate the intestinal wall and are carried to the various tissues where they develop to produce the human disease of cysticercosis and even neurocysticercosisIP - 8-14 weeksPeriod of communicability - T saginata is not directly transmitted from person to person but T solium may be Eggs may remain viable in the environment for monthsSusceptibility and resistance - susceptibility is general Clinical Manifestation (for both species)

Symptoms of cysticercosis may appear after some days and stay for 10 years after infection

Passage of proglottidis (segmented adult worms) in the faeces and perianal discomfortMinimal or mild abdominal pain or discomfort nausea change in appetite weakness and wt loss Epigastria discomfort nausea a sensation of hunger wt loss nervousness and anorexia Diagnosis - Identification of proglottidis (segments)

- Eggs in faeces or anal swab - Palpable subcutaneous cysticercus in microscopic exam of an excised tissueTreatment - Single dose of praziquantel is highly effective

- Niclosamide or - Dechlorophil or- Mebendazole or- Albendazole

T SoliumRx is the same as to T saginata but praziquantel can evoke an inflammatory response in the CNS if cysticercosis is present in CNSCysticercus Mgt - Combination of praziquantel and Albendazole

- Surgery and supportive medical MGT- High dose of glucocorticoid can be used to decrease inflammation

Prevention and control 1 prevent faecal contamination of soil water human amp animal food2 Cook beef and pork thoroughly3 Use latrines4 Identification and immediate RX of Cases5 Freezing of pork beef below -5oc for more than 4 days kills the cysticerci

effectively or cooking to a To of 56oc for 5 minutes destroys cysticerci6 Deny swine access to latrines and human faeces

BrucellosisDefinition Brucellosis is a systemic bacterial disease with acute or insidious onset transmitted to humans from infected animalsInfection agent

- Brucella melitensis (most common world wide) acquired primarily from goats sheep and camels

- B Abortus from cattle- B Suis from pigs- B Canis from dogs

EPI Occurs world wide Predominantly an occupational disease of those working with infected animals or their tissues especially farm workers veterinarians and abattoir workers which is more frequent among males Reservoir- cattle swine goats and sheep pet dogs Mode of transmission by contact with tissues blood urine vaginal discharges aborted foetuses and especially placentas (through breaks in the skin) Most commonly through 45

ingestion of raw milk and dairy products from infected animals (raw meat or bone marrow) Airborne infection occurs rarely Incubation period - usually 1-3 weeks Period of communicability - no evidence of communicability from person to personSusceptibility and resistance - GeneralClinical Manifestation

- Abrupt onset of Fever chills diaphoresis head ache myalgia fatigue anorexia joint and low back pain wt loss constipation sore throat and dry cough

- Often no abnormalities and pt looks well- Some patients are acutely ill with pallor lymphadenopathy

hepatosplenomegally arthritis spinal tenderness epididymo orchitis skin rash meningitis cardiac murmurs or pneumonia

Diagnosis- Epidemiological amp clinical features- Serology-raised levels of B agglutinin- Blood or bone marrow culture

Treatment- Doxycycline + Streptomycin for 2 weeks followed by Doxycycline + Rifampcin for 4-8 weeks is the most effective regimen

- In pregnancy and in children less than 7 years bacterium and rifampcin for 8-12 weeks

Prevention and control 1 Educate people not to drink untreated milk or eat products made from untreated

milk2 Educate farmers and slaughter house workers and those in meat processing plants

and butcher shops as to the nature of the disease and the risk in the handling of carcasses and products of potentially infected animals

3 Educate hunters to use barrier precaution (gloves and clothing)4 Pasteurize milk cook meat and bone well 5 Proper disposal of placenta discharges or foetus from an aborted animal

Disinfect contaminated areas

ToxoplasmosisDefinition Toxoplasmosis is a systemic protozoal disease that can be either acute or chronic type with intracellular parasite Infectious agent -Toxoplasma Gondi(protozoa)EPI - It occurs world wide in mammals and birds Infection in man is commonReservoir The definitive hosts are cats and other felines They acquire the infection mainly from eating infected rodents or birds The intermediate hosts include sheep goats rodents cattle chicken birds amp man Mode of transmission

1 Ingestion of raw or undercooked infected meat containing Toxoplasma cysts2 Ingestion of food drink or from hands contaminated with faeces of an infected cat3 Tran placental 4 Blood transfusion amp Organ transplantation

The parasites form tissue cysts most commonly in skeletal muscle myocardium 46

and brain these cysts may remain throughout the life of the hostIP - from 10-23 daysPeriod of communicabilityNot directly transmitted from person to person except in utero Cysts in the flesh of an infected animal are infective if eaten uncookedSusceptibility and resistanceSusceptibility to infection is general Most infections are asymptomatic Pt taking immune suppressive therapy or pts with AIDS are at risk of developing the diseaseClinical manifestations Symptoms are generally mild except in immuno suppression or some rare cases The acute form of this disease is characterized by fatigue lymphadenitis chills fever head ache and myalgia In addition to chronic disease the pt may develop maculopapular rash encephalomyelitis and hepatitis retinochorditis with subsequent blindness has been known to occur on rare occasions Diagnosis - Clinical sign and symptom

- Serological test amp Cell cultureTreatment

1 No treatment for a healthy immunocompetent host except in sever disease2 The preferred Rx for those with severe symptomatic disease is pyrimethamine

combined with sulfadiazine or fansider and folinic acid for four weeks3 For pregnant women spirmycin is commonly used to prevent placental infection-

Treatment for infants1 Pyrimethamine2 Sulfadiazine3 Folinic acid

Prevention and control1 Avoid eating under cooked or raw meat and 2 Avoid cyst-contaminated materials3 Meat should be heated or frozen well4 Hands should be washed thoroughly after work in the garden and all fruits and

vegetables should be washed 5 Discourage cats from hunting6 Dispose cats faeces daily7 Pts with HIV AIDS who have severe symptomatic toxoplasmosis should receive

prophylactic Rx (pyrimethamine sulfadiazine folinic acid) throughout their life span

RabiesDefinition It is acute viral encephalomyelitis (attacking brain and meninges)It is almost 100 fatal if untreatedInfections agent-Rabies virus EPI-occur world wide It is primarily a disease of animals (zoonotic) Reservoir - Dog wild carnivores and bats Mode of transmission - Transmitted with saliva of rabid animal introduced by a bite or scratch IP- Usually 3-8 weeksPOC- 3-7 days before the disease and throughout the course of the disease

Susceptibility amp resistance - GeneralClinical Management

1 Prodromal phase-A sense of apprehension head ache fever and nausea abnormal sensation at the site of inoculation (bite)(paraesthesia tingling sensations at the bite site)

2 Excitatory phase or aerophobia slightest sound or wind excite the victim irritability restlessness nervousness tendency to bite are some of the symptoms

3 Paralytic phase - spasm of swallowing muscles leads to drooling of saliva and fear of water (hydrophobia) Delirium and convulsions Death is often due to respiratory muscle paralysis

Diagnosis- history of bite by known rabid animal - The rabid animal usually dies in 10 daysTreatment 1) Wound care

- Wash the wound with soap and water thoroughly to decrease the viral load- If there is bleeding cover the wound- Never suture the wound

2) Start anti rabies vaccine immediately if it is proved to be rabid animal bitePrevention and control

1 Immunize all dogs and cats2 Detain amp clinically observe for 10 days any healthy appearing dog or cat known

to have bitten a person 3 Post exposure prophylaxis4 Keep dogs and cats at home5 Destroy stray animals where rabies is endemic

Definition An acute bacterial disease usually affecting the skin amp rarely the oropharynx lowers respiratory tract mediastinum or intestinal tractInfections agent Bacillus anthracis spore forming bacteriaEPI-occurs world wide It is Primarily a disease of herbivores Humans and carnivores are incidental hosts Primarily an occupational disease who process amp hides hair (esp from goats) bone and bone products and wool and of veterinarians and agriculture and wild life workers who handle infected animalsReservoir - Animals normally herbivore The spores of B anthracis are very resistant to adverse environmental conditions and disinfectionsMode of transmission 1 Cutaneous anthrax contact with tissues of infected animals (cattle sheep goats

horses pigs and others) Contamination with hair wool hides or products made from them such as drums or brushes or contact with soil associated with infected animals

2 Inhalation anthrax - Inhalation of spores in risky industrial processes such as tanning of hides or wool or bone processing where aerosols of B anthracis spores may be produced

3 Intestinal and oropharyngeal anthrax ingestion of contaminated meat but not milk- Vultures have been reported to spread the organism from one area to another

IP - Most cases within 48 hoursPOC - Transmission from person to person is very rare Articles and soil contaminated with spores may remain infective for decadeSusceptibility amp resistance - Uncertain Clinical Manifestation ndash Is different according to the site of infection 1 Cutaneous anthrax - Approximately 95 of human cases of anthrax are cutaneous

- Small red macules amp papule appear- An ulcer with blackened necrotic eschar surrounded by oedema

-The lesion may be pruritic but painless - regional lymphadenitis is common - Spontaneous healing occurs in 80-90 of untreated cases but edema may persist for weeks - In 10-20 of cases infection progresses bacteria develops and is often associated with high fever sever shock and rapid death 2 Inhalation anthrax

- Increasing fever dyspnoea stridor hypoxia and hypotension usually leading to death with in 24 hrs

3 Gastrointestinal Anthrax- Fever nausea and vomiting abdominal pain bloody diarrhoea and

sometimes rapidly developing ascites- Diarrhoea is occasional and massive in volume- Usually death will occur within 48 hours

4 Oropharyngeal anthrax- Fever sore throat dysphagia painful regional lymphadenopathy

Inflammation of the tonsil toxaemia respiratory distress may be evidentDiagnosis

- Clinical data- Gram stain of wound discharge- Culture from the wound discharge or blood

Treatment For cutaneous anthrax1 Penicillin-G IV until edema subsides and with subsequent oral penicillin to

complete the course (adults) =gtFor penicillin-sensitive adults Ciprofloxacin erythromycin TTC CAF can be substituted

2 Clean and cover the cutaneous lesions

For inhalation anthrax GI and Anthrax meningitis - High dose of IV penicillin is recommended

Prevention and control1 Decontaminate wool and goats hair and improvement of working condition for

handlers of animal products 2 Vaccination of humans amp herbivores 3 Carcasses of animals should be buried intact or burned 4 Butchering of infected animals should be avoided

5 Dust control and proper ventilation in hazardous industries6 Treat all animals exposed to anthrax with TTC or penicillin

TetanusDefinition - Tetanus is an acute disease caused by a toxin produce by tetanus bacilli and is characterized by painful contraction of voluntary muscles It is also called lock jawInfectious agent

Clostridium Tetani It is Gram negative rods Spore forming amp anaerobe organismEpidemiology

- Move common in rural than town - It is almost 100 fatal if untreated - Normally tetanus bacilli live in the bowel of man amp animal

The source of infection is soil street dust amp Faeces containing spores Tetanus is more likely to develop is patents with deep penetrating necrotic wound Wounds which favor tetanus are

Umbilical stump in new born (necrosis) Crush wound (Necrosis poor blood supply) Stab wound (deep) Wound with foreign bodies (always infected) Human amp animal bite Burns (Necrosis poor blood supply ) Surgical wound (from dressing instrument) Chronic ear discharge Endogenous infection (during bowl surgery)

Tetanus bacilli harmful only when they are lodged in the tissue bc from there the toxin can be transported to CNS

Incubation period- The usual IP 5-21 days - But it can range from 3 days ndash 3 months

Susceptibility (high risk group) - New born - Children - Farmers - Any one with dirty wound - Soldiers

Clinical Picture Increased tone of the jaw muscle - causing trismus amp ldquorisus sardomicusrdquo (devilrsquos

grin) Later the spasm become generalized involving all muscles and painful Sever spasm results in pain disturbance of swallowing amp respiration Spasm of the neck muscle resemble neck stiffness of meningitis Negative neurological signs (no drowsiness no change in consciousness) Low grade fever

Arrhythmias Asphyxia Cyanosis pain at wound site Risus sardomicus (fixed smile )Hydrophobia photophobia Stiffness of jaw Sudden bradycardia Irritability Tachycardia Muscle rigidity amp sudden cardiac arrest can occur

= Death occurs due to asphyxia due to Spasm of glottis thoracic muscle amp diaphragm

= In the new born first sign of tetanus is- Inability to suck spasm Apnea amp cyanosis - Extended spine with clenched fists amp mouth and flexed toes

Dx - History of the pt - Culture from the wound

Complications - Respiratory arrest Air way obstruction - Cardiac failure Anoxia - Pulmonary embolism Urinary retention - Secondary bacterial infection constipation- Dehydration pneumonia

ManagementPatient must be referred to hospital quickly Spasm (caused by toxin of bacilli)

- Diazepam (valium) in high dose - Start with 10-40mg IV + chlorpromazine 20-50mg IM alternately 6 hourly - When spasm continue more diazepam should be given (max dose 500 mg day- Reduce the dose if the pt is over sedated - Or phenobarbitone(100mg 4 hourly) + chlorpromazine (20-50mg IM 6 hourly)

Secondary infection To combat secondary infection amp tetanus bacilli

- Doxycycline - Crystalline penicillin (1Mil IU) - Clindamycin - PPF(12 Mil IU) daily for 5 days

ATS (anti tetanus serum) ( also known as TAT)- 10000 units IM IV for both adultamp children - Do skin test first Have adrenaline at hand

Surgical RX - Look for wound amp clean with savalon - Tracheostomy ( sever case)

Intensive care unit(ICU) - Give care in dark amp isolated room - Mouth- mouth respiration if Pt develops breathing arrest (tetanus do not pass

through mouth to mouth contact) - Semi-prone position (never on his back) - Change position every 2 hrs - Rise to foot of bed to stimulate lug drainage to prevent pneumonia

Tetanus Toxoid (TT) - Patients with Tetanus do not develop immunity so they must be immunized with

TT after recovery to prevent re occurrence

Prevention amp Control Active Immunization (DPT) ( For Infants ) Active immunization with TT ( specially for pregnant women ) Passive protection ATS is only for 10 days so it should not be given with out

active immunization

UNIT 7Food Borne Diseases (Food Poisoning Food borne

Intoxications Food-borne infection)Introduction Food-born diseases including food borne intoxications and food-borne infections are terms applied to illnesses acquired by consumption of contaminated food Staphylococcal food poisoning (Intoxication) It is intoxication (not infection) of abrupt and some times violent onset Infections agent (toxic agent)Enterotoxins of staphylococcus aureusStaphylococci multiply in food and produce the toxinsReservoir Humans amp occasionally cows with infected udders MOT- By ingestion of a food product containing staphylococcal enterotoxin Food handlers infected with S aureus ( from purulent discharges of an infected finger or eye abscesses nasopharyngeal secretions) will contaminate the food When these foods remain at room temperature for several hours before being eaten toxin producing staphylococci multiply and elaborate the heat stable toxin Ip 30 minutes to 8hrs usually 2-4 hrsPOC- not applicable SR ndash Most people are susceptible Clinical Manifestations

- Sudden onset of vomiting and watery diarrhoea - Fever and abdominal cramp- If the illness is severe it may require hospitalization

Diagnosis- short interval between eating and the onset of symptoms - Culture amp detection of enterotoxin from food

Rx Fluid and electrolyte replacementPrevention and control

1 Strict food hygiene hand washing cleaning of finger nails cover wounds on the skin

2 Reduce food handling time to an absolute minimum with no more then 4hrs at ambient temperature Keep perishable food hot (gt600C or cold (below 100C)

3 Exclude people with boils abscesses and purulent lesion from food handlingBotulism( Intoxication )

A paralytic disease that begins with cranial nerve and progresses to the extremitiesIA - Toxin produced by clostridium botulinum (Neurotoxin)EPI - World wide occurrence Home canned foods particularly vegetables fruits and less commonly with meat and fish Outbreaks have occurred from contamination through cans damaged after processing Reservoir - The bacteria is found in the soil and in the intestine of animals MOT- Food infection in which the toxin is foundIP usually 12-36 hours some times several days after eating contaminated food POC not communicable S and R ndashSusceptibility is generalClinical Manifestations

- Illness varies from a mild condition to very severe disease that can result in death within 24 hours

- Symmetric descending paralysis is characteristic and can lead to respiratory failure and death

- Cranial nerve damage produce diplopia (double vision) dysphasia (difficult in swallowing) amp general body weakness

- Nausea vomiting abdominal pain occur following paralysis- Dizziness blurred vision dry mouth and occasionally sore throat- No fever- Paralytic ileus severe constipation and urinary retention are common

Dx - Afebrile mentally well patients who have symmetric descending paralysis - Demonstration of organisms or its toxin in vomitus gastric fluid or stool Treatment 1 Hospitalize the pt and monitor closely 2 Intubation and mechanical ventilation may be needed

3 Antitoxin administration after hypersensitivity test to horse serum 4 Emesis and lavage if short time after ingestion of food to decrease the toxin

Prevention and control1 Effective control of processing of canned and preserved food2 Education about home canning and other food preservation techniques regarding

the proper time pressure and temperature required to destroy spores 3 Adequate refrigeration amp boiling canned foods9 Specially vegetables) for at least

10 minutes to destroy botulinal toxin 4 Canned foods in bulging containers should not be used eaten or tasted

Salmonellosis (Infection)A bacterial disease commonly manifested by an acute enterocolitisIA- Salmonella typhimurium and salmonella enteritidis EPI It occurs world wideReservoir - Animals including poultry swine cattle rodents pets and humansMOT- ingestion of food ( specially raw fruits amp vegetables raw and under cooked eggs and egg products raw milk and its products poultry) contaminated by faeces of an infected animal IP from 6-72 hours usually about 12-36 hoursPOC- usually several days to several weeks

S R ndash Susceptibility is general and increased by achlorhydria antacid therapy GI surgery immuno suppression and malnutritionSS - Self limited fever and diarrhoea (Bloody or dysenteric when colon is involved) nausea vomiting abdominal cramp amp leukocytosisDX ndash Blood culture initially amp Stool culture laterRx ndash Symptomatic ( Mainly fluid replacement amp Analgesics)

- If there is an underlying immunosuppressive disease (condition like AIDS lymphoma immunosuppressive treatment) treat the underlying cause

Prevention and control1 Quality testing of the known and commonly contaminated foods 2 Avoid consuming raw or partially cooked ages3 Wear gowns and gloves when handling stool and urine and hand washing after

patient contact

VI Prevention amp Control of STISyndromic approach to the management of STIThe control of STI is based on three principles

1 Education on the mode and means of reducing the transmission of STI 2 Provision of effective Management for symptomatic pts with STIs3 Detection of infection in asymptomatic individuals by screening patients

attending routine services like family planning or antenatal clinics Advantages of syndromic case management over etiologic

1 Solves the problem of scarce human resources and lab facilities where these are significant limitations for mgt based on the identification of the etiologic agent of a specific STI

2 Saves the time spent to isolate the specific pathogen and the inaccessibility of such facilities

3 Saves financial expenditure to get lab services NB The syndromic case met requires identification of distinct syndromes that are known to be associated with STI rather than identifying specific diseases One of the means of controlling AIDS is effective control of STI Because

1 Both infections share similar epidemiologic determinants 2 STIs increase the susceptibility to infections as well as the spread of HIV

The public health importance of STIsThe occurrence of STI in an individual is an indicator of unprotected sexual activity that increases the chance of acquiring another STI including HIV There fore the epidemiological determinants of STI and HIV infection are similar bc both infections result from risky sexual behaviour STI promote the spread of HIV in the community for instance men with gonococcal urethritis have eight times higher concentration of the virus in their semen than men without it This increases the probability of infection in their partners Similarly women with vaginosis have large number of CD4 cells in the vagina resulting in high chance of acquiring HIV infection STIs are also important causes of cervical and penile cancer Infertility and other obstetric complications like ectopic pregnancy occur following inadequately treated STIs

Impact of HIV on conventions STIThe interaction of HIV and conventional STIs is bi-directional This is because HIV affects the Mgt of STI and conventional STIs predispose for HIV infection The clinical features of various types of STIs are affected by co-infection with HIV Syphilis can have atypical presentation with a tendency to rapidly progress to neurosyphilis Atypical lesions of chancroid are common and tend to be less purulent often with indurations mimicking primary syphilis The lesions could as well be extensive and multiple which could be associated with fever and chills Recurrent or persistent genital ulcers caused by herpes simplex virus are common among pts with HIV and they are often multiple and extensive The Rx of conventional STIs is also affected by infection with HIV The risk of Rx failure following single injection of benzathine penicillin is increased among pts with primary syphilis Topical antifungal drugs are less effective and hence oral drugs like ketoconazole are frequently indicated

Examination of a pt with STI- Like any other disease the diagnosis of STIs relies on paper history taking and

physical exam This entails privacy and confidentiality in order to promote health seeking behaviour and avoid stigmatization

- The demographic characteristics of the pt that include age sex and marital status are important components of the history

- The occupation of the pt is also important because long truck drivers and solders are at increased risk for STIs Multiple sexual partnership and history of STIs in the pt or hisher partner are also important risk factors for STIs

Urethral discharge or burning on micturation in men - Onset unprotected casual sex the amount of discharge should be inquired

Vaginal discharge in women- Vaginal discharge is abnormal when the women notice change in colour amount

and odour History of STI in her partner multiple sexual partners and change in Partner is important risk factor to consider in the history Genital ulcer in men and women

The onset history of recurrence presence of pain location and whether the ulcer is single or multiple should be described in the history

Lower abdominal pain in women The onset quality of pain radiation severity presence of vaginal discharge last menstrual period and systemic symptoms like fever nausea and vomiting are essential components of the history

Scrotal swelling The health worker should ask the onset presence of pain history of trauma and for concomitant urethral discharge

Inguinal bubo Presence of pain ulceration discharges and the locations of the swelling are essential components of the history

Common syndromes in STIs1 Urethral Discharge andor burning on urination in men

Burning on micturation and urethral discharge are common symptoms of urethritis

Aetiology N gonorrhea C Trachomatis Commonest causes of urethral discharge amp dysuriaM Genitalium T Vaginalis Rare causes of urethritis U Uraelyticum

Urethritis caused by N-gonorrhoea has usually an acute onset with profuse and purulent discharge while that of C trachomitis will be of subacute onset with scanty mucopurulent discharge However mixed infections by both organisms can occur in 20 of pts Examination Look for evidence of spontaneous discharge -Note the colour quality and quantity of the discharge

-The evidence of mild discharge may be crusting at the meatus and meatal redness should also be sought

-Milk the urethra to bring the discharge forward if no discharge is found on meatus

Complications - Disseminated gonoccocal infection (Ng) - Prostatitis (Ng) - Conjunctivitis (both) - Urethral stricture (both) - Enhanced transmission of HIV (both)

Mgt 2 Genital Ulcer

- Primary syphilis genital herpes chancroid LGV and granuloma inguinale are common ulcerative lesions of the genitalia in men and women

Aetiology Common causes of genital ulcer are

1 Treponema palidum ndash syphilis 2 Herpes simplex virus ndash herpes genitalia (genital herpes) 3 Haemophilus ducreyi-chancroid4 Chylamidia trachomatis serovars L1 L2 and L3 ndash LGV 5 Chlymmatobacterium granulomatis ndash GI

Clinical Features Syphilis (Hard chancre)

- A disease characterized by a primary lesion a later secondary eruption on the skin and mucus membranes then a long period of latency and finally late lesion of skin bones viscera CNS and CVS

Etioiopy ndash Treponema pallidum a spirochete Three stages are described in the clinical presentation of syphilis Genital ulcer occurs in the primary stage of the disease It starts as a small papular lesion that rapidly ulcerates to produce a non ndashtender indurated lesion with a clean base and a raised edge known as hard chancre

Clinical manifestations The clinical presentation is divided in to three stages

1 Primary syphilis Consists of hard chancre the primary lesion of syphilis together with regional lymphadenitis The hard chancre is a single painless ulcer on the genitalia or elsewhere (lips tongue breasts) and heals spontaneously in a few weeks with out Rx The lymph glands are bilaterally enlarged and not painful There will not be suppuration

2 Secondary syphilis After 4-6 weeks of the primary infection a generalized secondary eruption appears often accompanied by mild constitutional symptoms These early rashes tend to be symmetrical quickly passing and donrsquot itch These early skin lesions are highly infective and many spirochetes are demonstrated in them

3 Tertiary syphilis This stage is characterized by destructive non-infectious lesions of the skin bones viscera and mucosal surfaces Other disabling manifestations occur in the CVS (aortic incompetence aneurysms) or CNS (dementia paralytica tabes dorsalis)

Herpes genitalia (Genital herpes) Latency and frequent recurrence characterise herpes genitalias producing a life long infection after the primary infection The lesions are painful initially presenting erythematous macules which then progress to vesicles pustules ulcers and finally crusts Prolonged and severe disease with extensive tissue involvement and higher rate of dissemination occur in patients with HIV infection First episode primary genital herpes is x-zed by fever head ache malaise and myalgias Pain itching dysuria vaginal and urethral discharge and tender inguinal lymph adenopathy are the predominant local symptoms

Chancroid soft chancre- It is a bacterial infection characterized by single or multiple painful necrotizing

ulcers at the site of infection The lesions are painful progressing from a small papule to pustule and then ulcer with soft margins described as soft chancre Inguinal adenopathy that becomes necrotic and fluctuant (buboes) follow the ulcer It is endemic and the commonest cause of genital ulcer in many developing countries Most frequently diagnosed in men especially those who frequently prostitutes

LGVThe diseaese starts as a small painless papule that develops to an ulcer After a week or so painful regional lymphadenopathy develops with symptoms of fever chills head ache malaise anorexia and wt loss Elephantiasis of genitalia scrotum and vulva occur in either sex

Granuloma Inguinale 57

It is a chronically progressive ulcerative disease with out systemic symptoms The pt usually presents with a non-supportive genital lesion which develop from a small firm papule to a painless ulcer with a beefy red appearance and non ndash purulent base

Complications 1 Syphilis ndash Secondary syphilis

- Latent syphilis - Aortitis with valvulitis - Aortic aneurysm - Gumma- Neurosyphilis

2 Genital herpes ndash Recurrence - Aseptic meningitis and encephalitis

3 Chancroid ndash Penile auto amputation

4 LGV ndash Genital edema - Salphingitis - Infertility - PID

5 GI ndash Genital pseudo elephantiasis - Adhesion - Urethral vaginal or rectal stenosis Recommended Rx for genital ulcer B Penicillin 24 miu lm stat

or ( in penicillin allergy) Doxycycline 100mg BID for 15 days Plus Erythromycin 500 mg po QID for 7 days 3 Vaginal DischargeCauses of vaginal discharge

1 Neisseria gonorrhoea 2 Chylamydia trachomatis3 Trichomonas vaginalis4 Gardnerella vaginalis5 Candida albicans

The first three are sexually acquired and the last two are endogenous infections The first two cause cervicitis while the last three cause vaginitis

The presence of vaginal discharge may represent either cervical or vaginal pathology There fore the initial evaluation of a pt that has vaginal discharge includes risk assessment and clinical examination with a speculum to determine the site of infection Vaginitis Bacterial vaginosis vaginal thrush or trichomoniasis are the usual causes of vaginitis Bacterial vaginosis and trichomoniasis are more frequent among sexually active women while vaginal thrush occurs when there is impairment of local or systemic defence

mechanisms Risk assessment is usually negative and cervix looks healthy and discharge is not coming from the cervical opening in isolated vaginitisCervicitis The presence of purulent or mucopurulent exudation from the cervical os frequently indicates gonococcal or chlamydial infection The risk factors include age less than 25 yrs single status multiple sexual partners a change of sexual partner recently and history of STI previously either in the pt or in the partner On speculum examination the presence of redness contact bleeding spotting and endocervical discharge suggests the diagnosis of cervicitis Complications

1 PID2 PROM

3 PTL (preterm labourRecommended treatment for V discharge

Risk assessment positive Ciprofloxacin 500 mg po stat

Or Spectinomycin 2g Im stat

Plus Doxycycline 100mg po BID for 7 days

Plus Metronidazole 500 mg po BID for 10 days

Risk assessment negative Metronidazole 500 mg PO BID for 7 days

PlusClotrimazole vaginal tab 200mg at bed time for 3 days

4 Lower abdominal pain due to PIDPID refers to an acute clinical syndrome that results from ascending infection from the cervix and or vagina The upper structures of the female genital organs are affected The term PID includes endometritis parametritis salphingitis oophoritis pelvic peritonitis tuboovarian abscess and inflammation around the liver spleen or appendix The common pathogens associated with PID which are transmitted through sexual route include N gonorrhoea C trachomatis M Homonis and bacteroides Other organism like streptococcus species Ecoli and H influenza may some times cause PID but their transmission is not via the sexual route PID and STI share many of the same risk factors and in most instances PID is caused by STIs

Clinical Features- The occurrence of vaginal discharge may be an antecedent event and supports the

diagnosis of PID- Bilateral lower abdominal pain or pelvic pain is the most common clinical

complaints but ranges from abrupt and fulminant presentation to a sub acute form with mild symptoms often described as dull pain

- Lower abdominal and adenexal tenderness together with cervical excitation tenderness are indicative of PID

- Other causes of lower abdominal pain like appendicitis ectopic pregnancy and cholecystitis should be ruled out by proper examination

Recommended Rx for PID0utpatient Ciprofloxacin 500 mg PO stat

Or Spectinomicin 2g Im stat

Plus Doxycycline 100mg PO BID for 14 days Plus Metronidazole 500mg PO BID for 14 days

- Remove IUD and do counselling for contraception - Admit if there is no improvement with in 72 hrs

Inpatient Ciprofloxacin 500mg PO BID

Or Spectinomicin 2g IM BID

Plus Doxycycline 100mg PO BID for 14 days

Plus Metronidazole 500mg PO BID for 14 days

Inpatient regimen is given for at least 48 hrs after the pt clinically improves

After discharge from hospital the pt hast to continue with the oral Rx

5 Scrotal swellingThe cause of scrotal swelling can vary depending on the age of the pt Among pts who are younger than 35 years the swelling is likely to be caused by N gonorrhoea and c trachomatis However scrotal swelling among patients older than 35 yrs is commonly caused by gram-negative organisms and rarely TBc Other infectious causes of scrotal swelling could be brucellosis mumps onchocerciasis or infection with w bancrofti

It is important to exclude other causes of scrotal swelling like testicular torsion trauma and incarcerated inguinal hernia as they may require urgent referral for proper surgical evaluation and Rx

Complications - Epididymitis- Infertility - Impotence- Prostatitis

Recommended Rx of scrotal swelling The Rx of scrotal swelling suspected to be of STI origin is similar to that of a urethral discharge Ciprofloxacin 500mg PO stat

Or Spectinomycin 2gm IM stat

Plus Doxycycline 100mg PO BID for 7days

Or TTC 500mg PO BID for 7 days6 Inguinal buboIt is swelling of inguinal lymph nodes as a result of STI it should be remembered that infections on the lower extremities or in the perineum could produce swelling of the inguinal lymph nodes The common sexually transmitted pathogens that cause inguinal swelling include T pallidum C trachomatis (serovars L1 L2 L3) H ducreyi and C granulomatis However unlike other causes of inguinal bubo syphilis doesnrsquot cause necrosis and abscess collection in the lymph nodes In conditions where the clinical examination doesnrsquot reveal fluctuant bubo syphilis should be considered and be treated accordingly Surgical incisions are contraindicated and the pus should only be aspirated using a hypodermic needle Recommended Treatment B Penicillin 24 MIU IM stat

Plus Erythromycin 500mg PO QID for 15 days

Or Co-trimoxazole double strength tablet PO BID for 15 days

7 Neonatal infections due to STIs1 Congenital syphilis

Infection of the fetus by T pallidum usually occurs starting from the second trimester of pregnancy The infection may result in still birth or produce multiple

systemic complications which affect the infant after birth Early manifestations of congenital syphilis occur in the first two years of life and may include fever nasal discharge hepatosplenomegally or failure to thrive The late onset manifestations of congenital syphilis include keratitis deafness Hutchinsons teeth or bone damageTreat any infant whose mother had untreated or inadequately treated syphilis at delivery regardless of signs and symptoms in the infantTreatment crystalline penicillin 50000 iukg IV daily for 10 days

Or PP50 000 iukg lm daily for 10 days

2 Neonatal conjunctivitis It is acquired during birth as a result of genital infection of the mother by N gonorrhoea and C trachomitis The clinical features include periorbital swelling redness of the eyes with sticky eye lids and purulent discharge from the eyes Treatment Spectinomycin 50 mg kg IM stat

Plus Erythromycin 50 mgkg PO in 4 divided doses for 10 days

3 Neonatal herpes Neonatal herpes occurs after birth of a neonate from a mother with active herpes genitalis In fact vaginal delivery is CI if the mother is found to have active genital herpes in order to avoid neonatal infection The neonate may develop aseptic meningitis or encephalitis and it is frequently fatal Treatment Acyclovir 5-10 mgkg IV daily for 10 days

Prevention and control1 Treatment of cases2 Treatment of contacts and source of infection3 Health education on safe sex (sex education for high risk groups) 4 Controlling STIs among commercial sex workers

ndash Monthly check up and Rx of casesndash Provision of condom

5 Screening of clients (eg VDRL in pregnant to prevent congenital syphilis) 6 Screening of blood before transfusion (syphilis) 7 Thorough washing of genitalia with soap and water promptly after intercourse is

very effective (chancroid) 8 Consistent use of condoms (herpes genitalia) 9 Application of 1 TTC in both eyes of new borne as soon as delivered

(Gonorrhoea)

Reference1) Jan Eshuis and peter Manschot communicable diseases a manual for rural

health workers African medical and research foundation Nairobi copy 19782) Abram S Benson 14th edition control of communicable disease in man

interdisciplinary books pamphlets and periodicals Washington 19853) National guide line on HIV AIDS MOH Addis Ababa 19984) National guide line on selected epidemic diseases in Ethiopia MOH

Addis Ababa 5) National guide line on MTCT MOH Addis Aabab 6) National Management guide line on Malaria for health workers in Ethiopia

MOH Addis Ababa7) National Guide line on prevention and control of malaria in Ethiopia MOH

Addis Ababa 8) Mansons tropical diseases 4th edition UK

Principles of communicable disease control

Mode of transmission

Airborne droplets released when an infected person sneezes or coughs

Contact with nose and throat secretions of infected people

Cases can infect others for several days before and after they develop symptoms

Spreads easily in over crowded areas (schools military barracks health facilities etc)

Signs and symptoms

High fever which begins approximately 10 -12 days after exposure and lasts for

several days

Runny nose conjunctivitis coryza cough red and watery eyes and

Complications

Unimmunized children under 5 years and infants are at highest risk of measles and its complications

Pneumonia is the most common cause of death as the virus weakens the immune system

General nutritional support and Rx of Dehydration

Antibiotics are given only to ear and severe respiratory infection

Vitamin A two doses in 24 hours

Definition An acute disease of the respiratory tract caused by bacteria

Many children that contract pertussis have coughing spells that lasts for eight weeks

Vaccination (DPT)

Patient may recover within 6 ndash 10 days

Abnormal heart beats which may lead to heart failure

Inflammation of heart muscles and valves (lead to chronic heart disease and heart failure)

The most severe complication is respiratory obstruction as a result of laryngotracheobronchitis (croup) followed by death

The clinical presentation is divided in to three stages

Clinical Features

Types of reservoirs1 ManThere are a number of important pathogens that are especially adapted to man such as measles typhoid M meningitis gonorrhea and syphilis The cycle transmission is from man to man2 AnimalsSome infective agents have their reservoir in animalEg Bovine TBc - cow to man Brucellosis ndash cow pigs and goats to man Anthrax ndash cattle sheep goats horses to man Rabies ndash dogs foxes etc to man3 Non-living things as a reservoirEgCbotulinum etiology of botulism Ctetani etiology of tetanus Cwelchi etiology of gas gangrene all of them use soil as reservoir Carrier -It is an infected person or animal that does not have apparent clinical disease but is a potential source of a diseaseTypes of carriersA Healthy or asymptomatic carriers -These are persons whose infection remains unapparent through out its course B Incubatory or precocious carriers -These are individuals or persons who excrete the pathogens during the incubation period (before the onset of symptoms)C Convalescent carriers-These are those who continue to harbor the infective agent after recovering from the illnessD Chronic carriers -The carrier state persists for a long period of timeEg Typhoid fever Hepatitis B virus infectionPortal of exit (mode of escape from the reservoir ) -The site through which the agent escapes from the reservoir Eg GIT = bacillary dysentery amoebic dysentery cholera etc Respiratory = TBc common cold etc Skin and mucus membrane = syphilisPortal of entry -The site in which the infectious agent enters to the susceptible hostEg Mucus membrane = syphilis HIV Respiratory tract = TBc pertusis GIT = bacillary dysentery amoebic dysentery cholera etcPeriod of communicability or communicable period-The period during which an infectious agent is transmitted from the infected person to the susceptible host Susceptible host -A person or animal not possessing sufficient resistance against a particular pathogenic agent Incubation period -The time interval between infection of the host and the first appearance of symptoms and signs of the diseaseProdromal period -The time interval between the onset of symptoms of an infectious disease and the appearance of characteristic manifestations Eg In measles from the onset of fever and coryza to the development of characteristic signs like koplickrsquos spots and rashes

21 Airborne

22 Vehicle borne

UNIT THREE

TYPHOID FEVER

Life cycle

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

21 Airborne

22 Vehicle borne

UNIT THREE

TYPHOID FEVER

Life cycle

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

21 Airborne

22 Vehicle borne

UNIT THREE

TYPHOID FEVER

Life cycle

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

UNIT THREE

TYPHOID FEVER

Life cycle

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

UNIT THREE

TYPHOID FEVER

Life cycle

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

UNIT THREE

TYPHOID FEVER

Life cycle

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

TYPHOID FEVER

Life cycle

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Life cycle

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Life cycle

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Life cycle

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Life cycle

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Life cycle

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Life cycle

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Life cycle

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Unit 4 20

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Influenza 21

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Signs and symptoms

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

months of age

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Complications

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Introduction

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

-Diagnosis

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

active immunization

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

patient contact

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Mgt 2 Genital Ulcer

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

1 PID2 PROM

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

(Gonorrhoea)

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Signs and symptoms

several days

Complications

Vaccination (DPT)






Clinical Features

Documents

Cominicable Abebaw