Effects of infection on the body

Effects of infection on the body

Infection has many effects on the body. These are summarised in the first information box on page 60 and may be acute, chronic or allergic. Chronic effects are seen especially in children in tropical countries.

Pathology of infection

Disease due to infection is the result of interaction between a microorganism and the defence mechanisms of the body. The outcome of this interaction can range from no demonstrable effect to death, and will depend on the number and

Killers of children, preventable but variably prevalent
  • Measles
  • Diphtheria
  • Pertussis
  • Poliomyelitis
  • Tetanus
  • Hepatitis B
  • Gastroenteritis
  • Malaria
  • Meningococcal disease
Chronic disabling infections, widely prevalent
  • Leprosy
  • Tuberculosis
  • Trachoma
  • Malaria
  • Trypanosomiasis cruzi
  • Amoebiasis
  • Intestinal helminths
  • Schistosomiasis
  • Filarial infection
Epidemic diseases, actual (marked *) and potential
  • Louse-borne typhus and relapsing fever
  • Cholera*
  • Malaria
  • Visceral leishmaniasis*
  • Human immunodeficiency virus infection*
  • Tuberculosis *, in association with HIV epidemic
  • Influenza
Infections liable to focal outbreaks (zoonotic or vector-borne)
  • Dengue fever, e.g. Thailand
  • Plague, e.g. Vietnam
  • Cutaneous leishmaniasis, e.g. Sudan
  • African trypanosomiasis, e.g. Zambia
  • Yellow fever, e.g. Kenya, Nigeria
  • Anthrax

virulence of the organisms, physiological and anatomical effects that they induce, and the effectiveness of the natural defences. It is now demonstrated that there are strong genetic influences which determine the response to infection. A clear example of this is the genetic polymorphism in expression of cytokine release (tumour necrosis factor-α, TNF-α) and cytokine receptor expression (interferon γ;).

The mechanisms by which microorganisms cause disease are summarised in the second information box on page 60 and discussed in other sections of this book. Organisms act directly and/or through their toxins. Many of these effects are general, but some act at specific anatomical sites-for example, poliomyelitis virus in anterior horn cells, hepatitis virus in hepatocytes, pneumococcus in the lung alveoli, and tetanus and diphtheria toxins at nerve terminals.

Shock is an especial problem in severe infections. Its aetiology is complex and results from reduced systemic vascular resistance brought about by dilated small vessels

  • Fever: anorexia, protein catabolism, negative nitrogen balance, acute-phase protein response, hypoalbuminaemia, low serum iron sequestration of iron, anaemia, neutrophilia
  • Inflammation, pain, dysfunction, tissue damage
  • Convulsions, especially in children
  • Shock; sustained fall in circulating blood volume associated with lowered systemic vascular resistance
  • Haemorrhage; haemolytic anaemia, intravascular coagulation
  • Organ failure: kidneys, liver, lung, heart, brain, necrosis of skin
  • Weight loss and muscle-wasting
  • Malnutrition; especially associated with diarrhoea
  • Retardation of growth and intellect in children
  • Anaemia; iron sequestration, maturation arrest in marrow, folate deficiency
  • Tissue destruction; e.g. lung in pneumonia or tuberculosis, nerves in leprosy, liver in hepatitis B
  • Post-infective syndromes: e.g. lactose intolerance, malabsorption, irritable colon, depression, post-viral fatigue syndrome
  • Rash; e.g. erythema with streptococci, urticaria with helminths, maculo-papular in typhoid and endocarditis, erythema nodosum in tuberculosis
  • Arthritis; e.g. in rheumatic fever, Reiter's syndrome
  • Pericarditis; e.g. in meningococcal infection
  • Encephalitis; e.g. in measles or following vaccines
  • Peripheral neuropathy; e.g. in post-infective polyneuritis
  • Haemolytic anaemia; e.g. in infectious mononucleosis
  • Nephritis; e.g. in streptococcal infection
Microbe-mediated Host-mediated
  • Direct cell destruction, e.g. poliomyelitis, rabies, hepatitis
  • Exotoxin, e.g. tetanus, cholera, botulism, diphtheria
  • Endotoxin, e.g. typhoid, Gram-negative septicaemia, meningococcal infection
  • Neutrophils and macrophages
  • Complement activation
  • Activation of clotting Cascade
  • Immune mechanisms
  • Secondary autoimmune mechanisms

and leaky capillaries under the influence of several mediators, which include kinins, complement components, histamine, cytokines and endogenous opiates (see Ch. 1). Endotoxin from Gram-negative bacteria is one of the known mediators causing release of these agents. However, Gram-positive shock is caused by other cell wall components and by lipoteichoic acid, and is clinically indistinguishable from Gram-negative shock. The cycle of shock, tissue anoxia and organ failure is difficult to break and may kill the patient within hours.

Host response to infection

Non-specific defences

The body has a number of 'natural' antimicrobial defences, especially on the skin and at mucosal surfaces (e.g. lysozyme secretion, gastric acid, intestinal enzymes, vaginals secretions). However, these non-specific systems are not entirely adequate and pathogenic microorganisms can breach them under conditions such as trauma and intense exposure to pathogens. The colonisation of host tissues by pathogens is then counteracted by the body's immune response. Host immunity is expressed through several different mechanisms which depend upon antigen-specific lymphocytes and their products. Polymorphs and macrophages play an important part in defence against microorganisms, especially bacteria (see Ch.1).

Immune response

The immune system has evolved largely to block the access of pathogenic organisms to host tissues and, where this fails, to limit their colonisation and spread. Microorganisms carry molecules which are foreign to the host, and some bacteria secrete toxins. Both antibody and cell-mediated immune mechanisms may be directed against these antigens (see p. 30). T lymphocytes can kill virus-infected cells, and they also secrete a variety of cytokines which attract and promote the antibacterial and antiviral activity of other inflammatory and immune cell , particularly macrophages. Eosinophil granulocytes are important in host defence against parasites, e.g. worm infestations. Antibodies can neutralise bacterial toxins and bind to the surface of microorganisms, where they inhibit spread and initiate complement fixation which promotes phagocytosis of micro

Source and spread of infection
Source/route of transmission Method of spread Examples of infection
  • Contact
  • Person to person
  • Soil
  • Water
  • Skin or mucous membrane contact
  • Via wounds and abrasions
  • Penetration of skin
  • Impetigo, scabies, wound infection, infectious mononucleosis
  • Sexually transmitted diseases (including HIV and hepatitis B)
  • Tetanus, Buruli ulcer, hookworm, mycetoma
  • Schistosomiasis, leptospirosis
Air-borne spread
  • Respiratory droplets or dust
  • Water aerosols
  • Measles, rubella, whooping cough, scarlet fever, mumps, meningococcal infection Upper respiratory tract infection, influenza
  • Legionellosis
Faecal/oral spread Faecal contamination of food or drink Salmonella infection, bacillary and amoebic dysentery, enteroviral infections, cholera, giardiasis, hepatitis A. Campylobacter infection
Transplacental Maternal blood Rubella, cytomegalovirus (CMV) infection, toxoplasmosis, syphilis, malaria, HIV infection
Medical and nursing procedures Needles, ventilators, infusion fluid Hepatitis B, staphylococcal infection, Pseudomonas infection
  • Zoonoses
  • (Animal, fish or bird to humans)
  • Beef or pork
  • Poultry or eggs
  • Milk
  • Cheese
  • Rats' or dogs' urine
  • Dogs' faeces
  • Dog bite
  • Birds
  • Fish
  • Tapeworms, toxoplasmosis, Trichinella infection
  • Salmonellosis
  • Tuberculosis, Campylobacter infection, brucellosis
  • Listeriosis, brucellosis
  • Leptospirosis, Lassa fever
  • Toxocara infection, hydatid disease
  • Rabies
  • Psittacosis
  • Tapeworms, mycobacterial infections

organisms. The complement membrane attack complex may destroy certain bacteria, especially Gram-negative organisms.

Microorganisms may be transmitted by several Autogenous infection may develop as a result of local e.g. from bowel to peritoneum, or by the blood stre i f the latter type is endocarditis cau reanisms. The complement membrane attack complex may menerially Gram-negative organisms.

Source and spread of infection

Infection may originate from the patient (autogenous), usually from skin, nasopharynx or bowel, or from outside sources (exogenous), often another person who may either be suffering from an infection or carrying a pathogenic microorganism. Carriers are usually healthy and may harbour the organism in the throat (for example, diphtheria), bowel (salmonella) or blood (hepatitis B or HIV). Non-human sources of infection include water (cholera), milk (tuberculosis), food (botulism), animals (rabies), birds (psittacosis) and also the soil (legionnaires' disease).

Microorganisms may be transmitted by several routes.

Autogenous infection may develop as a result of local spread, e.g. from bowel to peritoneum, or by the blood stream. An example of the latter type is endocarditis caused by Streptococcus sanguis originating in the patient's mouth and entering the blood during dental procedures. Exogenous infection may be acquired directly or indirectly by one of the routes.

Incubation period is the period between the invasion of the tissues by pathogens and th appearance of clinical features of infection. Period of infectivity is the time that the patient is infectious to others. Details of the incubation periods of major infections and periods of infectivity in childhood infectious diseases are summarised .

Concepts of infection
Major manifestations of infection
Principles of management of infection
Diseases due to viruses
DNA viruses
Diseases due to chlamydiae
Diseases due to rickettsiae
Diseases due to bacteria
  • Streptococcal infections
  • Staphylococcal infections
  • Corynebacterial infections
  • Bacillus infections
  • Bordetella infections
  • Salmonella infections
  • Food poisoning
  • Dysentery
  • Other true bacterial infections
  • Mycobacterial infections
Diseases due to spirochaetes
  • Leptospira infections
  • Borrelia infections
  • Treponema infections
Diseases due to fungi (mycoses)
  • Cutaneous fungal infections
  • Subcutaneous fungal infections
  • Systemic fungal infections
Diseases due to protozoa
Diseases due to helminths
  • Trematode (fluke) infections
  • Cestode (tapeworm) infections
  • Nematode (roundworm) infections
  • Zoonotic helminth infections
Diseases due to arthropods
Sexually transmitted diseases
  • Sexually transmitted bacterial diseases
  • Sexually transmitted viral diseases
  • Miscellaneous conditions