Tropical and Infectious Diseases Important Question and Answers

Tropical And InFectIous Diseases

Question.1. Enumerate the causes of enteric fever.

Answer. Enteric fever is an infectious disease

Causative Agent

• Salmonella typhi and Salmonella paratyphi
• The organisms are gram­negative nonspore forming bacilli.

Predisposing Factors

• Organisms: A large number of organisms are ingested by the healthy person to suffr from typhoid.
  Smaller inocula may produce the disease.
  If the organisms are very virulent or if the resistance of host is poor.
• Stomach acidity: Acid in the stomach destroys Salmonella.
  Hence, patients having achlorhydria or who take large amount of antacids to neutralize the acid in stomach suffr more often from the typhoid.
• Intestinal flora: Normal intestinal flra produces shortchain fatt acids which are lethal to Salmonella.
  When these are reduced by antibiotics the patient is more prone to typhoid.

Read And Learn More: General Medicine Question And Answers

Question.2. Describe clinical signs and symptoms of enteric fever.

Answer. Clinical signs and symptoms of enteric fever.

Invasion (1st Week)

• Onset: Lassitude, headache, bodyache and anorexia.
• Tongue is coated with raw tips and edges.
• Abdominal discomfort and distention occurs with nausea,
  vomiting and constipation which are followed by diarrhea.
• Hepatomegaly
• Fever: It may show step ladder rise.
• Signs of bronchitis are common. Epistaxis may occur.
• Pulse: Relative bradycardia and *dicrotic pulse.

Advance (2nd Week)

• General state: Listlessness and *apathy.
• Abdomen:
• Spleen become palpable
• Increased abdominal distention and discomfort
• Usually there is diarrhea.
• Temperature: It is high with slight morning remissions.
• Rash (Rose spots): These are erythematous maculopapular lesions 2–4 mm in diameter which *blanch on pressure usually seen on the upper abdomen, back and chest.

Decline (3rd Week)

Mild case: Toxemia *abates and gradual fall of temperature.
Severe case: Increased toxemia, intestinal hemorrhage or perforation.

 

Question.3. Describe briefl complications of enteric fever and their management.

Answer. Complications of enteric fever with their management.

Hemorrhage
Seen at the end of 2nd week and early 3rd week from gastric ulcer.

Treatment

• Absolute bed rest.
• Repeated blood transfusion
• Morphine. 15 mg SC.

Shock

Treatment

• Plasma transfusion
• Oxygen
• Vasopressor drugs
• IV hydrocortisone or dexamethasone.

Perforation

It is most dangerous complication leading to peritonitis.

Treatment

• Gastric suction
• IV flids
• Broad spectrum gram­negative agents.

Hepatitis

• It is represented by hepatomegaly and jaundice.
• Treatment is symptomatic.

Cholecystitis

Salmonella typhi has affity for gallbladder and can produce inflmmation.

Treatment

Ampicillin or ciproflxacin is required.

Cholecystectomy is done if above treatment fails.

Toxemia

Treatment

Hydrocortisone 200 mg or Dexamethasone 8 mg parenterally followed by 45 mg prednisolone.

Meningitis

Treatment

Cefotaxime 2 gm IV 4 hourly or ceftazidine 2 gm 6 hourly and gentamicin.

 

Question.4. Write short note on typhoid.
Or
Write short note on enteric fever.

Answer. Typhoid is an acute systemic illness caused by infection due to salmonella typhi.

Epidemiology

Typhoid germs are contracted from food or drink contaminated with excreta from carriers or patients. Spread is facilitated by poor environmental hygiene.

Clinical Features

Invasion (1st Week)

• Onset: Lassitude, headache, bodyache and anorexia.
• Tongue is coated with raw tips and edges.
• Abdominal discomfort and distention occurs with nausea,vomiting and constipation which are followed by diarrhea.
• Hepatomegaly
• Fever: It may show step ladder rise.
• Signs of bronchitis are common. Epistaxis may occur.
• Pulse: Relative bradycardia and *dicrotic pulse.

Advance (2nd Week)

• General state: Listlessness and *apathy.
• Abdomen:
• Spleen become palpable
• Increased abdominal distention and discomfort
• Usually there is diarrhea.
• Temperature: It is high with slight morning remissions.
• Rash (Rose spots): These are erythematous maculopapular lesions 2–4 mm in diameter which blanch on pressure usually seen on the upper abdomen, back and chest.

Decline (3rd Week)

• Mild case: Toxemia *abates and gradual fall of temperature.
• Severe case: Increased toxemia, intestinal hemorrhage or perforation.

Investigations

First Week

• Normochromic normocytic anemia, leukopenia and albuminuria
• Blood culture may be positive in 70–90% of cases.

Second Week

• Anemia, leukopenia may persist
• Widal test become positive, may show four fold rise in agglutinins against somatic ‘O’ antigen. It is not specifi but rising titers are diagnostic.
• Blood culture may be positive only in 50%.

Third Week

• Anemia and leukopenia persist. Leukocytosis occur in severe septicemia
• Blood culture is positive in 30–45% of cases.
• Positive WIDAL test with rising titers
• Positive stool culture and urine test for S. typhi.

Complications

Following are the complications oftyphoid fever:

Intestinal complications:

• Hemorrhage
• Perforation
• Paralytic ileus
• Peritonitis

Extra intestinal complications:

• Meningitis
• Bone and joint infection
• Cholecystitis
• Encephalopathy
• Pneumonia
• Granulomatous hepatitis
• Nephritis
• Myocarditis

Treatment

Specific

• Ciproflxacin: It is given in the dose of 500 mg BD for 7 to 10 days it is avoided in children because of risk of cartilage damage and tendonitis.
  If absolutely required, low dose can be used for not more than 3 days.
• Ceftriaxone: It is 3rd generation cephalosporin and improves the condition rapidly. It is given in the dose of 1 gm BD for 10 to 14 days.
• Azithromycin: 1 gm OD for 5 days.

Supportive Treatment

• Treatment of fever paracetamol
• Good nursing care.
• Nutritious diet should be given. 3000 calories per day should be given
• Fluid and electrolyte balance should be maintained.
• For severe toxemia and peripheral circulatory failure:
  Dexamethasone 3 mg/kg stat followed by 8 doses of 1mg/kg 6 hourly for 48 hours each given by IV infusion over 30 min.

Treatment Of Carrier

Patients who are asymptomatic, but constantly releases bacteria in stool because bacteria are persisting in gallbladder.

• Ampicillin 500 mg QID for six weeks.
• Ciproflxacin 500 mg BD for 2 to 4 weeks.
• Cholecystectomy if above measure fails.

 

Question.5. Describe briefl typhoid vaccination.

Answer. Following are the typhoid vaccinations present:

• Anti­triple typhoid vaccine containing in each mL. 1000
  million typhoid organisms, 250 million each of paratyphoid ‘A’ and ‘B’ organisms.
  Course of 3 injections of 0.5 mL, 1 mL and 1 mL subcutaneously at intervals of not less than 7 days or not more than 28 days. Immunity lasts for about 12 months.
• V1 capsular polysaccharide typhoid vaccine: 25 mg in each dose. Single dose (0.5 mL) SC or IM gives protection for 3 years.
  However, the V1 antigen does not invariably provoke V1 antibody. Booster every 2 years.
• TY21a—oral vaccine: TY21a is 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 at least 3 years.
  Booster is given every 5 years.

 

Question.6.Describe briefl management of malaria.
Or
Write short note on treatment of malaria.

Answer. Malaria is a common topical disease caused by protozoa,Plasmodium.

Acute febrile illness characterized by paroxysms of fever as a result of asexual production of Plasmodium within the red cells.

Management

General Management

• Measurement of glucose and if possible lactate and arterial blood gases.
• Fluid balance should be maintained because both dehydration and overhydration can occur as a result of disease or treatment.
• Treatment of convulsions with diazepam.
• Attention should be given to hypoglycemia and hyponatremia.
• Blood should be taken for cross­matching and coagulation studies
• Parameters for monitoring treatment include twice daily parasite counts, regular pH and blood gas measurements and when appropriate, measurement of glucose (during iv quinine therapy), lactate, CRP and kidney function.

Specific Treatment

• Treatment of chloroquine susceptible P. vivax,
  P. falciparum, P. ovale, P. malariae chloroquine:
  This is given in the dose of 600 mg base followed by 300 mg at 6th, 24th and 48th hours.
  It is useful in trating all types of malaria.
  It is curative for P. falciparum malaria but cannot prevent relapses due to exoerythrocytic cycles of P. vivax malaria.
• Treatment of chloroquine resistant P. falciparum:

• Quinidine IV 10 mg/kg dissolved in 300 mL normal saline infused over 1 to 2 hour.
• Quinine hydrochloride: 600 mg TDS for 3–7 days is useful.
  If required for cerebral malaria, this drug can given IV the dose is 7 mg/kg over 30 min, followed by 10 mg/kg over 4 hours and then 10 mg/kg over 8 hours or until the patient can complete a week of oral treatment.
• Meflquine: It provides rapid schizonticidal action in single dose of 15 mg/kg orally maximum dose is 1000 to 1250mg.
• Halofantrine:
  Dosage: Adult 500 mg BD for 4–6 days.
  Children: 8 mg/kg
• Artemether: This drug is rapidly acting, safe and is effctive against multidrug resistant infections.
  Artemether 3.2 mg/kg IM is given followed by 1.6 mg/kg IM every 12 to 24 hours until patient wakes up. Artesunate 2 mg/kg IV stat followed by 1 mg/Kg 12 hourly.
• Sulfadoxine and pyrimethamine: Combination of sulfadoxime 1500mg and pyrimethamine 25mg helps to cure an acute attck ofchloroquine resistant malaria.

• Treatment of chloroquine resistant P.vivax
  Oral meflquine and halofantrine.
• Treatment of persistent hypnozoites in P. vivax or P.
  Ovale Infection
• Primaquine: It is given in the dose of 7.5mg BD for 14 days usually after doing a G6PD test
• Bulaquine: It is given 25mg OD for 5 days.

Question.7. Outline the management of F. malaria.

Answer.

1. Treatment of chloroquine susceptible P. falciparum

Chloroquine: This is given in the dose of 600 mg base followed by 300 mg at 6th, 24th and 48th hours.

2. Treatment of chloroquine-resistant P. falciparum:

• Quinidine IV 10 mg/kg dissolved in 300 mL normal saline infused over 1 to 2 hours.
• Quinine hydrochloride: 600 mg TDS for 3-7 days is useful.
• Meflquine: It provides rapid schizonticidal action in single dose of 15 mg/kg orally maximum dose is 1000 to 1250 mg.

3. Treatment of complicated P. falciparum malaria

• Cerebral malaria caused by P. falciparum infection is a medical emergency.
  So depending on prevailing sensitivity of P.falciparum to anti­malarial drugs, i.e.
  Quinine or chloroquine is given as an intravenous infusion over 2 to 4 hours to avoid acute circulatory failure or acute malarial encephalopathy.
  Quinine should be used in chloroquine­resistant cases.
  The starting dose of chloroquine is 5 mg/kg and of quinine is 10 mg/kg.
  The dose should be repeated at intervals of 8–12 hours until the patient can take the drug orally.
  The total dose of chloroquine is 25 mg/kg.
  The quinine is continued orally in the same dose for 7–10 days.
  Recently artemisinin (artemether) has become fist line treatment of severe malaria as mentioned by WHO. Artesunate 2.4 mg/kg IV then 1.2 mg/kg/day or artemether 3.2 mg/kg, then 1.6 mg/kg IM daily is given for 3–5 days.
• Single dose of parenteral phenobarbitone 5–20 mg/kg is given to prevent convulsion.
• If severe anaemia is present then transfusion with packed red cells is done.
• If oliguria develops, frusemide or an infusion of mannitol is given to prevent renal failure.
• Intravenous flids are given, if necessary should be guided by central venous pressure because pulmonary edema may develop if the patient is over­infused.
• Exchange blood transfusions is life saving in complicated very severe infection (over 10% of RBCs are infected).
• Hypoglycemia and septicemia may be treated appropriately. All patients treated with quinine should be monitored for blood sugar and should receive 5–10% glucose as continuous infusion during treatment.
• If renal failure develops dialysis should be done.
  Care of unconscious patient or if patient undergo coma.

 

Question.8. Write short note on diphtheria. 

Answer. Diphtheria is an acute infectious disease caused by Corynebacterium diphtheriae and is characterized by the local exudates on the mucous membrane of nose, throat and larynx and systemic toxemia.

Types Of Diphtheria
Pharyngeal diphtheria

• It is characterized by the toxemia, *congestion and edema of palate.
• There is formation of a membrane in pharynx which is generally thin glistening pearly white in early stage and become thick, grayish and opaque later on.
• There is lymphadenopathy in neck and breath is foul smelling.
• In second week there is lethargy and restlessness. Pulse becomes irregular.
  Respiration is rapid and shallow.
  Repeated vomiting takes place.

Nasal Diphtheria

• There is presence of unilateral and bilateral nasal discharge, at fist serous and often blood stained, later thick, mucopurulent and foul smelling.
• A thick membrane may be visible on the mucosa of the anterior part of nasal septum.

Laryngeal Diphtheria

• It is common in young children
• It is characterized by the hoarseness, brassy cough followed by attck of inspiratory stridor and laryngeal spasm
• The membrane is usually limited to larynx.

Cutaneous diphtheria

When corneum bacteria enters into the abrasion or wounds they produced punched out ulcers which is covered by the grayish membrane.

Facial diphtheria

Mild:

• Reddening of one or both the tonsils.
• Small membrane formation on one or both the tonsils.

Moderate:

• Membrane on both tonsils.
• Localized tonsillar lymph node enlargement.

Severe:

• Rapidly spreading fimly membrane on the palate and roof of the mouth.
• There is gross edema of facial and palatal tissue.

Conjunctival Diphtheria

• Due to direct involvement of the eyes by the organism or spread from the nose.
• It is characterized by the severe congestion in the eyes and discharge.

Clinical Features

• Patient complains of presence of sore throat.
• Low grade fever is present.
• Presence of headache and malaise.
• Hoarseness of voice, dyspnea in cases with laryngeal diphtheria.
• Presence of gross cervical lymphadenopathy.
• Formation of b luish white or grayish green pseudomembrane at the site of infection.
• Punched out ulcerations are present if skin is involved.
• Foul smelling serosanguinous discharge in cases of nasal diphtheria.
• Cyanosis is seen in cases with laryngeal diphtheria.

Management of diphtheria

• Bed rest: Usually bed rest is required for 3 to 6 weeks
• Antitoxin: Anti­diphtheria serum is given subcutaneously or IM in the dose of 10,000–1,00,000 units depending on the severity of the disease.
  A test dose is usually given before giving the injection to exclude hypersensitivity.
• Antibiotics: A course of ampicillin or erythromycin 500 mg 6 hourly should be given to eradicate the diphtheria bacillus.
• General management:

Diet: In mild cases, normal diet may be allowed

• In moderate to severe cases initially flids are given orally.
• If there is palatal palsy semisolid diet is preferred to liquids because
• liquids may be regurgitate from nose.
• If swallowing is affcted, feeding should be with Ryle’s tube.

Care of Mouth: The mouth should be cleaned.

Treatment of complication:

• Cardiac failure: Diuretics and digitalis may have to be given.
• Palatal palsy: Head low position may be given to drain secretion of the mouth.
• Laryngeal obstruction: Tracheostomy may be required.
• Respiratory paralysis: Oxygen and ventilator may be required.
• Prophylaxis: Acute immunization should be given to all the children at age of 4th, 5th and 6th month in form of DPT.

Question.9. Mention the complications of diphtheria.

Answer.

Complications

Acute Circulatory Failure

• Toxic myocarditis.
• It is characterized by the tachycardia, feeble heart sounds,cardiac enlargement, tic­tac rhythm and arrhythmias.
• Sudden death may occur.
• Congestive heart failure.

 

Respiratory Complications

• Bronchitis
• Bronchopneumonia
• Respiratory obstruction
• Respiratory paralysis.

Toxic Neurological Damage

• Paralysis of palate
• Paralysis of accommodation
• Facial paralysis
• Bulbar paralysis
• Paralysis of muscles of respiration
• Peripheral neuropathy.

Renal complications

• Toxic nephritis.
• Vascular involvement especially middle cerebral artery leading to a picture of thrombosis or monoplegia.
• Other complication include otitis media and arthritis.

Question.10. Enumerate the causes of hyperplasia of gums.

Answer. According to etiologic factors and pathologic changes,gingival enlargements are:

Inflmmatory Enlargement

• Chronic
• Acute.

Drug Induced Enlargement

Enlargement Associated With Systemic Disease

Conditional enlargement:

• Pregnancy
• Puberty
• Vitamin C defiiency
• Plasma cell gingivitis
• Non-specific conditional enlargement.

Systemic diseases causing gingival enlargement:

• Leukemia
• Granulomatous disease.

Neoplastic enlargement

• Benign tumors
• Malignant tumors

False enlargement

According to location and distribution gingival
enlargement are classifid as:

• Localized: Gingival enlargement limited to one or more teeth.
• Generalized: Entire mouth, gingiva is enlarged.
• Marginal: limited to marginal gingiva.
• Papillary: Confied to inter-dental papilla.
• Diffse: Involves all parts of gingiva that is marginal,attched and inter-dental.
• Discrete: Isolated sessile or pedunculated tumor like enlargement.

According to degree of gingival enlargement

• Grade 0: No sign of gingival enlargement.
• Grade I: Enlargement confimed to inter-dental papilla
• Grade II: Enlargement involves papilla and marginal gingiva.
• Grade III: Enlargement covers three quarters or more of the crown.

 

Question.11. Enumerate causes of bleeding gums.
Or
Enumerate fie causes of gum bleeding.

Answer.

Causes

Local Cause:

• Minor injury: Use of hard new tooth brush may cause minor local injury to gums and leads to bleeding.
• Dental caries: It may be obvious or hidden between the teeth and get irrigating the gums.
• Tartar
• Pyorrhea alveolitis is the result of septic infection extending down into the sockets, loosening the teeth, causing the gum margins to recede by erosion and leading to purulent discharge.
  In severe cases gums bleed on the slightest touch.
• Tuberculous gingivitis
• Stomatitis.

General conditions:

• Scurvy: Spongy bleeding of the gums, teeth covered by exuberant blood is the prominent feature of scurvy due to lack of vitamin C.
• Syphilis: In second stage will produce bleeding from the gums.
• Purpura
• Blood dyscrasis.

 

Question.12.Briefl describe hookworm infestation.

Answer. Hookworm is a small, grayish white and cylindrical in form.

The egg is oval in shape and contains four blastomeres.

There are three species of hookworm which are pathogenic:

• Ankylostoma duodenale
• Necator americans
• Ankylostoma brazilenses

Habitat: Adult worm lives in jejunum. Here they suck,the blood from jejunal wall.

Clinical Features

Diagnosis

• Stool examination: It shows adult worm or characteristic hookworm eggs.
• Blood examination: Hypochromic anemia and eosinophilia.

Treatment

• This consists of expulsion of the worms and treatment of anemia. If anemia is severe, it should be treated fist.
• Anemia: Anemia should be treated with oral iron therapy along with vitamin B complex and folic acid.
  If it is severe blood transfusion should be given.

Effective drugs

• Tetrachloroethylene 5 mL is given after an overnight fast and may be repeated in heavy infestations.
• Bephenium hydroxynaphthoate 5 gm is given orally with fruit juices because it is very bittr.
• Mebendazole 100 mg twice daily is given for 3 days.

 

Question.13. Outline the management of tapeworm infestation.

Answer. Tapeworms are ribbon like segmented worms.

The common tapeworm affcting human are Taenia saginata, Taenia solium.

Humans are defiitive host.

Clinical Features

• Mild abdominal pain
• Nausea
• Change in appetite
• Weakness
• Weight loss.

Management

• Niclosamide
  Adults: Single dose of 2 gm.
  Children: 0.5 to 1 gm
  The tablets should be given onempty stomach, chewed thoroughly and washed down with a litte water.
  A purgative is recommended if the dead segments are not passed out within few years.
• Praziquantel: Single dose of 5–10 mg/kg after a light breakfast.
• For cerebral cysticercosis praziquantel 50 mg/kg/day for 15 days or albendazole 15 mg/kg/day for 30 days.

 

Question.14. Outline treatment of threadworm infestation.

Answer. Threadworm is also called as pinworm or seatworm.

It is enterobius vermicularis.
It is a nematode and sexes are separate.
Adult worm is small, spindle shaped and white in color.

Mode of entry

Eggs entry into mouth through contaminated figers during scratching in the perianal region. This is auto­ infection.

Clinical Features

• Pruritis, i.e. itching in the perianal regions.
• Salpingitis: Inflmmation of fallopian tube.
• *Nocturnal enuresis.
• Appendicitis.

Treatment

• Mebendazole: Single dose of 100 mg.
• Pyrantel: Single dose of 10 mg/kg
• Sporadic infections are usually cured by one treatment.
• In intensive and symptomatic infection drug therapy should be repeated after 2 weeks, and then if necessary every 2 months.

 

Question.15. Write short note on chickenpox prevention.

Answer. Chickenpox is an acute infectious disease.

Etiological Agent

Chickenpox is caused by varicella virus which is closely related to the herpes simplex virus, cytomegalovirus and Epstein­Barr virus.

Prevention of chickenpox

Varicella­zoster immunoglobin is given to the following, i.e.

Indication

• Following signifiant exposure to chickenpox in immunocompromised and susceptible children.
• Susceptible adolescents and adults particularly pregnant women.
• Newborn infants mothers have chickenpox within 5 days before delivery.
• Premature infants of less then 28 weeks gestation.
• Premature infants whose mother do not have a history of chickenpox
• Dose: 125 units per 10 kg body weight IM within 48 hours and not later than 96 hour after exposure
• Maximum suggested dose is 625 units.

Vaccine

• Live attnuated Varicella-zoster.
• Safe and highly protective in both healthy and immunocompromised children.
• Dose: In children of 2 to 12 years, who have not had chicken pox, two doses are recommended fist at 12 to 15 months of age and second at 4 to 6 years of age.

 

Question.16. Write short note on measles.

Answer. It is highly infective disease.

Measles are caused by RNA paramyxovirus group.

Clinical Features

Prodromal stage (4 to 5 days)

• Fever is present and there is abrupt rise in temperature to 400 C.
• *Catarrh: *Coryza, conjunctivitis, photophobia and hacking cough
• Koplik’s spots: They appear on second day as minute pin point bluish white specks with slight reddish motted areola around them, on buccal mucosa usually opposite to lower molars.
  They looks like grain of salt.
  They are variable in number.
  These spots begin to fade with appearance of rash.
  Red blotches may be seen on soft palate.
  Koplik’s spots may sometime occur on lover lip in front of lower incisors, in severe cases of palate and rest of mucosa are peppered with these spots.
• Laryngeal involvement: Hoarseness and laryngeal stridor is present.
• Gastrointestinal: Persistent vomiting and diarrhea.
• Fleeting rashes: Either urticarial or erythematous.

Exanthematous stage:

• On 5th day red macules appear fist behind the ear,along hair line, posterior part of cheeks and spread rapidly in few hours all over the body. Macules appear in crop which by conflence form blotches with crescentric or thumb nail edge.
• In severe disease rashes are conflent, face get swollen and disfigured and along with photophobic eyes creates typical measly appearance.
• Mucous membraneinvolvement: It includes conjunctivitis,rhinitis, stomatitis, laryngitis, tracheitis and bronchitis.

Stage of Defervescence

• Temperature falls by crisis or rapid lysis in 24 to 48 hours.
• Rashes fade from face and leaves brown staining followed by branny desquamation.
• At times normal rash of measles instead of fading become deep purple and this can persists for week or two.

Types Of Measles

• Toxic: This is malignant form of disease and is manifested by high fever, delirium, circulatory, fever and may be fatal.
• Pulmonary: Respiratory infection with high temperature and rapid respiration.
• Hemorrhage: It is rare. There is hemorrhage into the mucus membrane, skin and subcutaneous tissue.

Laboratory Findings

• Leukopenia is frequent. If leukocytosis is present it is indicative of superadded bacterial infection.
• In stained smears of sputum or nasal secretions or urine there is presence of multinucleated giant cells in which measles virus is isolated on appropriate cell cultures.
• Measles antigen is detected by florescent antibody test in stained respiratory or urinary epithelial cell.
• In patient having encephalitis along with measles, CSF examination is done which show rise in protein with cell count along with normal range. CSF shows lymphocytosis.

Management

• Bedrest is given.
• Frequent flid intake.
• Paracetamol for the fever.
• Irrigation of eyes with the boric lotion.
• Cough linctus to suppress the dry cough.
• Antibiotics such as amoxicillin if there are complications such as Otitis media or pneumonia.
• Vitamin A 200,000 IU orally for 2 days will prevent ocular complication and respiratory infections.

 

Question.17. Write short note on mumps.

Answer. Mumps is a widely prevalent infectious disease.

Etiology

It is caused by mumps virus which belongs to group of paramyxovirus.

Humans are the only natural host and infection spreads by droplet infection as well as by direct contact with respiratory secretions of the patient.

Incubation period usually ranges from 12 to 22 days average being 16–18 days.

Clinical Features

Onset of disease:

• Presence of moderate fever, sore throat, drawing or puckering feeling at angle of jaw.
• Swelling of face fist draw the attntion.
• Onset with rigor or convulsion.
• Onset with meningeal reaction, i.e. cerebral mumps

Early signs:

• Presence of pain or tenderness on pressure beneath angle of lower jaw.
• Redenning of parotid duct orifie

Other features:

• Usually one parotid gland is affcted followed by the other gland after varying interval or only one gland is affcted throughout.
  Swelling reaches to its maximum in 3 days, remain its peak for 2 days and slowly receds.
  Lobe of ear is in center of swelling which is tender on pressure.
• After appearance of parotitis fever rise to 400 C. Fever falls by lysis in 3 to 7 days.
  Other symptoms are diminished salivation, furred tongue and foul breadth.
• Enlargement of parotid may cause trismus and deafness.

Diagnosis

• Viral isolation: From saliva or nasopharynx in acute illness or from CSF in mumps meningitis.
• Antibody titer: Four fold rise in 1 to 2 weeks after infection.

Treatment

• It is mainly supportive and symptomatic.
• Child is put to bed rest.
• Mouth hygiene must be maintained meticulously.
• Analgesics and antipyretics are the main stay of treatment,i.e. paracetamol/nimulid syrup 1–2 teaspoonful two to three times a day
• Diet should be soft, bland and preferably in liquid form.
• In cases where complications like orchitis or neurological complications develop, prednisolone 40–60 mg per day in divided doses for about seven days is given along with antibiotics, i.e. Ampicillin/Amoxycillin/Cefazolin/Ceftizoxime.

Complications

Common complications:

• Orchitis and epididymitis: It is unilateral. Common in young adults, may occur without parotitis.
  Fever return and go up to 40–50°C.
  Testis is swollen, tender and tense with or without epididymitis. Last for 10 days. Can result in sterility.
• Meningitis: It follows parotitis and can occur at same time or before salivary gland enlargement.
• Oophoritis: It is less common than orchitis.
• Acute pancreatitis: Occur in 2nd week. Occasionally disease can be present with pancreatitis without salivary gland involvement.

Rare complications:

• Neurological: Meningoencephalitis, cranial nerve involvement, polyneuritis, other CNS problems, i.e. cerebellar ataxia, facial palsy, transverse myelitis, hydrocephalus, flccid paralysisand behavioral changes.
• Arthritis: Occassionally one or more large joints, but there is no permanent damage.
• Mastitis: Mild and transient enlargement of breasts.
• Prostatitis in males
• Thyroiditis
• Nephritis
• Fetal endocardial firoelastosis

Question.18. Write diffrential diagnosis of lock jaw.

Answer. Lock jaw or tetanus is caused by the powerful neurotoxin,i.e. tetanospasmin which is released by the C. tetani.

This disease is characterized by the muscular rigidity and spasms.

Differential Diagnosis

• Other causes of trismus: Irritant local lesions of teeth, throat,temporomandibular joint, masseter muscle and cervical lymph nodes.
• Meningitis: Neck rigidity can occur in both tetanus and meningitis, signs of meningeal irritation, diagnostic CSF.
• Rabies: Dysphagia associated with spasms of inspiratory and pharyngeal muscles also occur in rabies. History of dog bite is present
• Tetany: Spasm starts in periphery with carpopedal spasm.
• Drug dystonia: Dystonic relations to drug such as phenothiazines and metoclopramide.
  Grimacing,spasmodic and neck retraction and torticollis, wide opening of mouth and eyes.
  Dystonia prolong muscular contractions that may cause twisting of body parts,repetitive body movements and increased muscular tone.
• Acute peritonitis: Board like abdominal rigidity as in tetanus, but in tetanus there is litte or no tenderness.
• Functional muscle spasms: Bizarre movement of posture,absence of constant rigidity of involved muscles, history of previous personal disorders.
• Catatonic schizophrenia: It might cause confusion in absence of background information.

Question.19. Write clinical examination of tetanus patient.

Answer. Tetanus initially presents with muscle stiffness.

The distribution may vary with the type of tetanus.

The masseter muscles are commonly involved with an accompanying headache.

Neckstiffess, diffiltyswallowing, generalized muscle spasms including the abdominal and back muscles and sweating may be seen later in the disease.

In severe cases, respiratory paralysis may develop, which presents with apnea, hypoxia and hypercapnia.

Physical examination of a patient with tetanus may reveal the following:

General Appearance

• Severe muscular spasm (location varies with the type)
• Opisthotonos
• Leg extension with arm flxion
• Risus sardonicus
• May be in respiratory distress

Vitals

• Fever
• Tachycardia
• Elevated blood pressure

Musculoskeletal

• Spasms of the diaphragm and intercostals
• Stif abdominal wall

Respiratory

• Tachypnea
• Dyspnea

Cardiovascular

• Normal S1 and S2
• Hypertension
• Arrhythmia

Autonomic

Intervals of bradycardia and hypotension are accompanied by that of tachycardia and hypertension.

Abdominal

Stiffning of the abdominal muscles.

The physical examination may vary according to the type of tetanus. Specifi fidings associated with the various types of tetanus may include:

local tetanus

• Limited area of spasm
• The affcted area is in close proximity to a contaminated wound
• Contraction is usually painful and associated with swelling
• Generalized tetanus may follow localized tetanus

Cephalic tetanus

• Ear infection or head injury may be seen
• Trismus
• Signs of CN III, IV, VI, VII and XII involvement including:
  Tilting of the mouth
  Inability to close the eye
  Inability to move the tongue
  Diplopia
• Abnormal eye movements: Dysphagia
• Confusion
• Symptoms of stroke

Generalized tetanus

• Descending spasm
• Trismus may present initially:
  Followed by stiffess of the neck
  Diffilty in swallowing
  Stiffess of abdominal muscles
• Other symptoms include:
• Elevated temperature
  Sweating
  Elevated blood pressure
  Episodic rapid heart rate
• Spasms may occur frequently and last for several minutes
• Spasms may continue for 3–4 weeks
• Complete recovery may take months

Neonatal tetanus

• Unhealed, unhygienic umbilical stump
• Trismus (spasm of masseter muscle)
• Risus sardonicus (spasm of facial muscles)
• Clenched hands
• Dorsiflxion of the feet
• Opisthotonus (spasm of spinal muscles)

The Spatula Test

The “spatula test” is a clinical test for tetanus that involves touching the posterior pharyngeal wall with a sterile, soft­tipped instrument, and observing the effct.

A positive test result is the contraction of the jaw (biting down on the “spatula”), and a negative test result would normally be a gag reflx attmpting to expel the foreign object.

Question.20.How will you diffrentiate tetany from tetanus?

Answer.

Question.21.How will you diffrentiate rheumatoid arthritis from rheumatic arthritis?

Answer.

 

Question.22. Write short note on viral exanthema.

Answer. Viral infections associated with skin lesions are known as viral exanthems.

Viral exanthems lead to maculopapular rashes sparing palms as well as soles.

Following are the viral exanthems:

• Measles
• Rubella
• Varicella-zoster infection, i.e. chicken pox and
  shingles
• Exanthem infectiosum
• Exanthem Subitum
• Enteroviruses
• Infectious mononucleosis
• Adenovirus
• Reovirus
• Arbovirus.

Exanthematous Stage In Measles

• In exanthematous stage on 5th day the red macules appear behind the ear, along hair line and on posterior parts of cheeks and spread rapidly in a few hours all over the body. Macules appear in the crops which by conflence from bloatches with crescentric or thumbnail edge.
  Fully erupted rash deepens in color, petechiae may occur.
  In severe measles rash is conflent, the face is swollen and disfiured and together with photophobic eyes create typical measly appearance.
• Mucous membrane involvement: It consists of conjunctivitis,rhinitis, stomatitis, laryngitis, tracheitis and bronchitis.

Exanthema In Chicken Pox

• Evolution: In form of crops, first at back, then chest,abdomen, face and lastly limbs.
• Character: At fist macule appear then in few hours dark pink papule which soon turn into vesicle. They also get collapsed if pierced and vesicles turn into pustules in 24 hours and to scabs in 2 to 5 days.
• Distribution: It is centripetal, i.e. more on upper arm and thighs, upper part of face and in concavities and flxures.
• Cropping: Rash mature quickly and most spots dry up within 48 hours of appearance. For 2 to 3 days new spots continue to appear on any area of body vesicles,pustules and scabs are found side by side.

Exanthema In Rubella

In exanthema rash occurs more often in older children and adults on fist or second day of illness, fist on face and behind the ears, and then spreads downwards to trunk and limbs.

The rash is variable, but commonly starts as discrete, pink,punctate, erythematous, perifollicular macules that rapidly become conflent.

Alternatively, there may be blotchy pink rash or conflent blush.

Rash seldom persists for more than 4 days and is not followed by staining or desquamation.

Rubella without rash is common in young children.

In a dark skinned patient all that may be seen is prominence of hair follicles giving a goose pimpled appearance.

 

Question.23.Describe briefl AIDS.
Or
Write short note on AIDS. 

Answer. AIDS stands for acquired immunodeficiency syndrome

A CD4 count less than 200/µl in HIV infected individual is defied as AIDS.

Etiology

Both HIV 1 and HIV 2, members of lentivirus family of retroviruses causes AIDS, but HIV 2 appears to be less virulent progress slowly and is less commonly transmittd vertically.

Transmission

• Sexual: Most HIV infection occurs in homosexual man.
• Multiple heterosexual contacts often prostitutes.
• Contacts with blood and body flids, contaminated blood and blood products.
• Contaminated needles and syringes.
• Through organ and tissue donation
• From mother to child: In uterus at birth, breast milk.

Stages Of HIv Infection By WHo

Primary HIv Infection

• Asymptomatic
• Acute retroviral syndrome: Fever with maculopapular rash primarily on trunk with small aphthous lesions on oral and genital mucosa.

Clinical Stage 1

• Asymptomatic
• Persistent generalized Lymphadenopathy

Clinical Stage 2

• Unexplained moderate weight loss (< 10% of presumed body weight)
• Infections
• Recurrent respiratory tract infections
• Herpes zoster
• Fungal infections of figer nails: Oral lesions
• Recurrent oral ulcerations
• Angular cheilitis: Itchy dermatosis
• Papularpruritic eruptions
• Seborrheic dermatitis

Clinical Stage 3

Conditions where a presumptive diagnosis can be made on the basis of clinical signs or simple investigations.

Unexplained symptoms:

• Chronic diarrhea for > 1 month
• Persistent fever, intermittnt or constant for > 1 month

Severe weight loss (> 10% of presumed or measured body weight)

Infections:

• Severe presumed bacterial infections
• Pulmonary tuberculosis diagnosed in last 2 years

Oral lesions:

• Oral candidiasis
• Oral hairy leukoplakia
• Acute necrotizing ulcerative stomatitis, gingivitis or periodontitis

Conditions where confirmatory diagnostic testing is necessay

• Unexplained anemia (< 8 g/l or neutropenia (< 500 µl) or thrombocytopenia (< 50,000 µl) for > 1 month

Clinical Stage 4

Conditions where a presumptive diagnosis can be made on the basis of clinical signs and simple investigations

• HIV wasting syndrome
• Infections
• Pneumocystis pneumoniae
• Recurrent severe or radiological bacterial pneumonia
• Chronic herpetic simplex infection (oral, labial, genital or anorectal of > 1 month duration).
• Esophageal candidiasis
• Extrapulmonary tuberculosis

Neoplasms: Kaposi’s sarcoma

Neurological disease

• CNS toxoplasmosis
• HIV encephalopathy

Laboratory Diagnosis

Investigations for the diagnosis of HIV infection:

• HIV-ELISA: This is the most commonly used screening test for HIV infection. If this test is positive confimation should be done by western blot test.
• HIV-rapid antibody test: They are for rapid diagnosis,i.e. within 10 to 15 minutes. It is also a screening test,as if this test comes positive confimation is done by western blot.
• Western blot: It is the confirmatory test for HIV infection.
• Blood cell count: Since neutropenia, anemia and pancytopenia are associated with HIV infection, this test is done.

Investigations for monitoring progress of HIV infection:

• Absolute CD4 lymphocyte count: This is most commonly used. As its count decreases occurrence of opportunistic infection and malignancy is high, i.e. if count is less than 200 cells/µL.
• CD4 lymphocyte percentage: In this if count is less than 14% occurrence of opportunistic infection and malignancy is high, if treatment is not given to patient.

Investigations for virological monitoring: In this HIV viral load tests are done such as HIV RNA by PCR, HIV RNA by bDNA, HIV

• RNA by NASBA. These all tests measure the actively replicating HIV virus.
  These cells also deflct the response of antiretroviral drugs. These test are excellent for diagnosis of acute HIV infection before its seroconversion.

Treatment

The medical management of AIDS is done by HAART, i.e. highly active antiretro viral therapy.

It causes suppression of HIV replication and prolonging life as well as improving the quality of life of the patient.

The drugs used are:

Nucleoside reverse transcriptase inhibitors

• Zidovudine: Dose: 600 mg daily in two divided doses
• Didanosine: Dose: 400 mg OD. To be taken before meals
• Zalcitabine: It is used in combination with zidovudine:
• Dose is a 0.75 mg TDS.
• Lamivudine 150 mg orally BD

Nucleotide reverse transcriptase inhibitors

• Tenofovir: Dose: 300 mg orally OD

Non­nucleoside reverse transcriptase inhibitors

• Nevirapine: 200 mg orally daily for two weeks and
  then 200 mg BD
• Efavirenz: 600 mg orally daily

Protease inhibitors

• Amprenavir 1200 mg orally BD
• Atazanavir 400 mg orally daily
• Indinavir 800 mg orally TDS

Protease inhibitors boosted with ritonavir

• Lopinavir R 6 capsules per day
• Fosamprenavir 700 mg + 100mg ritonavir twice daily
• Ritonavir 100 mg BD orally

Fusion inhibitors

• Enfuvirtide 90 mg SC injection twice daily.

 

Question.24. Write clinical examination of advanced HIV disease in patient.

Answer. Clinical examination of advanced HIV disease.

External Examination

Patient is markedly cachectic with:

• Generalized lymphadenopathy
• Nodular skin lesion all over the body.
• White patches in the oral cavity.

Internal examination

• Skull: Meninges are congested and inflmed.
• Thorax: There was presence of dense adhesion between the pleura and the chest wall. Mediastinal lymph nodes were enlarged and mattd. Both lungs show marked destruction of parenchyma.
• Abdomen: Serosal surfaces of liver, spleen and kidney were studded with tubercle. Mesenteric lymph nodes were enlarged and mattd.
• Urinary bladder: Serosal surface shows presence of tubercles.
• Genital system: It is studded with tubercles.
• Adrenals: Enlarged, congested, shows presence of multiple tuburcles.

 

Question.25. Write short note on chickenpox.

Answer. It is an erythematous or vesiculopapular lesion caused by varicella­zoster virus.

It spreads through aerosol route.

Its incubation period is of 14 to 15 days

Clinical Features

Stage of invasion or prodomata:

• Presence of headache, sore throat and fever for 24 hours.
• Erythematous or urticarious prodromal rashes are seen.

Stage of eruption:

• Enanthem: Earliest lesions are on buccal and pharyngeal mucosa.
• Exanthem

• Evolution: In form ofcrops, fist at back, then chest,abdomen, face and lastly limbs.
• Character: At fist macule appear then in few hours dark pink papule which soon turn into vesicle.
  They also get collapsed if pierced and vesicles turn into pustules in 24 hours and to scabs in 2 to 5 days.
• Distribution: It is centripetal, i.e. more on upper arm and thighs, upper part of face and in concavities and flxures.
• Cropping: Rash mature quickly and most spots dry up within 48 hours of appearance. For 2 to 3 days new spots continue to appear on any area of body vesicles, pustules and scabs are found side by side.

Other symptoms:

• Pruritus of varying degree.
• Generalized lymphadenopathy may occur.
• Enlargement of suboccipital and posterior cervical lymph nodes.

Laboratory diagnosis

• A Tzanck smear, performed by scraping the base of an acute lesion and staining with Giemsa or Papanicolaou’s stain may demonstrate multinucleated giant cells having intranuclear inclusions.
• Other tests are florescent antibody against membrane antigen, immune adherence hemagglutination and ELISA.

Complications

• Cerebral ataxia
• Myocarditis
• Hepatitis
• Acute glomerulonephritis
• Pneumonia
• Arthritis
• Corneal lesion
• Bleeding diathesis.

Management

• No need to confie patient to bed unless symptoms are severe.
• For pruritus Calamine lotion with or without phenol (0.4%) and sedative antihistaminics by mouth. If there is much scabbing, gauze soaked in 1 in 5,000 solution of potassium permanganate which is changed every 4 hours may be applied to areas most affcted.
• For secondary infection antibiotics should be given.
• For true varicella pneumonia oxygen is given.
• For encephalitis oxygen and corticosteroids are given
• Paracetamol is given for fever.
• Oral acyclovir should be initiated within 24hours of rash results in a decrease in the duration and magnitude of the fever, and in the number and duration of skin lesions.
  Dose is 20 mg/kg qds.with maximum of 800 mg qds.

 

Question.26. Write short note on oral manifestations of HIV/AIDS.
Or
Describe oral manifestations of HIV

Answer. Classifiation of Oral Manifestations By EC-Clearing-house

Group 1: strongly associated With HIv Infection

• Candidiasis: Erythematous, pseudomembranous, angular cheilitis
• Hairy leukoplakia
• Kaposi’s sarcoma
• Non­Hodgkin’s lymphoma
• Periodontal diseases: Linear gingival erythema, necrotizing
  gingivitis, necrotizing periodontitis.

Group 2: less commonly associated with HIv Infection

• Bacterial infections: Mycobacterium avium-intracellulare,Mycobacterium tuberculosis
• Melanotic hyperpigmentation
• Necrotizing ulcerative stomatitis
• Salivary gland disease: Dry mouth, unilateral or bilateral swelling of major salivary glands
• Thrombocytopenia purpura
• Oral ulcerations NOS (not otherwise specifid)
• Viral infections: Herpes simplex, human papillomavirus,varicella­zoster

Group 3: seen in HIv Infection

• Bacterial infections: Actinomyces israelii, Escherichia coli,
  Klebsiella, pneumonia
• Cat­scratch disease (Bartonella henselae)
• Epithelioid (bacillary) angiomatosis (Bartonella henselae)
• Drug reactions: Ulcerative, erythema multiforme, lichenoid,toxic epidermolysis
• Fungal infections other than candidiasis: Cryptococcus neoformans, Geotrichum candidum, Histoplasma capsulatum,Mucoraceae (mucormycosis/zygomycosis), Aspergillus flvus
• Neurologic disturbances: Facial palsy, trigeminal neuralgia
• Recurrent apthous stomatitis
• Viral infections: Cytomegalovirus, Molluscum contagiosum

Description of oral Manifestations

• Candidiasis is the most common oral manifestation of HIV infection. All the three types. i.e. erythematous,pseudomembranous and hyperplastic forms are seen.
  Erythematous candidiasis is seen when the CD4 count drops below 400 cells/mm3 and pseudomembranous develop when CD4 count drop below 200 cells/mm3.
• Hairy leukoplakia: Presence of soft painless plaque on the lateral border of tongue with corrugated surface.
• Kaposi’s sarcoma: Single or multiple bluish swellings are seen with or without ulceration over gingiva and palate.
• Angular chelitis: Linear fisures or linear ulcers are seen at the angle of mouth.
• Linear gingival erythema: It is firy red band along the gingival margin and attached gingiva with profuse bleeding.
• Necrotizing ulcerative gingivitis: Destruction of inter­dental papillae is seen.
• Necrotizing ulcerative periodontitis: There is advanced necrotic destruction of periodontium, rapid bone loss, loss of periodontal ligament and sequestration.
• Oral ulcerations: Single or multiple major recurrent aphthous ulcers are seen with white pseudomembrane surrounding the erythematous halo.
• Non-Hodgkin’s lymphoma: It is the malignancy of HIV infected individuals. It occurs in extranodal locations and CNS is the common site. Intra­osseous involvement is also seen.
• Mycobacterial infection: Mycobacterial infection in form of tuberculosis is seen. When present tongue is affcted most commonly. Affcted areas show common ulcerations.
• Herpes simplex virus: Recurrent or secondary herpes simplex infection is seen in the patients. Herpes simplex lesions increase when CD4 cell count drops below 50 cells/mm3.
• Herpes zoster: It is common in HIV infected individuals.
  Orally, involvement is severe and leads to sequestration of bone as well as loss of teeth.
• Histoplasmosis: It is the fungal infection caused by histoplasma capsulatum. Sign and symptoms of disease are fever, weight loss, splenomegaly and pulmonary infitrate.
• Molluscum contagiosum: It is caused by pox virus. Lesions are small, waxy, dome shaped papules which demonstrate central depressed crater.

Question.27. Write short note on HIV importance in dental practice.

Answer. The HIV is the virus which results in the causation of the AIDS.

Prophylactic measures to be adopted by dental health care workers while treating AIDS patient.

• Care in handling sharp objects like needles, blades.
• All cuts and abrasions in an HIV patient should be covered with a waterproof dressing
• Minimal parenteral injections
• Equipments and areas which are contaminated with secretions should be wiped with sodium hypochlorite solution or 2% glutaraldehyde.
• Contaminated gloves, cottns should be incinerated.
• Equipments should be disinfected with glutaraldehyde.
• Disposable equipments (drapes,scalpels,etc.) should be used whenever possible.
• Walls and flor should be cleaned properly with soap water.
  Separate operation theater and staf to do surgeries to HIV patients is justifible
• Avoid shaving whenever possible before surgery in HIV patients.
• All people inside the theater should wear disposable gowns, plastic aprons, goggles, overshoes and gloves.
• Surgeons, assistants and scrub nurse should wear in addition double gloves.
• Suction botte should be half—filed with freshly prepared glutaraldehyde solution.
• Soiled body fluids should be diluted with glutaraldehyde.
• Accidental puncture area in surgeon or scrub nurse should immediately washed with soap and water thoroughly
• Theater should be fumigated after surgery to HIV patient.

 

Question.28. Write short note on HIV.
Or
Write on mode of transmission and clinical features of HIV.

Answer. HIV disease is an infectious disease caused by human immunodeficiency virus.

Late stage of HIV infection is AIDS when CD4 + T lymphocyte count is < 200/µL.

Etiology

Both HIV 1 and HIV 2, members of lentivirus family of retroviruses causes AIDS, but HIV 2 appears to be less virulent progress slowly and is less commonly transmittd vertically

Transmission

• Sexual: Most HIV infection occurs in homosexual man.
• Multiple heterosexual contacts often prostitutes.
• Contacts with blood and body flids, contaminated blood and blood products.
• Contaminated needles and syringes.
• Through organ and tissue donation
• From mother to child: In uterus at birth, breast milk.

Pathogenesis of HIv Infection

• HIV virus infects target cells (CD4 + T cells, monocytes,macrophages and dendrite cells) through CD4 receptors.
• On entering T cells, the virus integrates its RNA genome into the host cell genome by fist transcribing this genome into DNA (HIV provirus) with the help of enzyme reverse transcriptase.

 

• Provirus is then transcribed and translated along with the host cell DNA to synthesize specifi viral components, which eventually assemble to produce complete virus particles.
• At this time patient is seronegative, i.e. antibodies against the virus are not present. But patient is highly infectious. This period is labelled ”window period”.
• Although some virions are killed, HIV continues to multiply infecting increasing number of CD4 cells.

• In early stages of immune destruction, the patient is asymptomatic.
• As the immunosuppression progresses over a period of time patient becomes symptomatic.

Stages Of HIv Infection By WHo

Primary HIv Infection

• Asymptomatic
• Acute retroviral syndrome: Fever with maculopapular rash primarily on trunk with small aphthous lesions on oral and genital mucosa.

Clinical Stage 1

• Asymptomatic
• Persistent generalized lymphadenopathy

Clinical Stage 2

• Unexplained moderate weight loss (<10% of presumed
  body weight)
• Infections
• Recurrent respiratory tract infections
• Herpes zoster
• Fungal infections of figer nails
  Oral lesions
• Recurrent oral ulcerations
• Angular cheilitis
  Itchy dermatosis
• Papularpruritic eruptions
• Seborrhoeic dermatitis

Clinical Stage 3

Conditions where a presumptive diagnosis can be made on the basis of clinical signs or simple investigations.

• Unexplained symptoms
  Chronic diarrhoea for > 1 month
  Persistent fever, intermittnt or constant for > 1 month
• Severe weight loss (> 10% of presumed or measured body weight)
  Infections
• Severe presumed bacterial infections
• Pulmonary tuberculosis diagnosed in last 2 years
  Oral lesions
• Oral candidiasis
• Oral hairy leukoplakia
• Acute necrotizing ulcerative stomatitis, gingivitis or periodontitis
  Conditions where confimatory diagnostic testing is necessary
• Unexplained anemia (< 8 g/L or neutropenia (< 500 µL) or thrombocytopenia (< 50,000 µL) for > 1 month

Clinical Stage 4

Conditions where a presumptive diagnosis can be made on the basis of clinical signs and simple investigations

• HIV wasting syndrome
• Infections
  Pneumocystis pneumonia
  Recurrent severe or radiological bacterial pneumonia
  Chronic herpetic simplex infection (oral, labial, genital or anorectal of > 1 month duration).
  Esophageal candidiasis
  Extrapulmonary tuberculosis
• Neoplasms
  Kaposi’s sarcoma
• Neurological disease
  CNS toxoplasmosis
  HIV encephalopathy

 

Question.29.Give defiition, etiology, signs, symptoms, diagnosis,diffrential diagnosis and complications of enteric fever.

Answer.

It is an acute systemic illness caused by infection due to salmonella typhi.

Typhoid fever is characterized by fever, malaise, pain abdomen, rash, splenomegaly and leukopenia.

The untreated patients may develop complications during 2nd and 3rd week due to toxemia and septicemia.

In some cases it may be fatal.

Diagnosis

First Week

• Normochromic normocytic anemia, leukopenia and albuminuria
• Blood culture may be positive in 70–90% of cases.

Second Week

• Anemia, leukopenia may persist
• Widal test become positive, may show four fold rise in agglutinins against somatic ‘O’ antigen. It is not specifi but rising titers are diagnostic.
• Blood culture may be positive only in 50%

Third Week

• Anemia and leucopenia persist. Leukocytosis occur in severe septicemia
• Blood culture is positive in 30-45% of cases.
• Positive WIDAL test with rising titers
• Positive stool culture and urine test for S. typhi.

Differential Diagnosis

• Para typhoid fever: Mode of onset often acute and atypical; Wider remissions of temperature; Eruption is more profuse; less toxaemia; sweating and rigours more common; Intestinal complications rare
• Short fever: A fever lasting for 8 to 10 days; no associated signs, probably of viral origin. Subside spontaneously.
  No complications.
• Amoebic liver abscess: Pain in right hypochondrium and lower chest, moderate fever, enlarged tender liver or compression tenderness over right lower intercostal spaces. Right hemidiaphragm may be elevated and immobile on floroscopy.
• Viral hepatitis: In pre­icteric stage there is marked nausea and vomiting, hepatic tenderness, high colored urine.
• Tuberculous meningitis: Absence of abdominal discomfort, greater frequency of vomiting, persistence of headache after fist week, irritability, irregular pupils,CSF changes.
• Miliary tuberculosis: Increased respirations, irregular temperature, tachycardia, cough and cyanosis, symptoms referable to alimentary tract less pronounced. Early loss of flsh. Diagnostic CXR.
• Heat fever: Not uncommon in children and aged. Fever may be continuous or touch normal for some hours every day. Absence of other physical signs. Response to lowered temperature.
• Subacute infective endocarditis: Fever seldom continuous or high; Frequent chills with septic type of temperature; cardiac signs; anaemia; embolic phenomenon; positive blood culture.
• E. coli infection: Pyelitis or septicemia—high fever,though not of continuous type. May last for 2–3 weeks.
  Leukocytosis, tenderness in loins, pus in urine or positive blood culture.
• Malaria: Sudden onset, wide diurnal variation, early splenic enlargement, malarial parasites in blood, response to antimalarial drugs.

Question.30. Write short note on WHO criteria for diagnosis of AIDS.

Answer. WHO criteria for diagnosis of AIDS.

Primary HIv Infection

• Asymptomatic
• Acute retroviral syndrome: Fever with maculopapular rash primarily on trunk with small aphthous lesions on oral and genital mucosa

Clinical stage 1

• Asymptomatic
• Persistent generalized lymphadenopathy

Clinical stage 2

• Unexplained moderate weight loss (< 10% of presumed body weight)
• Infections
• Recurrent respiratory tract infections
• Herpes zoster
• Fungal infections of figer nails
  Oral lesions
• Recurrent oral ulcerations
• Angular cheilitis
  Itchy dermatosis
• Papular pruritic eruptions
• Seborrheic dermatitis

Clinical Stage 3

• Conditions where a presumptive diagnosis can be made on the basis of clinical signs or simple investigations.
• Unexplained symptoms
  Chronic diarrhea for > 1 month
  Persistent fever, intermittnt or constant for > 1 month
• Severe weight loss (> 10% of presumed or measured body
  weight)
  Infections
• Severe presumed bacterial infections
• Pulmonary tuberculosis diagnosed in last 2 years
  Oral lesions
• Oral candidiasis
• Oral hairy leukoplakia
• Acute necrotizing ulcerative stomatitis, gingivitis or periodontitis
  Conditions where confimatory diagnostic testing is necessary
• Unexplained anemia (< 8 g/l or neutropenia (< 500 µl) or thrombocytopenia (< 50,000 µL) for > 1 month

Clinical stage 4

• Conditions where a presumptive diagnosis can be made on the basis of clinical signs and simple investigations
• HIV wasting syndrome
• Infections
• Pneumocystis pneumonia
• Recurrent severe or radiological bacterial pneumonia
• Chronic herpetic simplex infection (oral, labial, genital or anorectal of > 1 month duration).
• Esophageal candidiasis
• Extrapulmonary tuberculosis
• Neoplasms
• Kaposi’s sarcoma
• Neurological disease
• CNS toxoplasmosis
• HIV encephalopathy

 

Question.31. Write short note on risk factors for candidiasis.

Answer. Following are the risk factors for candidiasis.

Any condition that weakens the immune system, such as:

• Diabetes
• Organ transplant
• Chemotherapy
• AIDS
• Daily corticosteroid use
• Breaks in the skin or mucous membranes
• Kidney dialysis
• Intravenous catheters
• Intravenous drug abuse
• Obesity
• Peptic ulcer disease
• Severe burns
• Urinary catheters

 

Question.32. Enumerate etiology, clinical features, investigations,complications and management of enteric fever.
Or
Discuss clinical feature, complication and management of enteric fever.
Or
Write etiology, clinical features, investigations, treatment and complications of enteric fever (Typhoid).

Or
Describe the complications and treatment of enteric fever
Or
Write enteric fever under following headings:

• Etiology
• Clinical features
• Complications
• Treatment

Or
Write etiology, clinical features, investigation and treatment of enteric fever.
Or
Describe enteric fever under following headings:

• Etiology
• Clinical features
• Complications
• Treatment

Or
Write etiology, clinical features, diagnosis and management of enteric fever.
Answer.

Treatment

Specific

• Ciprofloxacin: It is given in the dose of 500 mg BD for 7 to 10 days it is avoided in children because of risk of cartilage damage and tendonitis. If absolutely required, low dose can be used for not more than 3 days.
• Ceftriaxone: It is 3rd generation cephalosporin and improves the condition rapidly.
  It is given in the dose of 1 gm BD for 10 to 14 days.
• Azithromycin: 1 gm OD for 5 days.

Supportive Treatment

• Treatment of fever paracetamol
• Good nursing care
• Nutritious diet should be given
• Fluid and electrolyte balance should be maintained.
• For severe toxemia and peripheral circulatory failure.
  corticosteroids may be used, i.e.
  Dexamethasone 3 mg/kg stat followed by 8 doses of 1 mg/kg 6 hourly for 48 hours each given by IV infusion over 30 min.

Treatment Of Carrier

Patients who are asymptomatic, but constantly releases bacteria in stool because bacteria are persisting in gall­ bladder.

• Ampicillin 500 mg QID for six weeks.
• Ciproflxacin 500 mg BD for 2 to 4 weeks.
• Cholecystectomy if above measure fails.

 

Question.33. Write in brief on gum hypertrophy.

Answer. Gum hypertrophy means increase in the size of gums.

Classifiation

According to etiologic factors and pathologic changes, gingival enlargements are:

Infmmatory enlargement

• Chronic
• Acute.

Drug-Induced Enlargement

Enlargement associated with systemic disease

Conditional enlargement

• Pregnancy
• Puberty
• Vitamin C defiiency
• Plasma cell gingivitis
• Non-specifi conditional enlargement.

Systemic diseases causing gingival enlargement

• Leukemia
• Granulomatous disease.

Neoplastic Enlargement

• Benign tumors
• Malignant tumors

False enlargement

According to location and distribution gingival enlargement are classifid as:

• Localized: Gingival enlargement limited to one or more teeth.
• Generalized: Entire mouth, gingiva is enlarged.
• Marginal: limited to marginal gingiva.
• Papillary: Confied to inter-dental papilla.
• Diffuse: Involves all parts of gingiva that is marginal,attched and inter-dental.
• Discrete: Isolated sessile or pedunculated tumor like enlargement.

According to degree of gingival enlargement:

• Grade 0: No sign of gingival enlargement.
• Grade I: Enlargement confimed to inter-dental papilla
• Grade II: Enlargement involves papilla and marginal gingiva.
• Grade III: Enlargement covers three quarters or more of the crown.

Clinical Features

• Presence of slight ballooning of interdental papilla and marginal gingiva
• The enlargement progress slowly and painlessly
• It occurs as a discrete sessile or pedunculated mass resembling a tumor, it may be inter proximal or on marginal or attched gingiva
• The lesions are slow growing masses
• The lesions undergo spontaneous reduction in size,followed by exacerbation and continued enlargement
• Painful ulceration sometimes occur in fold between mass and adjacent gingiva.

Treatment

• Scaling and curettge: If the size of enlargement does not interfere with complete removal of deposits, the enlargement caused due to inflmmation is treated by scaling and curettge.
• Surgical removal: Indicated for two reasons.

• In enlargement with signifiant firotic component that does not undergo shrinkage following shrinkage and curettge.
• If size of enlargement interferes with access to root surface deposits.

 

Question.34. Write in brief signs, symptoms and treatment of diphtheria.

Answer. Diphtheria is an acute infectious disease caused by nonmotile, non­sporing generally aerobic Gram­positive rods C. diphtheriae.

Symptoms

• Patient complains of presence of sore throat.
• Low grade fever is present.
• Presence of headache and malaise.
• Hoarseness of voice, dyspnea in cases with laryngeal diphtheria.

Signs

• Presence of gross cervical lymphadenopathy.
• Formation of b luish white or grayish green pseudomembrane at the site of infection.
• Punched out ulcerations are present if skin is involved.
• Foul smelling serosanguinous discharge in cases of nasal diphtheria.
• Cyanosis is seen in cases with laryngeal diphtheria.

 

Question.35. Write in brief clinical features and treatment of syphilis.

Answer. Syphilis is a sexually transmittd disease caused by
Treponema palladium.

Clinical Features

Acquired syphilis is divided into three stages, based on this

Clinical Features Are As Follows:

Primary syphilis

• A single painless macule is seen over penis which later on become papular and then ulcerates forming punched out ulcer with well­defined margins,indurated base and fail to bleed on trauma. It is known as chancre.
• In men, the ulcer is found on the coronal sulcus or on glans penis and in women on vulva, vaginal walls or cervix.
• Bilateral inguinal lymphadenopathy occur. Lymph nodes are discrete, rubbery in consistency and are non­tender.
• In very short time, generalized lymphadenopathy occurs and as the lesion heals lymphadenopathy persists for a longer time.
• Untreated ulcers resolve spontaneously in 3 to 8 weeks, usually without leaving a scar.

Secondary Syphilis

• In one­third of patients, primary lesions are still evident when secondary manifestations occur.
• One to three months after appearance of primary chancre secondary stage develops.
• Patient complains of malaise, headache and fever.
• A macula­papular rash appears over trunk and extremities which is symmetrical, dull red in color and is nonitchy.
• Condylomata lata are seen over round the anus, on labia, between buttcks, on lateral aspect of scrotum and other warm moist areas of body.
• Ulcers are seen over mucous membrane of mouth,these ulcers may coalesce to form snail track ulcers.
• Laryngeal lesions involving the vocal cords may give rise to hoarseness of voice
• Either regional or generalized lymphadenopathy is present.

Late syphilis

It is divided into two, i.e. late latent syphilis and tertiary syphilis

Late latent syphilis
It is associated with no clinical manifestations, but time elapsed since acquisition of disease is more than 2 years.

Tertiary syphilis

• It takes years to develop.
• Gumma is a painless round swelling which is rubbery in consistency and involves deeper tissues such as muscle or bone and later on manifests as solitary, deep punched out mucosal ulcer.
• Mucosal gummas affct submucous tissues of mouth,throat, palate, larynx, pharynx and nasal septum. They can ulcerate with punched out appearance and lesions have a sloughy base.
• Bony gummas are diffse subperiosteal reactions which often occur in long bones, particular in anterior margin of tibia.
• Formation of lytic lesions can lead to perforation of hard palate or nasal septum which causes collapse of nasal bridge.

Treatment

Primary, secondary and early latent syphilis

• Benzathine penicillin G 2.4 million units IM usually in two sites (4 mL in each buttck) at a single visit.
  Additional dosages of 2.4 million units should be given 7 to 14 days later for latent syphilis of unknown duration..
• If patient is allergic to penicillin give ceftriaxone 125 mg IM OD for 10 days and azithromycin 1 gm orally OD Or oral doxycycline 100 mg BD for 14 days.

Tertiary Syphilis

• Benzathine penicillin G 2.4 million units IM weekly for three weeks.
• If patient is allergic to penicillin give oral doxycycline 100 mg BD for 14 days.

 

Question.36. Write short note on gonorrhea.

Answer. It is a sexually transmittd disease caused by Neisseria gonorrhoea.

Clinical Features

In males:

• Earliest symptom present is burning or tingling sensation in urethra followed by discharge which becomes muco­purulent.
• Dysuria is presence and increased frequency of micturition.
• Pus is greenish yellow in color.

In females:

• Presence of dysuria, vaginal discharge, abnormal menstrual bleeding and rectal discomfort are the symptoms.
• Leucorrhea is present and feature of pelvic infection are present. Pelvic infection may lead to abscess formation and toxemia.
• Extension of infection leads to salpingitis, bartholinitis and abdominal pain.

Diagnosis

• History of sexual contact with pus discharge from urethra in males and from vagina in females make diagnosis more likely.
• It is made by demonstration of intracellular gram­negative diplococcic in smears obtained from urethral discharge and staining with Gram stain.
• Immunofloroscent antibody test gives quick diagnosis
  ELISA is done to detect gonococcal antigens.

Complications

In males:

Local complications

• Epididymitis
• Prostatitis
• Inguinal lymphadenitis
• Periurethral abscess and later on periurethral
  fitula.

Systemic complications

• Arthritis
• Bacteremia.

In females:

Local complications

• Premature birth
• Salpingitis
• Pelvic infection.

Systemic complications

• Perihepatitis
• Pustular eruption.

Treatment

• IM injection of 2.4 g of procaine penicillin with 1 g of probenecid orally.
• Alternative therapy oral amoxicillin or ampicillin 3 g as single dose with 1 g of probenecid orally Or cotrimoxazole 4 g in single dose.
• For penicillin resistant gonorrhea ciproflxacin is given 250 to 500 mg orally as single dosage Or Cefotaxime 0.5 to 1 g IM as single dosage.
• For complicated gonorrhea patient is hospitalized.
  Penicillin G IV 10 million units is given for 5 days;
  ciproflxacin 500 mg BD for 5 days; ceftriaxone 1 g IV for 5 days is given.

 

Question.37. Write short note on risk factors and prophylaxis of HIV infection.

Answer. Following are the risk factors of HIV infection risk Factors

• People who have unprotected vaginal or anal sex.
• People who have sex with many partners, thereby increasing the chance that they will encounter a partner who is HIV infected.
• People who share needles, for example for intravenous drug use, tattoing or body piercing
• Babies of mothers who are HIV infected.
• People who have another STD, especially STDs that cause open sores or ulcers such as herpes, chancroid or syphilis.
• Hemophiliacs and other people who frequently receive blood products (this risk is now very much diminished,but there are still countries where blood is not adequately screened)
• Health care workers, where precautions are neglected or fail for example through not wearing gloves or accidental needle stick injuries.

Prophylaxis

• Practice safer sex. This includes using a condom unless you are in a relationship with one partner who does not have HIV or other sex partners.
• Never share intravenous (IV) needles, syringes, cookers, cottn, cocaine spoons, or eyedroppers with others if you use drugs.
• Do not donate blood, plasma, semen, body organs, or body tissues.
• Do not share personal items, such as toothbrushes, razors, or sex toys, that may be contaminated with blood, semen,or vaginal flids.
• The risk of a woman spreading HIV to her baby can be greatly reduced if she: is on medicine that reduces the amount of virus in her blood to undetectable levels during pregnancy; continues treatment during pregnancy; Does not breast­feed her baby.
• Healthcare workers should take universal precautions while treating HIV positive patient.

 

Question.38. Discuss the signs, symptoms, diagnosis and treatment of malaria.
Or
Write short note on malaria.

Answer. Malaria is the acute febrile illness which is characterized by paroxysms of fever as a result of asexual reproduction of plasmodia in red cells.

Symptoms And Signs
Onset of malaria is with lassitude, anorexia, headache and fever with chills.

Three clinical stages are present:

• Cold Stage: It remains for half an hour. Patient feels intense cold and shivers from head to foot, teeth of patient chattr.
  Patient cover himself with blanket.
  Fever raises rapidly and is as high as 41°C.
• Hot stage: It follows cold stage and last for 3 to 4 hours.
  Patient feels intense heat and throws blanket.
  Patient has flshed face, headache, vomiting, dry skin.
• Sweating Stage: Patient has excessive perspiration,temperature is declined and patient feels relief.

Diagnosis

• Clinical: Periodic fever with chills, sweating, anemia and splenomegaly.
• Blood fim: Malarial parasites are identifid in thick and thin blood smears. Common microscopic characters of falciparum malaria are high concentration of parasites, predominant thin ring­shaped trophozoites
• Malarial antigen spot test using parasite LDH: P. falciparum antigens are taken from blood by figer prick and are exposed to monoclonal antibodies to detect antigens and read out color bands.
• Immunofloroscent microscopy and PCR (Polymerase chain reaction)
• Latex agglutination assay.

Treatment

Treatment of chloroquine susceptible P. vivax, P. falciparum,P. ovale, P. malariae chloroquine: This is given in the dose of 600 mg base followed by 300 mg at 6th, 24th and 48th hours. It is useful in treating all types of malaria. It is curative for P. falciparum malaria but cannot prevent relapses due to exoerythrocytic cycles of P. vivax malaria

Treatment of chloroquine resistant P. falciparum:

• Quinidine IV 10 mg/kg dissolved in 300 mL normal saline infused over 1 to 2 hour.
• Quinine hydrochloride: 600 mg TDS for 3-7 days is useful.
  If required for cerebral malaria, this drug can given IV the dose is 7 mg/kg over 30 min, followed by 10 mg/kg over 4 hours and then 10 mg/kg over 8 hour or until the patient can complete a week of oral treatment.
• Meflquine: It provides rapid schizonticidal action in single dose of 15 mg/kg orally maximum dose is 1000 to 1250mg.
• Halofantrine
  Dosage: Adult 500 mg BD for 4–6 days.
  Children: 8 mg/kg
• Artemether: This drug is rapidly acting, safe and is effctive against multidrug resistant infections.
  Artemether 3.2 mg/Kg IM is given followed by 1.6mg/Kg IM every 12 to 24 hours until patient wakes up.
  Artesunate 2 mg/Kg IV stat followed by 1mg/Kg 12 hourly.
• Sulfadoxine and pyrimethamine: Combination of sulfadoxime 1500mg and pyrimethamine 25 mg helps to cure an acute attck ofchloroquine resistant malaria.
• Treatment of Chloroquine resistant P.vivex
  Oral meflquine and halofantrine.
• Treatment of persistent hypnozoites in P. vivex or P.
  Ovale Infection
• Primaquine: It is given in the dose of 7.5 mg BD for 14 days usually after doing a G6PD test
• Bulaquine: It is given 25 mg OD for 5 days.

Question.39. Write short note on clinical features and treatment of P. vivex malaria.

Answer.

Clinical Features

Onset of malaria is with lassitude, anorexia, headache and fever with chills.

Three clinical stages are present:

• Cold Stage: It remains for half an hour. Patient feels intense cold and shivers from head to foot, teeth of patient chattr.
  Patient covers himself with blanket.
  Fever raises rapidly and is as high as 41°C.
• Hot stage: It follows cold stage and last for 3 to 4 hours.
  Patient feels intense heat and throws blanket.
  Patient has flshed face, headache, vomiting, dry skin.
• Sweating Stage: Patient has excessive perspiration,temperature is declined and patient feels relief.

Treatment

• Treatment ofchloroquine susceptible P. vivax:
• Chloroquine: This is given in the dose of 600 mg followed by 300 mg at 6th, 24th and 48th hours.
• Treatment ofChloroquine resistant P.vivax:
• Oral meflquine with dosage of three 250 mg tablets which are repeated after 6 hours.
• Treatment ofpersistent hypnozoites in P. vivax infection:
• Primaquine 30 mg per day orally for 14 days is given.

Question.40. Write short note on causes and treatment of bleeding gums.

Answer.

Causes of Bleeding Gums

Following are the causes of bleeding gums:

• Gingivitis and gingivostomatitis
• Bleeding disorders, i.e. Thrombocytopenia,hemophilia, leukemia and anticoagulants.
• Abnormalities ofvessel wall: Scurvy, Henoch Schönlein purpura, dysproteinaemia
• Connective tissue disorders: Ehlers­Danlos syndrome,pseudoxanthoma elasticum.

Treatment Of Bleeding Gums

• Bleeding gums can be treated by the removal of the source of bacteria.
• Proper maintenance of the teeth by the patient is a must.
• Sore and bleeding gums can be aggravated by citrus fruits and juices, rough or spicy food, alcohol, and tobacco.
• Take vitamin C supplements, if citrus fruits and juices cannot be taken.
• If dentures make gums bleed, wear them only during meals.
• Gum bleeding can be controlled by applying pressure with a gauze pad soaked in ice water directly to the bleeding gums.
• Brush teeth gently after every meal. Use a soft brush, or a special vibrating brush to clean the teeth without irritating the gums.
• Use gumpaint regularly to control bleeding from the gums.

 

Question.41. Write short note on herpes zoster infection.
Or
Write short answer on herpes zoster infection.

Answer. It is also known as shingles.

Herpes zoster is the secondary form of infection.

After primary infection virus remains dormant in the dorsal root or cranial nerve ganglia.

The disease recurs in the localized form which remains to its dermatome innervated by spinal or cranial sensory ganglion or it can affct the motor nerve causing facial nerve palsy.

Predisposing Factors

Herpes zoster is more common in people with diminished cell mediated immunity.
This includes elderly people, patients with lymphoma receiving chemotherapy or steroids, and individual with HIV.

Clinical Features

• It consists of two stages, i.e.
• Pre-eruptive stage: Pain with hyperaesthesia along the course of the nerve and fever.
• Eruptive stage: May be the fist manifestation of disease in some cases.
• There are several edematous patches along the course of a nerve with intervening clear areas, these are very tender and painful.
• A few hours later these patches are surmounted with small vesicles in cluster. Vesicles occur in crops. The contents may become purulent. The vesicles crust over, and in absence of secondary infection, clear within a week.
• Chronic ulcerative lesions may be seen in HIV­infected patients.
• Regional glands are painful and tender.
  An attck lasts for 2–3 weeks.
• The rash is usually unilateral and leaves behind pigmentation and scarring.
• Thoracic and lumbar dermatomes are the sites most commonly affcted.
• An eruption in the mandibular and maxillary distribution of trigeminal nerve is associated with oral, palatal and pharyngeal lesions. If there is involvement of ophthalmic division, there can be keratitis or uveitis with presence of vesicles over the nose.

Complications

• Post­herpetic neuralgia
• Keratitis and corneal ulceration
• Neurological, i.e. encephalitis, meningitis and myelitis.

Management

• Acyclovir 800 mg orally fie times a day for a week is given.
• Acyclovir cream can be applied over the lesions also.
• Prednisolone 40–60 mg in tapering doses is given for 3 weeks.
• Calamine lotion or cream is given to the patient for prevention of irritation in the lesion.
• Anti­septic powder can also be applied for preventing the secondary infection. This should be applied after vesicles break
• Analgesics can be given as per need.
• For post herpetic neuralgia analgesics,amitriptyline,gabapentin, pregabalin, tramadol and carbemazepine is given.

 

Question.42. Write short note on postexposure prophylaxis in HIV/AIDS.
Or
Write post exposure prophylaxis in AIDS.

Answer. Following is the post exposure prophylaxis in HIV/AIDS:

• HIV post exposure prophylaxis is started within an hour or two.
• Depending on the type and seriousness of the exposure either a basic regimen, i.e. zidovudine with lamivudine is followed or expanded drug regimen,i.e. zidovudine + lamivudine + Indinavir is given.
• Following is the recommended HIV postexposure prophylaxis:

Question.43. Write etiology, clinical features, investigations and complications of HIV infection.

Answer. The presence of a reliably diagnosed disease, i.e.atleast moderately indicative of an underlying defect in cell­mediated immunity occurring in a person with no known cause for immunodeficiency other than the presence of HIV.

Etiology

• HIV infection is caused by the infection with virus HIV­1 and HIV­2.
• HIV­1 is most common worldwide. It has many strains due to the mutation.
• HIV-2 has 40% sequence homology with HIV-1 and is very closely related to simian immunodefiiency virus.

Clinical Features

Clinical features of HIV infection as per its stage are as follows:

Investigations

Investigations for the diagnosis of HIV infection

• HIV­ELISA: This is the most commonly used screening test for HIV infection.
  If this test is positive confimation should be done by western blot test.
• HIV-rapid antibody test: They are for rapid diagnosis,i.e. within 10 to 15 minutes.
  It is also a screening test,as if this test comes positive confimation is done by western blot.
• Western blot: It is the confirmatory test for HIV infection.
• Blood cell count: Since neutropenia, anemia and pancytopenia are associated with HIV infection, this test is done.

Investigations for monitoring progress of HIV infection

• Absolute CD4 lymphocyte count: This is most commonly used.
  As its count decreases occurrence of opportunistic infection and malignancy is high, i.e.if count is less than 200 cells/µL.
• CD4 lymphocyte percentage: In this if count is less than 14% occurrence of opportunistic infection and malignancy is high, if treatment is not given to patient.

Investigations for virological monitoring

In this, HIV viral load tests are done such as HIV RNA by PCR, HIV RNA by bDNA, HIV RNA by NASBA.

These all tests measure the actively replicating HIV virus.

These cells also deflct the response of antiretroviral drugs.

These test are excellent for diagnosis of acute HIV infection before its seroconversion.

Complications

Question.44. Write herpes simplex under following headings:

• Causative organism
• Manifestations/Clinical features
• Treatment

Or
Write short answer on herpes simplex

Answer.

Causative organism

Herpes simplex is caused by a DNA virus.
Virus consists of two strains, i.e. Type 1 and Type 2.
Type 1 virus enters through the mouth while Type 2 virus is sexually transmittd and leads to anorectal or genital infections.

Manifestations or clinical Features

Primary infection by herpes simplex

Mucous membranes:

• Acute gingivostomatitis: It is characterized by soreness of mouth, salivation, fever and malaise.
  Vesicles are present in the mouth.
• Keratoconjunctivitis: The condition is painful and is unilateral. Ulceration of cornea can occur which leads to chronic scarring.
• Genital herpes: In females, vesicles are present over the vulva, cervix or vagina. In males, vesicles are seen on glans penis or less commonly urethritis.

Skin:

• Disseminated herpes simplex: Seen in new born infants. Brain, liver, lungs and other vital organs are affcted.
• Eczema herpeticum: In cases with atopic dermatitis,herpes simplex develops in varicelliform.
• Herpetic whitlow: It manifest as indolent inflmmatory arising at site of minor skin trauma on figer in form ofdeep, painful multiple vesicles over the figer tip.
• Anal infection: In homosexuals there is intense pain, tenesmus and local vesicles are present.

Recurrent infection

• Herpes labialis: Lesions appear on vermilion border of lip and surrounding skin.
  These lesions are grey or white vesicles which rupture quickly leaving small red ulcerations with slight erythematous halo on lip covered by brown crusts.
• Eye infection: Recur as superfiial keratitis.
• Genital infection: They are mild and short as compared to its primary form.

Treatment

• 5% acyclovir cream, is applied in every 4 hours.
• For severe infection oral acyclovir 200 mg 5 times a day is given. Reduce the dose to half in children.
• IV acyclovir 5 mg/kg for every 8 hours by slow infusion is given.
• Anti­bacterial therapy is given in mucocutaneous herpes to reduce risk of secondary infection.

Question.45. Write short note on rose spots.

Answer.

Rose spots are the clinical sign for typhoid fever.

• As fist week of typhoid fever is over rose spots appear.
• Rose spots appear over the trunk. They can also be seen over back and chest.
• They are small macules which are 2–4 mm in diameter, red in color and on applying pressure they show blanching.
• Rose spots lasts for 2–3 days.

Question.46. Write in short treatment of esophageal candidiasis.

Answer.

Treatment of esophageal candidiasis

• Oral flconazole systemically 200 mg/day for 14–21 days is given.
• In cases with severe dysphagia, IV administration of Fluconazole is done.
• Patients who had previous infection of esophageal candidiasis, patient should be given Fluconazole 100–200 mg daily for prophylaxis.

Question.47. Write short note on infectious mononucleosis.

Answer. It is also known as glandular fever.

• Infectious mononucleosis is caused by Epstein-Barr virus (EBV).
• Incubation period for virus is 7–20 days.

Pathogenesis

EBV undergo replication in lymphoid tissues of throat and is transmittd to healthy person via saliva.

Clinical Features

• There is presence of acute onset of fever with chills, core throat, headache, malaise and tiredness.
• Lymph nodes become enlarged, discrete and slightly tender affecting cervical and submandibular lymph nodes.
• Non­tender splenomegaly is present.
• Petechial rash can occur at the junction of hard and soft palate on 4th day and can persist for 3–4 days.

Investigations

• Peripheral smear shows leucocytosis with atypical lymphocytosis.
• Paul-Bunnell test can be positive in 1:32 dilution.
• Liver transminases are raised.

Complications

• Fatigue
• Hemolytic anemia
• Hepatitis
• Meningoencephalitis
• Thrombocytopenia.

Management

• In acute phase of disease, patient should be on bed rest.
  Condition resolve in 4 weeks.
• Short course of steroids can be used, i.e. 10 mg prednisolone thrice daily with tapering dosages.
• Gargles with soluble aspirin are helpful for relieving sore throat.
• Antibiotics, i.e. erythromycin can be given, if secondary infection is present.
• Interferon-α administration, cytotoxic chemotherapy and radiation therapy can also be used.

 

Question.48. Write short note on complications of enteric fever.

Answer.

Intestinal complications

• Hemorrhage may occur at the end of the second week and is characterized by black stools, tachycardia,hypotension and diarrhea.
  There is no abdominal pain or rigidity or obliteration of liver dullness like in intestinal perforation.
  Transfusions may be needed, if there is massive blood loss.
• Perforation may occur at the end of the second week or in the third week. It is characterized by acute pain in the lower abdomen, vomiting, abdominal distension,hypotension and tachycardia.
  Liver dullness may be obliterated and the abdomen becomes tender, rigid and silent (absent peristalsis).
• Tympanitis
• Cholecystitis
• Splenic infarction
• Rarely, appendicitis, intussusception and pyogenic
  liver abscess

Extraintestinal complications

• Myocarditis, endocarditis
• Osteomyelitis, arthritis, typhoid spine and Zenker’s
  degeneration of rectus abdominis
• Pulmonary infection and embolism
• Thrombophlebitis
• Electrolyte imbalance, shock and acute renal failure
• Neurological: Meningoencephalitis, meningism,cranial nerve palsies, myelitis, ascending paralysis,Parkinsonism, athetosis, cerebellar ataxia, neuritis
• Typhoid state: This is characterized by coma vigil,muttring delirium, carphologia (picking up clothes in bed) and subsultus tendinosis
• Psychosis

Question.49. Enumerate the complications of typhoid fever.

Answer. Following are the complications of typhoid fever:

Intestinal complications

• Hemorrhage
• Perforation
• Paralytic ileus
• Peritonitis

Extra-intestinal complications:

• Meningitis
• Bone and joint infection
• Cholecystitis
• Encephalopathy
• Pneumonia
• Granulomatous hepatitis
• Nephritis
• Myocarditis

Question.50. Write etiology, clinical features, diagnosis and management of malaria. Mention complications of falciparum malaria.

Answer. Malaria is a common tropical disease.

Etiology

It is caused by protozoa, Plasmodium through the bite of a female anopheles mosquito.

Requirements for the causation of malaria are:

• Presence of suitable female anopheles mosquito
• Reservoir of malaria infection in the particular area.
• Suitable non­immune or partly immune hosts
• An environmental temperature with suitable humidity

Complications Of Falciparum Malaria

• Central nervous system: Cerebral malaria, i.e. convulsions and coma
• Renal system: Black water fever, acute renal failure
• Blood: Severe anemia, disseminated intravascular coagulation
• Respiratory: Adult respiratory distress syndrome
• Metabolic: Hypoglycemia, metabolic acidosis
• Gastrointestinal tract and liver: Diarrhea, jaundice, splenic rupture
• Miscellaneous: Hypotensive shock, hyperpyrexia
• Pregnancy: Maternal death, abortion, stillbirth and low birth weight

 

Question.51. Write short note on cutaneous and oral manifestations of AIDS.

Answer. Cutaneous Manifestations of AIDS

Following are the cutaneous or dermatological manifestations of AIDS:

• Superfiial fungal infection: Candidiasis, dermatophytosis,pityrosporum infection
• Disseminated fungal and protozoal infection: Cryptococcus neoformans infections, histoplasmosis, sporotrichosis,dermal leishmaniasis, coccidioidomycosis
• Bacterial and mycobacterial infections: Staph. aureus, M.avium intracellulare, M. tuberculosis, actinomycosis.
• Viral: HPV infection, molluscum contagiosum, herpes simplex virus, varicella and herpes zoster, cytomegalovirus,EB virus.
• HIV-related rash: Acute HIV exanthem, papular rash of HIV
• Pruritic papular and follicular eruptions: Folliculitis
  Eosinophilic pustular, pityrosporum, demodectic, insect bite reaction, Prurigo nodularis.
• Papulosquamous disorders: Seborrheic dermatitis, psoriasis,
  Reiter’s syndrome, atopic dermatitis, lichen planus
• Malignancies: Kaposi’s sarcoma, squamous cell and basal cell carcinoma, malignant melanoma
• Miscellaneous dermatoses: Acquired ichthyosis, chronic photosensitivity, granuloma annulare, vitiligo, immunobullous disorders, Sjögren’s syndrome, porphyria,telangiectases, leukocytoclastic vasculitis, scabies(Norwegian), hidradenitis suppurativa, palmoplantar keratoderma.

Oral Manifestations Of AIds By Ec-Clearinghouse

Group 1: Strongly Associated with HIV Infection

• Candidiasis: erythematous, pseudomembranous, angular cheilitis
• Hairy leukoplakia
• Kaposi’s sarcoma
• Non­Hodgkin’s lymphoma
• Periodontal diseases: Linear gingival erythema, necrotizing gingivitis, necrotizing periodontitis.

Group 2: Less Commonly Associated with HIV Infection

• Bacterial infections: Mycobacterium avium-intracellulare,
  Mycobacterium tuberculosis
  Melanotic hyperpigmentation
• Necrotizing ulcerative stomatitis
• Salivary gland disease: Dry mouth, unilateral or bilateral swelling of major salivary glands
• Thrombocytopenia purpura
• Oral ulcerations NOS (not otherwise specifid)
• Viral infections: Herpes simplex, human papillomavirus,varicella—zoster

Group 3: Seen in HIV Infection

• Bacterial infections: Actinomyces israelii, Escherichia coli,Klebsiella pneumoniae
• Cat­scratch disease (Bartonella henselae)
• Epithelioid (bacillary) angiomatosis (Bartonella henselae)
• Drug reactions: Ulcerative, erythema multiforme, lichenoid,toxic epidermolysis
• Fungal infections other than candidiasis: Cryptococcus neoformans, Geotrichum candidum, Histoplasma capsulatum,Mucoraceae (mucormycosis/zygomycosis), Aspergillus flvus
• Neurologic disturbances: Facial palsy, trigeminal neuralgia
• Recurrent aphthous stomatitis
• Viral infections: Cytomegalovirus, molluscum contagiosum

Question.52. Write short answer on candidiasis.

Answer. Candidiasis is a fungal infection caused by an opportunistic fungus known as candida albicans.

Predisposing factors

• Changes in oral flora: Marked changes in oral flora occur due to administration of antibiotics, excessive use of antibacterial mouth rinses, xerostomia secondary to anti cholinergic agent or salivary gland disease.
  These chages result ininhibiton of competitive bacteria leading to candidiasis.
• Local irritant: Chronic local irritants i.e. dentures,orthodontic appliances etc.
• Drug therapy: Various drugs i.e. corticosteroids, cytotoxic drugs, immunosuppressive agents and radiation to head and neck.
• Acute and chronic diseases such as leukemia, diabetes,tuberculosis etc.
• Malnutrition states such as low serum vitamin A,pyridoxine and Vitamin A.
• Endocrinopathy: Such as hypothyroidism, hyper parathyroidism and Addison’s disease
• Immunodefiiency states such as AIDS, Hypogamma­globulinemia

Clinical features

• It occur in both infants and adults. In infants, oral lesion occurs between 6th and 10th day after birth.
• Common sites for infection to occur are roof of mouth,retromolar area and mucobuccal fold.
• It is more common in women as compared to man.
• Patient can complain for burning sensation.
• Lesion appears as white plaque which is pearlish white or blue white in colour and are present on the oral mucosa.
  Lesions resemble as cottage chesse or curdled milk.
  Mucosa adjacent to the lesion appears red in color and is moderately swollen.
• White patches are easily wiped out with wet guaze which leaves normal or erythematous area.
  This area can be painful.
  Deep invasion of an organism leave an ulcerative lesion on removal of patch.
• In severe infection, the involvement of pharynx and oesophagus cause dysphagia.
• The fungus may travel to lower respiratory passage and may involve lungs in fulminant infection.

Investigations

• On staining with periodic acid Schiff (PAS) method,candidal hyphae are readily identifid.
  Organisms are identifid by bright magenta color.
  The candidal hyphae are 2µm in diameter, vary in length and may show branching.
• About 10–20% KOH is also used to identify organisms readily.
• Cultures can be obtained readily on Sabouraud’s medium and on ordinary bacteriological culture media.
  Colonies are creamy white, smooth with a yeasty color.
• On corn­ meal agar medium C. albicans form chlamydospores.

Diagnosis

Clinically the white lesion can be scrapped of by wet guaze.

Treatment

• Treatment includes antiseptic mouth wash with antiseptic solution for 4-5 days.
• Nystatin tablets may be retained locally in the mouth 3-4 times daily or may be crushed or mixed with glycerine for local application.
• Oral administration of nystatin is needed in severe or systemic infection.
  Nystatin is given 250mg TDS for two weeks followed by 1 troche per day for third week.