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Dr K Chaudhry
Medicine
For
Students & Practitioners
by
Dr K Chaudhry
 
Haemopoietic System
Endocrine Disorders
Alimentary System
Nervous System
Cardiovascular System
Respiratory System
Urinary System
Infectious & Tropical Diseases
Nutritional Disorders
Diseases of The Children
Mental Disorders
Skin Disorders
Sexually Transmitted Diseases
Miscellaneous Topics
Medical therapeutics
 
Chapter 8
Infectious & tropical diseases
 
TYPHOID 
Typhoid fever is a severe systemic infectious disease characterized by continued fever, splenomegaly, bacillaemia, involvement of intestinal lymphatic tissue and usually a reseolar eruption. 
Etiology 
Typhoid fever is caused by a Gram negative bacillus, Salmonella typhi. 
Predisposing causes 
1. Age: Chiefly 5-35 years. 
2. Sex : Males slightly predominate. 
3. Season : Chiefly in autumn. 
4. Overcrowding and bad sanitation. 
5. Absence of a previous attack. 
The disease occurs all over the world. It is spread by patients and carriers, through contamination of food and water. It is also spread by flies, by fomites, and by inhalation of bacilli, as from dried excreta. Incubation period is 7-21 days, usually 14 days. 
Clinical Picture 
The onset is usually insidious, the patient complaining of lassitude, frontal headache, backache, constipation, anorexia, epistaxis, malaise and insomnia, associated with a gradually rising temperature. In some cases there is a sudden onset with fever, vomiting, rigors and delirium. The disease runs an average course of four weeks which is divided into four stages of one week each. 
A. Stage of Invasion 
1. Face flushed. 
2 Tongue with white fur at the surface 
3. Pupils dilated. 
4. Abdominal pain or discomfort. 
5. Temperature rises in a ladder step fashion with a progressive evening rise and 0.5-1.0oF drop each morning. 
6. Relative bradycardia with dicrotic pulse. 
7. Abdomen swollen with gurgling on palpation over caecum; abdominal reflexes usually absent. 
8. Spleen just palpable. 
9. Rose spots, seldom seen in this country; may appear about the sixth day. 
B. Stage of Fastigium, 
1. Patient more prostrated. 
2. Headache less marked. 
3. Deafness may develop 
4. Tongue dry and coated in the centre with clean tip and edges. 
5. Insomnia or delirium. 
6. Sustained temperature (101 -103oF). 
7. Relative bradycardia (pulse about 100 per minute). 
C. Stage of Defervescence 
1. Patient still more exhausted. 
2. Delirium and muscular twitching. 
3. Dry and shiny tongue. 
4. Muscular wasting. 
5. Haemorrhage and perforation may occur. 
6. Abdomen more distended. 
7. At the end, temperature begins to fall by lysis and rarely by crisis. 
 
D. Stage of Convalescence 
1. Temperature normal in the morning, a little higher in the evenings. 
2. Abdominal reflexes reappear. 
3. Spleen not palpable. 
Diagnosis 
Typhoid fever may be mistaken for influenza, gastro-enteritis, pneumonia, nephritis, or meningitis. The following investigations are helpful at different stages :- 
First week: 
(i) Blood culture 
(ii) Leucocyte count - Leucopenia relative lymphocytosis. 
Second week: 
     Widal's test 
Third and fourth week: 
(i) Widal's test 
(ii) Stool and urine culture. 
Complications 
1. Intestinal 
(i) Haemotrhage 
(ii) Perforation and peritonitis 
2. Venous thrombosis ; left femoral vein susually affected. 
3. Respiratory 
  (i) Laryngitis and ulceration of laryngeal cartilages. 
(ii) Bronchitis 
(iii) Pneumonia 
(iv) Pleural effusions. 
4. Cardiac 
  (i) Myocardial degeneration. 
 (ii) Endocarditis and pericarditis 
5. Neuritis, especially causing tender toes. 
6. Otitis and parotitis. 
7. Meningitis. 
8. Cerebral thrombosis or embolism 
9. Myelitis. 
10. Nephritis. 
11. Periosteitis. 
12. Acute cholecystitis. 
13. Infarction of the spleen. 
Treatment 
 1. Bed rest until temperature has been normal for two week. 
 2. Adequate diet of 2,000-3,300 calories per day with enough fluid to prevent water depletion. The daily diet should include half a litre of milk. 
 3. Drugs 
a. Chloramphenicol (Chloromycetin) 500 mg 4-hourly (50-75 mg/kg body weight a day for young children) till temperature gets normal ; subsequently 250 mg. 6 hourly (conveniently given at 5 and 11 O'clock) for 2-3 weeks. Treatment with chloramphenical reduces typhoid fever mortality from approximately 20% to 1% and duration of fever from 14-28 days to 3-5 days. 
Chloramphenicol therapy has been  associated with emergence of : 
- A high relapse rate (10-25%) 
- Resistance 
- A high rate of chronic carriage 
- Bone marrow toxicity5  and aplastic anemia 
- High mortality rates in some recent series from the developing world. 
Chloramphenicol is bacteriostatic both for clinical isolates and against salmonella typhi cultured in human macrophages. 
b. Cotrimoxazole. It is a second line drug for typhoid fever but resistance is an increasing problem.. In adults Cotrim appears to be effective in dosage of 800 mg of Sulphamethoxazole plus 160 mg of trimetoprim every 12 hours for 15 days. 
c. Quinolones 
(i) Ciprofloxacin. 500 mg orally twice daily for 10 days 
(ii) Ofloxacin 5-7.5 mg/kg twice daily for 2 to 3 days 
Complications of quinolines in children are arthropathy and cartilage damage. 
d. Cephalosporins 
- Cefixime 10 to 15 mg/kg twice daily 
e. Aminoglycosides 
 - Azithromycin 500mg every six hours for 7 days 
 4. If the fever goes beyond 104oF, it should be lowered by cold sponging. 
 5. If constipated, Herbolax Strong one tablet at bed time. 
Prophylaxis 
 T.A.B. veccine 1 ml. subcutaneousfy, repeated after 10 days. 

DIPHTHERIA
 Diphtheria is an acute infection and communicable disease characterized by involvement of respiratory system, the local formation of membrane, and general symptoms produced by absorption of toxin. 
Etiology 
The disease is caused by a gram-positive bacillus, Corynebacterium diphtheriae. The organism is usually divided into three groups, gravis, intermedius and mitis, however, a fourth type minimus is also described. 
Predisposing factors 
1. Age. Chiefly in children (1-15 years). 
2. Season. Common in cold months of the year 
3. Sex. Both sexes are equally affected in childhood; later females predominate. 
4. Climate. More in the temperate zones. 
5. An operation about the nose or throat. 
6. Low socio-economic status. 
Immunity is short-lived, subsequent attacks being common. The incubation period is usually 3-4 days but may vary between 2-10 days. 
Clinical Types 
1. Tonsillar diphtheria. 
2. Pharyngeal diphtheria. 
3. Laryngeal diphtheria. 
(i) Primary 
(ii) Tracheo-bronchial. 
(iii) Mixed. 
4. Nasal diphtheria. 
5. Haemorrhagic diphtheria. 
6. Cutaneous or wound diphtheria. 
7. Diphtheria involving the conjunctivae, the ears, the umbilicus and/or the genitals. 
Clinical Picture 
Tonsillar and pharyngeal diphtheria 
(i) Headache 
(ii) Pain in extremities 
(iii) Rarelv diarrhoea and vomiting. 
(iv) Toxaemic look. 
(v) Exudate, in the early stages, as isolated greyish yellow patches on the tonsils or pharynx; later these coalesce to form a membrane extending to the soft palate, uvula and posterior wall of the pharynx. 
(vi) Bleeding spots on stripping the membrane. 
(vii) Submaxillary and cervical lymph glands enlarged. 
(viii) Tongue furred. 
(ix) Temperature 99-100oF; returns to normal in 3-4 days. 
(x) Pulse rapid (110-120 per minute). 
Laryngeal diphtheria 
Common upto 5 years of age. 
(i) Hoarseness of voice ; 
(ii) Dyspnoea in paroxysmal attacks 
(iii) Cough ; 
(iv) Signs of laryngeal obstruction 
(a) Cyanosis. 
(b) Laboured breathing with accessory respiratory muscles in action. 
(c) intercostal recession. 
(v) Membrane extending to trachea or main bronchi. 
Nasal diphtheria 
(i) Watery or mucous nasal discharge; usually blood stained. 
(ii) Membrane in the posterior part of the nose; may be visible in nostrils. 
(iii) Small follicular spots on the upper lip under the nose. 
Diagnosis 
1. Naso-pharyngeal or laryngeal swab 
(j) Direct smear ; 
(ii) Culture on Lofflers' medium 
(iii) Fluorescent antitoxin test. 
2. Schick test., 
Differential diagnosis 
1. Acute tonsillitis; 
2. Vincent's angina; 
3. Streptococcal sore throat; 
4. Infectious mononucleosis; 
5. Catarrhal laryngitis. 
Complications 
1. Peritionsillar abscess. 
2. Myocarditis-two types; early and late. 
3. Peripheral nerve paralysis A 
4. Acute laryngeal obstruction. 
5. Pneumonia 
6. Allergic shock - due to serum therapy and may occur about the ninth day  after its administration. There is loss of plasma into tissue space and urticaria. This results in a diminished blood volume and haemoconcentration. In some cases, death immediately follows the infection. 

Table : Types of Diptheritic Myocarditis
 
Early Myocardltis
Late Myocarditis
Time of Occurrence  3rd to 7th day 5th-14 day
Colour of skin  Slight pallor  Extreme pallor, cyanosis late
Systolic blood pressure Normal, or slightly higher  Far below normal 
Pulse  Full and rapid  Weak, thready, difficult to obtain; slow
Heart sounds Normal, easily heard Softening or absence of first sound; softening of second sound 
Heart rhythm Normal, or occasional irregularity Total irregularity; gallop rhythm; heart block
Abdominal pain  None Severe 
Blood circulation  Normal ; collapse at end Peripheral and splanchnic dilatation

Table : Nerve Involvements
Paralysis
Time of Occurrence 
Signs 
Palatal  10th day or later Nasal voice
Oculomotor 3rd week or later  Strabismus
Ciliary  3rd week or later  Dilated pupils, blurred vision
Facial  3-6th week Loss of tone of facial muscles; inability to blow out cheek equally 
Pharyngeal 3-4th week Dysphagia
Laryngeal  3-5th week  Hoarseness or aphonia
Extremities 5-6th week Weakness, numbness, tingling
Diaphragm 5-6th week Dyspnoea, cyanosis 
 
Prevention 
1. Notification and isolation of patients. 
2. Regular gargling with potassium permanganate or saline. 
3. Immunization. 
Treatment 
A. General. 
 1. Bed rest for 4-8 weeks with minimum wovement. For first two weeks, only one ; low is allowed; a second pillow is then given, and gradually he is allowed to sit up. 
 2. Fluid diet ; if feeding by mouth is not nc3sible, intravenous glucose, 
B. Specific 
 I. An Y- diphtheritic serum should be adAdnisteredas early as possible unless the Patient is sensitive. The amount of serum administered varies according to the severity and number of days elapsed since onset. The following dosage is generally used 
0) Unitonsillar or bitonsillar ...... 
 20,000 units. 
 00 Pharyngeal  ....... 
20,000,40,000 units. 
(iii) Tonsillar and uvular ........ 
 40, 000 u n i ts. 
 Ov) Nasopharyngeal  ..... 
60,000-100A0 units. 
 (v) Laryngeal  ......... 
20,000 units. 
(vi) Laryngeal, with others ..... 
 20,000-100,000 units. 
 Patients suspected of having diptheria should be administered a full single dose of serum without awaiting the laboratory reports. 
 2. . Procaine penicillin 0*5 megaunit per day intramusculary for 7 days. 
3. Ascorbic acid (Sukcee) 500 mg, daily. 
C. Treatment of complications. 
 D. Special measures in laryngeal diphtheria : 
 1. Aspiration- Withdrawal of mucus, pus, membrane from the larynx and trachea by means of an aspirator connect to a suction pump. 
 2. Intubation. Direct or Indirect placing of a tube in the larynx. 
3. Tracheostomy. 

SCARLET FEVER
 Causative Organism. Streptococcus haemolyticus of Lancefield group A. 
Modes of Infection 
1. Airborne infection, 
2. Through infected milk or ice-cream. 
Incubation Period. 2-4 days. 
Common Age. 3-10 years. 
Clinical Features 
 1 . Ons9t sudden with sore throat, shivering, headache and vomiting. 
 ,2. Fauces inflamed ; tonsils enlarged and covered with follicular exudate which is yellow and easily wiped off (c.f. diphtheria), 
 3. Rash appears first behind the ears on the second day ; rapidly becomes a generalised punctate erythema ; most intense in the flexures of arms and legs ; face not affected. 
 4. Face may be flushed due to fever; paleness around the mouth. 
 5. Tongue initially furred with prominent red papillae (white strawberry tongue) ; in 2-3 days the fur peels off (red strawberry tongue). 
 6. Rash fades away in one week followed by desquamation of skin. 
Complications 
1. Acute suppurative otitis media, 
2. Cervical adenitis. 
 
 
10T Rhinitis and sinusitis. 
4. Rheumatic fever. 
I I 
~ I 
Ij 
t, i 
 
1. Rest in bed for 2-3 days after tempera­ture is normal. 
2. Antibiotic e g. phenoxymethylpenicil- Paroxysmal stage lin 250 mg orally every six hours. 
WHOOPING COUGH
 Pertussis or whooping cough is an acute, infectious, communicable disease affecting the respiratory tract, characterized by spasmodic attacks of coughing, and accompanied by an inspiratory whoop. 
 predisposing factors 
 11. Age, Mostly under the age of 5 years. 
 2. Sex. Females predominate. 
 3. Race. Mortality higher among the 
Negroes. 
 4. Season. Prevalent in colder months.  Transmission is by droplet infection, and cough being the prominent feature, the organism is Pasily disseminated to others. Carriers may act as continuous source of the disease. On3 attack confers a lasting immunity but ~econd attacks ate occasionally reported. The 
incubation period varies between 7-21 days. 
Catarrhal stage : 
(i) Duration. 1-2 weeks with insidious  onset. 
00 Dry cough, occurring at any time during day or night ; gradually pro­gressing to severe and uninterrupted cough particularly troublesome at night. 
(iii) Vomiting occasionally following a 
 severe bout of cough. 
(iv) Anorexia and insomnia. 
(v) Sneezing, coryza and lacrimation. 
NO Moderate fever. 
(i) Duration. 2-4 weeks or shorter. 00 
Paroxysms of cough, 10-15 per day. A paroxysm ensues, with expiratory efforts which may be 5-10 or more in number, short and sometimes raspy in character, 
(iii) Early in the paroxysm, the patient's face becomes deep red in colour, changing to purple red with a tinge of cyanosis as the expiratory coughs increase in number. 
"Whoop" immediately following the expiratory phase. The whoop is pro­duced by a deep inspiratory breath taken in rapidly, air passinq suddenly over the vocal cords. 
(v) After the paroxysm lasting often 5-10 minutes, copious amounts of thick, viscid mucus expectorated or swallowed. 
(vi), Post-paroxysmal vomiting. 
Convalescent stage : 
(i) Usually begins within 4 weeks after the acute onset. 
(ii) No paroxysm or whoop ; a bout of cough may be initiated by a slight irritation. 
(iii) Vomiting may rarely occur as a matter of habit. 
~iv) Improving appetite. 
 5. Acute nephritis. 
Differential Diagnosis 
1. infectious mononucleosis. 
2. Measles. 
3. German measles. 
4. Drug reaction. 
Treatment 
Etiology 
The disease is.caused by a gram-negative 
bacillus, Bordetella portussis, It occurs in  Ov) 
both epidemic and endemic forms. 
 
Clinical Picture 
 The disease may be divided into three stages, the catarrhal, the paroxysmal, and the convaiescent. 
ntia!_Diaanosis : 
 
 examination 
Tma~ !eucocyte count, 15,000-20,000  & 
'OF:-K cu. mm. 
-AMMNMK 
 Diffe,ential count - Lymphocytosis. 
1 solation of organism 
(i) Abrupt onset ; 
(ii) Greater prostration 
(iii) Cough not common and not in paroxysms ; (iv) No whoop. 
(i) Slow progress 00 No whoop; 
(iii) Polymorphonuclear leucocytosis. 
3. Foreign body in larynx or trachea 
 (i) Sudden onset 
 (ii) Normal temperature 
(iii) No lymphocytosis. 
4. Parapettussis. Distinguished by the !~=_cteriological methods. 
1. Bed-rest in a well ventil~tea room during catarrhal stage and fora timeduring paroxysmal stage. 
2. Diet. Liquids and semisolid diet. Feeds should be given after the paroxysms and should be small and frequent. 
3. A cough linctus e.g. Phensedyl (pro­methazine, codeine, ephedrine) I tbaspoon-ful thrice a day. 
 4. Sedative - triclofos (Tricloryl) 
syrup 250 mg. thrice a day. 
5. Antibiotics e.g. tetracycline 50 mg. per kg. body weight daily in divided doses. 
6. Hyperimmune convalescent serum 20 mi. intravenously at 2-3-days intervals. 

MENINGITIS
Meningitis is an inflammation of the pia and arachnoid membrane. 
Cough plate cultures 
NasopharVngeal swab 
Florescent antibody technique. 
(iii)- Toxic encephalitis; (iv) Cerebral haemorrhage. 
Gastrointestinal : 
(i) Umbilical hernia ; 
(ii) Prolapse of rectum 
(iii) Frenal ulcer 
(iv) Enteritis. 
Complications 
1. Respiratory (i) Pneumonia (ii) Atelectasis 
(iii) Emphysema (iv) Bronchiectasis (v) Pneumothorax. 
(i) Otitis media ; 
(H) Acute nephritis 
(iii) Fulminant tuberculosis. 
4. Others: 
influenza : 
Nervous 
(i) Convulsions 00 Menin4itis,; 
Treatment 
Etiology 
A. Infecfive : 
f, Bacterial : 
7- Bronchitis ; 
(i) Pneumococcus 
(ii) H. influenzae 
(iii) Meningococcus 
(iv) E. coli 
(01 Staphvlococcus 
 
 
NO MYcobacterium tuberculosis 
(vii) Streptococcus. 
 Viral : 
 (I) Poliomyelitis 
0i) Coxsackie virus A & B 
(III) Lymphocytic choriomeningitis (IV) Herpes simplex (V) Herpes zoster NO mumps 
(vii) Viral hepatitis 
MID Infectious mononucleosis 
3. Fungal : 
 (I) Cryptococcus 
00 TOXOPIasmosis. 
4. Parasitic : 
 (I) HistOPlasmosis 
00 Trypanosomiasis. 
5- SPirochaetal 
 (I) Syphilis 
0i) Leprospirosis 
Sterile (Afenjngjsm) 
(I) Acute tonsillitis 
(!I) Cervical adenitis 
(III) APical Pneumonia 
(IV) Typhoid 
~(v) Influenza 
NO Salmonella gastroenteritis. (") Otitis media 
(viii) SubaraChnoid haem Modes Of Infection 
orrhage. 
Signs 
 
(IV) Septic lumbar Puncture. 
2. Local spread: 
W RU'Pture Of 6erebral abscess 
00 Tubercul0ma. 3, Haematogenous : 
(i) Bacteraemias 
00 Miliary tuberculosis. 
Clinical Features 
symptoms 
1 - Fever 
2. Headache 
3. Vomiting 
4. Irritability 
*5* Weakn3ss Of limbs 
6. Rigidity 
7. Visual defects 
8- Convulsions 
9 , Constipation 
10. Unconsciousness 
Stage Of irrigation 
(I) Neck rigidity, 
00 Kernig's sign Res the hip with Isted flexion of  Bikele's - the knee extended. 
sign : Pain on extension 
 of the shoulder t 
 extended. Wi h the elbow 
v) Brudzinski's sign : Flexion Of the 
 n~ck causes flexion Of one or both 
 hIPs and knees. 
(v) Temperature 101-1031F. (vi) Pulse 100-120/minute, (vii) Deep reflexes exaggerated. 
Stage Of compression 
Extrinsj, : 
(I) Fracture Of skull 
(ii) -Penetrating wound of c 
 vault. 
 Infection Of mastoid and nasal 3i 
 sinuses r 
 
Delirium r4r- 
coma -siness, stupor, or 
Table : Changes in Meningitis 
 
Normal
Pyogenic meningitis 
Tuberculous meningitis 
Viral meningitis
Pressure 60-150 mm of water  Raised Raised Raised
Appearance Clear and colourless Turbid  Cob-web coagulum Clear and colourless 
Protein 20-24 mg/100 ml  Raised Raised Raised
Chloride Lowered  Lowered  Normal 
Sugar Absent Lowered  Normal 
Cell count (Mostly lymphocytes) Beyond 500/cu mm (mostly polymorphs) 100-500/cu mm 140-150/cu mm (Mostly lymphocytes)
Bacteriology Gram Positive cocci  Acid fast bacilli  -
(ii) Localized or general muscular convulsions ; 
(iii) Marked head retraction; back rarely arched; 
(iv) Pupils dilated and often unequal; 
(v) In infants, anterior fontanelle may buldge; 
(vi) Pulse slower with premature systoles; 
(vii) Temperature about 99oF 
Paralytic stage : 
      (vi) Abdominal and deep reflexes 
       abolished. 
      (vii) A general flaccid paralysis. 
    Laboratory Investigations 
     1. C.S.F. examination. 
     2. Blood culture. 
    Treatment 
     A. General 
     1 . Good nursing care ; nasal feeding or 
    IN. drip may be needed when the patient is 
    not able to swallow. 
     2. Phenobarbitone (Gardenal, 30 mg. 
 0) incontinence of faeces and urine.  thrice a day to control restlessness and con­ 
 (i i) Temperature remains low ; just vulsions. 
  before death, it may rise to 105OF 
  or more. 
(iii) Pulse more frequent. 
Ov) Pupils dilated, not reacting to 
  light. 
 (v) Anterior fontlahella becomes flat 
3. Analgesic such as paracetamol (Calpol) 
0.5 Gthrice a day, for relief of headache. 
4. Care of bladder and bowels. 
B. Specific : 
 1. Tuberculous meningitis. Triple d-rug 
therapy till relief frcm. rreningitis ; then IWO 
700-750 mg1J00 ml 
50-80 mg/100 ml 
0-5/cu. mm 
(mostly lympho­cytes) 
Three antigenicallY distinct Influenza viruses are recognised vI types A, El and C. 
8. Symptoms disappear within a week 
9. Leucocyte count normal or low Treatment 
There is no specific treatment. Only sym­ptomatic treatment is given in the form analgesics and decongestants 
POIVValent influenza vaccine 0.2 mi. intra­dermally repeated after 10-14 days, during the epidemic. 
Clinical Picture 
1. Prodromal stage: 
(i) Moderate fever upto 101*r 
00 'Headache 
drugs in changing combination for at least Clinical Features 18 months. 
2. 
(i) Streptomycin I G (20-40 mg./kg. for 
 children) i.m. daily. 
(i 0 Isoniazid (Isonex) 300 mg, (10-20) 
 mg.lkg.for children) once daily. 
(iii) PAS 5 G. (0.1 GJkg. for children) 
 thrice a day. 
Ov) Thiacetazone 150 mg. once a day. 
Corticosterolds such as betamethasone (Celestone) may be given 1 mg. thrice a day till remission of symptoms, and then gradually tapered off. Xantinol nicotinate (Complamina) is helpful and may be given in divided doses of 37.5 mg./day. 
(i) 
Pyogenic meningitis : 
Benzylpenicillin (Crystapen) 10,000 units in 10 MI. of patients C.S.F. injected intrathecally at the start of treatment, thereafter 1-2 mega­units i.m. 4-houdy. 
00 Sulphasomidine (Elkosin) 6G orally atonce; then 2 G 4-hourly, with plenty of fluids. 
(iii) An alkaline mixture to keep the urine 
 alkaline. 
3. H. influenzae meningitis 
(i) 
Chloramphenical (Chloromycetin) 
500 mg. six hourly by month or 
500 mg. i.m. daily in divided doses 
or 
(ii) Ampicillin (Roscillin) 50) mg. six 
 hourly. 
4. Herpes simplex meningitis. 
5. lodoxyuridine in intravenous drip. 

INFLUENZA
Influenza is a self-limited viral disease characterised by constitutional symptoms and signs with respiratory tract involvement of varing severety and extent, 
Etiology 
6. Nasal discharge and cough 
7. Conjuctivae red ; photophobia 
Chickenpox or varicella is an acute, infec­tious and highly communicable disease, characterized by mild constitutional symp­toms, a short prodromal period, and a rash which passes through the stage of macule, papule, vesicle and crust. 
The disease is caused by a filtrable virus which is probably the same as that causing herpes zoster. It is usually endemic but some­times epidemics do occur. Mostly the children are affected but the disease also occurs in young adults. Infection spreads by direct contact and the fomites. The period of infec­tivity is from the day before the first symp­toms appear to six days after the appearance of rash ; crusts do not appear to be infectious. one attack confers lasting immunity ; relapses are uncommon. The incubation period is, 14-21 days, with 17 days as the average, 
1. Incubation period 1-3 days 
2. Onset sudden 
3. Fever with chills 
4. Headache 
5. Bodyache and prostration 
Prophylaxis 

CHICKEN POX
Etiology 
GO Vague body pains 
(iv) Malaise or shivering 
(v) Haematuria 
(vi) Ill-defined rashes 
Z Stage of eruption. 
Macules, appear on second day, pink­colour and of pinhead size. In a few macules get changed to papules. 
'-i) Papules, at first small but later r-,: --ase in size forming vesicles. 
j Vesicles, well rounded, without area 
dness ; thin covering readily yielding to -mate presure. 
,jv) Crushing and dropping of the scab, a, 1b slight indentation which soon aajgipears. 
Within a period of 2-4 days, the pocks ime gone through the various stages of -acule, papule, vesicle and crust. Additional crcos appear from time to time. All the stages :f the rash are present after the second day. Treatment he lesions are usually discrete but may be­wne so numerous that in some areas they 
Differential Diagnosis 
1. Smallpox 
2. Pustular dermatitis 
3. Impetigo contagiosa 
4. Infected scabies 
5. Erythema multiforme 
Complications 
1. Secondary infections of skin 
2. Encephalitis 
3. Pneumonia 
4. Pulmonary infarction 
5. Otitis media 
6. Bullous impetigo 
7. Orchitis and testicular atrophy 
Bed rest till temperature is normal and all the rashes have reached the crusting stage 
 
Table : Smallpox Vs. Chickenpox
Smallpox
Chickenpox
Incubation period 8-12 days 14-21 days
Prodromal stage :
Duration 2-4 days 0-2 days
Symptoms Severe Mild or moderate
Temperature High Moderately elevated
Eruptive stage :
Appearance 2nd-4th day 0-2nd day
Temperature About normal; Secondary rise during postulation Same level
Distribution Centrifugal Centripetal
Character Monomorphous Polymorphous
 
SMALL-POX
Smallpox or variola major is an infectious and highly communicable disease, characte­rised by marked symptoms during the prodro­mal period and the appearance of a skin erup­tion, which progress through the stages of macule, papule, vesicle, pustule, and crust, to end in pitting or scar formation. 
Etiology 
The disease is caused by a filtrable virus and frequently occurs in epidemic form. It affects all the age-groups and both sexes. The disease is more prevalent in the colder months but may be encountered in, any season, A patient is infectious from tho onset of prodromal period till all the crusis nave dropped off, particularly from the palms and soles. Transmission is direct, mainly by droplet infection. Indirect transmission may be carried on a person or in clothes. The incubation period is 8-16 days with 10 days as the average. One attack confers lasting immunity, second attack being exceeeding rare. 
Clinical Picture 
1. Prodromal stage : 
(i) Abrupt onset : duration 2-4 days. 
(ii) High temperature, 102-105'F. 
(iii) Headache. 
(iv) Severe muscular and joint pains 
(v) Nausea and vomiting, 
NO Abdominal pain, in severe cases. 
(vii) Prodromal rash, petechial or ery­ 
 thematous. 
(viii) Spleen may be palpable. 
2. Eruptive stage 
(i) Temperature drops to about nor­ 
 mal. 
00 Lesions first appear on the face, 
neck, upper chest, or hands and 
forearms; most marked on the exposed surfaces of the body and centrifugal. 
 
 2. For itching calamine lotion. Lesions snould be kept clean by permanganate wash. 
3. Antipruritic drug e.g. cyproheptadine (Periactin) 4 mg. thrice a day. 
4. Antibiotic to control secondary infec- 
tions. 
 
Fig. 8.1. Classical Smallpox 
Courtsey : About.com : Dermatology
 
(d) Pustule. Forms by the sixth day when white blood cells enter the vesicle ; umbilica­tion prominent ; larger and discrete or confluent and shotty. 
(e) Crust. Appears on 8-10th day by erosion of the centre or rupture of the pustule ; dry and drop off, last from the palms and soles ; leave permanent pock marks. 
Ov) Secondary rise of temperature 
 during pustular stage : 
(iii) Eruptions : 
(a) Macules, light red spots. 
(b) Papules, by the second day the macule becomes raised and forms apapule. 
(c) Vesicles, Papule becomes filled with clear fluid and forms a vesicle ; it is firm to touch and forms a definite blister ; shows umbilication on sections. 
 
sixth 
cells 
ilica­ 
and 
and 
Ild on th 
Pre-erupilve. Ine typical eruptions ot K do not appear, either because the :m is so mild that the eruptive stage -it occur, or to severe that the patient Am -7"~re the typical lesions become mr, ~; - -* 
r ram Severe. This form is characterized by 
 S 
  kzs ed and stormy prodromal period, by 
 becorr*:z s lesions, which may be discrete or 
id a.", Z;;_~nerc, 
 nerous that they become conf luent. Pit­ 
firm to innonly occurs followinq an attack of 
Haemorrhagic. Haemorrhagic smallpox most severe dull-blown form encoun­It is of two types. Purpura-varioiosa In the prodromal stage and is invari­al. Variola pustulosa occurs in the 
ar stage and is less fatal. The lesion& invaded by red cells as well as by es. 
Alastrim. This form is considerably than the classical smallpox. It is doubt- 
edwther the same strains of virus produce severe and alastrim types of smallpox. 
from the variola major produces pocks 
:the chick chorio-al lantois in eggs incubat­at 25-38'C whereas virus from the alastrim 11ces not. The prodromal symptoms are gene­less severe and of shorter duration than 
e of severe smallpox. The lesions are less =xnerous and more differ6nt' from those of :--"ckenpox. Pock marks are common and, udwn present, are shallow. 
. Varioloid. It is a modified form of lpox occurring in persons who are par- 
fially immune to smallpox, as a result of I-revious vaccination. In general, the disease is milder than severe smallpox and may be as alastrim. 
 1. Microscopic examination .*of the smears. Material from maculopapular lesions, vesicles, or pustules may be obtained by needle, placed on clean slides,' stained by Giemsa method, and examined for , elementary bodies. 
2. Complement fixation reaction. Fluid from lesions or crusts is tested against hyper­immune rabbit serum by utilizing the heat stable antigen. 
3. Paul Test. The cornea of a rabbit is scarified by sharp needle which has been pas­sed through'small amount of material obtain­ed from suspected lesions. If the infection is smallpox, minute vesicles appear within 24-48 hours, and from them the virus may be reco­vered. The test is not always positive in alastrim. 
4. Isolation and identification of the virus. Virus from cutaneous lesions may be propaga­ted on the chorioallantoic membrane of the chick embryo. 
Treatment 
1 - Tepid sponging of the skin, with bich­loride of mercury 0 1,000) or postassium Permanganate (1 : 10,000). 
2. Severe itching controlled by the apoli­cation of magnesium sulphate solution. 
3. For headache, and other pains, parace­tdmof (Aspap) 0.5 G thrice a day. 
4. For vomiting and dehydration, normal saline and hypertoniiz~ilucose solution. ' 
5. For suppurative complication, procaine penicillin G, 0 6 megaunit intramuscularly once a day. 
6. Liberal diet, plenty of fluids, and good nursing care. 

MEASLES
Measles or roseola is an acute, infectious, and highly communicable disease characteri­zed by prodromal catarrhal symptoms, Koplik's spots, and a typical rash. 
Complications 
1. Furunculosis. 
2. Abscess. 
3. Cellulitis. 
4. Gangrene. 
5. Pneumonia 
6. Laryngitis. 
7. Pleurisy. 
B. Empyema. 
9. Otitis media. 
Diagnosis 
 day 
  or 
 dry 
 the 
,leave 
r ure 
Etiology 
The disease is caused by a filterable virus and may occur in sporadic, cndemic, or epide­mic forms. All ages are susceptible, young 280 UMCINS 
children being particularly more prone. Both !he sexes are equally affected. A patient is infectious from 1-2 days before the first symptom to 5-6 days after the appearance of rash. The transmission is direct, by means of dioplat infections. Articles freshly contaminated by discharges from the nose and throat of an Ifected person may also be infections. The 
 cubation period varies between 8-12 days, with an average of 10 days. 
Clinical Picture 
 Illness of infection. A few hours after exposure to infection, the patient may develop symptoms of measles and even a transient fleeting rash. This illness disappears in a day or so and symptoms then develop after the incubation period. 
Prodromal stage : 
(1) Onset sudden ; duration 2-4 days. Diagnosis 
(I I) Temperature 100-104' F. 
(iii) Coryza and sneezing. 
(iv) Conjunctivitis and photophobia. 
(v) Laryngitis. 
NO Prodromal rash. 
coiour, until by the fifth or sixth day of the rash, a brownish discoloration has replaced bright pink and red noted at the onset. Fading and pigmentation of the lesions occur 7-14 days after the appearance of rash. 
Complications 
1. Otitis media 2. Mastoiditis 
3. Pneumonia 
4. Appendicitis 5. 6. 

Brcnchitis Cervical lymphadenitis 7. Catarrhal laryngitis 8. Encephalitis 9. 
Encephalomyelitis 
 1 - Examination of nasal secretion fo epithelial giant cells. 
2. Complement fixation reaction. 
Differential diagnosis 
(a) On second or third day, generaliz- 1. Rubella  ed erythematous rash which fades 
 away quickly. 
b) On third and fourth day, macular eruptions of the mucous memb rane ; and on the buccal mucous 
 membranes, Koplik's spots, bluish white spots surrounded by a red aroela, giving a granular, rough 
 appearance. 
(i) Prodromal symptoms milder and brief. 
00 Rash more macular. 
(iii) Lesions smaller than those of measles. 
(iv) Desquamation uncommon. 
2. Typhoid: 
Eruptive stage 
 Skin rash, first noted about the face and neck, behind the ears, on the forehead, and later on the chest. Thereafter it spreads to the remaining portions of the body, progressing from above downward to include upper and lower extremities and trunk. The rash is Treatment of a light pink colour and is first macular, the individual lesions become pinhead in size. The spots increase in size and number, and become maculopapular. In some areas they remain discrete, but in others they coalesce and become progressively deeper red in 
Rose spots localized to trunk and usually few in number. 
Serum sickness. 
4. Drug rash. 
 1. Bed rest till 2-3 days after thetemperature is normal. 
 2. Tepid sponging of the skin with potassium permanganate (11 : 10,000) solution. 
 7s should be bathed with warm 
  -don 2-3 times daily and vaseline 
mr -~-ie ~:ids : sulphacetamide (Locula) 10 
Etiology 
 The virus is present in the saliva and spreads by droplets. It has a predilection for certain gland tissues. The common site of infection is one or both parotid glands, but sometimes there is involvement of the submandibular or sublingual salivary glands, the testicle, the pancreas or ovary, alone or in combination. 
(Rubella) 
 -0, tive Agent. Rubella virus. 
 roubat~on Period. 14-21 days (average 
    By droplet infection. 
 ~arturi&s 
  Mild constitutional symptoms 
  Nasal catarrh 
  Conjunctivitis days. 
  Stiffness in the neck; tender and eniar ;csierior cervical lymph glands. Symptoms  Rash appears on second day. In child  disease is mild and rash may be the indication. Pink macules appear" first 
  the ears and on the forehead, spread 
Predisposing causes 
1. Age and 18-25 years 
2. Sex Males predominate 
3. Season : Winter and spring. 
 4. Absence of previous attack ; second attack rare 
5. Overcrowding. 
,iiiii--ky !o the trunk and the limbs. 
1L Generalised lymphandenopathy at 
Illness disappears in 2-3 days. 
I ications 
Tihe disease during first trimester of pregproduces malformations in the foetus. 
I- I 
 No treatment is usually needed except in pregnant women (first trimester) who should be administered 750 mg human gammaglo- - in. 

MUMPS
 Mumpsorepidemic parotitis isanacuteinfectious disease characterized byenlargementof the salivaryglands, usuallytheparotid. 
Clinical Picture 
Incubation period. 12-23 days, usually 18 
 
Headache Malaise Sore throat Epistaxis Stiff neck Pain and Swelling in parotid region. Inability to open the jaw. Increased salivation. 
Signs 
 1. Fullness behind the angle of the jaw, spreading forward over the masseter and down into the neck ; parotid rapidly . becomes enlarged. 
 2. Tonic spasm of the muscles of mastication (trismus). 
 3. 01rifice of Stensons' duct usually swollen. 
4. Lacrimal glands rarely enlarged. 
5. Spleen often just palpable. 
 
 6. Temperature I 01'F or over; usually When the environment is unfavourable for 
gets normal in 3-4 davs. growth of the organism, spores are formed 
Pulse usually slow, 50-60 per minute. 
Complications 
1 . Orchitis : rare before puberty 2. Oophoritis 3. Myocarditis 4. 5. 6. 7. 8. 9. nerves 
Acute pancreatitis 
Mastitis 
Otitis media 
Labyrinthitis 
Peripheral neuritis 
Neuritis of 11, VII, VIII and III cranial 
10. 
11. Meningism. 
12. Meningitis. 
Meningo-encephalitis 
Treatment 
I . Bed rest for 10 days 
2. Fluid diet till mastication is painless 
3. Antiseptic mouth washes 
4. Fomentations 
 5. Stilboestrol 1 mg 4 times a day to prevent orchitis. 

TETANUS
 Tetanus is infectious disease affecting the motor nervous system and complicating the wounds. 
Etiology 
 The disease is caused by a spore forming organism, Clostridium tetani which is a commensal in the intestines of man and cattle. The organism finds its entrance through a contaminated wound. The wound may be very trivial or a deep penetrating one. The organism remains localised at the wound and produces an exotoxin which has affinity for the motor nerve endings and motor centres. When the exotoxin affects the motor nerve endings it produces local tetanus. When it reaches anterior horn cells of the spinal cord through blood stream it produces generalized tetanus. 
which may remain dormant for years. 
The portal of entry may be : 
 1. Through the umbilical cord-Tetanus neonatorum. 
2. Trauma : 
0) Abrasions 
(i i) Lacerations (iii) Incisional 
Ov) Penetrating 
(v) Compound. fracture 
(Vi) Post-operative. 
3, Otitis media 
Clinical Picture 
 The incubation period may be as low ai, six days or as high as several years. 
 1. Trismus. Painless spasm of masseter muscle causing lockjaw. 
 2. Risus sardonicus. Contraction of frontalis and muscles at angles of the mouth. 
 3. Rigidity of muscles of the neck and trunk : neck arched. 
 4. Board like rigidity of abdominal muscles with little tenderness. 
 5. Sudden violent spasms lasting 1-4. minutes inducled by minimal stimuli. 
 6. Local tetanus. Spasm of the muscles near the wound. 
Prognosis 
 1. The wound. The prognosis is good in cases of unnoticed minor wounds and bad in cases of infected deep wounds. Mortality is highest in tetanus neonatorum and least in tetanus associated with otitis media. 
 2. Incubation period. Longer incubation period indicates better prognosis. 
 3. Age. Children (upto 10 years) and old persons (beyond 50 years) are more vulnerable to death. Mortality is least in the age group of 11-20 years. 
pdriDd. The lockjaw-spasim periodlion -1 between the development oflmgiiemw 1 generalised spasm. Prognosis is Me 11iftrval is lesser than 48 hours and_=17 . . - of n the duration. L-S period  hours carries good prognosis.10611111~-re of spasm. Absence of spasm indicate good prognosis zpasmst are severe and 
rrt 
JWnd toilet. body 
~A_T.S.- 1500 units Per kilogram 
§trtFbiotics. Inj. crystalline Penicillin ur~t3 per kilogram bod y weight. In sensitive patients, injection oxymg. per kilogram body weight uscular route. Sedatives and muscle relaxants 
) At 3 P.M., 9 P.M., 3 A.M., and 9 
a W r 
IV 
(a) Inj. promethazine (Phenergan) 
 1 mg*g body weight i.m. 
(b) Ini. diazepam (CaImpose) 0.2  mg/kg body weight i.m. 
(ii) At 6 P.M., 12 midnight, 6 A.M. and own. 
(a) Ini. chlorpromazine (Largactil)  2 mg/kg body weight i.m. 
(b) Inj. trifluperazine (Eskazine) 0.2  mglkg weight i. M. 
(c) Inj. methocarbamol 10 mg/kg  body weight i.m. 
 (iii) In case severe spasm persist despite 3Dove medication, Inj. paraldehyde 5-10 ml i m, 4-hourly should be added till the spasm me controlled. 
 Before the administration of every dose of sedatives the patient should be carefully examined and the c~ose avoided if there are any signs of card io - respiratory failure. 
 5. Nutrition. It should be maintained by intravenous route till spasms persist and thereafter by Ryle's tube. 
6. Care of bladder, bowel and back. 
 7. Low molecular weight dextran (Lomodex) 500 mg daily intravenously at the rate of 50 drops per minute for 3 consecutive days. 
Prophylaxis 
 Young children are routinely protected against tetanus along with diphtheria and pertussis through common triple antigen. Three 
doses at monthly intervals should be given during 3rd, 4th , and 5th month followed by booster dose at the age of I j' and 3 years. Now for older children duel antigen for prophylaxes against tetanus and diphtheria is also available. For active immunity against tetanus only, tetanus toxoid may be administered before possible exposure. Passive immunisation with A.T.S. should be avoided as the balance between protection and hazards is unfavourable. In case the ampoules have been properly transported and stored, 1500 units A.T.S. may be given i.m. after sensitivity test. 

BRUCELLOSIS
(Undulant Fever, Malta Fever, Abortus 
 Fever) 
Causative organism. Brucella sP. 
Modes of Infection 
1. Infected milk. 
 2 Direct contact with infected animal. Incubation Period. Three weeks.. 
Clinical Features 
1. On-set gradual 
2. Sweating 
3. Weakness 
4. Headache 
5. Anorexia 
6, Pain in limbs, back and joints. 
 Constipation. 
7. 
8. Rigors. 
9. Cough and sore throat. 10. `11. 
Fever, intermittent or continuous. Spleen often palpable. 
284 mmicna 
'~_ 1 
 r 
I I I 
0 - 1i 
12. Occasional rash of variable type. 
 13. Neutropenia and lymphocytosis in ,severe cases. 
Complications 
1. Depression and irritability. 
2. Subacute arthritis. 
 3. Osteomyelitis of vertebra or paravertebral abscess. 
Diagnosis 
8. Blood culture, 
 2. Agglutination tests. Treatment 
 Antibiotic e.g. tetracycline 250 mg., orally every six hours. 

ACUTE POLIOMYELITIS
Acute poliomyelitis is an acute disease characterized by lesions having a special affinity of the gray matter of the anterior horns of the spinal cord and for the motor nuclei of the brain system. 
Etiology 
The disease is caused by a virus, of which there are three types - Brunhilde, Lansing and Leon. Infection is mainly transmitted from healthy carriers or in epidemic, from infected contacts, by droplet infection when it enters the body through the nasopharynx. It is also spread by food, water and milk through the gastointestinal tract. Cases occur sporadically throughout the year with epidemic in the late summer. The severity of the epidemics varies greatly. 
Predisposing causes 
1. Age. Chiefly 4-10 years. 
2. Sex. Males predominate slightly. 
3. Tonsillectomy. 
Clinical picture 
Incubation period. 7-30 days, usually 12 days. 
A. Minorillness 
 (i) Fever 
00 Headache 

 (iii) Vomiting 
 Ov) Sore throat 
B. Pre-paralytic stage 
(i) Headache 
0 i) Malaise 
(iii) Pains in the neck, back and limbs 
Ov) Nausea and vomiting 
 (v) Diarrhoea 
 (vi) Convulsions 
(vii) Temperature about 103' F 
(viii) Sometimes diplopia 
 (ix) Neck rigidity 
(x) Small involuntary movements in the 
 fingers and hands. 
Paralytic Stage : 
1. Spinal type (most usual) 
(i) Flaccid paralysis of muscles, more  often of legs than of the arms ; 
(ii) Deep reflexes generally sluggish or  lost ; 
(iii) Abdominal reflexes abolished 
(iv) Sensation normal 
(v) Muscles unduly tender on pressure  or on joint movement ; 
(vi) Spasm in the back of the neck, the  erector and hamstring muscles 
(vii) Maculopapular eruptions on the affected limb ; 
(viii) Bowels usually constimted. 
2. Brain stem type : 
(i) VII, VI and III cranial nerves most commonly affected 
(ii) Bulbar lesions 
 (a) Dysphagia 
 (b) Dysarthria 
 (c) Dysphonia 
 (d) Dyspnoea 
(e) Cardiac irregularities 
2. Progressive muscular atrophy. 
3. Relapse. 
kd ; 
k pressure 
k, the I the 
Oes most 

Severe pains in the arms or legs 
Dee-o reflexes diminished, 
35. Paralytic Polio of both lower limbs -Note the characteristic position. 
Cwebellar type Headache Vertigo Vomiting on moving the head Dysarthria (v) Ataxia of spinal muscles (vi) Nystagmus S_ Cerebrall type : (i) Generalized convulsions (ii) Spastic paraplegia ; 
(iii) Extensor plentar response (iv) Mental deterioration ; (v) Athetotic or cnoreic movements. Complications 
 1. Contractures and deformities e.g. swflosis 
Treatment 
1. Bed rest. Bed rest should be advised even in the mildest case as it is likely to prevent the onset of the paralytic stage. The patient should be isolated for three weeks after the temperature has become normal or for six weeks from the clinical onset of the disease. The limbs must be placed in such a position that the affected muscles are relaxed and the position maintained by pillow, sandbags, or celluloid splints. 
2. In cases with excessive sweating, plenty of fluids by mouth and sodium chloride 0.5-1.0 G thrice a day. 
3. If respiratory muscles are affected, artificial respiration in a respirator. 
4. Sedative such as phenobarbitone (Luminal) 30 mg. thrice a day. 
5 Analgesic such as paracetamol (Crocin)) 0.5 G thrice a day. 
6. Peripheral vasodilator such as tolazoline hydrochloride (Priscol) 25-50 Mg. four times a day. 
7. Orthopaedic treatment for contractures and deformities. 

INFECTIOUS MONONUCLEOSIS
(Glandular Fever) 
 Causitive organism. Uncertain but presumably a virus 
 Mode of Transmission. Not known 
Common Age. Children and young adults 
Incubation Period. 5-10 days. 
Clinical Features 
1. Tiredness and malaise 
2. Headache and general bodyache 
3 Pyrexia 
4. Enlarged superficial glands 
5. Sore throat with or without exudate 
6. Maculopen"lar rash appears within 10 days In adults. 
286 1 unaINX 
7. Spleen slightly enlarged, soft and 
tender. 
Diagnosis (iii) Tingling Paresthesia with dull or 
stabbi ng pain at the site Of bite radiating to other Parts Of the 
LeucOcyte count 10,000-30 000/cu. body. ' 
IM. but May be normal or low. I  Phase Of excitation DYsphagia precl' 
 2,  Pita3te. d by a ttemPts to swa * 
 "Ononuclears vi,,. lymphocytes, mono- Phobia)  flow fluids (hydro- 
c1tes and atypical Ytes cons 
'60-80% of total leuclYmphoc  titute 
Ocyte count. 4 Te 
 3. Paui-13unnel test. 
Treatment 
 Rest in bed with symptomatic treatment. 
 
RABIES 
 Rabies is a viral disease manifesting itsel as an acute encePhalomyeli nearly always fatal, transmitted through ttis'animals. he saliva of rabid 
Etiology 
The disease is, caused by rabies virus which is identified on presence of i POst-mortem as the inclusion bodies called negri bodies. The animal hosts wiry from country to country, the dog being the common one. this country the knot~n animal hosts are rOps, jackals, wild cats and mangoose. These animals secrete rabies virus in the saliwhen these  va OnIare clinically rabid. Durin Yincubation period, the animals are not * 9 Etiology 
fective. The clinical in course of rabies in animals is very short leading to death within ten days. The infection is through animal bites. Aerial infection from rabid bats is known to occur but in India bat - 
animal host of rabies.  is not an 
Clinical Picture 
This is divided in four Phases. 
 1. Incubation PeriOd The usual incubation period is 2-13 weeks. However it is known between 8 days and two years. Patients with multiple bites in the upper Parts of the body have S h O,teF incubation Period. 
2. PrOo'romal symptofns 
0) Fever 38-390C V 
malaise,  vith headache, 
 nausea and vomiting. 
00 Sore throat and Persistent cough, 
rminalPhas, 
G) Generalized flaccid Paralysis. 
 Muscle spasms and Pharyngeal 
 spasms cease. 
 Depres - 
Sion, ap?thY, hYPOreflexia 
Prognosis and coma leading to death. 
 The disease is invariably fatal Only one Survival has been confirmed so fa'r. 
Treatment 
 With no hope for survival the 
tic treatment is usually symPtoma- 
given'on :humanitarian 
ground or for academic interest. 
 
MALARIA 
Malaria is an acute and chronic infection characterized by fever, anaemia, splenomegalY and often serious or fatal complications and caused by the Protozoa of the genus Plasmodium. 
Four species Of genus Plamodium are pathogenic for man - P. vivax (benign Malaria), P. falciparum tertian malaria), P. malariae (qu (Malignan tertian ovate (Ovate malaria). Th artan matatria). p. Parasite consist  e life cycle Of the Phaso s Of an exogenouse,ual  (SPorogony) with Mu' female anoPheline ItiPlication in genous Phase mosquito, and an endotion in man. (schizOgony~ with The cted in the 
chart. life cycle is depi MultiPlica 
Clinical Picture 
Incubation Period  7-10 days (falciparum malaria). 10-14 days (other type.) 
Onset: 
(i) Lassitude 
(ii) Anorexia 
(iii) Headache 
(iv) Chillness. 
Classical bouts of fever appear at regular intervals. Each attack comprises three stages :- 
1. Cold stage. It lasts about half an hour. The patient feels intense cold and shivers from head to foot; his teeth chatter and he covers himself under blankets. He has severe headache and often troublesome vomiting. The temperature goes on rising. 
2. Hot stage. It lasts 1-6 hours. The patient feels burning hot and may be delirious. Vomiting often continues to this stage. The face is flushed, and the skin dry and burning. The temperature rises to 39-41oC. 
 3. Sweating stage. Profuse perspiration starts. The temperature drops and the patient becomes comfortable and falls asleep. Usually the spleen and, especially in children, the liver become palpable and tender. Herpes simplex usually around the mouth, is a common acompaniment. 
While the above description usually conforms to all the types of malaria, the distinguishing features are given below :- 
 1. Benign tertian malaria. (P. vivax). There is spontaneous remission and a greater tendency to relapse. 
 2. Quartanmalaria. (P. malariae). The attacks are"of short duration and occur every fourth day. Nephritis is common complication. 
 3. Malignant tertian malaria. The fever is rather remittent and the tertian periodicity of the infection is indicated by exacerbation of a continuous fever. Prostration is more marked and the tendency to delirium greater. Falciparum malaria is notorious for its tendency to produce, suddenly and without warning, severe and dangerous type of the disease to which the term, pernicious malaria is applied. This may be rapidly fatal if not promptly recognized and adequately treated. Several clinical types are known. 
(i) Bilious remittent fever. The onset is characterized by marked nausea and profuse continuous vomiting, Jaundice appears about the second day ; the urine frequently contains bile 
Fig 8.2 Life cycle of a malarial parasite
Table : Chemotherapy of Malaria
Drug
Features
Dosage*
Side Effects
Chloroquine (Resochin) Active against erythrocytic forms; less effective against P. malariae  1.0 G followed by 0.5 G hours later; 0.5 G daily for 3, more days Headache; Visual disturbances; Pruritus; Anorexia; Nausea; Psychic stimulation
Amodiaquine (Camoquin) (Similar to chloroquine) 0.6 G first day; 0.4 G daily for 3 more days Insomnia; Epigastric discomfort; Anorexia; Pigmentation of skin and  nail beds 
Quinine Less effective in quartan  
malaria 
0.6 G thrice a day - for a week  Abortion; mental depression; Tinnitus; Deafness; Amblyopia; Hypertension 
Pyrimethamine (Daraprim) Especially active in benign tertian malaria 25 mg. daily for a week Megaloblastic anaemia;  Leucopenia 
Mepacrine Active against erythrocytic forms  0.1 G daily for a week Epigastric pain; nausea; vomiting; diarrhoea; dermatitis
Proguanil (Paludrine) Inhibits chiomatin division in schizont; also inhibits development of macrogamete in the mosquito; slow in action  0.1 G daily for 10 days  Nausea; anorexia; diarrhoea; haematuria
Primaquin Not effective in active phase 15 mg daily for 14 days  Abortion 
 *In indigenous population, during the epidemic, single dose of 1.00 chloroquine or 0.6 G amodiaquine is sufficient. 
Pigment. Epigastric distress and liver tenderness are marked. Haemorrhage from stomach may occur producing I# coffee ground" vomitus, dehydration and disturbance of the alkali reserve and of mineral balance may develop rapidly. 
(111) Cerebral malaria. The onset may be  sudden or gradual and the clinical  picture may be varied. There may be  progressively increasing headache  with little or no fever and then  gradually lapse to coma. In some  cases there is Sur! , den rise or tem  perature to above 1080F. In addition  to hyperpyrexis, convulsive seizure  are common. Involvement of the  cranial nerves may 15e evident. Ocessionally the onset may be sudden and characterized by mania or other acute psychotic manifestations. The initial stages may at times be mistaken for acute alcoholism. 
(iii) Algid malaria. Profound prostration, with a tendency to fatal syncope, marked coldness of the skin, subnormal temperature and circulatory collapse characterize this form. Jaundice and anaemia are frequently present. 
(iv) Gastric malaria. Characterized by 
 persistent vomiting. 
(v) Dysenteric malaria. Bloody diarrhoea due to excessive capillary thrombosis in the inte,.;tinal walls. 
 
 

I_ A 
[Yfects 
IsualdlAturritus ; AnoI 
a Ps~"chic 
gastric disexia ; pig. *In and 
L~a ' depresDeafness; erte nsion 
anaemia 
'I 

nausea 
hoea der- 
 diarra 
be sudden 
We or other 
tions. The 
ms be mis- 
,rostration, 
rsvncope' in, subulatory form. uently 
d by 
Oiarrhoea wombosis 
Oquine or 
Diagnosis 
 d films. Thick films are more help 
- thin films since rhe latter may not 
.,y parasites. However, it is necesexamine the stained thin filmsfor, 
Sternal Puncture 
11 not be found in the thin blood films. 
-6. General. 1. Bed rest with abundant 
Analgesics e.g. paracetamol (Calpol) thrice a day. 
When dehydration is marked, intraveinfusion of saline and glucose may be 
Chemotherapy. The dose and dura- 
of chemotherapy depends upon the nce of the disease in a particular area. description hereunder conforms to this try and others where the disease spreads 
emic or epidemic forms. The dose and on of chemotherapy in isolated cases is ed in the chaft. 
Suppressive Cure 
 Chloroquine phosphate (Resochin) ;A G to be taken as single dose or 
(ii) Amodiaquin (Camoquin) 0.6 G to be en as Eingle dose. 
megaly and often hepatomegaly, emaciation, anaemia, leukopenia, and hyperglobulinu.ria. 
Etiology 
 The disease is caused by Leishmania donovani. Transmission is mainly through a sandfly, in this country, Phlebotomus argentioes. Direct transmission is possible by personal contact via nasal secretion. L.D. bodies are found in nasal mucus, urine and faeces. Rarely transmission occurs through 
ecies 
)f the 
cytes 
th re- placenta. 
ara- 
 When medication cannot be administered 4wally, chloroquine phosphate may be given witramuscularly in the maximum dose of 5 wig kg of actual body weight. Intravenous acministratior, should be avoided because of  the risk of convulsions or cardio-vascular collapse. Oral therapy should be given as soon as possible. The suppressive cure results generally in 36-48 hours. The two drugs can safely be given in pregnancy in therapeutic doses. 
by Leishmania donovani,. ind characterized by ~Pdies. 
irregular prolonged fpver, chronicity, spleno- 3 P~ecipitation tests with serum positive. 
Clinical Picture 
The incubation period is usually 2-4 months ; rarely it may be as short as 10 days. The onset may be sudden or gradual. In some instances it is acute, accompanied by chills, high fever and vomiting. In others it manifests as general malaise with fever which reaches 103-104'F in about a week. In still others it is insidious and unaccompanied by any febrile reaction. 
 The patient is wasted. The spleen is enlarged and the liver may be palpable. The temperature is irregularly raised and may present 2-3 summits in 24 hours. The pulse is proportionately frequent. As the disease advances characteristic grayish colour of the skin develops. The pigmentation is most noticeable on the hands, the nails, the forehead and the central line of the abdomen. 
Laboratory Findings 
 1. Blood examination 
  0) R.B.C. count 2.5-4 million per cu. 
  mm. 
  (i i) Haemoglobin : 4-10 G per 100 
  MI. 
  (iii) Total leucocyte count : 500-3,000 
  per cu. mm. 
  (iv) ffE rc rl iF I leucccyte count 
  (E ) Eosinophils reduced; 
  (b) Lymphocytes and monocytes 
  relatively increased. 
  (v) Serum bilirubin raised ; Van den 
  Bergh reaction biphasic. 
  (vi) Blood culture on N.N.N. media. 
 KALA-AZAR 2. Smear examination from sternal, 
Kala-azar is a protozoal disease produced splenic and lymph node puncture shows L.D. 
'4% ViDi6NE 
Treatment 
1. Blood transfusion, if severe anaemia. 
 2. Pentavalent antimony preparation such as Pentostam 0.8 G 4v. daily for 14 days. 

INTESTINAL AMOEBIASIS
Treatment 
 1. Emetine 60 mg daily subcutaneously for 3-6 days followed by diloxanide furoate (Furamide) 0.5 G thrice a day orally for 10 days. 
 2. Chloroquine (Resochin) 4 tablets daily for 2 days followed by 2 tablets daily for 14-21 days, 
 Intestinal amoebiasis or amoebic dysentery 
is a subacute or chronic afebrile condition, 
characterised by diarrhoea and tenesmus, 3. Tinidazole (Fabizol) 1 g. twice a day 
which may be symptomless for months or for three days, 
even years. 
Etiology 
 The disease is caused by a protozoon, Entamoeba histolytica which is found in two phases. The motile vegetative phase is called trophozite and the resting phase, the cyst. The cysts are passed through stools ; the tranmissibn is through contamination of water and food. Maximum inidence is in 21-30 years of age. 
Symptoms 
2. 
3. 
4. 
6. 
7. 
8. 
Signs 
2. 
3. 
4. 

BACILLARY DYSENTERY
Etiolcgy 
 Bacillary dysentery is caused by local infection of the large intestine by the bacilli of the genus Shigella. Three main pathogenic forms are described ; S. shigae, S, aexneri and S. sonnei. The shigellae are gram negative bacilli. non-sporing, non-motile and are easy to grow on ordinary culture media. 
Pathology 
 There is a generalised inflammation of the large bowel, which sometimes involves the lower part of the small intestine. The mucosa is red and swollen with a layer of mucopus ; there are patchy haemorrhagic areas. Ulcers may form and the adjacent lymph nodes are enlarged. 
Diarrhoea -Continuous or intermittent 
Pain in abdomen Flatulence Blood and mucus in stools 
Tenesmus Hyperactive gastro-colic reflex Incomplete evacuation Anorexia occasionally fever and nausea 
Aneemia Glossitis Palpable colon Hepato-splenomegaly. 
Investigations 
k, 
cope.. 
1. Stool examination 
2. Sigmoidoscopy 
3. Mucosal biopsy through sigmoldos- 
Symptoms 
I. Diarrhoea wit~ small stools. 
2. Colicky pain. 
3. Tenesmus 
4. Blood in the stools. 
5. Fever with prostration. 
6. Headache and muscular aching. 
S','gns 
 1. Signs of dehydration e.g. dry tongue, inelastic skin, sunken eyes, etc. 
 2. Tenderness over the whole colon, elicited more easily over the sigmoid part in the left iliac fossa. 
Complications 
I., Intestinal haemorrhage ; 
Man 
ide fur."I 
r oLlo 
ally f 
blets daily daily for 
ia day 
ce 
local inba 
) cilli* 
hoger* Specific chemotherapy 
aexneri rn negaand are ia. 
Fknfoiration rOw"tonitis ; Rec!al prolapse 
Ar'britis. 
it 
3ed rest to prevent embarassment and of infection. Semifluid low roughage diet. Plenty of fluids orally ; if dehydration 
 . 5 per cent glucose in normal saline be given intravenously, 
Potassium citrate 4 G thrice a day. 
n Of the ves the I 
nmucosa opus ulcers 
S are 
~Ongue, 
I colon, 
~art in 
I V 
absent. 
 9. Voice weak, high-pitched, almost inaudible. 
10. Tachycardia and tachypnoea. 
11. Bodytemperature subnormal. 
12. Hypotension. 
13. Heart sounds faint ; bowel sounds 
Investigation 
1. Blood examination 
 0) PCV elevated 

 (i i) Specific gravity high 
 (iii) Plasma protein raised 
 Ov) Plasma bicarbonate reduced 
 (v) Arterial pH lowered 
 (v i) Plasma sodium normal 
(vii) Plasma chloride slightly increased 
(viii) Plasma potassium moderately 

CHOLERA
1. Vibrio cholerae. 
2. Vibrio eltor. 
Mode of infection. Through water and 
Incubation period. ?-48 hours. 
Clinical Features 
 1. Onset abrupt with painless, watery diarrhoea. 
 2. Effortless vomiting producing ricewatery material. 
 3. Severe muscle cramps in gbstrocnemius musc!es. 
4. Prostration. 
5, Cyanosis. 
6. Peripheral pulses not palpable. 
7. Pinched facies. 
8. Scaphoid abdomen. 
elevated. 
2. Stool and vomit culture. 
 3. Flourescent antiboby technique. Treatment 
 1. Fluid and electrolyte replenishment. 0) Normal saline and sodium lactate are infused in the ratio of 2 : 1, initially rapidly till radial pulse is normal, then speed of infusion regulated to maintain normal pulse. 
 (ii) Potassium 15-20 m. Eq. for each litre of stool passed. 
 2. In uncontrolled cases, antibiotics e.g. ampicillin 500 mg. every six hours. 
Vaccination 
Cholera vaccine 0.4-1.0 ml i.m. 

PLAGUE
Causative organism. Pasteurella pestis. 
 Modp of Infection. From rats and mice; primarily it is a disease of rodents. Infection is by rat fleas which carry and convey the bacilli through inhalation. 
 Rarely, transmission is through abraded skin of feet as in cowdung-floored houses or - I I I 1 11 
through laboratory handling of infected animals. 
Incubation Period. 2-4 days. 
Clinical Features A. Bubonic plague 
 1. Onset abrupt with chills and rapidly rising temperature ; occasionally onset insidious with malaise and headache. 
2. Tachycardia and tachypnoea. 
3. Mental dullness followed by anxiety 
D. Primary septicaemic plague 
 1. Rapidly developing cerebral symptoms progressing to coma. 
 2. Death within 3 days, before demonstrable enlargement of lymph nodes. 
Investigations A. Demonstration of baclli in 
or excitem"t. 
4. Eyes and face congested. 
5. Tongue coated. 
6. Nausea and vomiting. 
7. Constipation. 
8. Oliguria with moderate albuminuria. 
 Convulsions common in children. 
 '10. Localised pain in inguinal, axillary or cervical region followed by appearance of hard and tender bubo upto the size of an egg, 
 11. In fatal cases, bubo remains indurated; in others it softens owing to suppuration. Death may occur within 5 days. 
 '12. Leuce-,yte count upto 40,000 per cu. mm. with increased polymorphonuclears. 
13. Blood culture positive in 45% cases. 
B. Peslds,minor 
1. Bubo in the groin, less commonly in 
axilla or neck. 
2. Little or no fever or toxaemia. 
 3. Bubo may suopurate or be gradually absorbed. 
C. Primary pneumonic plague 
 1. Onset usually abrupt with rapidly rising fever, 
2. Painless cough and dyspnoea. 
 3. Sputum at first mucoid, becoming blood tinged but not tenacious; finally thin and bright red. 
4. High leucocytosis, 
1. Bubo aspirate in bubonic plague. 
 2. Blood and spulum in septicaemic and pn6umonic plague. 
B. Culture and animal inoculation tests give too delayed results to be of -any clinical use. 
Treatment 
 1. Streptomycin 0.5 g.m, every 3-4 hours till temperature is normal, then twice a day till a total dose of 15 g. 
 2. Oxytetracycline ('rerramycin) 250 mg i.m. every four hours in addition to streptomycin in severe cases. 
3. Hot wet application to the bubo. 
4. Incision only on suppuration. 
DENGUE FEVER 
Causative oganiSm. Dengue virus. 
 Transmitted by Culex mosquito, Aedes aegypti. 
Incubation period. 5-8 days. 
Clinical features 
 1. Prodromal symptoms viz. headache, backache, fatigue, stiffness, anorexia, chilliness, malaise and occasional rash, 6-12 hours before fever in half the cases. 
 2. In other half, onset sudden with sharp rise in temperature, persisting for 5-6 days and terminating by crisis. 
 3. Headache, and pain behind the eyes bachache and pain in muscles and joints stiffness in neck. 
4. Anorexia and constipation, 
 5. Epigastric discomfort with colicky pain and tenderness. 
symptoms 
de 
ue. 
iC and 
 Ive u9s el. 
3-4 hours ce a day 
250 mg strep- 

S. 
Aedes 
eadache, 
1, chilli 
12 hours 
rsharp 6 days 
0 eyes, Joints ; 
Pain 
  lopapular rash on 3-5th day, lasts 
 first seen on chest, trunk and abdo 
 spreads to extremities and face, To 
 and of fever small petechiae appear 
  of feet, legs, in the axillae, 
hands, fingers, buccal mucosa and 
Weakness and dizziness. Photophobia. Drenching sweats. Sore throat and cough Epistaxis. Dysuria. Hyperesthesia of skin. Pain in groin and testicles. Delirium. 
Lymph node enlargement. t1gations; Blood counts initially normal, later nia with diminished neutrophils. Serological tests (i) Haemaggiutrnation inhibition 00 Complement fixation (iii) Neutralization of toxin. 
These tests are carried out against all the types of dengue virus. 
Clinical Features 
 1. Onset abrupt with fever with chills, nausea and weakness. 
 2. Bite site inflamed, oedematous or ulcerating ; draining lymph nodes enlarged. 
3. Superficial lymphadenitis. 
 4. Fever rises to 104*F by 2nd or 3rd day ; rapidly returns to normal after 2-4 days. 
5. Joint pains and arthritis. 
6. Conjunctival photophobia. 
7. Endocarditis may supervene. 
 8. Relapses are frequent simulating relapsing fever. 
Investigations 
 1. Moderate polymorphonuclear leucocytosis. 
 2. Culture of blood, synovial fluid, wound serum. 
3. Animal inoculation. 
 4. Agglutination tests. Treatment 
 Procaine penicillin 3 lac units i.m. twice a day or oxytetracycline 0'25 g. six hourly. 

HELMINTHIC INFECTIONS
Classification 

RAT-BITE FEVER
Causative organisms 
 1. Spirillum minus. 
 2. Streptobacillus moniliformis. 
Modes of Infection 
r  1. Through bite of infected rats. 
  2. Wound contamination with rat excreta. 
 Incubation Period 5-21 days. 
1. Phyllum Platyhelminthes 
 A. Class Cestoda (Cestodes) 
  1. Dibothriocephalus latus 
  2. Taenia saginata 
  3. Taenia solium 
  4. Taenia echinococcus 
5. Hymenolepsis nana. 
B. Class Tematoda (Trematodes) 
1. Schistosoma hematobium 
2. Schistosoma mansoni 
3. Schistosoma japonicum 
4. Clonorchis sinensis 
5. Fasciola hepatica 
6. Paragonimus westermanii. 
11. Phyllum Nematoda (Nematodes) 
1. Ascaris lumbaricoides 2. Enterobius vermicularis 3. Strongyloides stercoralis 4. Trichuris trichiura 5. Trichinella spiralis 6. 7. 8. 9. 
Ankylostoma duodenale Wuchereria bancrofti (Filarial worm) Loa loa Dracunuculus medinensis. 

TAPEWORM INFESTATION
Habitat 
Adult worm 
 1. Taenia saginata. Small intestine of man 
2. Taenia soleum. Small intestine of man 
 3. Taenia echinococcus. Intestine of dogs, jackals, woives, foxes, cats (not in man). 
Eggs 
In faeces of man or aforesaid animals. 
larvae 
1. Taenia saginata. In muscles of cattle. 
 2. Taenia solium. In muscles and other organs of pig and often man. 
. 3. Taenia echinococcus. In liver and other organs of sheep, cattle, horses and man. Life Cycles 
Taenia saginata 
Adult worm in man 
V, 
V, Eggs in human faeces 
Swallowed by cow 
Develop into larvae in muscle of cow 
 I ~nters man through eating insufficiently cooked meat 
Develops into adult worm. 
Taenle solium 
r ----Adult worm in man 
   4 
 Swallowed Eggs in human faeces 
 by man  4 
   Larvae 
   I 
  Swallowed by pig 
Swallowed by man 
Attaches to intestinal wall and develops into adult worm 
Taenie echinococcus 
Adult worm in intestine of fox and dog 
Eggs in faeces 
Eggs swallowed by sheep 
cattle or man 
Egg reaches liver and develops into hydated cyst containing daughter cysts, blood cells and scolices 
(cycle stops in man) 
Animal liver eaten by dog j each scolex becomes an adult in intestine of dog 
Clinical Features 
A. Due to adult (T. saginata, T. soleum) 
1. Usually asymptomatic 
2. Abdominal or epigastric pain 
3. Increased appetite 
4. Weakness or malaise 
5. VVeight loss 
6. Occasionally vertigo, nausea, vomit- 
ing, dyspnoea, headache and diarrhoea 
_~i 
i  I 
k -A- 
P I 
 

ROUNDWORM INFESTATIONS
(Ascariasis) 
matic initially ; later pressure Life Cycle 
Adult worms in man and pig 
Ir the liver (i) Bloating, indigestion, nausea, vomiting Mild pain in right hypochondrium 
often severe biliary colic 
Jaundice. An the bone, Spontaneous fracture --mity. 
In the brain. Epilepsy and blindness. In the lungs. Cough, haemoptysis, 
In the muscle. Muscular pain. 
Eggs passed in faeces 
Infective larva develops in egg 
Egg swollen by man ; larva 
escapes in intestine 
Enters blood stream 
Carried to lung 
Goes up the trachea to epiglo 
ttis, then down to intestine 
Develops into adult in six 
weeks. 
tool examination (not for T. echino- Clinical Featureb 
Fig. 37. Ovum of tapeworm. 
 2, X-ray and ultrasound scanning for brdatid cyst. 
 3, H aemaggl uti nation test for yclatid : ~ ~t 
4. Casoni intradermal test for hydatid 
LWL 
Treatment 
A. For adult worms 
 See chapter MEDICAL THERAPEUTICS under ANTHELMINTICS 
B. For hydatid cyst 
A. Due to larvae 
1. Intestinal haemorrhage (melaena) 
 2. Pulmonary alveolar haemorrhage (haemoptysis) 
3. Fever 103-105OF 
4. Cough, bronchial'rales 
5. Evidence of lobular consolidation 
D. Due to adult worm 
 1 . Abdominal pain, frequently colicky in the epigastrium and around umbilicus. 
2. Abdominal distention and tenderness 
3. Vomiting and constipation. 
4. History of passing worms: 
Surgical removal Fig. 38. Ovum of r?t4ndworm. 
Complication 
 Intestinal obstruction 
Diagnosis 



i: 


:i ~. 
Ova in stools 
Treatment 
 Piperazine citrate (Antepar) 150 mg. per kg. body weight (maximum 3 g). 

PINWORM INFESTATION
(Enterobiasis) 
I Life Cycle 
Adult worm in intestine of man 
Male dies after fertilization, female 
migrates to rectum and comes 
out at night 
 Eggs laid on perianal skin at night 
 and glu I ed to skin 
Infective larvae develop within 
eggs in 36 hours 
Egg transferred to nails on scratching 
perianal skin 
Transferred to mouth by 
fingers 
Infective larvae escape in 
intestine 

Develop into adult. 
Clinical Features 
1. May be asymptomatic 
2. Prufitus ani and pruritus vulvae 
 3. Anorexia, restlessness, insomnia in severe cases 
4. Rarely, appendicitis. 
Diagnosis 
Fig. 39. Ovum of pinwom 
Ova in perianal swab or at times in stools 

HOOKWORM INFESTATION
Etiology 
(Ankylostomiasis) 
 The disease is caused by the hookworm, Ankylostoma duodenale. The adult worm is about 10-15 mm. in length, and the moulh is provided with two pairs of sharp, hook-shaped teeth with which it pierces the mucous Tembrane of the intes'ine. The ova are passed inthe faeces. On the warm soil, ova develop into larvae which penetrate the intact skin. After entering the veins they pass upwards through the heart into the pulmonary circulation, from which they burrow into the bronchi. They then ascend through the trachea and after passing the larynx go down the oesophagus to develop into adult worms in the upper part of the small intestine. 
 Infection occurs in man if the feer are exposed to soil containing the larvae. This explains the high incidence among the agriculturists who pass stools and work in the fields barefooted. 
Clinical feature 
 1. Local lesions (ground itch) at the site of entry subsiding in a few days. 
 2. General debility, failure of nutrition and lassitude. 
 3. Anaemia with its clinical manifestations. 
4. Gastro-intestinal upset. 
 5. Sometimes symptoms of bronchial allergy. 
Diagnosis 
 The patients generally remain undiagnosed and exploited by peasant doctors till the disease advances to severe debility and referred to a place where investigation facili- 
1 :1  - . 
;kworm, worm is enmr, o u I h i s k- shaped s Tembrpussed indevelop tact skin. upwards circulainto the ough the go down 11 worms e. 
 feet a!e rae. This Pong the !o rk in the 
I the site 

, nutrition 
nifesta- 

konchial 
agnosed the and facili- 
ilable. The anaemia, microscopic 
romic has then advanced to 
&N. haemoglobin. 
.40. Ovum of hookworm 
diagnosis in confirmed by stool 
. n which reveals ova of hook 
ral. Correction of anaemia with iron leg. 
ons. In severe anaemia it is always 
to give total dose infusion of ironcomplex calculating the total iron 
nt by a formula. 
I iron required (in mg)=5xwxG. re w is the weight of the patient is kg 
the haemoglobin deficit in G% 
 cific. Tetramisol (Jetomisole-P) 150 after dinner repeated after breakfast next 
Bephenium hydroxynaphthoate (Alconules 5 G (2.5 G base) to be taken as dose. 
 Tetrachlorethylene (Avlon) three cachets J rid. each at two hourly interval followed a saline purge. 
Prophylaxis. Seeing the extent of the 
 e, the author suggests a dose of 
Iminthic to agriculturists in the prone at least once a year. 

FILARIASIS
Cycle of Wuchereria bancrof ti 
Adult worm in lymph glands, lymphatics, superficial abscesses, retro- 
peritoneal tissue and other sites in man I 
Gravid female liberate larvae into blood stream 
Into mosquito through bite 
Grow and reach mouth parts of 
mosquito 
To skin of man through biting 
Penetrate unbroken skin 
Reach lymph glands, etc 
Develop into adult worms 
Clinical Features 
Incubation period. Upto 12 months. 
A. Initial Phase 
1. Pain, swelling or redness of an arm or 
2. Pain and swelling in the scrotal region 
3. Commonly, stiffness of an extremity. 
 4. Enlarged lymph nodes, particularly the epitrochlear, axillary, femoral or inguinal. 
5. Often, mild fever. 
B. Inflammatory phase 
 1. Acute lymphangitis (i) Fever 101 -1 04'F with chills and severe toxaemla. 
 (ii) Focal spot of sharply circumscribed pain and tenderness, often around a malleolus then ascending upwards, at times it be~ins at a proximal spot and spreads centrifugally. 
 Oil) The affected part is swollen, often tender and painful with palpable lymphatics. 
(iv) Skin may be diffusely reddened. 
 2. InguinLIlymphadenitis. The inguinal lymph nodes are enlarged, painful and tender during the attack. 
 3. Filarial orchitis. Onset sudden with pain in testicle, fever with rigors, rapid enlargement of testicle. Hydrocele may develop. 
4. Funiculitis and epididymitis. 
 5. Filarial abscesses deeply seated in intermuscular facial planes ; may occur about infected lymph nodes. 
6. Elephantoid fever. Recurrent acuteInvestigations 
febrile condition often without inflammatory 
phenomena. Attacks last from a few hours to  1. Demonstration of microfilariae in night 
several days. blood smears, lymph fluid, abscess or hydro 
 cele fluid. 


C. Obstruction phase 
1. Lymph varices 
2. Lymph scrotum- 
3. Hydrocele 
4. Chyluria 
 5. Elephantiasis. Occurs particularly in the legs and scrotum and less frequently in arms, breast or vulva. The skin and subcutaneous tissues are greatly thickened and fibrotic. The draining lymph nodes are enlarged. This complication develops gradually following several acute attacks. 
2. Lymphangiography. 
Treatment  i 
 1. Diethylcarbamazlne (Hetrazan) 2 mg per kg body weight thrice aday after meals for 3-4 weeks, 
 2. Corticosteroid e.g. prednisolone 10 mg thrice a day for a month to be tapered off gradually. 
 3. Antihistaminics and analgesics, when necessary. 
Further Reading :-
Dutta, P,  Mitra, U,  Dutta, S,  De, A,  Et al Ceftriaxone therapy in ciprofloxacin treatment failure typhoid fever in children Indian Journal of Medical Research,  117:6 Jun 2001 
Sabu, Lucy,  Devada, K,  Subramanian, H Dirofilariosis in dogs & humans in Kerala Indian Journal of Medical Research,  121:5 May 2005 
Kurien, T,  Thyagarajan, S P,  Jeyaseelan, L,  Peedicayil, A,  Et al Community prevalence of hepatitis B infection & modes of transmission in Tamil Nadu, India Indian Journal of Medical Research, 121:5 May 2005 
Nalini Ramamurty, Lalitha C. Pillai, P. Gunasekaran, Varalakshmi Elango, Mohana Padma Priya & A. Khaleefathullah Sheriff  Influenza activity among the paediatric age group in Chennai Indian Journal of Medical Research, 121:6 June 2005 
 
 
 
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