Learn — Communicable diseases & control

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Diarrhoea and ORS management

Diarrhoea is the passage of three or more loose or watery stools in 24 hours, or more frequent stools than is normal for that person; it is acute when it lasts under 14 days, persistent at 14 days or more, and dysentery when there is visible blood in the stool. It matters because almost every diarrhoeal death in a child is a death from dehydration, and oral rehydration salts with zinc prevent it at a cost of a few rupees, which is why the classification and the three treatment plans are examined every year.

  • Low-osmolarity oral rehydration salts have a total osmolarity of 245 mOsm/L with sodium 75, chloride 65, glucose 75, potassium 20 and citrate 10 mmol/L; one sachet is dissolved in exactly 1 litre of clean water, nothing is added to it, and the solution is discarded 24 hours after preparation.
  • IMNCI classifies dehydration on two or more signs: severe dehydration if the child is lethargic or unconscious, has sunken eyes, is unable to drink or drinks poorly, or the skin pinch goes back very slowly (over 2 seconds); some dehydration if the child is restless or irritable, has sunken eyes, drinks eagerly and thirstily, or the skin pinch goes back slowly; no dehydration if there are not enough signs for either.
  • Plan A treats no dehydration at home on four rules: extra fluids including oral rehydration salts after every loose stool (50 to 100 mL under 2 years, 100 to 200 mL at 2 years and over), zinc for 14 days, continued feeding and breastfeeding, and a clear list of when to return immediately.
  • Plan B treats some dehydration at the facility with oral rehydration salts 75 mL/kg over 4 hours given by cup and spoon, with reassessment and reclassification at 4 hours; breastfeeding continues throughout and the mother is taught to give the solution herself.
  • Plan C treats severe dehydration with intravenous Ringer lactate 100 mL/kg: in an infant under 12 months, 30 mL/kg in the first hour then 70 mL/kg over the next 5 hours; at 12 months and over, 30 mL/kg in the first 30 minutes then 70 mL/kg over the next 2.5 hours; repeat the first bolus if the radial pulse is still weak or absent, reassess every 15 to 30 minutes, and start oral rehydration salts 5 mL/kg/hour as soon as the child can drink.
  • Zinc is given in every episode for 14 full days, 20 mg daily for a child of 6 months and over and 10 mg daily under 6 months, and it is continued even after the stools stop because it shortens the episode by about a quarter and reduces further episodes over the next two to three months.
  • Antibiotics are given only for dysentery (ciprofloxacin as per the IMNCI chart), for suspected cholera and for a proven systemic infection; antimotility drugs, antiemetics, antisecretory agents and antispasmodics have no place in childhood diarrhoea and can be fatal.
  • Prevention is rotavirus vaccine at 6, 10 and 14 weeks in the National Immunization Schedule, exclusive breastfeeding for six months, handwashing with soap at the critical times, safe drinking water, sanitation and safe complementary feeding; an extra meal a day for two weeks after the illness recovers the weight the child lost.

Malaria and vector-borne diseases

Vector-borne diseases are infections transmitted to humans by an arthropod, and in India the five that carry a national programme are malaria, dengue with chikungunya, lymphatic filariasis, kala-azar and Japanese encephalitis, all under the National Centre for Vector Borne Diseases Control. Malaria is the anchor topic because it has a defined national drug policy with species-specific regimens, a clear definition of severe disease, and a treatment that must start within hours of diagnosis if a falciparum case is not to die.

  • Five Plasmodium species infect humans, but only two matter in Indian practice: Plasmodium falciparum causes almost all severe disease and death, and Plasmodium vivax forms dormant hypnozoites in the liver that cause relapse months later, which is why vivax needs a radical cure and falciparum does not.
  • Diagnosis before treatment is the rule: every fever case is tested by a bivalent rapid diagnostic test, which detects HRP-2 for falciparum and a pan-species antigen for vivax, or by microscopy, where the thick film finds the parasite and the thin film identifies the species and estimates the parasite load.
  • National drug policy for vivax malaria is chloroquine 25 mg/kg over three days, given as 10, 10 and 5 mg/kg, together with primaquine 0.25 mg/kg daily for 14 days for radical cure; primaquine causes haemolysis in glucose-6-phosphate dehydrogenase deficiency and is withheld in pregnancy and in infants under one year, and the patient is told to stop it and return if the urine turns dark.
  • National drug policy for falciparum malaria is a three-day course of artemisinin-based combination therapy, artesunate with sulfadoxine-pyrimethamine in most of the country and artemether-lumefantrine in the north-eastern states because of sulfadoxine-pyrimethamine resistance, plus a single dose of primaquine 0.75 mg/kg on the second day to kill the gametocytes and stop transmission.
  • Severe malaria is defined by impaired consciousness or cerebral malaria, repeated convulsions, severe anaemia, hypoglycaemia, acidosis, shock, acute kidney injury with dark urine, pulmonary oedema, jaundice, abnormal bleeding or hyperparasitaemia; it is treated with intravenous artesunate 2.4 mg/kg at 0, 12 and 24 hours and then daily, followed by a full oral course of artemisinin-based combination therapy once the patient can swallow, and never with oral drugs or chloroquine.
  • Dengue passes through a febrile phase, a critical phase of plasma leakage around defervescence on days 3 to 7, and a recovery phase; the warning signs are abdominal pain or tenderness, persistent vomiting, clinical fluid accumulation, mucosal bleeding, lethargy or restlessness, liver enlargement of more than 2 cm and a rising haematocrit with a falling platelet count. NS1 antigen is positive in the first five days and IgM from about day five, fluid replacement rather than platelet transfusion is the treatment, and paracetamol is the only antipyretic because aspirin and ibuprofen worsen bleeding.
  • Lymphatic filariasis is caused by Wuchereria bancrofti carried by Culex quinquefasciatus and is diagnosed on a night blood smear taken between about 10 pm and 2 am when microfilaraemia peaks; control is annual mass drug administration with diethylcarbamazine and albendazole, with the triple-drug regimen adding ivermectin in selected districts, alongside morbidity management and disability prevention for lymphoedema and hydrocele.
  • Kala-azar is transmitted by the sandfly Phlebotomus argentipes, screened by the rK39 rapid test and treated first line with a single 10 mg/kg dose of liposomal amphotericin B, with an elimination target of fewer than one case per 10,000 population at block level; Japanese encephalitis is carried by Culex tritaeniorhynchus with pigs and ardeid birds as amplifying hosts and is prevented by the Japanese encephalitis vaccine given in endemic districts under the National Immunization Schedule.

Rickettsial disease

Rickettsial diseases are infections with small obligate intracellular gram-negative bacteria of the Rickettsia, Orientia and Coxiella groups, transmitted by mites, ticks, fleas and lice, that damage the small blood vessels and present as an undifferentiated fever with rash. They matter in India because scrub typhus is a common and under-recognised cause of acute febrile illness that is repeatedly mistaken for dengue or typhoid, and because the untreated case progresses to acute respiratory distress and shock while a cheap oral antibiotic given early ends the illness in two days.

  • Scrub typhus, caused by Orientia tsutsugamushi, is the commonest rickettsial disease in India; the vector and the reservoir is the larval trombiculid mite or chigger of Leptotrombidium, which maintains the organism transovarially, and cases cluster in the monsoon and post-monsoon months in scrub, foothill and terrace-farming areas.
  • The eschar, a painless black necrotic ulcer with an erythematous rim at the bite site, is the single most useful physical sign and is missed unless the patient is fully undressed and examined, because it hides in the axilla, groin, scrotum, under the breast and along the waistband.
  • Other Indian rickettsioses are Indian tick typhus from Rickettsia conorii carried by hard ticks, endemic or murine typhus from Rickettsia typhi carried by the rat flea, epidemic typhus from Rickettsia prowazekii carried by the body louse in conditions of crowding and cold, and Q fever from Coxiella burnetii, which is inhaled from infected animal birth products rather than bitten in.
  • The Weil-Felix test is the cheap and widely available screen and uses Proteus antigens, agglutinating OX-K in scrub typhus and OX-19 and OX-2 in the typhus and spotted fever groups; it is insensitive and non-specific, so IgM ELISA is the confirmatory test used in India, and treatment is never delayed for the result.
  • Doxycycline is first-line at all ages for this indication in India, 100 mg twice daily in adults and 4.4 mg/kg a day in two divided doses in children up to a maximum of 200 mg a day, for 7 days or until three days after the fever settles; azithromycin is the alternative in pregnancy, and defervescence within about 48 hours of the first dose supports the diagnosis.
  • Complications of untreated disease are acute respiratory distress syndrome, myocarditis, acute kidney injury, meningoencephalitis, hepatitis and multi-organ failure; the classic laboratory pattern is thrombocytopenia with raised transaminases, which is exactly why the case is mislabelled as dengue.
  • There is no vaccine, so prevention is environmental and personal: clearing scrub and rodent harbourage around houses, avoiding sitting or lying on grass in endemic areas, wearing long clothing, permethrin treatment of clothes, insect repellent on exposed skin, and bathing and changing clothes after field work.

Ascariasis

Ascariasis is infection with Ascaris lumbricoides, the giant intestinal roundworm, acquired by swallowing embryonated eggs from soil contaminated by human faeces. It is the commonest soil-transmitted helminth infection in India and matters less for the worm itself than for what a heavy load does to a child's appetite, iron stores and growth, and for the intestinal and biliary obstruction that a bolus of worms can cause.

  • Transmission is faeco-oral through soil: eggs passed in human faeces need two to three weeks in warm moist soil to embryonate and become infective, and are then swallowed on unwashed vegetables, in contaminated water or from soiled hands, so there is no direct person-to-person spread and no intermediate host.
  • The life cycle explains the symptoms: the larva hatches in the small intestine, penetrates the wall, travels by the portal blood to the liver, then through the heart to the lungs, breaks into the alveoli, is coughed up and swallowed, and matures in the small intestine, taking about two to three months from ingestion to eggs appearing in the stool; the adult lives one to two years and a female lays roughly 200,000 eggs a day.
  • Loeffler syndrome is the pulmonary phase, with cough, wheeze, fleeting patchy shadows on the chest film and marked eosinophilia about one to two weeks after ingestion, and it is regularly misdiagnosed as asthma.
  • Intestinal disease ranges from vague abdominal pain, anorexia and malabsorption with growth faltering to acute complications, namely a bolus of worms causing subacute or complete intestinal obstruction in a child, and a single migrating worm entering the bile duct, pancreatic duct or appendix.
  • Diagnosis is by finding the characteristic bile-stained, round, thick-shelled mamillated eggs in a direct stool smear; adult worms may be passed in the stool or vomited, and eosinophilia is present only during the migratory phase.
  • Treatment is albendazole 400 mg as a single dose, halved to 200 mg for children aged 12 to 23 months, or mebendazole 100 mg twice daily for three days, and a single dose cures the great majority of infections; the whole household is treated in the same round.
  • The National Deworming Day gives albendazole to all children and adolescents aged 1 to 19 years twice a year, on 10 February and 10 August, through schools and anganwadi centres with a mop-up day the following week, and this is the largest single-day public health programme in the country.
  • Prevention is sanitation and hygiene rather than repeated drugs: household latrines under the Swachh Bharat Mission, handwashing with soap after defecation and before eating, wearing footwear, washing vegetables, and never using untreated night soil as manure; reinfection follows within months if the soil remains contaminated.

Chickenpox

Chickenpox is the primary infection with varicella-zoster virus, a DNA herpesvirus, spread by droplets from the respiratory tract and by direct contact with vesicle fluid, with humans as the only reservoir. It matters because it is one of the most infectious diseases known and the patient is already infectious a day or two before the rash appears, so a ward or a school is exposed before the diagnosis is made, and because the virus stays latent in the dorsal root ganglia and returns years later as herpes zoster.

  • The incubation period is 14 to 16 days with a range of 10 to 21 days, and the period of communicability runs from one to two days before the rash until every lesion has crusted, usually about five to six days after the rash begins; the crusts themselves are not infective, and that period defines the isolation.
  • The secondary attack rate among susceptible household contacts is about 90 per cent, which is why an outbreak in a hostel, orphanage or paediatric ward spreads to almost every susceptible child before it is recognised.
  • The prodrome is short, about 24 hours of mild fever and malaise, and the rash appears on the first day of fever, unlike measles where the rash waits until the fourth day; this is a favourite discriminating point.
  • The rash is centripetal, dense on the trunk and sparse on the limbs, involves the scalp, axillae and mucous membranes of the mouth, evolves quickly from macule to papule to vesicle to pustule to crust, and comes in successive crops so that all stages are present in the same area at the same time, a pleomorphism that separates it from the monomorphic centrifugal rash of smallpox.
  • Complications are secondary bacterial infection of the lesions, which is the commonest and includes streptococcal cellulitis and necrotising fasciitis; varicella pneumonia, mainly in adults, smokers and pregnant women and the commonest cause of death; cerebellar ataxia and encephalitis; Reye syndrome after aspirin; congenital varicella syndrome when infection occurs in the first 20 weeks of pregnancy; and severe neonatal varicella when the mother's rash appears between five days before and two days after delivery.
  • Treatment for a healthy child is symptomatic, with calamine, cool baths, nails cut short, an antihistamine for itch and paracetamol for fever, and never aspirin; oral aciclovir started within 24 hours of the rash is given to adolescents, adults, pregnant women, people on corticosteroids and the immunocompromised, with intravenous aciclovir for pneumonia and for the immunocompromised.
  • Post-exposure protection depends on who was exposed: varicella-zoster immunoglobulin within 96 hours for a susceptible immunocompromised contact, a newborn of a mother with peripartum varicella and a susceptible pregnant woman, and the live varicella vaccine within 72 hours of exposure for a susceptible immunocompetent contact; the varicella vaccine is not part of the National Immunization Schedule in India and is given in the Indian Academy of Pediatrics schedule as two doses from 15 months.
  • Herpes zoster is reactivation of the same latent virus in one dermatome and occurs with ageing or immunosuppression; a person who has never had chickenpox can catch chickenpox, not zoster, from the vesicle fluid of a zoster patient, so a zoster case on a ward still needs contact and, if disseminated, airborne precautions.

Measles

Measles is an acute, extremely infectious viral illness caused by a Morbillivirus of the paramyxovirus family, spread by droplets and airborne particles, with humans as the only reservoir. It matters because it kills through its complications, chiefly pneumonia and diarrhoea, in exactly the children who are already undernourished, and because India is committed to measles and rubella elimination, so every suspected case is notifiable and must be investigated with a blood sample.

  • The incubation period is about 10 days to the onset of fever and 14 days to the rash; the period of communicability is from about 4 days before to 4 days after the appearance of the rash, and the secondary attack rate among susceptible household contacts is over 90 per cent, making it the most infectious of the common childhood exanthems.
  • The catarrhal or prodromal stage lasts three to four days with fever and the three Cs, namely cough, coryza and conjunctivitis with photophobia; Koplik spots, small bluish-white grains on a red base on the buccal mucosa opposite the second molars, appear one to two days before the rash, are pathognomonic and disappear within about 48 hours.
  • The rash is a dusky red maculopapular eruption that starts behind the ears and along the hairline on about the fourth day of fever, spreads downwards over the face, trunk and limbs across three days, becomes confluent, and then fades in the order it appeared leaving brownish staining and fine branny desquamation.
  • The surveillance case definition used for notification is any person with fever and a maculopapular, that is non-vesicular, rash together with cough, coryza or conjunctivitis; every such case is reported, investigated and a serum sample collected for measles IgM.
  • Complications are otitis media, which is the commonest; bronchopneumonia, which is the commonest cause of death; diarrhoea with dehydration; laryngotracheobronchitis or croup; corneal ulceration and blindness, driven by vitamin A deficiency; noma and stomatitis; worsening of existing malnutrition; post-measles encephalitis; and subacute sclerosing panencephalitis, a rare fatal degenerative brain disease appearing years after the acute infection.
  • Vitamin A is given to every child with measles at diagnosis and repeated the next day: 50,000 IU under 6 months, 100,000 IU at 6 to 11 months and 200,000 IU at 12 months and above, with a third dose two to four weeks later if there are eye signs of deficiency; this alone substantially reduces measles mortality.
  • Prevention is two doses of measles-rubella vaccine under the National Immunization Schedule, at 9 to 12 months and at 16 to 24 months, given as 0.5 mL subcutaneously into the right upper arm; the vaccine is live and heat-labile, must be discarded four hours after reconstitution, and coverage above 95 per cent with both doses is needed to interrupt transmission.
  • For a susceptible contact, measles vaccine given within 72 hours of exposure can prevent or modify the illness and immunoglobulin can be used within about a week; treatment of the case itself is supportive, with continued feeding, fluids, eye care, and treatment of the pneumonia and the diarrhoea, because there is no specific antiviral.

Bordetella pertussis (whooping cough)

Pertussis or whooping cough is an acute bacterial infection of the respiratory tract caused by Bordetella pertussis, a small gram-negative coccobacillus that attaches to the ciliated respiratory epithelium and paralyses it with pertussis toxin and tracheal cytotoxin. It matters because it is most dangerous in the infant who is too young to have completed the primary vaccine series, and because that infant is usually infected by an older sibling or an adult in the house whose only symptom is a long cough.

  • Spread is by droplets from a case, humans are the only reservoir, the incubation period is 7 to 14 days with a range of 4 to 21 days, and communicability is highest in the catarrhal stage before the whoop appears, lasting about three weeks from the onset of paroxysms if untreated but only five days after starting a macrolide.
  • The illness runs in three stages: the catarrhal stage of one to two weeks with coryza, a mild cough and little fever, which is the most infectious and the least recognised; the paroxysmal stage of two to four weeks or longer with bursts of short coughs in a single expiration followed by a crowing inspiratory whoop, post-tussive vomiting, cyanosis, subconjunctival haemorrhage and an ulcer under the tongue; and the convalescent stage lasting weeks to months, giving it the name of the hundred-day cough.
  • An infant under six months often has no whoop at all and presents instead with apnoea, cyanotic spells, poor feeding or a seizure from hypoxia, and this is the age group in which almost all the deaths occur.
  • Investigation shows a marked absolute lymphocytosis with a normal or raised total white count, which is a strong clue; a nasopharyngeal swab for polymerase chain reaction is the most sensitive confirmation and culture on Bordet-Gengou or Regan-Lowe medium is definitive but slow.
  • Treatment is a macrolide, usually azithromycin 10 mg/kg once daily for five days, which shortens infectivity and interrupts spread but alters the course of the illness only if it is given in the catarrhal stage; azithromycin is preferred in an infant under one month because erythromycin has been associated with infantile hypertrophic pyloric stenosis.
  • Supportive nursing is what saves the young infant: oxygen for cyanotic spells, gentle suction of secretions, small frequent feeds after a paroxysm rather than during one, minimal handling to avoid triggering a bout, and continuous observation because apnoea is silent.
  • Chemoprophylaxis with the same macrolide is given to all household contacts irrespective of age and immunisation status, and contacts under seven who are unimmunised or partly immunised also receive the due DPT or pentavalent dose.
  • Prevention is pentavalent vaccine at 6, 10 and 14 weeks with DPT boosters at 16 to 24 months and at 5 to 6 years under the National Immunization Schedule; the whole-cell pertussis vaccine used in the Indian public programme gives longer protection than the acellular vaccine, but immunity from either vaccine or from disease wanes, so adolescents and adults become the reservoir that infects newborns.

Hepatitis C and E

Hepatitis C is a blood-borne RNA virus of the Flaviviridae family that causes a largely silent infection which becomes chronic in most of those infected and ends in cirrhosis and liver cancer, while hepatitis E is a faecally transmitted RNA virus that causes self-limiting epidemic jaundice but kills pregnant women. They are taught together because they occupy opposite ends of the viral hepatitis table, one blood-borne and chronic and curable, the other waterborne and acute and preventable only by clean water, and both are covered by the National Viral Hepatitis Control Programme.

  • Hepatitis C is transmitted by unsafe injections and syringe reuse, unscreened blood transfusion, injecting drug use, unsterile tattooing and ear-piercing and by haemodialysis, with sexual and mother-to-child transmission occurring far less efficiently than for hepatitis B; the acute infection is usually silent, most of those infected become chronic carriers, and a substantial minority develop cirrhosis over about twenty years, on which hepatocellular carcinoma may follow.
  • Diagnosis of hepatitis C is a two-step process because the antibody persists after cure: anti-HCV antibody is the screening test and a nucleic acid test for HCV RNA is needed to confirm current infection and, twelve weeks after treatment, to confirm the sustained virological response that defines cure.
  • Treatment of hepatitis C is a 12-week oral course of direct-acting antivirals, usually a sofosbuvir-based combination, provided free under the National Viral Hepatitis Control Programme, and it cures more than 95 per cent of patients; there is no vaccine, so prevention rests on injection safety, blood safety, sterile procedures and harm reduction for people who inject drugs.
  • Hepatitis E is transmitted faeco-orally, mainly through drinking water contaminated with human faeces, and is the commonest cause of large waterborne epidemics of jaundice in India as well as of sporadic acute viral hepatitis in adults; the incubation period is about 15 to 60 days with an average of about 40 days, and the classic Indian outbreaks followed sewage contamination of a piped water supply.
  • Hepatitis E in pregnancy is the point that decides management: infection in the third trimester causes fulminant hepatic failure with a case fatality reported at 20 per cent or more, along with obstetric haemorrhage, preterm labour and fetal loss, whereas in everyone else the illness is self-limiting and does not become chronic except in the severely immunosuppressed.
  • Diagnosis of hepatitis E is by anti-HEV IgM, and management is supportive with rest, adequate calories, avoidance of alcohol and of hepatotoxic drugs and traditional remedies, and early referral of any pregnant woman or of anyone with encephalopathy, bleeding or a falling urine output.
  • Prevention of hepatitis E is entirely environmental: a protected and chlorinated piped water supply, safe excreta disposal, repair of cross-connections between sewage and water lines, handwashing, and boiling of drinking water during an outbreak; a vaccine exists but is not licensed for use in India.
  • The National Viral Hepatitis Control Programme, launched in 2018 under the National Health Mission, provides free testing and free treatment through model treatment centres, aims to eliminate hepatitis C by 2030, and works through injection safety, blood safety and universal hepatitis B birth-dose vaccination.

Brucellosis

Brucellosis is a bacterial zoonosis caused by small gram-negative coccobacilli of the genus Brucella, acquired from infected cattle, buffalo, goats, sheep and pigs through unpasteurised milk and milk products or through direct contact with animal blood, tissue, urine and birth products. It matters in India as an under-diagnosed occupational disease of dairy farmers, shepherds, abattoir workers, veterinarians and laboratory staff, and as a cause of prolonged undulant fever that is repeatedly treated as typhoid or tuberculosis while the herd that caused it is never investigated.

  • The species and their animal hosts are Brucella melitensis in goats and sheep, which is the most virulent and the commonest human infection in India, Brucella abortus in cattle and buffalo, Brucella suis in pigs and Brucella canis in dogs; there is no meaningful human-to-human transmission apart from rare spread by transfusion, transplantation, breast milk and sexual contact.
  • Human infection is acquired by drinking raw or unpasteurised milk and eating soft cheese or paneer made from it, by inhaling aerosols in barns, abattoirs and laboratories, by direct contact through cuts and the conjunctiva while handling aborted fetuses and placentas, and by accidental self-inoculation with the live animal vaccine strains used by veterinarians.
  • The clinical picture after an incubation of one to three weeks or longer is insidious fever with a characteristic undulant pattern, drenching night sweats with a musty odour, malaise, anorexia, weight loss, arthralgia and low backache, with hepatosplenomegaly and lymphadenopathy on examination.
  • Focal disease is what disables and kills: osteoarticular involvement, most often sacroiliitis and spondylitis, is the commonest complication; orchitis and epididymitis are frequent in men; endocarditis is uncommon but is the leading cause of death; and neurobrucellosis presents as meningitis or radiculopathy.
  • Diagnosis rests on blood culture, which is definitive but slow and needs prolonged incubation, with the Rose Bengal plate test used as the field screen and the standard tube agglutination test as the quantitative test, where a titre of 1:160 or above, or a rising titre on paired samples, supports the diagnosis in an endemic area; IgM and IgG ELISA and PCR are used where available, and the laboratory must always be warned because brucellosis is one of the commonest laboratory-acquired infections.
  • Treatment is always a combination given for a long course, because monotherapy relapses: doxycycline 100 mg twice daily for six weeks combined with either streptomycin intramuscularly for the first two to three weeks or rifampicin daily for the full six weeks, with co-trimoxazole-based combinations replacing doxycycline in children under eight and in pregnancy; relapse in the first year is common and is retreated rather than assumed to be resistance.
  • Prevention is at the animal end and in the kitchen: testing and segregation or culling of infected animals, vaccination of cattle and small ruminants, safe disposal of aborted material and placentas, gloves and protective clothing for those who handle them, and pasteurisation or boiling of all milk, which is the single measure that removes most household risk in India.
  • Brucellosis is dealt with under the One Health approach, so a human case is reported to the animal husbandry department as well, because the herd rather than the patient is the source and other households drinking that milk are at risk.

Anthrax

Anthrax is a zoonosis caused by Bacillus anthracis, a large gram-positive, capsulated, aerobic spore-forming bacillus that lives in soil and infects herbivores; people catch it from infected animals, their hides, wool, hair, bone meal or meat, and not from each other. It matters out of proportion to its numbers because the spores survive in soil for decades, because the inhalational form kills most of those who get it, and because it is a Category A agent of bioterrorism, so a single confirmed case is a public health event that must be notified the same day.

  • Cutaneous anthrax is about ninety-five per cent of human cases: a painless itchy papule on an exposed part becomes a vesicle and then a black necrotic eschar (the malignant pustule) surrounded by non-pitting gelatinous oedema, with regional lymphadenopathy and surprisingly little pain.
  • Inhalational anthrax (woolsorter's disease) begins as a flu-like illness, then after a few days brings fever, chest pain and breathlessness from haemorrhagic mediastinitis with a widened mediastinum and pleural effusions on the chest film, and it may end in haemorrhagic meningitis; gastrointestinal anthrax follows eating infected meat and presents as haemorrhagic gastroenteritis with ascites.
  • The incubation period of cutaneous anthrax is usually one to seven days, but spores inhaled into the lung can lie dormant for weeks, which is why post-exposure prophylaxis is given for sixty days and not for a week.
  • Laboratory pointers examiners like: square-ended bacilli in chains giving a bamboo-stick appearance on Gram stain of vesicle fluid, the pink capsule of McFadyean's reaction with polychrome methylene blue on a blood smear, Medusa-head colonies on nutrient agar and the string-of-pearls test on penicillin agar.
  • Treatment of cutaneous anthrax is ciprofloxacin 500 mg orally twice a day or doxycycline 100 mg orally twice a day for seven to ten days; systemic and inhalational disease needs intravenous ciprofloxacin combined with a protein-synthesis inhibitor such as clindamycin or linezolid, with antitoxin, for sixty days.
  • Prevention is animal-side: never open or skin a carcass suspected of anthrax, because exposure to air is what makes the vegetative bacillus sporulate; the carcass is burnt or buried deep with quicklime, contacts and herds are vaccinated with the veterinary vaccine, and the site is disinfected with a sporicidal agent such as formaldehyde or hypochlorite, since ordinary disinfectants do not kill spores.
  • Anthrax is a notifiable zoonosis reported through the Integrated Disease Surveillance Programme; the health worker's syndromic S form, the medical officer's presumptive P form and the laboratory L form are the reporting chain, and the animal husbandry department must be told on the same day so the source herd is traced.

Malaria species

Malaria is a protozoal disease caused by Plasmodium and transmitted by the bite of an infected female Anopheles mosquito, chiefly Anopheles culicifacies in the rural plains of India and Anopheles stephensi in towns. Five species infect human beings, and naming the species is not academic: it decides the drug, the length of treatment, whether the patient can relapse months later and whether the illness can kill within a day.

  • Plasmodium vivax causes benign tertian malaria with a 48-hour erythrocytic cycle, invades only young red cells so the parasitaemia stays low, and leaves hypnozoites in the liver that cause relapse months later; the infected cell is enlarged and stippled with Schuffner's dots.
  • Plasmodium falciparum causes malignant tertian malaria, invades red cells of every age so the parasitaemia climbs steeply, and sequesters in capillaries to cause cerebral malaria, severe anaemia, acute kidney injury, acidosis and hypoglycaemia; it forms no hypnozoite, so it recrudesces but never relapses, and its banana-shaped gametocyte is unmistakable on a thin film.
  • Plasmodium malariae causes quartan malaria on a 72-hour cycle, shows band forms on the smear, can recrudesce for decades and is associated with quartan malarial nephropathy; Plasmodium ovale is a benign tertian parasite of West Africa that, like vivax, makes hypnozoites and relapses; Plasmodium knowlesi is a zoonosis of macaques in South East Asia with a 24-hour cycle that looks like malariae on the smear but behaves like falciparum in the patient.
  • Diagnosis is by microscopy of a thick film for detection and a thin film for species identification, which remains the gold standard, or by the bivalent rapid test that the ASHA carries and which detects HRP-2 for falciparum and pLDH for vivax; treatment is never started on clinical suspicion alone where a test is available.
  • The National Drug Policy on Malaria treats vivax with chloroquine 25 mg base/kg over three days (10, 10 and 5 mg/kg) plus primaquine 0.25 mg/kg daily for fourteen days for radical cure of the liver stage; falciparum is treated with a three-day artemisinin-based combination — artesunate with sulfadoxine-pyrimethamine everywhere except the north-eastern states, where artemether-lumefantrine is used because of resistance — plus a single gametocytocidal dose of primaquine 0.75 mg/kg on the second day.
  • Severe malaria is treated with intravenous artesunate 2.4 mg/kg at 0, 12 and 24 hours and then daily, followed by a full oral course once the patient can swallow; primaquine is withheld in pregnancy and in infants under one year and given with caution and supervision where G6PD deficiency is suspected, because it causes haemolysis.
  • Vector control under the national programme is indoor residual spraying, long-lasting insecticidal nets, larvivorous fish such as Gambusia, anti-larval measures and source reduction, and the National Framework for Malaria Elimination (2016 to 2030) sets the target of a malaria-free India by 2030 with district-wise categorisation driving what is done where.

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