Infection – Last Moment Revision for exams

Dr  Sunila MD(Hom)
Medical Officer, Department of Homeopathy, Govt of Kerala.

  • Infection: Lodging & multiplication of the organisms in or on the tissues of host.
  • Primary infection: Initial infection of a host by a parasite.
  • Re-infection: Subsequent infections by the same parasite in the same host.
  • Secondary infection: Infection by another organism in a person suffering from an infectious disease.
  • Nosocomial infection: Cross infections occurring in hospitals.
  • Super infections: Infections caused by a commensal bacterium in patients who receive intensive chemotherapy.
  • Opportunistic infections: Organisms that ordinarily do not cause disease in healthy persons may affect individuals with diminished resistance.
  • Latent infections: When a pathogen remains in a tissue without producing any disease, but leads to disease when the host resistance is lowered.
  • Commonest infective disease: common cold.


When the temperature is raised above 38.3°C for more than 2 weeks without the cause being detected by physical examination or laboratory tests is PUO (FUO) 


a) Occult tuberculosis

b) Chronic suppurative lesions of the liver, pelvic organs, urinary tract, peritoneum, gall bladder, brain, lungs, bones & joints & dental sepsis (occasionally).

c)  Viral infections:

  • Viral hepatitis
  • Infectious mononucleosis
  • Cytomegalovirus infection
  • Aids

d) Connective tissue disorders:

  • Giant cell arteritis.
  • RA
  • Rheumatic fever
  • SLE
  • PAN (polyarteritis nodosa)

e)   Chronic infections:

  • Syphilis
  • Hepatic amoebiasis
  • Cirrhosis liver
  • Malaria
  • Filariasis
  • Leprosy
  • Brucellosis
  • Sarcoidosis

f)  Haematological malignancies

  • Leukemia
  • Lymphoma
  • Multiple myeloma

g)   Other malignant lesions: Tumours of lungs, kidney etc.

h)   Allergic conditions

i)    Miscellaneous conditions: Hemolytic anaemia, dehydration in infants etc.

j)    Factitious fever: Self induced fever in patients with psychological abnormalities..


Endotoxines of gram negative bacilli are responsible for most of the cases.

More frequent in men.

Toxic shock syndrome in women: caused by toxigenic strains of staphylococci (gram positive) contaminating vaginal tampons.

Clinical features:

  •  Features of shock: Hypotension, Weak thready pulse, Cold clammy skin, Tachycardia & Peripheral cyanosis.
  •  Death is caused by: pulmonary oedema, tissue anoxia, cardiac arrythmias & Disseminated intravascular coagulation 




  • Hypersensitivity reaction to group A streptococci.
  • Rheumatic fever follows 2-3 weeks after an attack of streptococcal pharyngitis.

Age group: 5-15 years (mean age- 6 years)

Pathology: 2 stages: 

  • Exudative stage: acute phase.
  • Proliferative stage: prolonged process. Hallmark of proliferative phase is Aschoff bodies.

Heart: Endocarditis, myocarditis & pericarditis (pancarditis). MacCallum’s patch is seen in posterior wall of left atrium due to scarring of mural endocarditis.

Pericardium: bread & butter appearance (fibrinous inflammation in pericardium). 

Joints: Acute synovitis. 


  • Throat swab culture.
  • Serodiagnosis
  • Anti-streptolysin O titer (ASO)
  • Anti-streptokinase (ASK)
  • AntiDNAse B
  • Anti- nicotinamide- adenine dinucleotidase (anti- NADase)
  • Anti- hyaluronidase (AH)
  • Anti- streptozyme test (ASTZ)
  • Acute phase reactants → lab tests helpful in acute phase.
  • ESR & C – reactive protein – increased.
  • ECG:
  •       Sinus tachycardia, ectopic beats & 1st & 2nd degree heart blocks.
  •       ST elevation in pericarditis.


  1. This may follow either cutaneous or pharyngeal lesion by group A streptococcus.
  2. 10- 15% of children getting recurrent skin infections may develop glomerulonephritis.
  3. Serotypes 12, 44, 2, 52, 55, 57 & 4 are more often nephritogenic.
  4. Latent period for the development of acute GN is 10 days after pharyngitis & 3weeks after pyoderma. 


Pneumococcal Pneumonia (Syn: Lobar pneumonia)

Most common pneumococcal lesion in adults is pneumonia.

Pathology: Formation of inflammatory exudate in alveoli.

Stages: Red hepatisation (alveoli are filled with red cells & fibrin), Grey hepatisation (neutrophil leucocytes predominate) & Resolution. 

Clinical features

  1. Fever, chills & herpes simplex.
  2. Pleuritic pain & Cough with pinkish or rusty sputum
  3. Signs of consolidation over the affected lobe.

Laboratory findings

  1. Rusty sputum
  2. Pneumococci can be demonstrated by gram staining, Blood culture is positive in 20-25% cases in early stage of the disease. Leucocytosis
  3. Skiagram of the chest shows a homogenous opacity corresponding to the lobe involved.


  • Local: atelectasis, lung abscess, delayed resolution
  • Due to spread of inflammation to adjacent structures: pleural effusion, empyema, pericarditis & peritonitis
  • Haematogenous spread: septicaemia, meningitis etc.


Agent: Salmonella paratyphi A, B, C.

Illness resembles typhoid, though the toxemia & complications are milder. 


Shigellae: 4 species

  1. Shigella dysentriae type 1 & 2(S. shigae & S. schimitzii)
  2. S. flexneri.
  3. S. sonnei.
  4. S. boydii.

Source: contaminated food or water.


  • The entire colon may be affected.
  • Toxins are responsible for secretory diarrhea.
  • Necrosed mucosa→ intestinal casts. 


  1. Dehydration
  2. Electrolyte imbalance
  3. Circulatory failure
  4. Renal failure
  5. Intestinal perforation & rectal bleeding
  6. Paralytic ileus.

ANTHRAX (Wool Sorter’s disease)

Agent: Bacillus anthracis (gram +ve)

Source: infected animals, contaminated wool, hair etc.

Clinical features

  1. Cutaneous form (malignant pustule)
  2. Pulmonary form: anthrax pneumonia (wool sorter’s disease)
  3. Gastrointestinal form
  4. Meningitic form


  1. Blood Culture: polymorph leucocytosis
  2. CSF: haemorrhagic in anthrax meningitis
  3. Agar gel precipitation inhibition test: a four fold rise in serum antibody titer confirms the diagnosis. 

Klebsiella pneumoniae: Freidlander’s bacillus 

Pseudomonas aeruginosa: produces a greenish pigment pycocyanin 

Proteus: 4 species: P. mirabilis, P. vulgaris, P. morganii, and P. rettgeri. 

They cause super infection in areas of tissue damage (eg. umbilical stump in newborn – bacteremia & septic meningitis) 


  • Group: Enterobacteriaceae.
  • Gram negative


  • Somatic (O)
  • Flagellar (H)
  • Capsular(K)

Clinical presentation

  1. UTI
  2. Peritonitis
  3. Septicemia
  4. Neonatal infection
  5. Biliary tract disease
  6. Gastroenteritis:

 Enterotoxigenic strains of E. coli (ETEC) cause gastroenteritis in children’s nurseries.
Traveller’s diarrhea 


  •  Coli serotypes O15, K7, and H7 cause haemorrhagic colitis.
  •  Watery diarrhoea→ bloody.
  •  Verocytotoxines are responsible for haemolytic uraemic syndrome 


  • Zoonosis.
  • Causative agent: Yersinia pestis (previously known as Pasteurella pestis); gram negative.
  • Vector:  Xenopsylla cheopis; infected rat flea.
  • Reservoir of infection: infected domestic rodents such as Rattus norwegius, Rattus rattus & Mus musculus. 

Pathogenesis: The organisms enter through the skin. The bacilli reach the local lymph nodes which enlarge & suppurate: Bubo. Bacilli proliferate and enter the blood stream to produce metastatic lesions. Spleen may be enlarged twice or thrice its normal size. In primary pneumonic plague, the organisms reach the lungs through the respiratory tract. 

Clinical manifestations:

Bubonic plague: 

  • a.  I. P: 2-6 Days.
  • b. Fever & lymphadenopathy
  • c. Buboes: in inguinal & axillary region.
  • d. Pestis minor: milder cases seen during epidemics. These present only with buboes.

Septicemic Plague:

  • a. Chills, fever, tachycardia, headache, vomiting and delirium
  • b. Death may occur with in a few days before localizing lesions are evident.
  • c.  Haemorrhagic manifestations may develop.

Pneumonic Plague:  Primary and Secondary

  • a.  Primary: More fulminant and rapidly fatal. Organisms reach the lungs by inhalation.
  • b.  Secondary: Organisms reach the lungs through the blood stream


  1. Diagnosis is confirmed by demonstrating the organisms by smear, culture or animal inoculation studies.
  2. Bubo-fluid can be aspirated and stained for the organisms.
  3. Sputum can be stained for the organisms and cultured.
  4. In septicemic plague blood culture yields the organism. There is neutrophil leukocytosis. Specific antibodies develop in patients who recover from the disease. 

Prevention: A heat killed vaccine (Haffkine) is available for immunizing the population at risk. 

BRUCELLOSIS (Undulent fever, Malta fever, Abortus fever) 

It is an infectious disease of animals which is transmitted to man by handling infective material.

Causative organism: gram negative coccobacilli.

  • Brucella abortus: causes abortion in cattle.
  • Brucella melitensis: infection spreads through goat’s milk
  • Brucella suis: obtained from pigs.

Pathogenesis: Organisms enter through GIT, RT, and conjunctiva or through the skin. They pass through the local lymph nodes into the blood stream to localize in the reticuloendothelial system. They multiply in RE tissues to produce granulomas.

Clinical features: 

  1. I.P: 2-3 weeks
  2. Fever, malaise, sweating, chills, arthralgia & backache.
  3. Spinal tenderness, arthritis & orchitis are common.
  4. Chronic brucellosis may present as PUO. 


  1. Endocarditis
  2. CNS: meningoencephalitis, myelitis & polyradiculoneuropathy.
  3. Nephritis
  4. Hepatic & splenic suppuration
  5. Calcification in the liver & spleen & cholecystitis
  6. Uveitis


  • Clinical features: typhoid like illness especially if associated with spondylitis or arthritis.
  • Diagnosis is confirmed by isolation of the organism from blood, bone marrow etc.
  • Special lab techniques are necessary to grow brucella.
  • Standard tube agglutination tests, Coomb’s antiglobulin tests, complement fixation test & ELISA test are used for detecting agglutinating antibodies. Coomb’s test & ELISA are more reliable. If the initial test is negative, test is repeated after 3-4 weeks. 



Causative organism:  Vibrio cholerae; gram negative. 92 serogroups are identified based on O (somatic) antigen. The strain producing epidemic cholera possesses O1 antigen; hence this vibrio is designated as vibrio cholerae O1.

  • Inaba, Ogawa & Hikojima are the most important pathogenic subtypes.
  • Others are collectively designated non- O1 V. cholerae.
  • Eltor biotype is a variant of V. cholerae O1; it is characterized by hemolytic activity & resistance to polymyxin. Differentiation between Eltor & V. cholerae is by phage typing.
  • Classic disease is caused by Vibrio cholerae, but the majority of outbreaks occurring in India are due to Eltor biotype.
  • Main vehicles of infection are water, cooked food kept unhygenically exposed to flies, sea foods, fruits & vegetables.

Pathogenesis: Vibrio cholerae multiply in the jejunum & small intestine & produce an enterotoxin. By the influence of this toxin the enterocytes (intestinal mucosal cells) secrete large amount of isotonic fluid. The result is watery diarrhea which leads to loss of isotonic fluid. Excessive loss of fluid & electrolyte gives rise to hypovoluemic shock & metabolic acidosis.

Cholera enterotoxin:

  • It is a protein of Mol. Wt: 84000.
  • 2 immunologically distinct regions: A (active) & B (binding).
  • Binding enables A region to penetrate the mucosal cells
  • This toxin leads to formation of adenylate cyclase which induces excessive production of cyclic –AMP (cAMP), which in turn is responsible for over secretion of electrolytes & water by the enterocytes. 

Clinical features:

  • Eltor cholera: usually mild & asymptomatic.
  • Moderate & severe cases: last for 3-5 days.
  1. Painless watery diarrhea & effortless vomiting (clear, watery fluid).
  2. Excreta: rice- water appearance due to the presence of flakes of mucus & large number of vibrios.
  3. Dehydration (when severe: sunken eyes, shriveled skin, collapsed neck veins), acidosis & shock. Thirst with dryness of mouth & tongue (earliest indication of fluid deficit); Oliguria & renal shutdown. Mental state is clear.
  4. Painful muscular cramps due to hyponatremia.
  5. Cold extremities.
  6. Abdomen: scaphoid.
  7. Cholera sicca: rarely large amount of fluid may collect in the intestinal lumen & a severe dehydration, shock & death may result even before evacuation occurs. 


  • Isolating he organism from stool sample.
  • Suitable medium for transporting specimen is: Venkataraman & Ramakrishnan fluid or Carry & Blair medium.


  1. Dehydration & severe shock leads to renal cortical necrosis & renal failure.
  2. Hypokalemia leads to fatal cardiac arrythmias, abdominal distension & muscle paralysis.
  3. Injudicious administration of electrolyte solutions intravenously without correcting metabolic acidosis may result in pulmonary oedema.
  4. Convulsions in children due to cerebral venous thrombosis.
  5. Severe hypoglycemia.
  6. Prolapse of rectum in children.
  7. Florid malnutrition.

Cholera is a notifiable disease.


  1. Rotavirus affects mainly infants & young children aged 6 months to 2 years.
  2. I. P: 1 to 7 days; usually less than 48 hours.
  3. Vomiting occurs early & it precedes diarrhea.
  4. Diarrhea extends over 5-7 days but virus is shred up for 10 days.
  5. Breast milk may have a protective role due to the presence of maternal Ig A antibodies.
  6. Rotavirus group A: major cause of endemic diarrhea in infants & young children worldwide. 

Norwalk & Norwalk like agents: Cause mild gastroenteritis in school, community & family settings.

Calcivirus:  Cause Rotavirus like illness in children & Norwalk like in adults.

Astrovirus:  Pediatric diarrhea reported in nursing homes.

Campylobacter jejuni (vibrio fetus):

Complications of campylobacter jejuni dysentery:

  • Reactive arthritis
  • Guillain-Barre syndrome(GBS) 

Pseudomembranous colitis: syn: antibiotic associated diarrhea. 

BARTONELLOSIS (Syn: carrion’ s disease, Oroya fever, Verruga Peruana) 

Bartonella consists of 3 main pathogens.

  1. Bartonella bacilliformis: Carrion’s disease. Disease is transmitted by sandfly phlebotomous verrucarum.
  2. Bartonella henselae: cat- scratch disease & bacillary angiomatosis in patients with AIDS.
  3. Bartonella Quintana: trench fever.

Clinical picture

2 distinct clinical syndromes:

A)    Oroya fever:

i.      Fever, rigor, headache etc. lasts for 3-4 weeks.

ii.     Organism can be demonstrated in blood smears stained by Giemsa’s or Wright’s strain.

iii.    Death may occur due to severe anaemia or super infection salmonella.

B)    Verruga Peruana:

i.      Hemangiomatous tumours of skin and mucous membranes

ii.     Mortality is very low


  • Causative agent: Legionellaceae; gram negative; natural habitat: water
  • Over 36 species; among them L. pneumophila is the most common human pathogen.

Clinical features:

Two main clinical syndromes

a)    Legionnaire’s disease

  • Infection is by inhalation of aerosols
  • I.P: 2-10 days
  • Pneumonia is the commonest presentation followed by GIT symptoms such as watery diarrhoea

b)    Pontiac fever

  • Brief febrile illness resembling influenza caused by other species of legionella


  • Culture of the organism from the sputum & direct fluorescent antibody staining: quick and ready method but less sensitive


TETANUS (Syn: Lockjaw) 

Exotoxin produced by Clostridium tetani.

Exotoxin: neurotoxin; tetanospasmin & hemolysin; tetanolysin.

I. P: generally less than 2 weeks; it may range from 2-60 days.

Clinical features:

  1. Diagnosis becomes evident when lockjaw sets in.
  2. Opisthotonous: hyperextension of the spine & neck due to rigidity and spam of back muscles.
  3. Risus sardonicus: grinning expression due to sustained contraction of facial muscles.
  4. Interval between first symptom & the first convulsion is called the onset period.
  5. Deep tendon reflexes are exaggerated but the plantar response is flexor.
  6. Local tetanus: symptoms confined to a part near the site of injury.
  7. Cephalic tetanus: local tetanus involves the facial muscles.
  8. Tetanus neonatorum: tetanus occurs within 10 days of birth; inability to suck the nipple, irritability & excessive crying associated with grimacing movements of the face. Muscles of the back, neck & abdomen become spastic.


  1. Respiratory obstruction &aspiration pneumonia.
  2. Hyperpyrexia
  3. Myocarditis leads to cardiac failure & hypotension.
  4. Decubitus ulcers &UTI due to prolonged immobility. 
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