1 During voluntary hyperbrtathmg stage, the PaC02, falU and PaO2 uses (A similar sort of ihings happen in high attitude; and lh& reader is referred

ring twelfth PaCO2 aid P*C02 begin (0 snub and return in normal or ri«» above normal values a trsn&ionl hyperpnp* correction of blood gas abnormalities due lo The phase of apnea normal respiratory rhylhrn Therefore, afler a bout of severe" voluntary hypervenMahOn. apnea follows then comes slighl hyperpmc phase and then Ihe respiration 15 back 10 normal The appearance of apnea in conscious hyperventilating subjects, is. however, nol regularly seen Enplanafton of symptom it ology
1 During voluntary hyperbrtathmg stage, the PaC02, falU and PaO2 uses (A similar sort of ihings happen in high attitude; and lh& reader is referred to (h* 'alveolai equal ion1 in high altitude sickness earlier in this chapter) 2 In normal persons and in non-nal environment 02 has practically no influence on Ihe frequency and amplitude of respiration H is only the C02. amongst Ihe gases, which has a strong influence Therefore law PaC02 withdrawal of the stimufation from ihe C02 sensitive chemoreceptoTS (fig 4 36) of medulla epnea 3 During the voluntary tiyperpnea. ihe subject may feel a:zness and visual biat kouT. This 15 due to low PeC02 When PiCO2 of ctmbril anenes fall they undergo vasospism This may b* called, msre'ore. hypocapmc cerebral vasospasm 1 Aflprwar-H unne may become slrongly alkaline This is because tht hfpoeapnis produces atkalosis. called, respiratory alkalosis The kidneys now eicrete the e'cess alhah ions and th*" homaostasrs of pH is maintained BREATH HOLDING Healthy persons, at Iht and of respiration can hold up his breath for •bout 50 seconds or so After 50 seconds ihe subject (a els distressed and develops a strong desire to breathe A] [his point,, (called ihe breaking point") ha is forced to breathe once again ae the 'breaking point1. typicaHy the PaO2 and PaCQJ are both about 60 mm Kg [normal, about 95 arid 4Q mm Hg respectively) The breaking paint depends mainly on ihe PaC02 Thus r lithe PaCO2 of 50 mm Hg i* reached quickly, as in breath holding Following muacular exercise, Ihe durihDn of breath holding will be short On the other hand if one holds up breath after a voluntary hyperventilation. Ihe duration may b* substantially prolonged This is because Ihe hyperventjlalion causes, washing out of CO2 so that buridmg up of PaC02" requires more lima Professional divers in the rive/is, who hive to stay under wstsi for sometime, often mike seven voluntary hypefvenl rial ten before diving so thai undarwater slay can be lengthened Thiv however, is dangerous, bacaus* the attainment of Ihe value of 60 mm Hg tor PaC02 it delayed no doubi but by this time the Pa02 mighi become dangerously \o*t and the subject may become unconscious due to hyprj*ia under waisr AHhough PaC02 value is Ihe mosii important influencing laclor for deiermming tr>e breaking point, oiher factors are also important Such (actors are (0 the concomitant hypoiemia. (n) neural factors like the role of vagus and the glosSOpharyngeal nerves They however will nol be drccusied hvre OXYGEN THERAPY The daiiical indcaTions of oirygtn therapy arB such condrtions like hypouc hypoxil. CO poisoning flic ip Ihe typical hypoiic hypoma, *verylhmg is normal bul The availably of O2n poor Whereas in CO poisoning, 02, particularly wtien given underpressure, replaces CO from ihe Hb molecule by mass action (in) In imonai-. edema. 02 therapy oflen trnpcoves the picture sharply/. This is because, inlhis condilion, there is ditlicully. m diffusion through thealveolo capillary membrane Inhalation of 1CK% 02 increases lh« PI02 lesulting in elevation of PAO2 and so .the alveolo capillary gradiBril of 02 greatly increases and the diffusion ofO2 improves (recall ihe Pick's Law. p 1EW) On ihe other hand., m anemia. The amounl of Hb or PBC fc poor, but the PaO2 is nomial Inhalation of 100% 02 and the following rse o( PIO2 and Pa02 therefore can increase only the 02m physical solution (normally about 0 3 ml/ 100 ml) but not Ihe 02 bound with the Kb, as Hb is praclicilly saturated wilh the 02 Therefore m anemia, the improvement by O2 therapy is only marginal In advanced cases of chronic bronchitis and corpulmcinale O2 therapy must be given with caution In these conrttionsr there Js chrome hypona as well as hypercapma The medullary CO2 sensitive celfs (central chemoreceplors, fig4 38), owing to chronic eicposura to the excess CO?, lose their sensitivity lo CO?, and O2tack remains the only dnve lefl to the patient for [h* breaihing 02 therapy, therefore, might kill ihe patient by withdrawing the only drive laftia ihe patient In CO poisoning and, with surgenes on hearl or lung, grealfy hyperbaTC 02 (i e 02 under high pressure) therapy is done where Such fec*lles e^isl Us dangers are given beow 1 When the PLO2 is very high, Ihe PaO2 ai*o becomes high and the amount of dissolved
02 (m physical solution) may rise greatly [say to values like 4 or 5 ml/100 ml from a normal value ofO 3 ml/IX ml), when Ihn occurs, for onygenatron of the tissues, this dissoked 02 alone is sufficient tnd tht HbO2 is not called for so that il remains imact This maeans, that Ihe carbamino Hb compounds cannot be formed and CO2 accumulates in the tissues (Retati. tht carbamioo Hb compounds, as shown m p 172 play a very crucial parr in transfer of CQ2) Accumulation of CO? can lead to. rather paradoxically, exaggerated respiration (panting for air due in excess O2'i) 2 High PaU2 produces cerebral vavot0*im Tins is id tame e'leni btntficial »s ihe hi »in ii»«uet ara protaciid from ihe mjur

) Emotional lability. Management of stroke and TIA: Hospitalization - for patients with suspected stroke Haemorrhage - Surgical evacuation of an intra

(f) Anxiety and depression. (g) Emotional lability. Management of stroke and TIA: Hospitalization - for patients with suspected stroke Haemorrhage - Surgical evacuation of an intracranial hematoma beneficial in selected cases: (1) Hemorrhage into cerebellum. This is characterised by relative retention of power and sensation (in contradistinction to pontine or capsular lesions), with small pupils, gaze palsy, cerebellar ataxia and peripheral facial palsy. (2) Surgically accessible clot in a patient with good level of consciousness but a persistent neurological deficit after a trial of medical management for a period of one week. (3) When progressive cerebral oedema and coning necessitates surgical decompression. Thrombosis and Embolism - A Supportive therapy -1. Position in bed - Patient should be nursed with the head in a flat position. Disturbance of autoregulation in patients with stroke results in decrease in cerebral blood flow (CBF) if the head is elevated. Semiprone position in order to avoid falling back of the tongue. Frequent change of position to prevent lung congestion and bed sores. 2. Maintenance of airway - if patient is unconscious. The tongue must be kept forward, if necessary by use of an airway and the mouth clear of pillows so that when the patient vomits obstruction is less likely to occur. 3. Maintenance of hydration and nutrition - In the unconscious patient by passing a nasogastric tube. In first 24 hours 5% glucose solution (2000 ml) is adequate. This can be replaced after 24 hours, when the danger of vomiting or active regurgitation is passed, by milk, sugar, eggs, salt and vitamins. Feeds are given 2-houhy preferably just after the patient's position is changed. 4. Care of the skin - Areas of reddening of the skin over heels, ankles, buttocks, shoulders and elbows are an indication of impending pressure necrosis. and indicate that the patient is not being turned frequently enough/ Care of the bladder and bowel - Incontinent patients may require sterile indwelling catheters and bowel care since dampness and infection predispose to the formation of decubitus ulcers. Appropriate antibiotics should be given at the first sign of pyuria. G. Care of the eyes -Antibiotic drops to prevent exposure keratitis/ 7. Passive movements - to be commenced from the first day to prevent contracture (especially at the shoulder) and also to decrease risk of leg vein thrombosis. B. Treatment of associated conditions - 1. Cardiac condition - Treatment of arrhythmias or of left ventricular failure. 2. Diabetes - Care should be taken to avoid hypoglycemia. 3. Hypertension - In acute stage mild to moderate elevation in BP requires no treatment. When associated with hypertensive encephalopathy or diastolic BP maintained at above 120 mm Hg. BP should be lowered cautiously using oral agents. 4. Hypotension-should be corrected by raising the foot of the bed and by fluid replacement. 5. Infection - Appropriate antibiotics for pulmonary or urinary infection. Paracetamol to lower temperature since with rise of body temperature there is an increase in metabolic demands and cerebral oxygen consumption. C. Specific measures - I. Measures to reduce cerebral oedema - (a) Mannitol- 350 ml of 20% aqueous solution IV. over 60-90 minutes. (b) Glycerol -1 5 g/kg of body weight every 24 hours in 3-4 divided doses mixed with fruit juice to mask the unpleasant taste or IV as 500 ml of 10% glycerol in 5% glucose or normal saline over a period of 3-4 hours daily for first 4 to 6 days of acute cerebral infarction. No rebound increase in intracranial. pressure after discontinuation as may occur after mannitol. (c) Steroid therapy - Dexamethasone 16-20 mg. IV or IM for first 5 days, followed by

AMPICILLIN SQDIUMC16HlsN3NaO4S Mol. Wt. 371.39 Ampicillm Sodium is sodium (6R)-6-(a-phenyl-D-glycyl-ammo)penicillmate. Category: Antibacterial. Dose:.

being examined and from the declared content of C16H19N3O4S in ampicillm trihydrate RS AMPICILLIN SQDIUMC16HlsN3NaO4S Mol. Wt. 371.39 Ampicillm Sodium is sodium (6R)-6-(a-phenyl-D-glycyl-ammo)penicillmate. Category: Antibacterial. Dose:. By intramuscular or intravenous injection, the equivalent of 1 to 3 g of ampicillm daily, in divided doses. Description: White, crystalline powder; hygroscopic. Solubility: Freely soluble in water; sparingly soluble in acetone; slightly soluble in chloroform; practically insoluble in ether, in liquid paraffin and in fixed oils. Storage. Store: in tightly-closed containers in a cool, dry place. If it is intended for use in the manufacture of injectable preparations, the container should be sterile, tamper-evident and sealed so as to exclude micro-organisms. Labelling: The label states whether or not the material is intended for use in the manufacture of injectable preparations. STANDARDSAmpicillm Sodium contains not less than 92. 5 per cent and not more than 100.5 per cent of C16HlsN3NaG4S, calculated with reference to the anhydrous substance. The sum of the percentage contents of ampicillm sodium and degradationproducts, calculated as C16HlsN3NaG4S, is not less than 97. 5, calculated with reference to the anhydrous substance. Identification Test A may be omitted if tests B, C and D are carried out. Tests B and C may be omitted if tests A and D are carried out. A: The infra-red absorption spectrum, Appendix 5.4, is concordant with the reference spectrum of ampicillm sodium or with the spectrum obtained from ampicillm sodium RS. If the spectra are not concordant, prepare another spectrum by the following method To a solution of 0 .25 g in 5 ml of water add 0. 5 ml of 2 M acetic acid, swirl the mixture and a How to stand for 10 minutes in ice. Filter with suction through a smtered-glass filter (porosity No. 3), wash the residue with 2 to 3 ml of a mixture of 9 volumes of acetone and 1 volume of water, dry the residue at 60° for 30 minutes and prepare a new spectrum of the residue. The infra-red absorption spectrum of the residue, Appendix 5.4, is concordant with the reference spectrum of ampicillm trihydrate or with the spectrum obtained from ampicillm trihydrate RS. B: Carry out the method for thin-layer chromatography, Appendix 4. 6, using silanised silica gel H as the coating substance and a mixture of 90 volumes of a 15.4% w/v solution of ammonium acetate and 1 0 volumes of acetone, the pH of which has been adjusted to 5. 0 with glacial acetic acid, as the mobile phase. Apply separately to the plate 1 ul of each of three solutions in a 4. 2% w/v solution of sodium bicarbonate containing (1) 0 .25% w/v of the substance being examined, (2) 0.25% w/v of ampicillm trihydrate RS and (3) 0.25% w/v each of ampicillm trihydrate RS and amoxycillm trihydrate RS. After removal of the plate, allow it to dry in air, expose it to iodine vapour and examine. The principal spot in the chromatogram obtained with solution (1) corresponds to that in the chromatogram obtained with solution (2). The test is not valid unless the chromatogram obtained with solution (3) shows two clearly separated principal spots. C: Complies with test C described under Ampicillm. D: A 5% w/v solution gives the reactions of sodium salts, Appendix 3. 1 .pH: Between 8: 9 and 10.0, determined 1 0 minutes after dissolution in a 10% w/v solution, Appendix 8.11. Clarity and colour of solution: A 10% w/v solution is clear, when examined immediately after preparation, Appendix 6.1, and the absorbance of the solution at about 430 nm is not more than 0.15, Appendix 5.5. Specific optical rotation: Between +253° and +237°, determined in a 0.25% w/v solution in 0.02M potassium hydrogen phthalate, Appendix 8.9. N,N. -Dimethylanilme: Complies with the test described under Ampicillm. Dichloromethane Not more than 0.2% w/w, determined in the following manner. Carry out the method for gas chromatography Appendix 4. 2; using the following solutions in water containing (1) 10% w/v of the substance being examined, (2) 10% w/v of the substance being examined and 0.02% v/v of 1,2- dichloroethane (internal standard) and (3) 0. 02% v/v of dichloromethane and 0.02% v/v of internal standard. The chromatographic procedure may be carried out using (a) a glass column (1.5 m x 5 mm) packed with acid washed, silanised diatomaceous support (100 to 120 mesh) coated with 1 0% w/w of polyethylene glycol 1000 and maintained at 60° with inlet port temperature at 100°, (b) a flame lonisation detector with detector temperature maintained at 150°, and (c) nitrogen as the carrier gas with 40 ml per minute as the flow rate. Calculate the percentage w/w of dichloromethane, assuming its weight per ml at 20 to be 1.325 g, Appendix 8.15. Heavy metals: Not more than 20 ppm, determined on 1.0,g by Method B, Appendix 3.12. Water: Not more than 2.0% w/w, determined on 0.3 g, Appendix 3.24 Assay: Weigh accurately about 50 mg,

. Role of adipose tissue hpoprotein lipase (ATLA). Recall, there are several types of lipoprolein lipases in our body, ATLA being one of them ATLA hyd

called diet courses for the obese. 3. Role of adipose tissue hpoprotein lipase (ATLA). Recall, there are several types of lipoprolein lipases in our body, ATLA being one of them ATLA hydrolyses the triglycerides of lipoprolem and the fatly acids (FA) thus released are incorporaled into the adipose tissue cells (adipocyles). Obese people, in general, have excessive concentrations of ATLA. 4. Role of brown fat. Brown fat (chap 7.10) has been discussed earlier In the adult, the amount of brown fat is usually meager. Nevertheless, brown fat activity causes development of great heat, ie, brown fat acltvities cause calorigenesis and this in turn raises the BMR, which in turn raises the energy output and reduction of body fat. Obese persons have no brown fal in their body (in contrast to normal persons who have some, although meager, quantity of il). 5. Psychological factors. Habits Many persons eat when il is time for the meal' no matter, whether he is feeling hungry or not This often leads to excess energy input. Some persons will eat whenever he finds 'good food', no matter whether he is hungry or not Some psychiatric persons (eg, some cases of depression) often over eat. It is important to remember depression n extremely common in Ihe present day society and many such cases are never suspecled even to be suffering from depression Dangers of obesity. Alherosclerosis, hypertension, diabetes mellitus, mammary cancer, gall slones are some diseases which are associated with obesity. Some well known adages, reflecting Ihe observation and wisdom of Ihe lay people may be quoted : (i) people dig Iheir own graves by their teeth, (ii) longer the belt, shorter is the life, (iii) (diabeles is), fat man's folly (iv) if you wanl to eal for longer number of days, eat less each day, and so on. Diabetes deserves special mention The maturity onset (NIDDM) diabetes (chap 6.6) commonly occurs in the obese persons. It is now known that in the obese (i) the insulin receptors, in the membranes of the target cells, are loo few in number and (ii) there is a deficiency of post receptor events - the two features precipitate the onsel of NIDDM type of diabetis. Body wt reduction usually reduces Ihe ferocity of the diabeles. In obesity, the blood vessels in tie adipose tissue, (i) have lo grow (to keep pace with Ihe growth of Ihe tissue), as well as (n) are compressed (by Ihe growing mass of the lissue) - the two factors combine to raise Ire peripheral resistance increase of BP. Reducton of body wt Ihus usually reduces the BP. Treatment, Physiological basis Obesity is very difficult to correct. Ullimately speaking, the aim is lo see thai energy input becomes less than the energy out put. (It is to be understood that there is no known method by which Ihe hypothalamic set point can be readiusted in man Therefore, basically the treatment of obesity is symptomatic). Common forms of treatment are 1 Energy input is reduced, either by short bouls of starvation (provided the person has no diabeles prone to kelosis or peptic ulcer) or mcessant reduced food intake. 1,2 or even 3 days of starvations are usually well tolerated. High calorie foods like fat, sugar etc must be slopped So called soft drinks often contain high calories Various diel courses (to reduce obesity) has now become a soil of industry in the affluent wesl. 2. Drugs are, for various reasons not popular. Thyroxme (almosl obsolete) and amphetamine (a banned drug in India, because of its addictive properties) were once very popular . Amphetamine, by acting on Ihe hypothalamus reduces appelite and is thus an well known anorexant. B. Surgical Various surgical procedures have developed to tackle extreme obesity. One commonly done is, small intestinal bypass surgery, where eunum is anastomosed with a loop of ileuin near its terminal (so that a good deal of small intestine is by passed). Result is, ultimately speaking, diminished energy input. Very oflen the patient becomes a chronic sufferer from various after effects of this operation. Role of exercise in Ihe treatment of obesity should be mentioned. All obese persons should increase his (her) energy oulput by increasing Ihe physical exercise, but only very hard work is needed lo reduce even a moderate amounl of fat. Therefore, one should not have great expectations from exercise alone STARVATION Though semistarvalion or under nutrition is very common in the developing world or in persons suffering from coma, cancer esophagus or psychological disorders, starvation until death is not so common Short term starvation (hunger strikes), however, is quile common. In the following passages, il will be presumed that the starving person continues to get hi§ water and mineral supply normally. Pathophysiology The glycogen reserve of an average man is only about 400 gm and in complete absence of food, it can supply Ihe calorie needs of the body for only a few hours. So fal mobilization from adipose tissue occurs early and continues until exhaustion Proteins of the body are also mobilized, primarily to supply the energy needs and also to meet various functions of ammo adds. The protein mobilization, called the endogenous breakdown of protein, occurs from the skeletal muscles, gastro intestinal trad and liver primarily but other organs also suffer. Heart muscle is relatively spared Loss of brain tissue is minimal (dealh due to starvation causes only about 5% loss from Ihe brain). As depot fat becomes more and more exhausted, more and more proteins are mobilized. As a result, blood urea (normal value, 20-40) mg/100 ml blood) begins to rise as starvation proceeds The high degree of lip id mobilization produces kelosis . The urine therefore now contains the ketone bodies (acetone, aceloacetc acid, hydroxybutyric acid) and becomes +ve to Rothera's Tesl The water conlent of Ihe body falls sharply Maximum possible duration of starvation is uncertain It obviously depends upon Ihe storage of body fal, and the ability lo combat acidosis and nitrogen retention Terence Mc Swiney, the Mayor of Cork, Ireland, undertook a fas unto death for political reasons in 1920, and died on Ihe 74th day. Acharya Vinoba Bhave, who stopped even water intake, died on the 5th day, and he was over 90 years. 1. Gross anatomy of the kidney. 2. Nephron and its structure. 3. Blood supply of the kidney. 4 Juxtaglomerular apparatus. 5. Juxta medullary nephron. Gross anatomy of the kidney (Fig. 8.1.1.) There are two kidneys,

Ty21a-oralvaccine-TY21ais a galactose epimerase mutant S. typhi given as oral enteric coated capsules. The bacilli invade mononuclear cells and underg

antibody (c) Ty21a-oralvaccine-TY21ais a galactose epimerase mutant S. typhi given as oral enteric coated capsules. The bacilli invade mononuclear cells and undergo 4-5 cell divisions in intestinal tract. This stimulates immunity, but the bacilli do not survive within the cells, as they lack the essential enzyme UDP-galactose^4- epimerase and are therefore avirulent. The vaccine stimulates cell mediated immunity and also stimulates intestinal IgA. Dose - One capsule on days 1, 3 and 5 irrespective of age one hour before meal with milk or water. Not recommended for children under 6 years of age. Protection commences 2 weeks after last capsule and lasts for atleast 3 years. Contraindications - Immunodeficiency states including treatment with immunosuppressive and antimitotic drugs, acute febrile illness and acute intestinal infection. Adverse reactions - Mild Gl disturbance, transient exanthema. 6. PLAGUE Epidemiology - Causative organism - Gram negative bacilli Yersinia pestis. Transmission - It is normally transferred from rodent to rodent (in whom it is enzootic) by fleas. Man can be infected through the infected flea or occasionally by louse or bedbug, and sometimes from droplet infection from cases of pneumonic plague. Permanent immunity results from an attack. Incubation period - 2-4 days. Clinical Features - 1. Bubonic plague - commonest variety. (a) Stage of invasion - Bodyache, mental confusion. Bubo appears on second or third day, usually in groin. Very tender and associated with cellulitis of surrounding tissues. (b) Febrile stage - Onset may be with high fever without prodromata. The temperature continues as a high remittent fever for 2-5 days and then falls suddenly, or gradually after 3-4 days, synchronous with the full development of the buboes. It may rise again if and when the buboes suppurate. Congested eyes, speech dull resembling alcoholic intoxication. Marked prostration, delirium, vomiting and oliguria, retention of urine, coma and convulsions may occur. Thready pulse, dilatation of heart and perhaps hemorrhages in later stages. Spleen and liver enlarged. Death may occur on third or fifth day. (c) Stage of recovery - Constitutional symptoms abate usually on 10th day with fall of temperature and perspiration. Bubo continues to enlarge and may burst, or suppuration may not occur. 2. Primary pneumonic - Rigor, malaise, vomiting, fever, and prostration. Chest pain, dry cough, dyspnoea and cyanosis with profuse, watery, blood tinged sputum. Hemorrhages frequent. 3. Septicemic - Systemic dissemination via blood stream with involvement of many organs. Hematogenous invasion of lungs results in secondary pneumonic plague. UNUSUAL PRESENTATIONS - Cervical bubonic plague - less common than inguinal, femoral or axillary forms. Carbuncular plague - presents with ulcerating skin lesion. Meningitis - may be the presenting feature and is diagnosed by isolation of Y pestis from CSF Laboratory diagnosis 1 White cell count - Leucocytosis with absolute predominance of neutrophils 2 Detection of Y pestis - in material from glands, blood (in septicemic form), sputum (in pneumonic cases), or discharge, by smear or culture. 3. Serology - Haemagglutinating antibodies appear within one week of onset of illness and specific IgM and IgG can be demonstrated by EL ISA techniques Management -1 Specific - (a) Streptomycin 30 mg/kg/day IM in 2 divided doses for 10 days to prevent relapse. (b) Tetracycline if allergy to streptomycin 2-4 g/day in 4 divided doses for 10 days (c) Chloramphenicol - for patients with meningitis 25 mg/kg loading dose IV followed by GO mg/kg in 4 divided doses and after clinical improvement continued orally for 10 days. 2. Local - In early stages buboes painted with iodine, or glycerine and belladona, or treated with infra-red rays. Opened only when they point, allowed to drain, and dressed with antibacterial powder. 3. General - Good nursing. Sedatives for pain and restlessness. Pneumonic plague patients must be strictly isolated to prevent droplet infection. Immunization - Vaccine containing 2,000 million killed organisms per ml. 0.5followed by 1 ml. after 7-10 days. Immunity lasts for G-12 months. Protection of contacts -Tetracycline 500 mg 6-houhy for 5 days for close contacts of plague patients or those believed to be incubating the disease. 7. BRUCELLOSIS Definition -Brucellosis is a zoonosis usually caused by Brucella melitensis, Brucella suis, or Brucella abortus (in decreasing order of virulence in man). Brucellae are small, non-motile, coccobacilli. Epidemiology - Organism - Intracellular parasite belonging to the genus brucella. Transmission - (a) Consumption of infected unsterilised milk, and its products. (b) Milking or tending infected animals, particularly those infected animals which have delivered or aborted Organisms may enter the body through cuts and abrasions on the hands, conjunctivae or respiratory tract. (c) Handling carcasses or meat of infected animals in abbatoirs, butchers. Veterinarians and microbiology workers are also at risk. (d) Sexual transmission may occur in man. Age - Rare below age of 15, three times more common in men. Incubation period 2-4 weeks. (7-10 days following accidental inoculation). Clinical features - 1 Acute brucellosis - fa) NON-SPECIFIC EARLY FEATURES - Period of ill-health for about 2 weeks with fever.

. Spread - by droplet route. Incubation period - 7-14 days. Clinical features - 3 stages, each lasting about 2 weeks. 1. CATARRFIAL (PRE-COUGH) STAGE

pertussis. Spread - by droplet route. Incubation period - 7-14 days. Clinical features - 3 stages, each lasting about 2 weeks. 1. CATARRFIAL (PRE-COUGH) STAGE - Insidious onset with coryza, moderate or mild cough and slight fever. The cough which is single at first, becomes progressively grouped and paroxysmal and more intense. No signs in chest, or bronchitic signs. 2. PAROXYSMAL (SPASMODIC) STAGE - follows with repeated episodes of short staccato cough during which the child is distressed, red faced or deeply cyanosed with bulging tearfilled eyes. As the glottis relaxes after the spasm, the older child takes a respiratory whoop which is often absent in the neonate. The paroxysm may comprise a single bout of coughs with terminal whoop, or the whole paroxysm may be punctuated by whoops and cease only when the child ejects mucus and food debris by vomiting, or coughing up, or swallowing large amount of thick mucoid sputum. After the attack, the child exhausted often goes to sleep or returns to play. Exciting causes - Feeding, excitement, activity, sudden change in temperature or sometimes no obvious cause. 3. CONVALESCENT STAGE - About the 4th week, paroxysms diminish in intensity, child ceases to vomit, then to whoop, and finally to cough. Appetite returns with improvement in general nutrition. Laboratory diagnosis - (i) Absolute lymphocytosis. (ii) Isolation of B. pertussis from upper respiratory tract taken after a spasm, by cough-plate culture method or preferably nasopharyngeal swab method on Bordet-Gengou medium. (iii) Normal ESR unless pulmonary complications. Differential Diagnosis - 1. Bronchiolitis or bronchopneumonia - In whooping cough there is history of contact, gradual onset of catarrhal symptoms progressing to spasmodic phase. 2. Enlarged tracheo-bronchial lymph nodes - usually tuberculous. Paroxysmal cough but no whoop. 3. Foreign bodies in larynx or trachea - Rapid onset Endoscopic examination reveals source of trouble. 4. Tetany with upper respiratory infection. 5. Fibrocystic disease in infants - Pulmonary lesion leads to paroxysmal coughing attacks. Family history, steatorrhoea, absence of trypsin from duodenal contents, increased concentration of sodium and chloride in sweat. Complications - 1. Pulmonary - (a) Pulmonary atelectasis - Common complication during paroxysmal phase due partly to viscid mucus secretion and bronchial blockage, and partly to bronchial and peribronchial inflammation. Degree of collapse varies from small segmental areas to collapse of a whole lobe. Recovery occurs in most cases in 2-3 weeks. Persistent low-grade infection accompanying atelectasis may lead to subsequent bronchiectasis. (b) Bronchopneumonia - usually due to secondary bacterial infection and closely associated with atelectasis. (c) Hilar adenitis and activation of tubercular disease may occur. (d) Asphyxia or cerebral anoxia are the common modes of death. 2. Mechanical or pressure effects - (a) Rise in intra-abdominal pressure -Inguinal and umbilical herniae and prolapse of rectum. (b) Rise of intrathoracic pressure -Subconjunctival hemorrhage common, occasionally petechiae on face, neck and upper trunk. (e) Cerebral hemorrhage or anoxic brain damage - may lead to convulsions, hemiplegia, cranial nerve palsies, mental retardation and coma (d) Fraenal ulcer - due to laceration by lower central incisors when the tongue protrudes forcibly during spasms. (c) Pneumothorax and mediastinal emphysema - rare. Management - 1. GENERAL MEASURES - (a) Isolation in a well ventilated room (b) Feeding - Food finely divided and in small feeds. Since feeding often provokes a paroxysm of coughing followed by vomiting in infants, it may be necessary to give a second feed after vomiting has occurred. (c) Management during a spasm - The child should be lifted from the cot and held in the head down position, patting the back until the spasm is over, to avoid inhalation of secretions and vomit. 2. DRUGS - (a) Sedatives - Phenobarbitone, or syrup of chloral hydrate, or antihistamine such as promethazine elixir 10-20 mg. per dose (b) Antispasmodies - Salbutamol or terbutaline t.d.s. may reduce frequency and severity of paroxysms. (c) Antibiotics -mildly effective in early catarrhal stage for reducing paroxysms, and to check secondary infection. Tetracycline or erythromydn -Dose per day - under 1 year 1 gm , upto 3 years 1.5 gm , upto 10 years 2 gm. , in four divided doses for 10 days. Ampicillin and cephaloridine for bronchopneumonia. (d) Anticonvulsants - such as IV diazepam or IM paraladehyde for fits, subsequent protection with sodium valproate or phenobarb. 3. OXYGEN - if convulsions or persistent hypoxemia. 4. PERIODIC GENTLE NASAL SUCTION -to remove secretions. Prevention - See immunization Chapter 10. Pertussis vaccination is not recommended over G years of age because vaccine reactions are more common in older children. Risk of pertussus vaccination (brain damage) can be reduced if vaccine is not given to infants with brain injury, CNS damage, personal or immediate family history of fits, or previous reaction to vaccine. Erythromydn 40 mg/kg/day into 4 divided doses may prevent or modify whooping cough in the non-immune neonate who has been exposed to the disease. 3. MENINGITIS Definition - Meningitis is inflammation of the

There is no known animal reservoir (in contrast to many Salmonella spp.). Shigella bacteremia is uncommon except in immunocompromised host (e.g. HIV i

disease they give rise to are Sh. dysenteriae, Sh flexneri, Sh boydii and Sh sonnei Shigella spp has been implicated as a cause of 'gay bowel1 syndrome in homosexual men. There is no known animal reservoir (in contrast to many Salmonella spp.). Shigella bacteremia is uncommon except in immunocompromised host (e.g. HIV infection). Cl. Fs. - Following an incubation period of 2-3 days, high fever, headache malaise and anorexia occur, along with frequent small-volume stools progressing to passage of blood and pus and severe abdominal cramps, tenesmus and abdominal tenderness on palpitation. Diag - Stool culture and identification of the organism by specific serological testing. Tr. -Fluid replacement. Antibiotics - Suprafloxacin is drug of choice in most adults, co-trimoxazole and ampicillin are alternatives in children. Escerichia coli - This Gram-negative organism is a major cause obacterial gastroenteritis. The identification of E.coli 0157:H7 as an important enteropathogen has helped understanding of bacterial diarrhoea. Transmission and pathogenesis - The 0157: H 7 serotype of E.coli is non-invasive and produces a toxin similar to that of Shigella which kills Vero cells; this organism is therefore known as verotoxin-producing E.coli (VTEC). Infection follows consumption of undercooked beef or untreated milk. Cl. Fs. - (a) Infection is classically associated with hemorrhagic colitis, but may be asmyptomatic or produce diarrhoea only. Illness lasts upto 12 days and usually resolves spontaneously but may prove fatal. (b) Hemolytic uremic syndrome as a complication in about 5% or more serious variant, thrombotic thrombocytopenic purpura. (c) Ischemic colitis - Mucosal disease due to VTEC resembles ischemic colitis in the elderly. Diag - Identification from stool culture can be confirmed by latex agglutination with specific antiserum. Tr - Fluid replacement. Ciprofloxacin if severe or prolonged disease for adults, ampicillin or co-trimoxsazole for children. Vibrio cholerae - the causative organism of cholerae, is a short, curved motile Gram-negative bacillus. The major pathogenic strain possesses a somatic antigen (01) with two biotypes - classical El Tor More recently, a strain with somatic antigen 0139, the Bengal strain has appeared. Pathogenesis - The major factor distinguishing 01 and 0139 serotypes from other 'non-cholera1 vibrios is the ability to produce an enterotoxin. This consists of a ring of five E' subunits around a central 'A' unit. This pentameric ring structure binds to GM1 ganglioside on the enterocyte cell membrane and the A subunit stimulates enterocyte adenylate cyclase, leading to conspicuous secretion of small intestinal fluid and ultimately diarrhoea. Cl. Fs. - (a) Stage of evacuation - Sudden onset with frequent loose stools, first yellow soon become colourless, watery and copious with flakes of mucus (rice water stools). Copious and incessant watery vomit. Subnormal temperature. (b) Stage of collapse - Depletion of water and salts occurs rapidly, leading to severe dehydration and hypovolemic shock, and ultimately to death Diag - is mainly clinical. The organism can be grown from stool either directly or after alkaline enrichment. Tr. - (a) Fluid and electrolyte replacement: Mild case - Oral rehydration therapy with glucose-electrolyte solution. Constituents (g/litre): Sodium chloride 3.5 Sodium bicarbonate 2.5 Potassium chloride 1.5 Glucose 20 Other solutions containing glucose polymers (e.g. rice water) and electrolytes are highly