Common Diseases Review - Community Medicine

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Lasanthi Aryasinghe Disease

Agent

Transmission

Signs & Symptoms

Complications

Vaccination & Treatment

RESPIRATORY INFECTIONS

Chicken Pox (Varicella)

-Varicella Zoster Virus (Human Alpha Herpes virus 3)

- Case - Droplet Infection (nuclei) - Oropharangeal secretions - Lesions of skin & mucosa POC: 2 days before rash 4-5 days after

Measles (Rubeola)

- RNA Paramyovirus - Only 1 serotype

- Case - No carriers - Droplet infection (nuclei) - Nose, throat & resp tract secretions during prodromal stage and early stages of rash (eruption time) POC: 4 days before rash 5 days after Isolate for 7 days after onset of rash

Rubella (German Mesasles)

- RNA virus - Togavirus family - Only 1 Antigenic type

- Case - Subclinical case - Droplets from nose, throat - Droplet nuclei (aerosols) - Max infectivity during eruption POC: 7 days before rash 7 days after rash fades

1. Pre-eruptive Stage 2. Eruptive Stage: - Symetrical, Centripetal rash - Rapid evolution of rash - “Dew drops” - vesicles filled w/ clear fluid - Pleomorphism

- Varicella Hemorrhagical - Encephalitis - Acute cerebellar Ataxia - Reye‟s Syndrome - Congenital varicella

- V-Z Ig - Live Vaccine (OKA strain)

IP 14-16 days

1. Prodromal Stage: - Koplik’s spots – small bluish, white spots on buccal mucosa, st nd opp 1 & 2 upper molars (2days before rash) -3Cs coryza cough conjuctivitis 2. Eruptive Stage - Dusky red, maculo-papular rash begins behind ears--face-neck--lower limbs 3. Post-Measles Stage

- Measles ass. diarrhoea - Pneumonia - Otitis Media - Febrile convulsions - Encephalitis - Sub-acute sclerosing panencephalitis (SSPE) - Keratomalacia & blindness from corneal scarring

- Reconstituted Measles Vaccine @ 9mts - MMR - NHIg

IP 10-14 days

- 50–65% are asymtomatic - Short duration (3 days) 1. Prodromal Stage 2. Lymphadenopathy - Postauricular & postcerival 3. Rash - Minute, discreet, pinkish, macular rash – spreds (and clears) rapidly to trunk and ext. faster than measles

- Arthralgia - Encephalitis - Thrombocytopenic purpura - Congenital rubella – virus inhibits cell division; st 1 trimester most dangerous= PDA + cataracts + deafness

- RA 27/3 Live vaccine - MMR @ 12-18 months giving life long immunity

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Lasanthi Aryasinghe IP 2-3 weeks

Mumps

- RNA virus - Myxovirus parotiditis - Genus; Rubulavirus

- Case - Subclinical case - Droplet infection & Direct contact - Max infectivity at onset of parotitis POC: 4-6 days before 6 days after illness

Pertussis (Whooping Cough)

- Gram negative bacilli: - Bordetella pertussis: - Clinical disease– encapsulatd, Phase 1 strains - 3 major agglutinogens (1,2,3) - B parapertussis (5% of cases)

- Case - Droplet infection & Direct contact - Nasopharangeal & bronchial secretions - Freshly contaminated formites - Max infectivity catarrhal stage POC: catarrhal and paroxysmal stage

- Ear ache - Parotid swelling, submandibular and sublingual glands may also be involved

IP 2-3 weeks

- Lasts for 6-8weeks 1. Catarrhal Stage (10days) Cough, coryza 2. Paroxysmal Stage (2-4 wk) Explosive cough, child is chocked, anxious, unable to breathe. Bout of cough ends w/ long drawn out inspiratory crowing sound- whoop, prod by air gushing thru half opened glottis. Bout ends in the child vomiting thick tenacious sputum. 3. Convalescent Stage (1-2 wks) Interval b/w bouts & severity 

- Meningoencephalitis - Orchitis - Epididymitis - Oopheritits - Pancreatitis - Nephritis - Myocarditis, thyroiditis, Mastitis, Arthritis, optic neuritis, keratitis & thrombocytopenic purpura

- Bronchitis - Broncopnemonia - Bronchiectasis - Subconjunctival hmrhgs - Epistaxis - Haemoptysis - Punctate cerebral hmrhgs - Hernias - Rectal prolapse

- Mumps Live vaccine - MMR - Rubella-Mumps vaccine

- DPT - Pertussis – Killed whole cell vaccine: contraindicated in H/O epilepsy, convulsions, febrile illness - No maternal Ab protection - Cases: - Erythromycin or ampicillin - Nebulization w/ salbutamol

IP 7-14 days

Diphtheria

- Corynebacterium diphtheriea: - Toxigenic strains- powerful exotoxin- responsible for S/S - Biotypes: gravis,mitis and intermedius 1. Respiratory Diptheria: - Pharyngotonsillar

- Case - Subclinical case - <
- Greyish/yellowish membrane on pharngotonsilar area “False Membrane” – cannot be wiped away - Marked edema of submandibular area + lymphadenopathy-“Bull Neck”  airway obstruction and

- Myocarditis - Loss of visual accomod. - Fluid regurgitation - Polyneuritis. - Fatality due to: Toxeamia Laryngeal stenosis Bronchospasm

- Cases: Dipth Antitoxin + Penicillin/ Erythromycin - Carriers: Erythromycin - DPT:

Lasanthi Aryasinghe - Nasal (mildest form) - Laryngotracheal 2. Nonrespiratory Mucosal : - Conjuntival & Genitals

- Droplet – N/P secretions

stridor

Respiratory failure

POC: 2-4 weeks

- Skin lesions/ulcer surrounded by erythema & covered with a membrane

- Provocative reactions = poliomyelitis

3. Cutaneous Diphtheria IP 2-6 days

- Nisseria Meningitides: - Sero-types A,B,C,W135 cause epidemics (A & C mainly) - Gram negative diplococci

Menigitis

- In Neonates: E. Coli, Proteus, Group B Streptococci - In Children: H. Influenza, N Meningitides, S Pneumoniae - In Adults: N Meningitides, S Pneumoniae, Lysteria, TB, H Influenza, Cryptococcus

- Gram positive, Acid fast bacilli - Mycobacterium lepre Leprosy (Hansen’s Disease)

Types: - Indeterminate - Tuberculoid (Lepromin +ve) - Borderline - Lepromatous (Lepromin –ve) Paucibacillary: 1-5 lesions

- Case –negligible source - Subclinical Cases: immunity mostly acquired by Subclinical infection - Carriers 80-90% in epidemics most imp. source of infection - Droplet Infection - N/P secretions Difficult to control b/c of subclinal cases and carries POC: Noninfective within 24hrs of treatment

- Cases of Multibacillary leprosy- main source - Subclinical Cases Animal Reservoirs: - Armadillos - Mangaba monkeys - Chimpanzees - Direct Contact - Droplet Infection

In children/adults: vomiting, fever, headache, stiff neck, light aversion, drowsy, joint pain, fitting, rash esp. on limbs and trunk *place glass over rash, if does not disappear it is menig. rash In babies: fever w/ cold hands/feet, fretful, refusing feeds/vomiting, neck retraction w/ arching back, lethargic, pale blotchy complexion On clinical exam, hypertonia w/ neck rigid, arthritis, Brudinski’s sign & Kernig’s sign = +ve

- Tertravalent Polysaccharide vaccine (A,B,C, W135) : Revaccinate 3-5yrs - Rash - Shock - Intravasculr coagulation - Renal failure - Peripheral gangrene - Arthritis - Pericarditis - Waterhouse Freidichsen syndrome: adrenal insufficiency

IP 3-4 days or 2-10 days

- Face: Mask face, leonine faceis, lagophthalmous (eye doesn‟t close completely- leads to corneal damage), loss of eyebrows, eyelashes, corneal ulcers & opacities, perforated nasal septum, depressed nose, nodules on the ear lobules and elongated ears - Hands: Claw hand, wrist drop,

-3contraindicated in H/O epilepsy, convulsions, febrile illness - Schick Test: - Presence of antitoxin (immunity status) - Hypersensitivity to dipth. toxin or protiens

- Cases: - Casefatality 95% - Penicillin or Chloramphenicol - Dexamethazone to  edema + neuro damage - IV mannitol for diuresis  intra cranial tension - Carriers: - Rifampicin - Ciprofloxacin

Intensive and extensive rehab centers: - Prevent physical deformities by early diagnosis and treatment “Preventive rehab”

Multidrug Therapy: 1. Multibacillary leprosy; 12months: - Rifampicin - Dapsone - Clofazamine

- Rehabilitation measures such as medical, surgical, educational & vocational

2. Paucibacillary leprosy; 6months: - Rifampicin - Dapsone

Lasanthi Aryasinghe Multibacillary: >5 lesions (Borderline & Lepromatous)

-4- Formites POC: Noninfective within 1 day of treatment

ulcers, absorbtion of digits, contractures, aollowing of interosseous spaces and swollen hand

Lepra Reactions: Immunologically mediated episodes of acute and sub acute inflammation, if not promptly treated may lead to serious deformities b/c peripheral nerve trunks are involved: - Type I reaction - Type II reaction

- Feet: Planter ulcers, foot drop, inversion of foot, clawing of toes. Absorbtion of toes, callosities and swollen foot - Others: Gynaecomastia and perforation of palate IP 9 months- 10 years

(erythema nodosum leprosum)

- Corticosteroids - Clofazamine

Tuberculosis

- Mycobacterium Tuberculosis

- Human Case - Bovine – Infected milk - Droplet Infection (nuclei) - 5000 bacilli/1mL: positive smear - 10,000 bacilli/1mL: 95% probability positive - Sputum smear +ve pts are major source of infection in community - Sputum smear -ve pts responsible for 15-20% of transmission (-ve in extrapulmonary TB) POC: Pt infective as long as he remains untreated; infectivity 90% within 48hrs of treatment

Rifampicin - Hepatotoxity, nephrotoxicity, gastritis, thrombocytopenia - Rapid & Slow multipliers - Fever with night sweats - Weight loss - Anorexia - Malaise - Chronic cough + expectoration - Chest pain - Blood streaked sputum to frank haemoptysis IP weeks, months or years From exposure to +ve Tuberculin Test takes 3-6 weeks

INH - Peripheral neuropathy, GI irritation, hepatotoxicity - Rapid multipliers Streptomycin - Vestibular damage and nystagmus - Rapid multipliers Pyrazinamide Hepatotoxicity, hyperuricemia - Slow multipliers (persisters) Ethambutol - Retrobulbar neuritis Thioacetazone (BS) -

- BCG @ birth DOTS strategy: -Intensive 2months: Rifampicin (BC) INH (BC) Pyrazinamide (BC) Ethambutol (BS) -Continuation 4mts: INH Rifampicin - Prophylaxis: INH for 1yr or INH + Ethambutol for 9months

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Lasanthi Aryasinghe Urticaria, GI irritation, blurring of vision INTESTINAL INFECTIONS

- RNA virus - Entero virus (Poliovirus): Type 1 (Brunhylde) Type 2 (Lansing) Type 3 (Leon) *Outbreaks of paralytic polio due to Type 1 Polio Myelitis

Types of Polio: - Subclinical infections: 95% - Abortive poliomyelitis: 4-8% - Aseptic meningitis / nonparalytic polio: 1% - Paralytic poliomyelitis: < 1%  Spinal  Bulbar and Bulbospinal  Encephalitic

- Case - <<Subclinical cases - Feco-oral - Droplet Infection - Feaces, orophayrengeal secretions Basis for eradication:  Man is the only host  Long term carrier state does not exist  Effective live vaccine  Vaccine mimics natural route of infection  Displaces the wild virus in intestines  If vaccination is 100% there is abrupt interruption of transmission of wild polio virus POC: 1-2weeks before and after the onset of illness

-Malaise, anorexia, abd pain, nausea, vomitting, headache, constipation, Meningeal irritation- stiff neck and back - Tripod Sign - sits by supporting hands at back, partially flexing hips and knees Spinal poliomyelitis: • Anterior Horn cells affected Paralysis is: • Flaccid • Patchy and asymmetrical • Descending • Proximal muscles more involved • Deep tendon reflexes are diminished • Sensory system intact Bulbar poliomyelitis: • Medulla affected • Facial asymetry (Cranial nv.) • Difficulty in swallowing • Weakness or loss of voice • Death  respiratory insuffeciency IP 7-14 days

Cholera

- Vibrio Cholerae: - Group O1: “epidemic strain” - O139: New strain

- Case - Subclinical cases: maintains endemic

1. Evacuation: - Sudden onset of profuse, effortless, watery diarrhorea

Provocative poliomyelitis: Risk factors precipitate an attack of polio in people who are infected by the virus:  Trauma  Operative procedures  Rigorous physical exercise  Painful IM injections or DPT (alum containing) Disability limitation and rehabilitation: - Pts w/ muscle paralysis benefit from frequent passive range of motion (PROM) - Splinting of joints prevent contracture & joint ankylosis. - Chest physical therapy (CPT)- pts w/ bulbar polio prevents any pulmonary complication (atelectasis) - Occupational Therapy: pts w/ paralysis of extremities: hand or arm splints, knee or trochanter rolls, footboards, or MultiPodus boots (prevent foot drop, ulcers, etc) - Speech Therapy

IPV (Salk): • Killed virus • SC or IM • No local immunity • Does not prevent reinfection • Not useful in epidemics • Difficult to make • Virus content > than OPV- costlier • No stringent conditions for storage OPV (Sabin): • Live virus • Orally • Local, humoral & Herd immunity • Prevents intestinal reinfection • Effective in epidemics • Easy to produce • Cheaper • Store: sub 0 temp NO secondary prevention

- Oral Cholera Vaccine (OCV) 2 doses 10-15 days

Lasanthi Aryasinghe - Killed by Gastric pH>=5 - Dose-related - Large dose 11 required for infection 10 - Biotypes of O-Group 1: - Classical - El Tor – greater “endemic tendancy” than Classical - 3 serotypes: • Ogava • Inaba • Hikojima

reservoir - Vehicle Borne: Water, food, drinks - Direct Contactcontaminated fingers - Feces, Vomit - Formites

(Exotoxin H stimulates adenylate cyclase  cAMP  drives fluids and ions into the lumen of the small intestine)  “Rice water stools” - Vomiting

Carriers: - Temp: maintains reservoir - Chronic (Gallbladder affected) - Incubatory - Convalescent - Healthy: imp in spread

2. Collapse: - Rapid dehydration (+ acidosis  Death) - Muscular Cramps - Suppression of urine ( renal failure Death) - Unrecordable BP - Intense thirst - Sunken eyes

POC: Case- 7-10 days Convals. Carrier- 2-3 wks Chronic Carrier- 1mt-10yr

-6apart mix with 150ml safe H2O - Lasts 6 months Treatment: • Plan A – Home therapy fluids • Plan B – ORS • Plan C – IV fluids ORS: • NaCl - 3.5 mg/L • NaHCO3 -2.5mg/L or Trisodium citrate - 2.9 gm/L • KCl - 1.5mg/L • Glucose - 20mg/L • Water - 1 liter

3. Recovery: - Increased BP, urine flow

IV Fluids: • Ringers lactate sol w/ 5% dextrose • Normal saline (Does not correct acidosis)

Above are S/S of the Classical type (5-10%) of Cholera, El Tor types causes mild & inapparent infection

Chemotherapy: • Doxycycline • Tetracyclin • Flurazolidine

IP few hours- 5 days

- Salmonella Typhi - Gram negative, nonsporing - Facultative anaerobic rod - Secondary attacks may occur Typhoid & Paratyphoid

- 3 main Ags- O, H & Vi: • Widal‟s Test for O, H, Vi Ags • Ab to O Ag > in pt. w/ disease • Ab to H Ag > in immunizd pts. Paratyphoid fever: • S. paratyphi A & B (rare) • I.P. is shorter • Clinical manifestations- Milder • Complications – Uncommon

- Man only reservoir - Case - Subclinical Case - Carriers: • Incubatory • Convalescent • Chronic (>1yr) – oraganism persists in gallbladder & biliary tract • Fecal >urinary carriers (Chronic urinary carriers are assoc. w/ urinary tract abnormalities)

1. First stage (1 week) Temp  step-ladder fashion, severe headache, malaise, coated tongue, relative bradycardia, abd. pain & constipation 2. Second stage (1-2 weeks) • Fever reaches plateau • Abd. discomfort & distention • Pt. exhausted and prostrated • Diarrhea- pea soup stools • Dicrotic pulse (double beat) • Occasionally meningismus

• Intestinal hmrrhgesudden temp, shock, dark/fresh blood in stool • Intestinal perforation • Urinary retention • Thrombophlebitis • Pychosis • Nephritis • Osteomyelitis • Cholecystitis • Hepatitis • Fatty liver & abscess • Bronchitis & pneumonia • Myocarditis

1 Prevention: Health education: Domestic, personal & environ. hygiene Vaccines: • Vi polysaccharide 1dose - parenteral • Ty21a Oral live vaccine capsule Day 1-3-5 Booster evry 3yrs

Lasanthi Aryasinghe • Rose spots MORE

-7• Female > Male carriers - 1 source of infection: Feces & urine of carriers - 2 source of infection: Contaminated water, food, fingers & flies

• Leukopenia • Blood, urine & stools test +ve for salmonella • Rose spots - 25% of white pts.- principally on trunk, fades on pressure • Splenomegaly & Toxemia

• Meningitis • Peritonitis

3. Third stage (over 7-10days) Condition improves, temp  in step-ladder OR complications start to appear

2 - Treatment: • Ciprofloxacin • Chloramphenicol • Cefexime • Amoxocillin • Cotrimoxazole • Azithromycin • Cortricosteroids –  mortality in critically ill pts Chronic carriers: • Ampicillin plus Probenecid • Cholecystectomy

4. Fourth stage: Recovery Relapse in 10-20% of cases

IP 10-14 days; 3 days-3 weeks IP is dose dependant

- Hepatitis A virus - Enterovirus - Picornaviridae family

Hepatitis A (infectious / epidemic jaundice)

Serological Diagnosis: • HAV particles or specific viral Ags in feces • Rise in anti-HAV titre – lifetime persistance • IgM appears early in illness and persists for over 90days • IgG appears more slowly, persists for many years – indicates past infection & immunity NO CHRONIC CARRIERS

- Case - Asymptomatic (Anicteric) < children, maintains chain of trans. - Feco-oral – food, water, milk, raw / inadequetly cooked shellfish (cultivated in sewage water) , hands, eating utensils - Parenteral – blood & blood products - Sexual – homosexuals, oral-anal contact - Fecal shedding > in later part of IP and early acute phase of illness - Feces, urine, blood, serum & other fluids are infective during breif viremia POC: 2wks before – 1wk

Non-specific symptoms: Fever, chills, headache, fatigue, generalised weakness, anorexia, nausea, vomiting, dark urine & jaundice - Benign disease – recovery w/in a few weeks

IP 15 - 45days (usually 2530days) – depends on dose ingested

Primary Prevention: - Food hygiene - Supercholrination

Prevention: • NHIg -  Globulin - Given before exposure or during IP prevents or attenuates clinical illness but DOES NOT prevent subclinal infection or excretion of virus Vaccines: • HepA Killed vacc. - 2doses parenteral - 6-18 months apart • Combined Killed Hep A & recombinant B - 3doses- 0-1-6 mts

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Lasanthi Aryasinghe after onset of jaundice - Hepatitis B virus - Hepadna virus 3 morphological forms: • Dane particles - 42nm - Double shelled DNA virus • Small spherical particles 22nm - Antigenic, stimulate prod. of surface Ag - Purified 22nm particles used to prepare Hep B vaccine • Tubules of varying length

Hepatitis B (Serum Hep)

Serological Diagnosis: HBsAg • Appears in serum during IP before biochemical evid. of liver damage or jaundice • Persists during acute illness • Cleared during convalesence • Present for 4-6 months

- Case - Subclinical - Chronic carriers: HbsAg > 9months 5-15% of cases; may cause chronic active Hep & hepatocellular carcinoma

HBeAg • Precedes onset of disease • Marker of virus replication, therefore  infectivity • Detectble 3-5days aftr HBsAg • Persists 2-6 weeks • Carriers - persists for yrs • Presence of HBeAg indicates pt. is highly infectious

- Contaminated blood (main source), saliva, vaginal secretions & semen

HBcAg - Core Ag Anti-HBs • Indicates past infection & immunity to HBV • From HBIg or immune response to HBV vaccine IgM anti-HBc

S/S similar to Hep A - Complicated in the carrier state by chronic liver disease, which may follow infection - Chronic liver disease may be severe, and progress to primary liver cancer or cirrhosis IP 6wks – 6 months (median IP = 100 days)

Pre / Post Exp.: • HBIg – asap w/in 6rs & not >48hrs - 2 doses – 30days apart - Hepatocellular cancer - Liver Cirrhosis

• Hep B – Plasma derived vaccine - 0-1-6 months • Hep B vac + HBIg

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Lasanthi Aryasinghe • Indicates recent infection • Positive for 4-6 months

Hepatitis C (Post Transfusion Hepatitis)

- Hepatitis C virus - Parenterally transmitted NonA, Non-B (PT-NANB) - Single stranded RNA virus - Similar to Flavivirus

- Case - Chronic Carriers - 50% of cases are asymptomatic - Transfusion - Contaminated blood & blood products - Maternal – neonatal, sexual transmission is small

- Clinical illness is often mild, usually asymptomatic - Chronic carriers are at risk of developing liver cirrhosis and liver cancer - Leading reason for liver transplantation

NO VACCINATION - Hepatocellular cancer - Liver Cirrhosis

- 50% of cases relapse when treatment is stopped - Only 25% have long-term remission

Treatment: Interferon (Very expensive)

IP 6 - 7 weeks

Hepatitis E

- Hepatitis E virus - Enterically transmitted Non-A, Non-B virus - RNA virus: 29-32nm - Calcivirus

- Water borne - Feco-oral

- Self-limiting acute viral hep for a period of several wks followed by recovery - Induces a fulminating form of acute disease in 80% of pregnant women

NO CHRONIC CARRIERS

Intrauterine infections w/ Hepatitis E: • Abortions • Intrauterine Death • High perinatal M&M

- Food hygiene precautions - Supercholrination - Recovery is always complete NO SPECIFIC TREATMENT

IP 2-9weeks - Hepatitis D virus - Delta virus

Hepatitis D

Serological Diagnosis: HDAg • Detectable in early acute infection Anti-HDV • Indicates past or present infection

Group A Streptococcal infections

- Group A beta hemolytic - Streptococci M type: 1,3,5,6,14,18,19 and 24

*See Hep B*

- ALWAYS occurs in assoc. w/ Hep B Carrier state

Immunization against Hep B also protects against delta infection

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Lasanthi Aryasinghe ARTHOPOD-BORNE / ZOONOTIC / PARASITIC - INFECTIONS

- Virus spreads from site of infection centripetally via the peripheral nerves towards the CNS- it “ascends”

Rabies (Acute viral encephalitis)

- Lyssa virus type I, RNA virus - Family Rhabdoviridae - Street virus: naturally occuring cases - Fixed virus: Serial brain-tobrain passage of street virus in rabits; used to prepare antirabies vaccine Duration of illness: - 2-3days - Dead-end disease (organism dies along with man) - Virus evades the immune system before the signs of encephalitis develops

Reservoir: - Urban Rabies - Wild (Slyvatic) Rabies - Bat Rabies - Animal bites - Licks - Aerosols – in bat caves - Person-Person: bites or organ transplantation - Carriers: only animals Variable qty of virus in saliva of rabid animals  only 50% of bites result in rabies

1. Prodormal stage: Fever, malaise, headache, sore throat, tingling at site of bite 2. Encephalitic stage: Sensory  Motor  Sympathetic  Mental - Intolerance to light, noise or air (Aerophobia)- sensory - Increased reflexes, muscle spasms- motor - Pupils dilated,  perspiration, salivation & lacrimationsympathetic - Fear of death, anger, irritability, depression- mental - Hydrophobia- sight or sound provokes voilent spasms of pharygeal and neck muscles

Maleria

- Female Anopheles Mosquito takes blood mealinjects sporozoites - Blood transfusions

Paralytic (dumb) rabies • 20% of cases • Less dramatic form of the disease • Death – 1 month • Flaccid muscle paralysis develops earlyprominent feature of this form of rabies. • „Dumb‟ rabies reflects the paralysis of the laryngeal muscles which inhibits speech. • Mild sensory disturbances

IP 3-8wks or 7 days to years depending on site & severity of bite, no. of bites and amount of virus injected

Treatment: • Isolation • Sedatives • Muscle relaxants • Hydration,diuresis • Resp & cardiac support • Barrier nursing

1. Cold stage – ¼ to 1 hr Lassitude (fatigue), severe headache, nausea, rigors, Temp 39-40C, vomiting, skin feels cold initially hot, pulse is

Falciparum: • Hyperparasitemia • Hyperpyrexia • Severe anaemia • Spontaneous bleeding

3. Coma  Death

- Plasmodium vivax - Plasmodium falciparum - Plasmodium ovale - Plasmodium malariae

Furious (classic) rabies • 80% of cases • Death – few days • Hyperactivity • Hydrophobia • Mood swings and aggressiveness • Convulsions

Pre-exposure: • 3doses- cell culture vaccine • 0-7-21-(or) 28 • Booster after 2yrs Vaccine: • HDCV or PCECV IM- 5doses x1ml Days: 0-3-7-14-28 • If previously vacc: Mild bites 1ml x 0-3 Severe 1ml x 0-3-7 ID- x 0.1ml Days: 0-3-7-28-90 2 x 0.1ml -Day0,3,7 Post-exposure: I No treatment II Vaccine III Vaccine +Ig • Clean- soap +H2O • Virucidal agent • Avoid suturing • Antibiotics • Tetanus • Ig 20 IU/kg infiltrated around the wounds, remains given at site anatomically distant frm vaccine

• Antirabies vaccine

Treatment: • Day 1 Chloroquine + Primaquin

Lasanthi Aryasinghe • Fetal Hb: supress Falciparum • Sicklecell (AS Hb) trait: Milder infection w/ Falciparum • Duffy –ve: resistant to Vivax

- 11 - Carriers: Human tht habor both male & female sexual forms (gametocytes) of sufficent density to infect a vector mosquito - Children are more likely carriers than adults - Definitive Host: Mosquito, Sexual Cycle

rapid & weak 2. Hot stage – 2 to 6 hrs Pt feels burning hot- removes clothing, skin hot & dry, intense headache, nausea dimishes, pulse full, respiration rapid 3. Sweating stage – 2 to 4 hrs Fever  w/ profuse sweating, temp  rapidly to normal, skin is cool & moist, pulse decreases

- Intermidiate Host: Man, Asexual Cycle

and coagulopathy • Cerebral malaria (Convulsions, Coma) • Acute renal failure (black water fever) • Hypoglycemia • Metabolic acidosis • Shock Vivax, Ovale & Malariae: Anaemia, Splenomegaly Liver enlargment, Herpes, Renal complications In pregnant women: • Intrauterine death • Premature labor • Abortion • Congenital maleria

Cutaneous forms: • Skin ulcers on exposed areas, face, arms and legs. • Heals within a few months • Leaves scars

Leishmania

- Protozoa: Leishmania: L. donovani- Kala azar/Visceral L. tropica/ L. major- Cutaneous L. braziliensis- Muco cutaneous

- Bite: infected female sandfly injects promastigotes

Diffuse cutaneous forms: • Disseminated & chronic skin lesions similar to lepromatous leprosy Mucocutaneous forms: • Lesions destroy mucous membranes of nose, mouth, throat cavities & surrounding tissues. Visceral leishmaniasis: • High fever, weight loss • Swelling of the spleen & liver • Anaemia

Vector Control: • Elimination of breeding places • Insecticide spraying • Personal prophylaxis

• Day 2 & 3 Chloroquine Vivax & Ovale: • Primaquin (5days) Chloroquin resist. Faciparum: Artesunate plus: • Mefloquine • Amodiaquine • Sulfadoxine/ Pyrimethamine Combined antimals • More effective • Prevent resistant. Chemoprophylaxis: • Cholorquin 1wk before travel to 4wks after return Control of reservoir: Early diagnosis: • Aldehyde test • ELISA • Isolation of parasite from aspirates of spleen, liver, bone marrow, lymph nodes and skin. Treatment: • Na stibugluconate 20days- Cutaneous 28days - Visceral • Pentamidine Isothionate- 10days nd - 2 line drug • Amphotericin B

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Lasanthi Aryasinghe • Untreated fatality rate as high as 100% within two years.

7-14 days

IP weeks-months

- Clostridium tetani - Gram +ve - Anerobic bacilli - Spore bearing Tetanus

- Exotoxin tetanospasmin: Acts on nervous system: • Motor endplates- skeletal sys • Spinal Cord • Brain • Sympathetic System

- Reservoirs: soil, dust, intestines of herbivorors (excreted in their feces) - Contamination of wounds with tetanus spores Types of Tetanus: • Traumatic - wounds • Perpeural - postabortion • Otogenic - foriegn body in ear • Idiopathic • Neonatorum POC: Not transmitted

• Stiffness and cramps around the area of wound • Deep tendon hyper-reflexia • Trismus lock jaw (masseters) • Dysphagia • Risus sardonicus (facial ms.) • Opisthotonus (back and neck) • Painful paroxsymal spasms of voluntary muscles  cyanosis  threatens resp. Auntonomic dysfunction (severe cases): - Toxin diffused to lateral horns - Increased basal sympathetic tone: tachycardia, bowel & bladder dysfunction - Sympathetic over activity (both alpha & beta receptors): • Labile hypertension • Pyrexia • Sweating • Pallor • Cyanosis of digits • Exhaustion, asphyxia or aspiration pneumonia  Death

Prevention: DPT @ 2-4-6+ 3 Booster doses: • DPT – 18 months • DT – 5-6yrs old • TT – every 10yrs Introduction of spore  germination & elaboration of exotoxin  blood stream  motor nerve endings  CNS via pheripheral nerves  Blocks the release of inhibitory (glycine) neurotransmitters across the synaptic cleft  Abolition of spinal inhibition  muscle rigidity & spasms

Treatment: • Isolation • Sedatives • Muscle relaxants • Hydration,diuresis • Maintain adequet airway

IP 6-10 days; depends on character, extent and location of the wound.

AIDS

- Retrovirus (lentivirus family) - RNA virus - HIV-1 - HIV-2 in West Africa

- Direct Contact: Sexually - Parenteral route - Transplacental/ Vertical - Blood Transfusions

1. Intial Infection Mild illness- fever, sore throat, rash. Window Period – period before HIV Abs (2-12wks)

Post Exposure: 1. Clean wound, remove debris & dead tissues 2. TIG/ATS + Benzathine Penecillin (long-acting) OR 3. TIG/ATS + TT (in pts. w/ incomp. imunization) + Benzathine Penecillin 4. TIG/ATS + PTAP/APT (absorbd tetanus toxoid) +Benzathine Penecillin + TT (in 6wks) + TT (in 1yr)  in pts never been immunized before

Human Tetanus HyperIg (TIG): • Human Antitoxin • 250-500IU • No serum rxn • Passive immunity upto 30days Antitetanus Serum (ATS): • Equine Antitoxin • 1500IU - SC • Allergic reactions • Passive immunity only 7-10days

Tests: • ELISA • Western Blot:

Treatment: Nucleoside Analog • Zidovudine (AZT)

Lasanthi Aryasinghe - Occupational: needlestick injury

appear in blood after infection. Pt. is highly infectious due to high viral conc. in his blood- pt. tests –ve on standard Ab tests.

Prophylaxis (4wks):

2. Asymtomatic Carrier state No overt signs- only persistent generalised lympadenopathy (nodes>1cm in 2 or more sites besides groin area for 3months)

• Zidovudine +Lamivudine + Nelfinavir (if source has AIDS) • Stavudine + Didanosine (if source failed AZT/3TC treatment)

Vertical Transmission: • HAART during pregnancy • Perinatal Antiretroviral prophylaxis • Caesarian section • Ziduvudine to neonate • Avoid breast feeding

POC: Highly infectious during „Window Period‟ and in advanced infection

3. AIDS related complex 1 or more of: diahorrea>1mt, wt. loss>10%, fever, night sweats, oral thrush, enlarged spleen, lympadenopathy. 4. AIDS • Opportunistic inf. + Cancers (Study table- infections related to falling CD4 count) • Slim disease - HIV wasting = Chronic diarrhoea + Wt. loss • AIDS dementia – HIV crosses BBB, resembles Alzheimer‟s

Confirmatory Test. Detects Ab to viral core protien p24 & envelop glycoprotien gp41. Indeterminate results w/ early HIV inf, HIV-2, Auto-immune disease, pregnancy & recent TT. • CBC – In advance HIV: Anemia, neutropenia, Thrombocytopenia • Absolute CD4 count: AIDS – CD4<200cells/L

Urinary Schistosomiasis • S. haematobium Schistosomia

Intestinal Schistosomiasis • S. masonii • S. japonicum. • S. Mekongi • S. intercalate

- Cercariae released by snails  penetrate skin

• Swimmer’s Itch @ site • Katayama fever (serum sickness like syndrome) w/ intestinal schistosomiasis, due to Ag-Ab complex • Acute & Allergic manifestation • Characteristic manifestations occur after oviposition Urinary: Dysuria, terminal painless haematuria. Protienuria, ulceration, thickening and

Protease Inhibitors • Saquinavir • Ritonavir • Indinavir Nonnucleoside rev. transcriptase inhbit. • Nevirapine • Delaviridine

• CD4 Percentage AIDS – CD4 % <20%

FirstLine CD4 <500 • 1 or 2 Nucleoside Analogs

• HIV Viral Loads: Amt. of actively replicating virus. Relates to disease progression and antiretroviral drugs.

Second Line • 1 Protease inhibit. + 1 or more Nucleo. Analogs

• B2 Microglobulin levels: >3.5mg/dL ass. w/ rapid progression of disease

IP Few months to 10 years

- Blood Fluke/ Trematode

- 13 • Stavudine • Lamivudine (3TC) • Didanosine

Urinary Complications: • Hydroueter • Hydronephrosis • Cancer bladder Intestinal Complications: • Portal hypertension • Liver cirrhosis • Esophageal varicies • Haematemesis • Colorectal polyps. • Epilepsy (S. japonicum)

Third Line • 1 or 2 Protease inhibit. + 1 or more Nucl. Analogs • Nevirapine + Zidovudine + Didanosine Reservoir Control: •Praziquantel •Mass chemotherpy for highrisk children 10-15yrs •Artemether anticercarial drug •Topical anticercarial ointment DEET insecticide repellent.

- 14 Snail control: • Mechanical method- removal of aquatic vegetations & increase flow of water in canals • Biological method- snail eaters. Ducks and geese • Chemical methodmolluscicides

Lasanthi Aryasinghe calcification of urinary bladder Intestinal: Intermittent diarrhea, abdominal pain, melena, intestinal polyposis, hepatomegaly, spleenomegaly and ascites. Manifestations more severe w/ S. japonicum b/c no. of eggs.

IP 2- 6 weeks

- Yersinia pestis - Gram-negative cocco bacilli - Typical bipolar staining - Non-motile and non-sporing.

Plague

Virulence due to: • Exotoxin and endotoxin • Fraction 1 • Many other Ag & toxins Bacilli occur in: • Buboes- Cannot spread person-person as bacilli are locked in buboe • Blood • Sputum (pneumonic) • Spleen, liver & other viscera of infected pts

• Natural reservoir: rodent • Source: infected rodents fleas & pneumonic case • Vector: Most efficient vector is the rat flea X.cheopis - Bite of infected flea - Direct contact with tissues of infected animal - Bite of human flea Pulex irritans from plague pt. (rare) - Droplet infection: when primary case of bubonic plague develops secondary pneumonic plague

A. Bubonic Plague • Buboes - greatly enlarged, tender lymph nodes in groin area w/ erythema and edema of the overlying skin. • Fever, suddenchills, headache, prostration, painful lympadenitis • If left untreated followed by disseminated infection  complications  secondary pneumonic plague & meningitis. Bacteremia can occur, some develop sepsis B. Pneumonic Plague • Primary  inhalation of organism frm other humans • Seconday  hematogenous spread as a complication of pneumonic or bubonic plague • Cough, hemoptysis, chest pain, tachypnea and dyspnea • Thin, watery, blood-tinged sputum becomes frankly bloody and mucopurulent as the disease progresses. C. Septicemic Plague

Comlications of Bubonic: • Secondary septicemia • Pneumonia • Meningitis. • Polyarthritis • Lung abscesses • Superinfection of lymph nodes Septicemic Plague: • DIC • Menigitis x4 more common than in bubonic • Multi organ failure

IP Bubonic 2-7 days Septicemic 2-7 days Pneumonic 1-3 days

Formalin-killed: • 2doses SC • Day 0 & 14 • Booster evry 6mts • Immunity starts 57days • Infants <6mts not immunized Treatment: 10days • Streptomycin • Tetracycline • Doxycycline • Chloramphenicol • Gentamicin • Trimethoprimsulfamethoxazole Prophylaxis: • Tetracyclin • Sufonamide

- 15 -

Lasanthi Aryasinghe • Primary- flea bite. S/S similar to bubonic plague but absence of palpable buboes. • Secondary - complication of pneumonic or bubonic plague. • Some pts develop nausea, vomiting, diarrhea & abd. pain. - Wild reservoir: monkey - Urban reservoir: Man & Aedes aegypi mosquito - Vector- Mosquito - Clinical cases - Subclinal cases

Yellow Fever

- RNA virus - Family Togavirus - Flavivirus fibricus - group B Arbovirus - Pantropic virus- can invade & affect different tissues of the body, w/out showing affinity to any of them - Shares specific Ag w/ other members of the genus eg. West Nile & Dengue

- Jungle (Slyvatic) Cycle Transmission of disease b/w monkeys. Americas: Haemagogus Africa: Aedes africanus & simpsoni - Urban Cycle Person to person transmission by Aedes aegypti mosquito POC: -Man: blood of paitent infective during first 3– 4 days of illness - Mosquito: infective for life

1. First phase: 72 hrs Headache, malaise, weakness, nausea and vomiting 2. Remission: 24 - 48hrs 3. Intoxication phase: 7-10day • Jaundice w/ hemorragic manifestations; mucosal hmrhgs & GI bleeding: black vomit, epistaxsis and melena • High fever • Albuminuria or anuria- acute renal failure • Shock • Agitation • Stupor/ Delirium • Seizures • Coma • Death within 7-10 days IP 3-6 days

Vector Control: 1. Anti larval measures Apply larvicide to actual or potential breeding places. 2. Anti adult measures Residual spray and space sprays with insecticides like malathion and lindane. 3. Personal protection Mosquito repellants, nets, coils and fumigation mats.

17-D vaccine: • Freeze-dried • Reconstituted w/ cold physiological saline diluent • Sub 0 temp • Immunity begins 7th day and lasts >35yrs • Revacination every 10yrs